Новое исследование подтверждает эффективность концентрации объема низкоинтенсивных тренировок в одну неделю

A new study landed in my feed last week, and I will admit the algorithm has my number. It steered me toward a question I have chewed on more than once here at FasterSkier: when it comes to low-intensity training, are you better off concentrating volume into one big week, or spreading the same volume evenly across several weeks? The easy move is to enjoy a paper that agrees with you and click away. I try not to do that. A study only earns its keep if I am willing to read the ones that argue against me with the same care I give the ones that pat me on the back. This one sits close to my own view, which is exactly why I want to handle it carefully. What the researchers tested Walther and colleagues, writing in the International Journal of Sports Physiology and Performance, set out to test whether concentrating low-intensity training into a high-volume block produces any adaptation that even distribution does not. They worked with 20 well-trained junior cross-country skiers in a crossover design, so every athlete completed both approaches and served as their own comparison. Total training volume was matched across the two protocols. Before and after each intervention, the researchers ran a battery of tests: VO2max, peak velocity at VO2max, lactate responses, submaximal economy markers, and subjective measures of recovery and fatigue. The two protocols differed only in shape: BLOCK: one week at 160 percent of normal endurance volume, followed by three reduced-volume weeks. EVEN: the same total volume spread evenly across four weeks. The point worth holding onto is that the totals were identical. Only the organization of the four weeks changed. The performance results Concentrating the volume into a block had no effect on performance. Both protocols nudged some variables in the right direction, and the improvements were statistically similar. VO2max, maximal aerobic speed, and lactate-threshold measures all moved to a comparable degree whether the work was stacked into a block or laid out evenly. That matters because block periodization is so often assumed to be the stronger option. Here, concentrating on a low-intensity load produced no extra adaptation beyond what consistent training already delivered. The two approaches did not feel the same, though. During the high-volume week and the recovery week that followed, the BLOCK group reported lower mood, reduced feelings of recovery, and greater fatigue. The athletes tolerated the work, and there was no indication of increased injury or illness risk, though four weeks is a short window in which to base that claim. The concentrated approach simply costs more on the recovery side without being repaid in results. I would have liked to see heart rate variability tracked across both protocols. Autonomic data might have put real numbers to that recovery cost, rather than leaving it to a subjective report. Why this matches what I have seen This lines up with something I have watched play out across endurance sport for years. Adaptation comes from repeated exposure, not from the occasional enormous week that flattens recovery and chips away at the very adaptation you are chasing. A training model deserves to be judged on more than whether it works. Time to adaptation matters. So does recovery cost, psychological and autonomic strain, and whether an athlete can actually keep the thing going for months and years. The block protocol led to greater fatigue and poorer perceived recovery without a better outcome. From a coaching chair, that is not a small detail, and it weighs even heavier with junior athletes. There is a fair counterargument, and it deserves room. Proponents of block periodization will point out that overload blocks build fatigue first and may reveal their benefits only over a longer horizon, and that a four-week window can miss those delayed adaptations. I see the logic, but I lean the other way. The longer the timeline an adaptation needs, the greater the room for overtraining and the thinner the signal you are actually working with. If a block needs four weeks to show its hand, there probably wasn’t much adaptive signal to begin with. Why low intensity is the key qualifier For low-intensity work, the physiological stress of any single session is modest by design. The adaptation seems to come from stacking many of those sessions on top of one another over time, not from cramming volume into a short window. When the totals match, the body appears to respond to how much training got done, not to how it was parceled out. That helps explain why athletes who lean on the occasional big week rarely pull ahead of the ones who just train, month after month, without drama. The big week feels harder. Harder is not the same as more adaptive. The authors are careful not to overreach, and so am I. Their findings should not be stretched to cover every form of block periodization. The earlier work showing real benefits from block training generally concentrated high-intensity sessions, where the stimulus is far larger. This study looked only at low-intensity volume. Block periodization may well earn its place when the stimulus itself is potent. There is just little evidence that piling up low-intensity volume creates a stronger adaptive signal. What it means for junior coaching For junior endurance athletes, the practical read is straightforward. Do not expect a high-volume, low-intensity camp or an overload week to produce superior adaptations simply because the work is bunched together. Camps still earn their place for logistics, technique, and the team-building that holds a season together. They just do not appear to hand you a physiological edge once total volume is matched. So here is where I land. Concentrating low-intensity volume into overload blocks does not seem to yield better short-term aerobic adaptation than spreading the same volume out, at least when the total volume is equal. I am not claiming block periodization does not work, or that all concentrated loading is a waste. What the evidence keeps pointing at, for aerobic base development, is that showing up consistently does more for an athlete than the occasional heroic training week. Over a season, the consistent skier and the big-week skier can bank the same hours. Only one of them pays the fatigue tax to get there. Help Support Our Coverage! If you value the thoughtful work and access FasterSkier provides, please consider becoming a Voluntary Subscriber. Your support directly fuels our work to cover the people, places, and moments that make our sport special. The staff from the U.S. Ski and Snowboard Cross Country Team will host a 2022 Cross Country National Coaches’ Symposium this next week on October 28th and 29th. Please click on the previous link to register. The Symposium will take place via Zoom to keep costs low and facilitate greater participation by our community. Here is a link to the Presentation Schedule and Presenter Bios. The Symposium will count towards 8 Continuing Education Credits for U.S. Ski and Snowboard coaches and is open to any interested individuals, not only cross-country coaches. Presenters will include U.S. Ski Team coaches and experts from our U.S. Ski & Snowboard Sports Science and Medicine departments, as well as international experts, including Olympic and World Champion Johan Olsson. Topics will range from athlete health and wellness to athlete development paradigms and training plan optimization. This should be a highly inspiring and edifying Symposium; please join us! Due to the start of the rollerski season, we are republishing this story to help promote best practices when rollerskiing on the open road. Making yourself visible while rollerskiing is a must. And with a recent reminder from U.S. Ski Team (USST) World Cup coach Matt Whitcomb, the time of year has come when many skiers are training on roads in lower angle sunlight as we tip away from the Sun in the Northern Hemisphere. Below we are including the rollerskiing safety bullet-points and slides from Whitcomb’s presentation on the topic at the recent National Coaches’ Symposium. Before that, we recognize that rollerskiing on roads open to car traffic poses risks. For several years now, rollerskiers have been encouraged to wear high-visibility shirts. The next progression in rollerskiing safety will likely come from the cycling community where researchers have studied how cyclists can become even more visible on the road. The safety debate has evolved beyond simply wearing a high-visibility shirt to further exploring “static-vs.-active dynamic” means to make drivers aware of athletes on the road. In other words, it appears high-visibility clothing worn on active dynamic parts of the body while cycling, like the legs and feet, more effectively alerts drivers. The same goes for rear-facing bike lights: blinking lights are safer than static lights. (Any light is safer than no light.) For now, we don’t know of any ski-specific water bottle carrier manufactured with simple attachments for a lightweight blinking light. We imagine that with some simple modifications, affixing a blinking light would be no big deal. Here’s a Wall Street Journal Video summarizing some of the 2017 findings to improve cyclist visibility. Current recommendations from the USST on rollerski safety. The U.S. Cross Country Ski Team is determined to win more Olympic medals. To do this, we all must train hard and smart. For us to move forward as a nation, we seek to keep every member of our skiing community as safe as possible while roller skiing. Safety must be the primary consideration of every roller ski session. No exceptions. No mistakes. The following is the roller ski safety protocol created by athletes and coaches of the U.S. Ski Team. Before a skier can share the road, they must be able to snowplow, stop quickly, and maneuver their skis to avoid hazards. The skier must be comfortable skiing off the road into the dirt or grass when necessary. An approved helmet in good condition must be worn at all times while roller skiing. Athletes and coaches should wear at least one of the following high-visibility articles as a way of alerting drivers: Shirt, safety vest, shorts, socks, helmet, water bottle holder. Highly visible bike light that can be seen clearly in bright sunlight. Skiers must practice single-file skiing at all times. Coaching support vehicles should utilize proper cautionary signage – g., “Athletes Training”. Minimize the number of support vehicles, as coach’s vehicles can be equally hazardous to athlete safety. Limit group size. A small, single-file pack of skiers is easier for passing cars to manage than a large group. All athletes and coaches must know the route. Avoid or walk dangerous sections. Train during non-peak traffic hours, and avoid holidays and busy weekends when possible. Skiers and coaches must know and abide by driving laws. Use hand signals to indicate direction to both cars and fellow skiers, and make eye contact with drivers at intersections. When not skiing (water breaks or coaching sessions), all athletes and coaches should be off the road. Wheels in the dirt – don’t get hurt. Sunglasses or clear lenses are mandatory at all times to prevent poles and debris from damaging the eyes. Improve roller ski awareness in your community, including publishing something in the local paper every year. Working with the local government to have “Athletes Training” or other signage helps alert drivers. Inspect equipment often. Properly tighten nuts, and inspect wheels, shafts, poles, and helmets. This article is part of a series regarding female athlete specific physiology and nutrition. To get started, you can find a primer on the menstrual cycle here and listen to this podcast on Nordic Nation discussing female athlete specific nutrition with registered dietician and professional runner Maddie Alm. The survey analyzed here is an extension of the conversation with Guro Strøm Solli on her research on female athlete specific physiology and effects that the menstrual cycle has on training and performance, which can be found here. Over the last five years, Dr. Stacy Sims book ROAR and the work of the team behind the FitrWoman app, cited by the US Women’s National Team soccer athletes as a key to their World Cup victory, have sparked conversations on how female athletes might take their unique physiology into account to optimize their training. However, the application of this research is far from ubiquitous. Research into the implications of hormonal fluctuations across the menstrual cycle to strength, inflammation, fatigue, nutritional demands, and the myriad of other training considerations is relatively new to the exercise physiology scene, partly because women tended to be excluded from research as their cycle might cause anomalies in the data. While this area has seen a boom in research over the last decade, the individual variation women experience coupled with the prevalent use of various forms of hormonal contraceptives makes it challenging to provide concrete generalized recommendations that will serve all female athletes. However, as the area gains more attention, trends have emerged that may help athletes who feel they could benefit from aligning their training or nutrition to their cycle. Some examples include periodizing hard strength training and intensity sessions earlier in the cycle when the ratio of estrogen, a steroid hormone, to other sex hormones is optimal, including a greater emphasis on hydration and electrolyte supplementation in the later half when elevated levels of progesterone trigger a rise in body temperature, or consuming anti-inflammatory foods during the pre-menstrual phase to mitigate inflammation and other PMS symptoms. For women desiring to troubleshoot or better attune their activity to their cycle, tracking is recommended as a first step to illuminate patterns in mood, fatigue, sensations during training, et cetera. Diving into the information presented in ROAR or tracking tools like the FitrWoman App that present findings on how training or nutrition might be aligned to the cycle may be a good next step to access information on existing research. Then, through self-experimentation or communication with a coach and/or registered dietician to apply these strategies, an athlete can learn which strategies might make the greatest impact in optimizing their training and overall health. As the topic of female-specific physiology gains traction in exercise physiology research circles, we began to ask how it is being used amongst elite athletes? And, how does this apply to the FasterSkier community? To look for parallels to this research closer to home, FasterSkier distributed a similar anonymous survey to assess the extent to which elite American skiers and biathletes track their menstrual cycle alongside their training, adjust based on cycle, experience side effects, and feel they have sufficient access to knowledge in this area. FasterSkier’s survey can be found here for reference. And now for the takeaways: the similarities to Solli’s research and the trends in responses, including featured responses that best represent common themes or differing viewpoints, and what coaches and athletes might gain from this insight. The Basics: The survey saw 16 respondents, all of whom were national team members and/or trained with elite-level clubs such as Alaska Pacific University, Stratton Mountain School, Craftsbury Green Racing Project, or the Bridger Ski Foundation Pro Team. 68.8% were between the ages of 22 and 30, with 18.8% in the category of 18-22, and 12.5% between 30-35 years old. 62.5% of these athletes experienced 8-12 menstrual cycles per year, 6.3% experienced 4-7 cycles and 31.% fewer than 4. The respondents were evenly split between hormonal contraceptive users and non-users (this question was not further broken down by type), and of athletes who used a tool like FitrWoman to track their cycle. Of the 50% who used a tracking tool, 87.5% had done so for 1-3 years, with the remainder of athletes tracking for less than one year. Q: In your experience, what affect, if any, do the phases of your cycle have on your training adaptations and/or performance? In line with Solli’s research, most athletes identified the week leading up to menstruation as the most common to experience detrimental symptoms, such as bloating, fatigue, lethargy, or mood changes. Some athletes also expressed positive impacts, which are featured in the next section. Three athletes expressed that due to the nature of ski racing every weekend during the winter, they either chose not to focus on the impacts of the cycle since they would need to be mentally and physically primed to race during all phases, and maybe preferred not to plant the seed that there might be factors that may hold them back on race day. “I have noticed that when I feel unwell due to my period, I am less inclined to train hard; however, I think if anything it is more mental than performance related (more related to just feeling unwell, tired, PMS symptoms, etc.)” “I don’t really change anything or adapt my training during a cycle, and haven’t noticed an impact on my performance.” “I use the pill and often find my best races are when I’m not taking it (I.e. when I’m on my period).” “Hard to really see patterns but sometimes detect a few. We have to train and race through all phases, so it’s detrimental from a mental perspective to think that any phase, in particular, is “bad” – they’re just different. I try to be extra nice to myself with training/rest/shortening workouts if I’m going through a rough phase of a cycle, which for me is usually in the lead up and when I have my period. However learning that the time on your period is when your hormones are most ideal for high performance has helped me get through it, because even though I may be feeling icky, I know that my body should be ready to go underneath it.” Q: During which times within your cycle do you feel your performance potential and/or ability to train hard and recover well are maximized? Explain. Most athletes indicated that the best sensations in training and racing occurred in the first half of their cycle, after their period had started. During menstruation, female sex hormones estrogen and progesterone are low, then estrogen independently rises in the second week of the cycle. Both “ROAR” and the FitrWoman app identify this as a sweet spot for high intensity training, heavy strength training, and decreased recovery time between sessions. “I tend to agree with the FitrWoman app predictions, of increased strength performance during my period and decreased activation beforehand. I know that I’ve had very strong races at all times of my cycle so I’m not sure it affects the very top end performance, but more affects my body’s willingness to activate and work hard. My main concern is dealing with cramps during my period. I have to take a lot of pain medication, which sometimes doesn’t seem good for racing or for general health when combined with hard efforts. Cramps also make it very hard to activate my lower abs and have stability through my torso, which makes it difficult to ski well unless I’m very motivated.” “I can tell that I’m more apt to lift well in the weight room while I’m on my period, after the cramps are gone. I think that also correlates to racing well. The wild mood swings before my period can occasionally be helpful in racing motivation, i.e. when I can be angry and keyed up. But moods swing both ways.” “Right when my period starts and the week after, I feel less bloated and I tend to feel faster in training. I don’t notice a difference in recovery time, but in overall feelings I tend to feel better.” “There are so many variations in a normal training cycle, and just from life, that I wouldn’t say I noticed any particularly maximized phases related to my cycle. However it is easier to embrace hard training and expect normal highs and lows when I’m not on my period, so the other 3 phases I guess.” Q: During which times within your cycle do you feel your performance potential and/or ability to train hard and recover well are most diminished? Explain. Thirteen of the respondents identified the week leading up and the first few days of their period as the time their training and overall feelings were most impacted, both physically and mentally. Note that registered dietitian and professional runner Maddie Alm, who is concurrently collaborating with coaches and experts on a project surrounding female physiology, offered suggestions for mitigating the effects of PMS during her interview on NordicNation. “I usually feel pretty drained mentally before and during my period, as well as feel effects on my body (bloating, cramps, cravings). Right after is when I feel the best since my body is back to ‘normal’.” “When I am on my period- I just feel very tired, irritable, bloated, and often relatively nauseous. Even with an IUD and not having normal cycles, I can feel hormonal fluctuations that make me feel unwell.This overall effect on my mental state makes me less motivated to train hard, but I am not sure if in terms of performance or recovery I actually perform worse or am less capable of adequate recovery (like in terms of race results and intervals I don’t think my performance is diminished while on my period, I just feel worse).” “Sometimes when I’m on my period, it feels like it affects my ability to train hard, to perform well, and to recover, as well as my mood and outlook on life. This can be in the few days leading up to the cycle starting, and the few days when it’s happening. However it doesn’t happen every month – while I get my period every month, the intensity and difficulty of it vary significantly. Unfortunately, I haven’t been able to track any patterns with this, otherwise, I would always do what makes it less severe. And as I mentioned before, hormonally the body is strong when you’re on your period, so I try to give myself extra positive thinking, pep talks, shorten workouts, and not be too hard on myself if I’m not super fast in a training session on the bad months, because that’s just what happens. Most of the time if I am gentle on myself I can still perform quite well, but there have been notable occurrences when I’ve had terrible performances that are almost directly attributable to feeling terrible from the intensity of my period.” “Before and during my cycle it is difficult to recover because I experience mood swings that affect the ability to recover properly. I often use ibuprofen to deal with cramps which I feel sometimes compromises how my body feels during training.” Q: What adjustments, if any, do you make to align your training and/or nutrition with your cycle? Examples could be: postponing or increasing recovery between hard sessions, increasing volume or intensity during a specific phase, increasing/decreasing carbohydrate or fluid intake, etc. No athlete reported strategically aligning her training or nutrition to their menstrual cycle, though several responses included the idea of listening to their body and dialing back when needed. “I don’t adjust because I have to race every weekend, and I want to be used to having to perform no matter what my body is feeling. That said, I always try to have good hydration and make sure I’m adequately fueling my body.” “I think nutritional adjustments could be made to make me feel less bloated and nauseous, but I would need education in this area (and I think there is a really big need for it). I think that much of the negative effects are from feelings of nausea, cramps, etc.- so if there are things that could be done nutritionally to help, that would be great. In terms of adjusting training, I think it’s more difficult because a race schedule won’t adjust to your cycle so it’s good to get used to pushing hard during different times of your cycle. However, if it were found that there is a training benefit associated with training a certain way during different times of your cycle (i.e. intervals at a certain time, etc.), I think it could be an awesome training tool… if only more research were done in this area!” “I mostly look at it mentally. I don’t make any adjustments to my training and/or nutrition, however, when I’m feeling sluggish or low-energy I reflect if this could be because of my period. Then I try to justify it and remember that it will only last a few days and that I shouldn’t be too hard on myself.” “I do notice that I need to eat more during PMS, so I try to follow that. I also try to let down after my period and eat less when I don’t need as much. We don’t officially change training, I guess I listen to the Fitr App about when it’s a good idea to reach a little in the weight room, but mostly I micro-adjust training to how I feel.” Q: Do you communicate with your coach regarding how you feel during different phases of your cycle? If so, explain how you and your coach use and discuss that information. Thirteen athletes responded that they do not communicate with their coaches about this topic, though some added that they did feel they could if they were to initiate the conversation. The remaining three athletes state that they sometimes or occasionally talked with their coaches about their cycle, usually when it pertained to feeling negative side effects that impaired their training that day. “I do not, but I would be comfortable doing so, since both my coaches are women. I would address if my period cramps were making me nauseous.” “Sometimes I’ll explain that I need space or less coaching if I’m feeling down or off because of my cycle, and my coach has always been really great at understanding and respecting that.” “No, I don’t communicate. I think I could if I needed to, but I also have a male coach and it is not brought up much for awkwardness level. My teammates and I communicate openly about periods and if someone has cramps, etc. and I find their support and ideas as helpful as a coach.” “Most phases are just normal life and training, ups and downs, but my coach and I definitely talk about it when I’m on an intensely bad cycle. Sometimes if it falls on an intensity day I’ll do fewer intervals than otherwise planned, or else use it as a wake-up workout rather than really pushing hard. More often I’ll carry on as planned, because ups and downs of feeling are just part of the training life.” Q: What information, if any, have you received or read regarding how normal hormonal fluctuations may influence training adaptations, nutritional requirements, and performance? Five athletes reported that they had never received information about the menstrual cycle as it pertains to female athletes. Six athletes expressed they had received some information, and five expressed that they had attended presentations put on by U.S. Ski & Snowboard or regularly used the FitrWoman app as an educational resource. “None! Ever! Huge need for this!!!!” “I have received information but chosen to ignore it.” “The Fitr App mentions characteristics of each phase, like when it’s good to train heavy weights for example. I generally agree with it. I’ve been to one lecture by the Fitr App creators at US Ski Team camp, which gave me the most information I’d ever gotten. Previously I’d noticed some trends myself, but didn’t understand the different phases and what hormones caused which effects.” “Working with Fitter Woman and using their app, I’ve learned that these fluctuations in body temperature, sleep and recovery are normal, which helps me to be less concerned by them and be able to focus on performance. It was also super helpful to learn that right before my period starts I’m most at risk for getting sick, so I try to be extra careful with my immune system that week.” “I have been tracking with the Fitr app the past year plus, and that has some helpful suggestions. I eat and hydrate with care and healthy habits all the time, so I can’t say that I’ve made many changes as a result of tracking or reading about it. Sometimes I do notice cravings that make sense in the context of the cycle. As I mentioned before, I prefer to believe that there are good and bad parts about each phase, and as there are ups and downs in all parts of life, it’s something I adapt to on the fly while training and don’t make too big a deal about. As we nordic racers will compete during the entire winter and just about every weekend, it’s not possible to race in the same phase of the cycle every time – we have to be adaptable and ready to handle what the body throws at us, and I find that is mostly mentally knowing that it might feel bad but I can still have a great performance if I ease into my warmup and maybe recover a little extra.” Q: Additional comments? “I think effects on the body and overall experience of a cycle is not discussed enough in the ski community. I have had some ‘girl talks’ with teammates or coaches but nothing more than once or twice a year, and nothing significant to make a difference in how I train or deal with it.” “I would like information on nutrition/hydration/recovery and other ways I can deal with cycle side effects. Some simple tips to start and maybe more info for those interested. I also think noting birth control methods and effects for athletes would help young women make choices that they often go blindly into.” “This is definitely a great survey and a topic that should be discussed much more frequently!” “I’ve always been curious about the effects of hormonal birth control on performance. The hormonal birth control I’ve tried (Sprintec pill and NuvaRing) changed my personality somewhat, made me more compliant and non-ambitious or depressed. They also made me gain weight. None of those were good things for skiing, so I’ve been unable to find a good solution. The Fitr App lecture talked about progesterone-only options being better, but I haven’t been able to find a good one. Apparently, I’m not a good candidate for an IUD, and wish there was another very low dose progesterone-only option. I also feel that people with ‘overly healthy’ menstrual cycles are a minority at my level in this sport, so I don’t have a lot of other athletes with heavy periods to brainstorm with…” Conclusions: So, what can we gain from these responses? It is noteworthy that over 80% of the responses stated that they had never spoken with a coach regarding their cycle or female physiology. As absence or irregularity of a menstrual cycle can also be thought of as a “canary in the coal mine” for the damaging condition referred to as Relative Energy Deficiency in Sport (RED-S), providing resources and initiating conversations about this topic might help female athletes not only optimize their athletic performance but also prioritize their overall health and wellbeing. One athlete commented that it was awkward to discuss her cycle with her coach as he was male, one said she did feel comfortable because her coach was female, and another commented that their conversations about the topic were in the form of “girl talk” with teammates. This is consistent with Solli’s journal article, where athletes were quoted as citing “because he is a man” as a reason for not discussing the topic with their coaches. The respondents in this article also expressed that their coaches lacked general knowledge about the menstrual cycle and the differences between male and female athletes. “I think there may be differences due to the MC that he is not aware of,” one athlete wrote. Female coaches are underrepresented at the elite level. In the United States, roughly 20% of Division 1 ski programs are led by a female coach, and the Craftsbury Green Racing Project stands alone as the only postgraduate elite team with a female coach, namely Pepa Miloucheva. U.S. Ski & Snowboard has recently hired a female coach to lead the D-Team, Bernie Nelson for the 2010-2020 season, who passed the baton to Kate Barton. Though male coaches can certainly be informed in the subject matter and engage in appropriate conversations with their athletes about this topic, per the athletes’ comments, more effort may be required to normalize these conversations. (Read how Diljeet Taylor, head coach of the 2021 NCAA title winning BYU women’s cross country running team, approaches these conversations with her athletes head-on in this Runner’s World article.) Coaches should educate themselves on these topics to help support their athletes and, if they do not feel comfortable initiating conversations with athletes directly, consider bringing in professionals to provide education to their athletes. Ensuring females are represented in a program’s coaching or support staff, or relying on female team captains to initiate these conversations may also be valuable. As we wrap up this series (at least, for now), we remind readers that this is an evolving topic as the impacts athletes experience take place on a spectrum and research is ongoing. We hope this information has started conversations, given women tools to start their own inquiry and self-experimentation, and raised awareness for the work being done to learn more about the female athlete body. Are you a well-trained endurance athlete? Do you know your resting heart rate, maximal heart rate, average weekly training hours, and – tough one here – age? If you’re reading this website, the answer to all four of those is probably “yes.” If you have a moment to spare, Stephen Seiler would like your help. Seiler is a longtime professor of sports science, currently at the University of Adger in Kristiansand, Norway. We’ve spoken with him for the site before about training and intensity. Seiler is currently seeking responses to this questionnaire. As he says on Twitter, “I bet most of you can complete it in less than the time it takes for your heart to beat 60 times.” One quick mathematical note, one of the questions, albeit specific to runners (to be fair, even some avid skiers may identify their primary training activity as running), asks about the best pace you could hold for six minutes running, as given in seconds per kilometer. If you’re an American reader and you know your pace in the more common minutes-per-mile, you should: (1) convert the whole thing to seconds, then (2) multiply that figure by 0.6214 to derive that pace in seconds per kilometer. Finally, one gender-specific note: Seiler writes on Twitter, “PLEASE get more women to complete this survey! 98% men so far with soon 100 responses. I want to collect data that serves male and female athletes, but I just fail miserably at achieving any kind of male/female balance in the data.” Female athletes, please take note. On May 29, the latest research paper to dive into Marit Bjørgen’s training logs from 2000-2017 was announced in Gemini, the research news publication from NTNU and SINTEF, two research institutions in Norway. The authors are described in Gemini as “Guro Strøm Solli of Nord University and NTNU and a former xc-ski team member herself, Espen Tønnessen from Kristiania University College in Oslo, and Øyvind Sandbakk, from NTNU’s Centre for Elite Sports Research.” The latest paper in their series explores Bjørgen’s use of two distinct types of high intensity training (HIT) and how they impacted her performance. Gemini describes the two HIT methods as the following: “The first approach was block training, where she clustered her HIT sessions into blocks, interspersed with recovery periods with fewer HIT sessions. Later in her career she switched to a traditional model, where HIT sessions are spread more or less evenly throughout a training period.” Bjørgen’s block HIT method, used from 2005-2006, involved numerous periods of intense HIT sessions and fewer hours in what many would consider a traditional long-duration low-intensity program. From 2014-2015, another HIT segment the researchers zeroed in on, Bjørgen used a more “traditional” approach to her HIT training. Gemini describes the “traditional” methodology as what many athletes have become familiar with: “Typically, the researchers said, the traditional approach means that an athlete relies on a mix of low, moderate and high intensity training, gradually transitioning from high volumes of training — meaning number of hours — to higher training intensity and training that is more specific to the sport the athlete is competing in.” Looking for where to play Crazy Time slot ? Go to the official website of the game https://crazytimegame.com/en/ The scientist do not answer which method is more effective? It is also important to remember this is Bjørgen, and it remains a sample size of one. “To get progression you need to change something,” Sandbakk told Gemini. “It’s not always that if something works, then more of it is better. That’s an important message.” Mix it up may be the take-home lesson. The three research papers derived from Bjørgen’s training logs are linked above and provide some great reading and insight. Sammy Izdatyev is the pen name of a Finnish sports enthusiast and unaffiliated amateur historian, who has been interested in endurance sports since the turn of the millennium. He hopes that his pro bono – research can provide more information into the body of literature of earlier underresearched areas of the history of sports. Epilogue Blood doping – a persistent research subject When Björn Ekblom’s opinion of his 1972 paper was that more research was needed in the arena of blood doping to understand nuances of the subjects, this was to be the case even up to our days. Even when the efficacy of blood doping became the mainstream view by the 1980s, Björn Ekblom’s research on in the arena of blood doping and on the limiting factors of maximal oxygen uptake didn’t end there and his research in both arenas is very extensive. One question of interest was the interplay between hemoglobin concentration and Vo2Max and total hemoglobin and Vo2Max, which actually was more important in the end? ”Prior research has shown that acute increase in blood volume as such has very little or no effect on work capacity”, Ekblom had written in 1972, and when he looked at the statistical correlations in his first published blood reinfusion study, he had seen that changes in hemoglobin concentration correlated better with Vo2Max than changes in total hemoglobin. The one rare attempt to research how acute blood volume expansion affected performance failed to show any increase in Vo2Max when a large amount of 1000 to 1200 of blood was infused. (Robinson et al, 1966) Whereas Bengt Saltin had been interested in seeing how cardiovascular system reacted if red blood cells had to flow in less plasma and he dehydrated his subjects in the early 1960s, Ekblom and his coauthor Inge-Lis Kanstrup did the opposite and tested how blood removal and reinfusion and blood dilution with dextrose infusions affected Vo2Max and performance in different combinations. (Kanstrup & Ekblom, 1984) The results were actually different than what Ekblom had written earlier because even when after dilution (dextrose infusion) each given unit of blood carried less blood, Vo2Max tended to remain the same because body increased cardiac output, indicating that total hemoglobin was more important for Vo2Max than concentration as such. Still working capacity was slightly lower after dilution. One unintentional conclusion for future blood dopers was that blood dilution was quite an effective in masking blood-doping induced elevation of total hemoglobin, because if one compares the subjects after they had been treated with blood infusion and saline, all the relevant parameters such as total hemoglobin (+6 %), Vo2Max (+ 4 %) and time-to-exhaustion (+13 %) are higher when compared to the control level indicating that they get almost full benefit of the extra RBCs. But the dextrose infusion clearly hides that the blood infusion took place because resting hemoglobin concentration is actually some 7 % lower than the original value (13.7 g/dl vs. 14.7 g/dl). Another item of interest was the theory of optimal hematocrit, the presumed ”best” value from oxygen delivery viewpoint which was assumed to be roughly hematocrit value of 45 % corresponding hemoglobin concentration of 150 g/l. While particularly Anglo-Saxon blood doping researchers were interested in the optimal hematocrit issue, there is barely a word of speculation about the ”real” optimal hematocrit in any of Ekblom’s writings. To research this, Ekblom and his coauthors researched how reinfusion of five blood bags (2250 ml) affected Vo2Max and took intentionally subjects with a large variation in their natural values. When a subject with a hemoglobin value of 178 g/l donated blood, his Vo2Max fell significantly even when his Vo2Max could’ve been increased had the optimal value of 150 g/l had any validity. ”The same subject increased his maximal oxygen uptake after the same linear pattern when [Hb] was raised above 200 g/l as one individual with a normal [Hb] around 120 g/l”, the authors observe somewhat surprisingly. (Celsing et al, 1987) It doesn’t automatically follow that if the 120 g/l subject would increase his/her hemoglobin to 200 g/l that Vo2Max would increase linearly all the way through, only that the baseline value is only somewhat unimportant. It could be that every red blood cell increased performance up dangerous zones of blood thickness, and sometimes the ”higher-the-better” idea became the consensus view of the sports circles, true or not. Not every second athlete could reinfuse five blood bags, but the implication was still troubling, particularly when the prestigious New England Journal of Medicine published brand new information about the new hormone erythropoietin in its January 1987 issue, the exact same month as Ekblom’s newest research was published. When the advent of a synthetic version of hormone erythropoietin sent shockwaves to the sports world in the late 1980s, it still wasn’t quite certain whether a gradual increase in hemoglobin concentration elicited a similar effect as an instant increase. As it is well known, erythropoietin speeds up the production of red blood cells in bone marrow, but it takes weeks until hemoglobin concentration is increased and the human system bolsters mechanisms to fight against this increase if red blood cells are increased above natural level. While scientists of other countries were interested in the issue as well, Björn Ekblom was the first scientist to research how the red blood cell hormone affected sports performance, when he gathered a group of volunteers with anti-doping specialist Bo Berglund and injected them regularly with the hormone and subjected them to various tests, including Vo2Max and endurance tests. The results showed that there was little difference between blood transfusion and administration of synthetic erythropoietin (rHuEPO) and both blood doping methods improved performance in an almost identical manner regardless of whether the increase in hemoglobin concentration was gradual (hormone) or instant (autotransfusion). (Ekblom & Berglund, 1991) ”This wasn’t unexpected, but still horrible”, Ekblom described the findings to journalist Omar Magnergård who had written one of the first articles about blood doping almost two decades earlier. ”It also makes it difficult to believe in the future of sports”. (Magnergård, 1989) Ekblom was particularly shocked that only a handful of injections could boost performance so much. Despite the pessimism of the early-1970s, Ekblom had predicted in the early 1980s that the method to detect autotransfusions would be developed by the 1988 Olympics if there was proper funding and whereas his coauthor Bo Berglund had participated into detection of blood doping with athlete’s own blood, the research ended when EPO replaced transfusions almost altogether by the 1990s. Now Ekblom took part in the scientific research to develop a method to detect the abuse of the hormone and the team concluded that it was possible to differentiate the natural and synthetic version of the hormone in urine. The method researched and published in 1995 by a group of exclusively Swedish researchers was based on differences of electric charge between naturally occurring hormone and the synthetic version manufactured in a laboratory. “The method became approved by the journal, but was never used because it was expensive and took up to three days to use being unusable at an Olympics games, championships, etc.”, Ekblom recalls the limitation. When the idea of how blood doping could even be detected was beyond anyone’s imagination when the issue was discussed first time in media in 1971, there were various approached proposed by the late 1980s and when it became clear that blood samples would be drawn, there was optimism that a few blood samples with good parameters would reveal its abuse. These hopes turned out to be futile even when indirect monitoring of the blood of athletes have at least curtailed the excessive use. While most of the modern detection methods have been based on how the body reacts to the shortage (blood removal) or abundance (blood reinfusion) of red blood cells, Ekblom’s student and friend Christer Malm from the Umeå University took another type of approach on the issue, looking exactly the blood itself changed during the storage period. While there hasn’t yet been a breakthrough and the first peer-reviewed published paper showed that the method wasn’t completed, Björn Ekblom is today certain that there will be a method that will detect the abuse. “It feels very good that there will be a method that detects autotransfusions to a 100% degree”, he sees the future prospects of the work of Christer Malm. Innovator or conveyer or zeitgeist? As expressed throughout the essay, Björn Ekblom and Per-Olof Åstrand have always maintained that “blood doping” was only as a scientific venue and that the sports application was only an unpleasant ”byproduct” of this research. “In summary, it is with some regret that I conclude that our basic exercise physiology experiments on manipulation of hemoglobin concentration have some consequences for sport”, wrote Björn Ekblom in 1982 about the subject matter. The evident question is whether these consequences could’ve been postponed or avoided had he not started the ”basic physiology experiments” and the research project on blood reinfusion? (Ekblom, 1982) While there is almost something biblical about a venomous serpent causing the chain of events that led blood doping to be invented, Ekblom sees that his role in the research is almost accidental and that he was only conveying the ideas of the zeitgeist of the 1960s, because other researchers had also access to the same pre-existing data. “Probably somebody else would’ve done this experiment around that time”, Ekblom thinks modestly about the significance of this blood doping work. “It would be natural that people would think of infusing blood to boost performance. That was something natural at that time”. Based on the lukewarm reception and the skepticism and on the fact that it took until 10 years before the consensus view shifted conclusively towards the opinion that the method worked, it isn’t that certain how many years attempt in another place would’ve taken. On the other hand, it is true that altitude trained athletes started to break their way into the Olympic arena from late 1960’s onward and athletes showing interest in altitude training, it is possible that the method would’ve been invented even had the research not taken place in Sweden, if the method wasn’t already been “invented” accidentally or in a clandestine research somewhere. In addition, while Ekblom was quite known and regularly quoted physiologist even in the 1960’s before the blood doping research became the “hot topic”, he still had no idea how overblown the issue would become: No – I had no idea that this would gather such a speed. I’ve been on the first page in Sports Illustrated which many would give their left hand for. Not even Bengt Saltin or Peo Åstrand has done so. Not that I think it is important – it is more than strange and also shows how the results of the research became taken by the mass media. Blood doping wasn’t the only seemingly random item turning out something bigger and he finds an interesting parallel from the beginning of the 21st century: In the summer of 2005 I conducted with a student a little pilot study with administering nitrate on GIH students. We measured many things and the effect was not noticeable except one thing – average blood pressure fell by about 3 mm. Some half years later a little article was published in the New England Journal of Medicine – which is the world’s respected medical journal. Today there are propably some 1000 articles on the effect of nitrate administration on performance, health and mental capabilities. The subject has even its own sessions in large conferences. This history is very similar to that of blood doping, if not bigger. Ekblom finds this research line “historically very interesting”, and since then, almost every other endurance athletes consume beetroot juice, and there has been research on the effect of nitrates on various other things such as efficiency. And one should remember that despite the meshing of science and sport with its questionable byproducts, the world of endurance sports wasn’t a pristine paradise before blood doping was invented, and blood doping didn’t “end” it altogether even when there are time periods and sports where it became more a rule than an exception particularly after the introduction of the blood-boosting hormone erythropoietin commonly known as EPO. Then how much does blood doping increase performance? When in the introduction we saw that half of the medallists of the 2001 FIS Ski World Championship had highly abnormal values indicating blood doping use, MD Jim Stray-Gundersen who was among the team researching the data read it differently. “Roughly 50 percent of the medalists had such abnormal blood profiles that they almost could only be due to doping”, he commented the issue, ”Half the people who won medals were clean”. (Fitzgerald, 2006) When blood doping was debated right after the games, Björn Ekblom coauthored an article at that time where the authors claimed the measured hemoglobin values were normal and the differences between (available) ON- and OFF-season data of the Scandinavian skiers didn’t reveal blood doping use. “Nothing talks that Swedish (and Norwegian) skiers would’ve been hematologically doped at the World Cup in Lahti in 2001 or in the last ten seasons”, is their conclusion based on the available data. (Ekblom et al, 2001) This is somewhat surprising because blood doping considered to be an effective way to boost performance. In fact the handful of published research papers have showed some 2-5 % improvements in time-trial type of performance when hemoglobin concentrations have been increased only by some 10-15 % keeping the values within the healthy ”normal range”, which is in itself an enormous benefit in a race where differences between are usually are occasionally fragments of one percent. It has also been known that athletes haven’t been so risk averse and some of them have taken multiple of these 10-15 % elevations going far above the normal limits. For instance, from the hematological data from the 1990’s we do know that one successful cyclist had his hematocrit (hemoglobin) increased from 35.7 % (~120 g/l) to 60.7 % (~200 g/l) between winter training season and spring which means that a given unit of his blood theoretically carried some 70 % more oxygen. Even when it is easy to think that these athletes get roughly similar speed improvement with each consecutive 10-15 % elevation, Björn Ekblom isn’t that convinced: I am not sure about how the other links can keep up. If you go from 140 or 150 g/l to 220 g/l, there must be some compensation in the distribution of flow or perhaps increased blood pressure and so forth. Björn Ekblom has always maintained that peripheral factors don’t appear to be the main limiting factor if enough muscle mass is recruited, which is illustrated by the fact that maximal ”forced” breathing is almost always higher than the highest values reached during exhaustive exercise points that there is ”idle” capacity in lungs and in addition, the blood returning from the muscles has a very low oxygen concentration, so the oxygen is pretty completely used at the peripheral level. While blood doping with all the methods has consistently elevated performance in the research papers and Ekblom always has stressed that heart and hemoglobin concentration are the main bottlenecks for most of the people most of the time, it is interesting that Björn Ekblom has occasionally discussed the possibility that the physiology of elites might be different and the key limiting factor might not be the heart and oxygen carrying capacity with elite level athletes. He brought up this possibility in the mid-1980s in a memorial lecture he gave when his coauthor and even an occasional critic Lars Hermansen had passed away at a relatively young age. ”In some extreme well-trained top athletes with very high maximal aerobic power in relation to the dimensions of the respiratory system the ventilatory/discussion/perfusion complex may be a critical factor – especially at altitude”. (Ekblom, 1986) He held a similar type of opinion quite recently when writing in relation to the ”central governor”-debate that occasionally lungs could limit oxygen delivery of which an ”obvious instance is oxygen desaturation of the hemoglobin in arterial blood during maximal exercise, which seems to be more common in well trained performers who have high Vo2Max”. (Spurway et al, 2012) In this light, it is also noteworthy that almost all the blood doping research has been conducted with sub-elite level athletes, and improvements can’t be directly extrapolated to elite level athletes.* *One paper that addressed this issue in 1987 compiling the data from four reinfusion studies with roughly similar protocol actually concluded that participants with 50-65 ml/kg/min were most ”responsive” to blood transfusions whereas subjects with higher or lower baseline Vo2Max increased their Vo2Max only half of the value of that group. (Sawka et al, 1987) Ekblom’s take on multiple Olympic champion Eero Mäntyranta is also interesting and expresses that he always looks beneath the surface even when anecdotal evidence would support his case. While it is also almost universal consensus view by expressed by geneticists, bioethicists, popular writers and anti-doping activists that Eero Mäntyranta benefited from his super-high hemoglobin concentration, Björn Ekblom isn’t totally convinced about this: I am not sure about Eero Mäntyranta. His superior ski performance may not be caused by his high hemoglobin. I know that Peo was very much in favour of the idea that his hemoglobin was the reason or his performance. While there are some issues in making too direct conclusions in comparisons between individuals, Ekblom has noticed a tendency that athletes with very low hemoglobin concentration had extremely efficient blood delivery. He thinks that the opposite could also hold true: Nobody measured the cardiac output of Mäntyranta, I think. About people who have high hemoglobin concentration at rest, they may have low cardiac output at maximal exercise for other reasons than viscosity reasons. I can say that we found two runners from the Stockholm area who had the same problem as Mäntyranta, so we measured cardiac output in one of these guys and he had fairly low maximal cardiac output, but he had reasonably good oxygen uptake. So there are some strange things going on in the oxygen transport chain. Ekblom may be on the right track in his skeptical account and there might be other factors explaining the success of the Finn and it is noteworthy that Mäntyranta had good genetics regardless of his high hemoglobin and his nephew Pertti Teurajärvi was an international caliber level cross-country skier who won many medals as a part of the Finnish cross-country relay team, most notably the 1976 gold medal at Innsbruck Olympics. Even when some authors such as author David Epstein (author of The Sports Gene) have stated that he had the same blood phenomenon as his uncle had, this is not the case. Despite all the media fuss about him, there is very little we know about his aerobic capacity. But as one interesting anecdote, his Vo2Max was discussed in passing in 1971 when he was trying to return to perform at top level for the 1972 winter Olympics and it was mentioned in passing that his Vo2Max had been measured with direct methods only once, in 1965. According to the journalist, the figure came then back surprisingly low, only 72 ml/kg/min. (Bremer, 1971) That is a good figure – no doubt about it, but nothing enormously high.* *Well-respected Finnish physiologist Heikki Rusko claimed that the Vo2Max of MaÅNntyranta was estimated to be in excess of 100 ml/kg/min based on an indirect bicycle ergometer test and claiming that it was never measured with direct methods. (Raevuori, 1977) Case closed on the timeline? If the reader wondered why the essay is titled “a genesis” and not ”the genesis”, it is because there could’ve been other paths to innovate the method. In fact, the narrative described in this essay on how blood doping became ”invented” is prone to reevaluation even far in the future if and when new information emerges. It is also difficult to pinpoint a moment when something is ”invented”. Blood doping wouldn’t even be the only hemoglobin concentration – related item that might’ve earlier than widely assumed. Even when there is a lot of truth in the claim that exercise physiologists James Stray-Gundersen and Benjamin Levine invented the so-called “live high/train low”- exercise method in the 1990s, one could argue that the idea was “really” invented some two decades earlier. Because blood doping researchers Norman Gledhill and Alison B. Froese, in essence, noticed the detraining-problem some fifteen years earlier in their essay. “A problem with altitude training, however, is that while acclimatizing to altitude, the athlete’s maximum work capacity is reduced approximately 10 %, and therefore, since the intensity at which the athletes can train is slightly reduced, a small amount of detraining can occur”, Gledhill and Froese wrote almost in passing in their 1978 paper. “However, it has been illustrated that it is possible to avoid this problem by transporting the athletes to a lower altitude for their daily training session or by having them train in an oxygen-enriched environment” (Gledhill & Froese, 1979) The study they refer to where these shortcomings were avoided was published in 1980 and the preliminary report in 1976. If one looks for trails of the idea of intermittent hypoxia even further in time, the idea is mentioned before the 1968 Olympics in a transcript of a discussion that took place about high altitude training between the scientists from nordic countries. ”There is one interesting aspect which is not clearly answered as yet, and that is the effect of intermittent living on a high altitude”, physiologist Kaarlo Hartiala mentioned in passing in 1966 when discussing the matter with his nordic colleagues. “It might be to some benefit to keep the training on a lower and the living on a higher altitude”. Still, it took until the 1990s before the Stray-Gundersen and Levine ”invented” the idea and gave it the scientific validation. About blood doping, the situation is slightly different because there is some smoking gun research, but in addition, there is also some gossip and evidence about the method actually been used before the 1970s and it is possible to locate some references of athletes having blood doped before the 1970’s even in academic publications. One theory actually is that Ekblom, Åstrand, Goldbarg and the others only gave the scientific validation to the method already in use. “Among other variables, Åstrand and his Swedish colleagues paid attention to blood values, in particular, the oxygen-carrying ability of hemoglobin”, wrote Finnish historian Erkki Vetteniemi recently about the origins of the blood doping research. “In 1971, one of them (Björn Ekblom) discovered the blessings of blood transfusion for athletes – or, he claimed to have discovered the benefits of blood packing”. Referring to the earlier gossip about transfusions taking place before that, the historian continues that a ”more probable scenario is that the Swedish scientists published their blood packing paper as soon as the method had become commonplace in skiing and other sports”. (Vettenniemi, 2017b) Vettenniemi has occasionally brought up the case Jonny Nilsson, for whom when Ekblom allegedly offered a transfusion in 1966, but another alleged blood doping case of interest he has mentioned took place early as 1948 before the London Summer Olympics. The incident was mentioned in one of his articles by MD Inggard Lereim, who was since the 1970s has been a Norwegian team doctor and later a member of the FIS Medical Commission. (Vettenniemi, 2017a; Lereim, 2001) It is equally true that there is some confusion about the timeline amongst the ”in-the-know” Nordic MDs. For instance anti-blood doping activist researchers Tapio Videman, Inggard Lereim and James Stray-Gundersen (and coauthors) wrote about the origins of blood doping in passing in one of their research papers in 2000 that “[r]umors about the use of blood doping have been circulating since the 1960s” (Videman et al, 2000). Only three years later the same trio contradicted this timeline by a decade, writing that ”rumors and reports of transfusion use in endurance sports did not surface until the late 1970s” (Stray-Gundersen et al, 2003). Bengt Saltin on his part coauthored paper in 2012 stating that ”[b]lood doping practices in sports have been around for at least half a century”, indicating the starting point closer to the early 1960s if not earlier. (Lundby et al) This hasn’t precluded Saltin stressing occasionally the importance of the GIH-research line that Ekblom and Åstrand had started in the mid-1960s. (Saltin, 1995) The case that the GIH-scientists knew about the benefits of blood doping before Björn Ekblom started the research around 1966 is a possibility but still somewhat unlikely one because why would Bengt Saltin have discussed transfusions publicly in 1965 if administering transfusions was the exclusively secret weapon of the Swedes? And why were there many foreign researchers involved in the research and why were the findings discussed as early as 1966 with some 200 nordic physiologists possible hearing about the line-of-inquiry even if the results were inconclusive at best? If there is one lesson from this lengthy essay, it is that all transfusions aren’t created equal and even if individual athletes had been administered transfusions, it didn’t necessarily mean that the rationale was to ”blood dope” in the same intellectual tradition that later (1971-) athletes performing similar operations did, because anemia was a medical condition treated with transfusions and it could’ve been used for altitude adaptation. It is still noteworthy that the gossip about these pre-1970’s transfusions are a few in number and later impressions of teammates and competitors can be deceptive. About evolving recollections, multi-time Olympic gold medallist Eero Mäntyranta was furious in 1972 after the Finnish team underperformed at the Sapporo winter Olympics demanding an explanation why the Finnish sports bodies were reluctant to test how blood doping worked to “sacrifice” one of the eight Finnish male cross-country skiers as a guinea pig for the games. “Such a test would’ve been extremely valuable, but still a very modest one, when compared to the enormous medical testing one, hears having been conducted in the modern sports world by the big sports countries”, he wrote in the spring of 1972 shortly after the unsuccessful winter games. (Mäntyranta, 1972) When blood doping practices were discussed once again in the media in 1985, some thirteen years later, he had a very different timeline and suspected that his Finnish compatriots had blood doped even for the 1966 FIS World Championships, some six years before he wanted the method to be tested. “I don’t want to insult anyone, but there was something strange when some Finnish skiers were in top form at the 1966 Oslo Championships but vanished after the games altogether”, he said. (Mörä, 1985) It isn’t even certain that even honest recollections about transfusions are sound, because anemias were regularly treated with iron shots and the Swedish daily newspaper Expressen went so far to even describe the treatment of cyclists of the 1970 Tour de France as “blood through drop” while still describing the actual content as “sugar solution and iron”. In addition, there existed some blood reinjection treatments such as ozone therapies that were already in use in the 1960s, and it is known that perhaps the best cyclist of the era Jacques Anquetil believed in the method. “While Anquetil did engage in a form of blood manipulation, it would probably be incorrect to refer to it as a transfusion”, was journalist Feargal McKay’s reading of the treatment in his essay on the history of transfusions in cycling. “What he was actually playing with was super-ozone therapy, whereby a small amount of blood is extracted, treated with ozone and immediately re-injected”. (McKay, 2013) It isn’t even certain that all the post-1972 transfusions were conducted in order to assume supranormal hemoglobin concentration was beneficial in every condition. Interestingly even cyclist Eddy Merckx (who was offered a transfusion in 1972) mentioned later that his “target” hematocrit was only 52 % when was planning to succeed in his attempt to break the hour world record at altitude, which was in the normal range of residents of 2200 meters and meant that his quest to thicken his blood wasn’t open-ended with the almost “higher-the-better” attitude of the 1990s. (Thirion, 2012) If one also follows the roots of many known blood doping circles, the roots are usually one way or another traceable to the research conducted at the GIH. The Finns were aware of the Swedish research on some level by the late 1960s and endurance running coach and anti-doping activist Alessandro Donati has also claimed that the Italians didn’t ”know” about blood doping all along but started their research on the subject in the 1970s. There is a negligible amount of material about the blood doping use by the East Germans, and when the evidence of the Soviet Union blood doping program was revealed, it also looks as if they started their clandestine blood doping research in secret in the mid-1970s as a response to the Swedish research. (Kalinski, 2003) If they had known it all along, why reinvent it again? End words As far as I know, this has been a first deep look into the origins of blood doping, which is somewhat surprising, considering that the blood doping research at the GIH began over fifty years ago, and the first published research paper on the subject was published some forty-seven years ago. The reason might be that the method of blood doping is so simple and tautologically true that many commentators looking the subject with the modern knowledge erroneously assume that there was not that much to be researched at all in the subject and correspondingly there was barely any debate at all about its efficacy. If the first blood research paper published in 1972 was an interesting and somewhat unpolished paper on an arena not much researched before, opening the subject for further interest, I do hope that this essay will serve somewhat similar purpose for the subject of the history of blood doping, stimulating intellectual curiosity for “real” historians and researchers either to confirm or debunk my findings and conclusions and to pursue new avenues of research. Regardless of what the response will be, I do hope that I’ve done justice for the research work that took place at the GIH and elsewhere many decades ago about the topic. And when I have a huge respect towards Björn Ekblom, I do hope that I’ve proven him wrong when he once remarked that only a physiologist understands the research they are doing. The author wishes to thank Dr. Björn Ekblom without whose help this essay would not have been possible and also Alex K. and Chelsea L., both of whom went through parts of the first version of the manuscript and corrected grammatical errors and made some improvements into the structure. This is part five of a multi-part series titled “Limiting Factors – A Genesis of Blood Doping”. The full bibliography for this research can be found at the end of Limiting Factors – A Genesis of Blood Doping (part one). Sammy Izdatyev is the pen name of a Finnish sports enthusiast and unaffiliated amateur historian, who has been interested in endurance sports since the turn of the millennium. He hopes that his pro bono – research can provide more information into the body of literature of earlier underresearched areas of the history of sports. Part VI: “Endgame” Answering the critics While blood doping research caused a variety of opinion about its efficacy worldwide, the reception wasn’t unanimously positive among even Björn Ekblom’s closest GIH colleagues and coauthors. While P.-O. Åstrand was convinced about the results and never expressed doubts about the veracity of the findings expressing this opinion in lectures, media and journal articles throughout the 1970s, all weren’t so enthusiastic. Ekblom’s GIH colleague Ulf Bergh is an example of the middle-of-the-road un-enthusiastic approach that wasn’t dismissive either. ”Theoretically, increasing blood hemoglobin concentration would lead to increased oxygen binding capacity”, Bergh wrote about the subject in his shortish 1974 pamphlet on cross-country skiing. “The research has shown that acute increase in Hb concentration can in some cases increase performance”. Bergh clearly wasn’t fully convinced that hemoglobin concentration was universally the key limiting factor and he even warned about the increased viscosity negating the benefits of increased hematocrit and that there must exist an optimal value. (Bergh, 1974) He would pay some interest in the theories about different muscle types correlating with maximal oxygen uptake. (Bergh et al, 1978) Bengt Saltin – who had defended his thesis in 1964 – was also a curious case, because while he coauthored some significant research on the peripheral adaptation, Saltin was very reserved in those papers not directly criticizing Ekblom and made no public post mortem about what was presumably wrong with the 1972 research paper and he even indirectly helped Ekblom’s case by researching how exercising at higher atmospheric pressure affected performance questioning findings of Lennart Kaijser’s who found no benefit. (Fagraeus et al, 1973) Björn Ekblom recalls that there was a minor competitive situation at the GIH, not between him and Saltin, but between and Saltin and Åstrand. The younger researcher didn’t want to be only “Peo’s student” without his own students and subsequently, in 1973 he took a professorship at the August Krogh Institute and moved to Denmark. One who encouraged him to do so was Eric Hohwü-Christensen, the same Danish physiologists who had founded the GIH decades earlier. Lars Hermansen, who was Ekblom’s coauthor of the 1968 paper measuring cardiac output of elite athletes, was also on the skeptical side. In the late 1960s and the early 1970s, he had paid a lot of attention to the relation between hemoglobin concentration and maximal oxygen uptake, studying comparisons between individuals and longitudinal studies how increase and decrease in hemoglobin concentration affected maximal oxygen uptake. Based on his own research on the pre-existing literature he observed practically no connection between hemoglobin concentration and Vo2Max and he wasn’t even fully convinced that even severe anemia causes fall in maximal oxygen uptake and there are various possible compensatory factors explaining why hemoglobin concentration isn’t that important from Vo2Max viewpoint such as increased blood velocity when the blood was thinner. (Hermansen, 1973) Whereas when Ekblom didn’t see any correlation between Vo2Max and hemoglobin concentration, he concluded that the speculations about ”viscosity problem” and “the optimal hematocrit” were wrong and that blood doping could in theory work. Hermansen drew the exactly different conclusion about the material. Because there was no correlation between the two, hemoglobin concentration was almost meaningless figure because almost every value was as good as the next one from Vo2Max viewpoint, and elevating hemoglobin would just bring the subject to another equally good value. As a case study, Hermansen even refers to a cross-country skier who was tested at the GIH on two different occasions, five years apart. When Åstrand and Saltin had tested subject ”ÅH” in 1962, his maximal oxygen uptake was 5.39 l/min and his hemoglobin concentration was 16.5 g/dl. But when Ekblom and Hermansen tested the same subject five years later for their cardiac output paper, the number of oxygen carriers per a given unit of blood had fallen from 16.5 g/l to 14.7 g/dl, by 11 percent. But unlike one could’ve expected if the blood doping hypothesis was sound, his Vo2Max had actually increased by 4 % from 5.39 l/min to 5.60 l/min. (Hermansen, 1973)* *Physiologist Loring B. Rowell – who had researched how blood donation affected performance – shared the opinion of Hermansen when writing about the subject matter in 1974 pointing also to the incapability of altitude training to elicit increase in Vo2Max and noticing that like Ekblom et al in their 4x300ml group, there had been a vague blood doping-related blood reinfusion research paper from 1966 (Robinson, 1966) where an infusion of 1200m of blood failed to elevate Vo2Max. In summary, Rowell concluded that ”[t]he constancy of Vo2Max in the face of substantial changes in blood 02-carrying capacity is an important but poorly understood human cardiovascular adjustment that maintains Vo2 max”. (Rowell, 1974) Of course, nobody formed their views in isolation and as Hermansen and Saltin were coauthors of many papers and Ekblom notes that Hermansen’s hemoglobin concentration views also influenced Saltin on the matter. Alberto N. Goldbarg and Björn Ekblom were fully aware and even brought up a few anomalies and contradictions in their breakthrough research paper, most of which could be explained by the small group of subjects. In retrospect, it looks as if some hematologists and cardiologists dismissed the findings out of hand without bothering to look at the material, but looking the issue almost five decades later, Ekblom feels that the scientific criticism from the exercise physiologists was in essence sound and sincere and the 1972 study left many questions unanswered: Those who were against the results didn’t believe in the effect for a variety of reasons. But more research was of course needed, either to prove or disprove the findings. That we got it right makes me feel happy but not malignant – that is how science just works. One sees something to prove – and if there are people who think that it is wrong then they take their attempts to disprove it in some way even when it is always difficult to prove things. Still there were those voices who dismissed the research out of hand and felt that just the ”unnaturalness” of blood doping meant that it couldn’t work, a case that made then intuitive sense particularly if one hadn’t researched or followed the subject closely, a case that became evident when Ekblom himself had to comment on anabolic steroids even when he hadn’t researched them and questioned whether they were of much benefit: I can pretty much agree that one viewpoint then was that what wasn’t normal should not have any positive effect. I have myself made the same mistake in undermining the effect of anabolic steroids as performance enhancer.* *Ekblom wasn’t alone in Sweden with this attitude. When accusations of anabolic steroid use were directed against two Finnish endurance runners in 1973 from Sweden, Bengt Saltin defended the runners. ”Neither of them would benefit from larger muscles”, he told emphasizing that steroids only benefited strength athletes and runners up to 400 meters and wasn’t even 100 % convinced about them. ”I want to emphasize that this benefit is in the limits of possibilities”, he stated and told that the scientific literature about the efficacy of steroids was nonexistent. (Ilta-sanomat, 1973) In the light of the oft-repeated – albeit in essence correct – statement, that blood doping was “invented” by the 1972 research paper, one should still pause for a moment about the implications of the paper, because it is easy too read too much into its conclusions. What was actually the new information from the 1972 study? As the paper states, the goal “was to investigate the influence of relatively small changes in the hemoglobin concentration on human physical performance capacity and on the different variables in the oxygen transport system”. First, it took no position whether it would be beneficial to increase hematocrit level beyond the “normal” physiological range and the highest hematocrits measured after blood infusions were still around 46-47 % and thus it wasn’t obvious that it could be beneficial to increase hematocrit to 50 % or 60 %. The only finding was that the “adapted” hematocrit was suboptimal for one reason or another. Even with a few random inconsistencies, it is still noteworthy that each one of the seven subjects tested their highest maximal oxygen uptake in the test conducted shortly after the blood reinfusion. In the group receiving 800 ml blood, maximal oxygen uptakes also returned to control level in the following weeks in tandem with hemoglobin concentration as should’ve been expected if the increase in Vo2Max was explained by the increased amount of oxygen carriers. When discussing the matter while lecturing in 1973 in the United States, Per-Olof Åstrand expressed as his opinion that the work data alone wasn’t totally convincing in itself, (Pate, 1976) but the maximal oxygen uptake figures weren’t prone to subject bias, a view that Ekblom himself expressed a decade later. “There are no reasons to believe that a subjective bias could explain the ‘overnight’ increase in maximal oxygen uptake, but on the other hand, psychological factors may have modified the magnitude of the changes in ‘physical performance’ as evaluated from time to exhaustion on the standardized maximal exercise”. (Ekblom, 1982) Other two problems brought up against blood doping were more technical than fundamental. One problem brought up also by Lars Hermansen wasn’t the capability of the stored red blood cells to carry the oxygen for the muscles, but its capability to release the oxygen to the muscles. This put a lot of emphasis on the enzyme 2,3DPG, a blood component that was identified in 1967. While the 2,3DPG is today more-or-less an item most researched by clinical hematologists, but for a brief time period in the 1970s, 2,3DPG became one item of importance for exercise physiologists when researchers measured how its amount changed relating to training status, at high altitude and during and after exercise. There were voices within the exercise physiology community, that the beneficial effect of high altitude training wasn’t the increase in hemoglobin concentration, but the increase in 2,3DPG-level when red blood cells released more oxygen for the muscles. Ekblom’s view is that 2,3DPG doesn’t play a significant role in oxygen delivery and the discussion around it in the 1970s didn’t bother him that much even when some illness could render it relatively more important. The other alleged problem was that exercise capacity was reduced during the relative anemia between blood removal and reinfusion and correspondingly a blood doper couldn’t give the 100 % effort during the weeks preceding a major competition. While the observation had its practical implications, this problem didn’t address the “workability” of blood doping from a fundamental viewpoint but was more related to the applicability for doping purposes. Still particularly the 2,3DPG and “viscosity problem” were so pertinent questions, that Ekblom and Per-Olof Åstrand conducted in 1974 a second published blood reinfusion study dealing with the issue. They coauthored this research with Jerold Wilson, a famous Canadian sports doctor and the team doctor of the ice hockey team Winnipeg Jets, who was spending a sabbatical year in Sweden and conducting research.* *Wilson followed closely the ice hockey circles of the nordic countries, and the first Swedish and Finnish ice hockey players had their professional contracts shortly thereafter with the Winnipeg Jets team. They used essentially the earlier 800 ml reinfusion protocol but lengthened the storage time by roughly a week. As the main criticism of the 1972 study was that the extra hemoglobin increased also viscosity and lowered cardiac output, cardiac output was measured to test how it responded to blood removal and reinfusion. Maximal oxygen uptake was also measured, but there was no performance test conducted. (Ekblom et al, 1976) The results came back roughly similar to the 1972 study. While no ”overnight” data was measured, maximal oxygen uptake fell after blood removal and was elevated by an enormous 8 percent after reinfusion when compared to the pre-removal data. The latter figure coincided with hemoglobin concentration going some 5 % above the normal. If critics had assumed that viscosity would negate most of the benefits, this didn’t hold true. While the body compensated some of the lowered hemoglobin by elevating cardiac output after blood removal, the heart could keep the blood flow unchanged after blood reinfusion. The 2,3DPG level didn’t fall and muscles could use the oxygen offered and it looked as if the opposite held true because a relatively higher portion of the ”offered” oxygen was used by the muscles because the blood returning from periphery had lower oxygen content than before blood donation. ”The benefit of an increased Hb concentration is easily understood, but the reason for a reduction in calculated [venous oxygen content] is unknown”, Ekblom, Wilson, and Åstrand write about the interesting phenomenon.** **Reviews of this 1976 study are difficult to find, but at least one later commentator concluded erroneously that the stable cardiac output was detrimental to the blood doping hypothesis even when it specifically meant that heart could keep up with the presumed extra viscosity. ”After that [1972] study, they repeated the protocol while measuring cardiac output as well”, wrote MD Jim Stray-Gundersen in his 1988 essay on blood doping. ”Unfortunately, they were not able to repeat their initial results and also found no difference in maximal cardiac output.” (Stray-Gundersen, 1988) Even when performance wasn’t measured as a part of the research paper, there is anecdotal performance data also from this study. The subjects were physiology students, of whom one was Artur Forsberg, who was a student at GIH and who would become a physiologist specializing in cross-country skiing. During the course of the study, he conducted a parallel time-trial test recalling the experience eleven years later. Forsberg’s personal record on a regular nine-kilometer cross-country route was 33:35 and he ran three control runs with times 34:25, 34:32 and 34:12 before the reinfusion. After he received back the blood, his time was 32:28 and therefore he was two minutes faster and also shattered his earlier record by a minute and seven seconds. Forsberg also observed that his resting heart rate was lower than usual after he got his blood back. (Lodin, 1985; Ekblom, 1982) While their new research had been submitted and waiting to be published, a team of West German researchers had also paid interest into the subject matter relatively quickly after the 1972 paper and secured funding and a mandate to research the subject. They had their research published in 1975. Whereas Ekblom and Goldbarg had only 7 subjects, the Germans had a total of 17 subjects and conducted various measurements on heart function, total hemoglobin count, etc. While the protocol was slightly different and there were more cohorts, the authors concluded that their findings coincided pretty much with those of the 1972 study when they noticed that Vo2Max increased by 9 percent and maximal working time by 37 percent after reinfusion of 900 ml of blood. One limitation of the study was that whereas Ekblom’s subjects were fit students, the subjects in this research weren’t that fit. (Rost et al, 1975) The West German researchers weren’t also just random guys, but very eminent scientists. The most recognized name is Wildor Hollmann, whose research on maximal oxygen uptake and heart was quoted widely internationally and Heinz Liesen who would become an eminent coach in many types of sports including football and cycling. It has been since claimed that the third researcher Richard Rost had tested the method with elite level swimmers already in 1972 (Spiegel, 1990) and interestingly Ekblom also had mentioned a West German swimmer having broken the national record with the help of blood doping. Ekblom’s thinks that on a general level, the German language research was undervalued and the to illustrate this, research paper vanished almost into the memory hole and Richard Rost is almost without exception misspelled as ”von Rost” when the study has been briefly mentioned in some blood doping literature reviews. “For us, the issue was completely clear after the 1976 research”, is the significance of this confirmation study according to Ekblom, when 2,3DPG and cardiac output were now measured. Bengt Saltin also becomes later convinced about the blood doping issue and became an anti-blood doping activist commenting on the issue in media and taking it as one of his focuses as a member of many sportorganizationsns. Hermansen, on the other hand, remained unconvinced. “Lars Hermansen dissertation showed no connection [between hemoglobin and Vo2Max] and that was his opinion until the end”, Ekblom recalls. His Norwegian friend and coauthor of many papers died unexpectedly in 1984, only a few weeks before his 51st birthday. The Mysterious Finn infuses new interest into the topic Even when the blood doping literature reviews list only three published blood doping research papers between 1972 and 1975 and the few reviews were very ambiguous about interpreting the available evidence, the issue gained a huge amount of media attention in 1976. The first instance was when the Norwegian Olympic team wrote an official letter to the International Olympic Committee (IOC) warning them about the practice only a days before the Olympics. The idea for the letter came from the team doctor Paul Lereim, who was also a member of the medical commission of the International Speed Skating Federation and had noticed that east European skaters rose rapidly in the early 1970s and broke the traditional hegemonies. During the games, there circulated also claims that several countries took benefit of the method and while the accusations were directed more against the triumphant communist countries, the geographical origin of the method didn’t go unnoticed and Nordic countries got a part of the heat. One French sports journalist of the Le Monde indeed found sinister motives behind the letter claiming that ”it is probably not a coincidence that the complain originated from Norway” because athletes from Nordic countries have been alleged to have benefited from the method. The journalist continues assuming that now that their ”advantage” is gone, they want to ban it for everyone. (Le Monde, 1976) The Norwegian Olympic Committee contacted the French media outlets and denied using the method as well as emphasized that their blood doping condemnation wasn’t directed against the Soviet Union as was claimed in some media outlets. (Helsingin Sanomat, 1976) There are always many variables in cross-country skiing affecting the outcome and while the Soviet athletes were triumphant, no ”hard” evidence was presented against them, and even the circumstantial evidence wasn’t that much better and only a few can even recall today the few names that circulated in passing in the media as suspected ”blood dopers”. Not that many people even followed winter sports and it took until the Montreal summer games until a perfect blood doper was found in the character of endurance runner Lasse Viren, who not only came from Finland but whose year-to-year performance progression was so abnormal and in many eyes consistent with blood doping. There are always some athletes that are just good and there was nothing overtly suspicious about Viren’s early career, when he progressed gradually from the late 1960’s onward becoming clearly the best endurance runner of the year 1972, when he broke three world records (2 miles, 5000m and 10000m) and he was also double Olympic gold medalist (5000m, 10000m) when he during the 10000m finale he simultaneously won Olympic gold and broke the world record despite falling during the race. Then he vanished almost altogether and there are no significant achievements during the years that followed. Whereas he was the best runners of 1972, he managed to win bronze at the 1974 European Championships in athletics and in 1975 for 10000m – the year preceding the Montreal games – he was 24th and over half a minute slower than his own record only three years earlier. Then Viren made a triumphant comeback for the 1976 summer Olympics repeating his 1972 performance by winning gold both in the 10000m and 5000m. He even tried his first marathon race only a day after the 5000m finale and managed to become 5th which is an astonishing achievement when he was competing against a group of fresh competitors of whom almost all were marathon specialists. When the Swedes were also triumphant in endurance events with Anders Gärderud winning the Olympic gold at the 3000m steeplechase breaking the world record, and his countryman winning the 175 km individual road cycling race, many people wondered what was happening in Scandinavia. Middle-distance running specialist Marty Liquori – who was injured and couldn’t compete – was a commentator on television and discussed blood doping during the ABCTV coverage on the 10000m finale, and some of Viren’s competitors accused him directly of blood doping. Correspondingly Associated Press and many international news agencies also wrote stories about the method that were republished and translated internationally and many people read ABC-TV Chris Brasher claiming that an unnamed ”Swedish star” might be using the method.* *This was almost certainly a reference to Anders GaÅNrderud, who was a student at GIH. Him paying some interest in blood doping in 1971 was republished in the American media, but Ekblom is convinced that the didn’t blood dope. ”When I tested him at the GIH, I didn’t even want to take the lactic acid test blood from his fingertip”, Ekblom recalls. If the case against Viren was only circumstantial, there was also no consensus view whether the method was beneficial at all, a question that many researchers wanted no to settle once and for all. Correspondingly there were several dissertation theses and research papers originating particularly from the English-speaking world in the wake of the Montreal games. Some of these weren’t published at all and some were published only in a short abstracted summary or random news items. Almost all of these were very carefully conducted with double-blind procedure and control group and some had even questionnaires to exclude the possibility that the participants had any idea whether they had been blood doped or infused only with saline. Perhaps the first one was the master’s thesis of one Andrea J. Frye’s submitted in April 1977, only some eight months after the Olympics. It is essentially the same experiment conducted by Melvin Williams and his coauthors some four-five years earlier (16 subjects, males and females), but the author measured maximal oxygen uptake and gave a more detailed look into the preexisting literature, with the unpublished thesis running some 80 pages. In the end, there was no improvement noticed and the author concludes that ”the data indicates that the technique of RBC reinfusion does not produce significant changes in aerobic capacity” and correspondingly “hemoglobin is not independently responsible for the delivery of oxygen to the tissues”. (Frye, 1977) Melvin H. Williams also recalls how interest in the subject intensified after the 1976 games and he also decided to conduct another reinfusion paper measuring this time hemoglobin concentration and making some minor changes into the protocol. The amount of blood infused was still on the low side (460 ml), so there was no statistically significant improvement observed in the paper published in 1978 that was widely referred to in the media. The authors acknowledge that their findings are ”in sharp contrast” to some earlier papers and “the major criticism” of these studies where the benefit was seen as the absence of a control group or double-blind procedure. (Williams et al, 1978) Marty Liquori had been a commentator of the ABC-TV at the 1976 Montreal Olympics and he commented blood doping issue both during the 10000m finale and gave comments later to various media accounts throwing some suspicion on Lasse Viren. Now he had a change of heart if he had ever truly believed in the blood doping thing or only discussed it as a possibility.” Its the consensus of most American doctors that I have talked to that [blood doping] doesn’t help,” he commented on the issue now in the media. “I think that people are just starting to realize that Viren just trained, to peak at the time of the Olympics.” Even when international news agencies were eager to publish these findings debunking the efficacy of blood doping and many authors referred to them, it is noteworthy that even the researchers themselves were acutely aware of the limitations and even might’ve noticed the problems. ”During Ekblom’s study 60 % to 140 % more blood was infused than in Williams’ [1973] study or the current study”, wrote Andrea J. Frye in her unpublished 1977 thesis. ”Also, the time between [blood removal] and reinfusion was significantly greater, allowing time for more thorough regeneration of cells in vivo”. Melvin H. Williams and his coauthors also noticed that a ”possible criticism” could be the low amount of blood infused because they used only half of what Ekblom had used in two of his published studies. Williams has later emphasized that the negative conclusion was most likely only a statistical issue because even when there were no ”significant” differences between the control and reinfusion groups, there was something interesting in the data: I should note that the statistical analysis showed no difference. However, almost all of the subjects who received the blood, as compared to the saline placebo, experienced an improvement in performance. But, since the difference between the groups was not statistically significant, we had to conclude that blood doping was not effective to increase running performance. However, that may have been a type II statistical error, in which the findings failed to reject the null hypothesis. Because the positive effect was almost seen in the raw data, Williams decided at this point to conduct a third study to settle the question once and for all using a higher amount of blood. There were also at least two unpublished dissertations that tackled the question using a roughly similar protocol, of which one showed no benefit (Woods, 1977) whereas similar method in the other one could produce at least a substantial increase of RBCs after blood infusion. (Weese & Hermiston, 1977) If the reader is confused about why at least four researcher teams used the ”early” Swedish protocol already proven having issues, there were two reasons for this. First, US Food and Drugs Administration limited storage period to 21 days and secondly most of the English-speaking had no idea about the earlier inconclusive attemps of the late-1960’s and they might’ve been under the impression that blood doping was easy and that Björn Ekblom and Alberto Goldbarg immediately succeeded in causing the surplus of red blood cells in their 1972 study. While Björn Ekblom had mentioned this preceding research occasionally in Swedish media outlets, the Anglo-Saxon world had to rely heavily on the two published blood doping research papers originating from Sweden in which there is not one word about the earlier inconclusive attempts. Thus the media outlets that were eager to report these ”inconclusive” findings showing no benefit were under the wrong impression that this research was 100 % original breakthrough research and actually superior to the Swedish research with placebo control groups (which was partly correct). While Melvin Williams and Ekblom knew each other well and even exercised together when Ekblom was visiting Palo Alto in the 1970s, Williams has since explicitly stated that even he wasn’t aware of these earlier 1960s blood doping attempts at the GIH. State of Confusion There were roughly a dozen published blood doping studies by 1978-79, and the literature was far from conclusive. Only Swedes and the West Germans were able to show a clear benefit and even and more damning for these findings, it at least appeared that more careful the conduct was, less effect there was seen. As anti-doping activist and prominent exercise physiologist James Stray-Gundersen wrote some the years later: ”The situation at that time was one where the athletic world felt the procedure was effective and the scientific world was showing the most recent data to the contrary”. (Stray-Gundersen, 1988) It is true that if an impartial arbiter weighed in the sheer amount of pro- and con studies on blood doping, the case was very open and even slightly against the efficacy. While skeptics hadn’t questioned the data itself, there were some who took a deeper look into the source material itself and questioned both the inner consistency and how the data was reported. Some researchers had pointed out that the ”overnight” improvement wasn’t the whole truth about the performance enhancement, and Russell R. Pate of the Human Performance Laboratory, University of South California stressed this point when writing for The Runner’s World about blood doping in 1976. Whereas it was widely publicized in the media that there was the 9 percent ”overnight” increase in Vo2MaX and it is usually reported even today with the 23 percent improvement in performance, very accomplished marathon runner Pate (personal record world-class level time 2:15) spotted an flaw in how the data was usually presented, because an athlete interested in blood dope wouldn’t be interested in the ”overnight” change but in change when compared to the pre-blood donation period. ”When Ekblom’s results are viewed in this manner, the increases in performance are still present but much smaller – a 15.6 % increase in work time and only 4.8 % increase in maximal oxygen uptake”. (Pate, 1976) While there was a point, Ekblom didn’t find this criticism totally valid: My view was that even if [our subjects] were not really fully recovered in hemoglobin concentration, the change after reinfusion would be enough from day-to-day to see the effect even if we were from lower-than normal value, and that was also the case that some of the guys we have had had not been recovered during 30 days. One could say [that] some of the performance effects could have been that they had restored an anemia situation, on the other hand, there are a lot of – at least a few – subjects who were normal when they got the blood back and still you could see this effect on performance and so forth. Even if one compares improvements to the pre-blood donation data, the improvement in maximal oxygen uptake was 4.8 % in the first published study and 8 % in the 1976 research paper, which are significant figures and the latter was even statistically significant (statistical analysis wasn’t conducted on the first one between the two values). Of later blood doping specialists particularly Professor Norman Gledhill from York University has later also questioned whether the data on maximal oxygen uptake and hemoglobin concentration is fully consistent in these first studies where the benefit was seen. His main problem with the three Swedish and West German studies wasn’t that the absense of increase in maximal oxygen uptake, but that the increase was too large when compared to the elevation of the amount of oxygen carrying red blood cells. But how come Vo2Max increased more than hemoglobin concentration if causally the link was that oxygen delivery caused the increase in Vo2Max? Even when the observation raises the question about the training effect and a fraction of improvement, Ekblom found part of Gledhill’s criticism strange because the oxygen delivery chain is a very complex one and there are always variables that can ”interfere”, and correspondingly there are almost always some seemingly unexplained anomalies in the measured data. In addition, hemoglobin concentration isn’t always the best predictor of how much red blood cell count has been increased after blood infusion, because it is only a relative figure and while usually blood volume returned to normal and there was higher hemoglobin concentration, occasionyll blood volume remained elevated, masking the increase in total hemoglobin, which is a variably more closely related to Vo2Max than hemoglobin concentration. While it is totally true that hemoglobin concentration was only slightly elevated (2-5 %) in the three reinfusion showing benefits associated with blood reinfusion, total hemoglobin was elevated on average by some 5-10 percent in these same studies. In addition of knowing a few anecdotal insights from the field about successful blood dopers, Ekblom – who had become a full professor in 1976 – later wrote that there had been 30-35 reinfusion tests conducted at the GIH in the 1970s, so he had access to more laboratory data than almost all the ”skeptical” researchers, because only a fraction of this material had been published in the two reinfusion studies in the 1970s. (Ekblom, 1982) Thus he had good reasons to be convinced that he and his fellow GIH researchers were on the right track despite a few irregularities in their research papers. They had also interest in proceeding with the blood doping research on track, but the research never materialized. “As I have stated, there was a lot going on at that time”, Ekblom recalls how busy the era was. The Consensus View Shifts If Ekblom planned a final research paper to convince the remaining skeptics, he never had the opportunity to do so, because at least three teams addressed the issue already in the late 1970s with the most sophisticated technology. Norman Gledhill didn’t just armchair speculate the issue, because he had planned to show ”definitely” that blood doping ”really” worked. He had actually written in June 1978 with his coauthor MD Alison B. Froese that ”research on blood-boosting has been inconclusive and in fact confusing” and that ”overviews of these studies have generally concluded that blood boosting has no effect on aerobic capacity and endurance performance”. Gledhill and Froese reveal in the same paper that they will soon be publishing a new study showing the efficacy of blood doping hoping that ”these results will prompt sport governing bodies to take a firm position on the use of blood boosting in athletic competition”. (Gledhill & Froese, 1979) The first report of the findings was delivered at the 1978 meeting of the American College of Sports Medicine in Washington, DC where coincidentally another team finding benefits of blood doping presented their findings. These lectures were delivered only a few hours after one MD had first given a lecture about athletes abusing methods and substances and mentioning anabolic steroids and blood doping as ”discredited” methods. (Barnes et al, 1978) Whereas almost all the research thus far had stored the removed blood in refrigerated form, the Canadians employed relatively new high-glycerol freezing technology, also known as cryopreservation, a technique more known from the world of science fiction. Instead of storing the blood at +4 degrees in a refrigerator, they separated red blood cells from the plasma and added glycerol to keep the ”dry” cells in liquid and froze the mixture at -90 degrees after which the aging process halted altogether. This technique allowed them to wait as long as possible before reinfusing the blood because the blood remained in high quality regardless of whether the blood remained stored for one day or for ten years. This allowed the research team directly to use a high amount of blood and the authors took some 1000 milliliters for later reinfusion. (Buick et al, 1980) Even when Ekblom and his coauthors had used well-trained subjects in all of their blood infusion research, they were still far from international level athletes. Now the subjects of the Canadians are described as ”highly trained male track athletes of national or international caliber” with the mean relative oxygen uptake being 79.5 ml/kg/min and the highest value being level 87 ml/kg/min, which would’ve been ”world record” only a decade earlier. They were also familiar with the rigorous training program and had a body fat percentage of around 6-8 %. This Canadian study would actually be one of the few blood doping research papers with elite level athletes because anti-doping regulations would make it practically impossible to use competing athletes for doping research of this type. The third improvement was that the testing protocol itself was also very sophisticated and there were a control group and double-blind protocol. One group received blood infusion first whereas the control sham infusion of saline and a day later the roles were reversed. Vo2Max increased constantly by 5 % and maximal working time on a treadmill increased by 35 % in the reinfusion group and there was no improvement in the sham group receiving only a miniscule amount of saline. Fred J. Buick – one of the authors and a graduate student of Gledhill – also told later that the participants were breaking their earlier personal records during the time period, so the improvement in Vo2max had some real life implications as well and it wasn’t just a statistical artifact. Then how to compare this paper to the earlier blood doping papers where an increase in Vo2Max was seen? One clear improvement in the paper was that both hemoglobin concentration and total hemoglobin increased very significantly, by more than 10 %, but the other results came back roughly similar. The 5 % improvement in Vo2Max measured in the 1980 research paper was very much in line with what the Swedes and West Germans had measured several years earlier as well as the 35 % improvement in a time-to-exhaustion test. In light of the current knowledge, it is almost impossible that training effect was the cause of the Vo2Max and performance boost of the Swedish research papers, but we do not know if it was a contributing factor in the Vo2Max increases. And indeed, this time there was very little room for speculation about placebo effect or training effect and both the authors and commentators could pretty conclusively conclude that the hemoglobin elevation caused the increase in Vo2Max and performance. But if the Canadians had in the first place objected to some strange anomalies in the Swedish and West German research papers, their own research paper has at least one strange anomaly. Whereas hemoglobin concentration had returned to normal in 16 weeks, surprisingly the maximal oxygen uptake hadn’t followed, but remained still elevated and hadn’t fallen at all. The same phenomenom took place in both of the groups. The authors speculate about increased maximal cardiac output achieved through above normal training load during the time period when hemoglobin was artificially elevated. This research had an enormous impact on the Anglo-Saxon world. R. Russell Pate, PhD., of the Human Performance Laboratory, University of South Carolina had been skeptical on the efficacy of blood doping in the mid-1970s and took an attempt to solve the issue in 1979 with 15 trained female distance runners. When there was no statistical benefit seen, the authors could’ve taken victory laps and poured water into the efficacy of the method, but instead they specifically note that the finding is relevant only to ”the specific blood reinfusion procedure employed” being more interested in why hemoglobin concentration wasn’t elevated with his procedure than making any general conclusions about efficacy of blood doping. ”We were using about half the blood that other workers use, we weren’t freezing it, and 21 days probably isn’t long enough for a return to normocythemia,” Pate stated emphatically seeing the shortcomings. (Barnes & Mealey, 1979) Whereas International Association of Athletics Federation (IAAF) had specifically warned before the 1974 European Athletics Championships that blood doping was dangerous and wouldn’t improve performance, Norman Gledhill had met Arnold Beckett of the IOC Medical Commission in 1978 and discussed with him about his findings convinced Beckett that the method would work in practice. “Since Ekblom’s original study, a number of other similar experiments have produced conflicting results so that the technique and the academic and ethical questions it raises were rapidly becoming a dead issue”, wrote Tim Noakes – a future opponent of Ekblom with his ”central governor” theory– in 1982. ”But now, unfortunately, the issue is again current because the most detailed and carefully-controlled study has confirmed that blood doping does, in fact, do exactly what Ekblom said it would”. (Noakes, 1982) The roots of the Los Angeles 1984 cycling blood doping scandal can also be traced to this Canadian research, because team physiologist Ed Burke got interested in the issue having read a 1983 article by Norman Gledhill published in The Physician and Sports Medicine where the hematologist explain his works with the shortcomings of the earlier research in a great detail. (Gleaves, 2015; Gledhill, 1983) On his part Melvin Williams had conducted two blood doping research papers and written regularly reviews on the issue of efficacy based on the available published research, concluding each time that the evidence wasn’t unambiguous and tilted towards the inefficacy. When he dealt the issue in the 1980 summer issue of Journal of Drug Issues, he came to the same conclusion. While he reviewed also the short summary of the Buick et al paper was published, he still concluded that “one may only speculate as to the validity of the results reported in abstract form”. (Williams, 1980) Williams had never questioned the validity of the data of the Swedes and West Germans, on the contrary, he was truly puzzled why the maximal oxygen uptake was elevated whereas the other research gave so inconclusive results. Now he came up with a possible theory relating to the testing protocol itself because the Swedes had used Vo2Max test as the same test where performance time was measured. Vo2Max test is an incremental test and his armchair speculation was that the subjects hadn’t reached their true potential Vo2Max in the first tests and when they ran for a long time after reinfusion, they also reached their real Vo2Max. “Thus, if subjects realized they were receiving an experimental treatment they may have been motivated to perform to a more exhaustive level, possibly increasing their Vo2max recordings”, he speculated. ”In some of the studies, increases in Vo2max were on the order of 300-400 ml, which might possibly be explained by the greater endurance time in these same studies. The question is, ”’Is the increased V02max the cause or the effect of the increased endurance time?’”. There was a noticeable gap between Melvin Williams sending his article to Journal of Drug issues and when it was published because by the summer of 1980 he had pretty much finished his third study on the subject and had changed his opinion about the inefficacy/efficacy issue almost 180 degrees. The issue had clearly been bothering him since the spring of 1972 when his student Jerry Bocrie had shown him a journal issue where the subject was discussed. After the two earlier inconclusive attempts, he had taken in 1979 his third take on the issue and wanted now to be absolutely certain that there would be as little ”possible criticisms” this time. The methodology he used was almost exactly the same as Buick and his coauthors had used from the number of subjects to the amount of blood reinfused (920 ml) to the storage technique and to the sham infusions. Williams had already two years earlier shown interest in testing the method in connection to a grand marathon, and this time he also didn’t measure Vo2Max figures at all, but instead used a simulated 5 mile-run on a treadmill, which would be a rare experiment attempting to measure the effect of elevated hemoglobin concentration on actual speed. (Williams et al, 1981) And unlike in his two earlier blood doping studies, something really noticeable took place this time. Only seven out of twelve athletes ran faster after saline infusion, whereas everyone but one improved after blood infusion. The mean improvement was statistically significant 2.5 %, almost exactly the same value that Ekblom predicted some ten years earlier that Anders Gärderud could improve his performance via blood doping. ”Blood doping appears to be an effective method to increase distance running performance, and its place in the sports world should be determined by the medical and rules governing bodies of athletic associations throughout the world”, Williams wrote in his ”update” review on the existing literature. (Williams, 1981) While time-trial type research on blood doping has been scarce, the improvement is roughly in the same range in the later handful of blood reinfusion studies and the improvement is significant, because it is the difference between the 1st and 35th at the 10000m world list for 1980. While famous exercise physiologist James Stray-Gundersen described later this Williams et al research paper the ”definitive study” (Stray-Gundersen, 1988) and Williams and his coauthors tried to avoid any ”possible criticisms”, the authors point out that ”several thoughts should be kept in mind”. The subjects were only good local runners and the results may not be applicable to elite level athletes. In addition, “results from laboratory test cannot always be generalized to an actual athletic competition where a number of other variables may influence performance”. Williams speculated to The New York Times that he planned to take his fourth take on the subjects. ”I’d like to set up a laboratory study in the field. It would be like looking at it during an actual run. Hopefully, we can plan something like this for next year”. (Amdur, 1980) Tapio Videman had been the coauthor of the first known study conducted outside the GIH to test whether blood doping worked in 1971 and didn’t find much benefit with the method. In 1977 he had sent the study to be published in a prestigious journal, but now in 1979, he coauthored a letter to the International Olympic Committee proposing blood doping testing in order to curtail its use. The history will always see Björn Ekblom as the eminent physiologist who came up with the ”blood doping” research line in the mid-1960s and conducting the major studies on the subject that opened the way for other researchers to follow his footsteps. Still, these mainly North American researchers such as Fred J. Buick, Norman Gledhill, Robert Robertson, and Melvin H. Williams have their place in the history, pushing the discussion forwards after it being in the intermediary limbo caused by all the conflicting literature. When the pertinent question of the 1970s was whether it worked at all, the focus shifted on what procedures constituted blood doping, should it be banned and what relative importance should be placed on its detection. I can propably say that I got the impression that the IOC changed its position because our research became more credible. The problem earlier was that Americans had much influence on the top people inside the organizations and we were considered just some “in Europe” who just did research on this and that. Even when it was the Anglo-Saxons who on some level convinced the sports governing bodies, Ekblom wants to emphasize that it was P-O Åstrand who did a lot of effort in making the GIH research known in the United States when he visited the country lecturing about blood doping, for instance in 1973 at the Berkeley University. *** Because this has been an essay on the intellectual origins of blood doping, we are slowly but surely approaching the end of this essay. The new decade gave also another interesting development. While there had been gossip about the use of the practice for roughly a decade and one Dutch cyclist had even admitted taking transfusions in the mid-1970’s after he had developed a persistent anemia after a crash where he lost a lot of blood, the early 1980s is usually considered the time when the first solid evidence of blood doping practice came into light. Peo Åstrand wasn’t convinced that the method had been used and he wasn’t alone. ”Blood doping – that is to say – that a sportsman before a competition fill himself with stored blood he has stored before in a ‘blood bank’ is more of theoretical than practical interest”, was the view of anti-doping activist Arne Ljungqvist in an interview in 1976. ”On one hand is the effect doubtful and on the other hand it needs a lot of resources, and one cannot meddle with blood doping as easily as pills in the locker room.” (Nordisk Medicin, 1976) While Finnish sports doctors hadn’t particularly denied in the 1970s that some anemic Finnish sportspeople had been treated with transfusions, they had claimed throughout the decade that the method was not beneficial for ”real” doping purposes. MD Pekka Peltokallio actually told in 1972 having heard of a ”few cases” of transfusion taking place emphasizing in 1975 that he knew with 100 % evidence of three cases – a wrestler, a cross-country skier, and a track & field athlete. ”I do not think anyone would dare to administer a transfusion to a top runner ahead of a major competition”, he emphasized. ”There are too many risks, the athlete may become feverish or yellow. Who takes such a risk?”. (Aromäki, 1975) While even The New York Times published in 1981 the news item about Finnish endurance runner Kaarlo Maaninka admitting having used the method at the 1980 Summer Olympics where he won two medals, more interesting confession had taken place a month earlier when the retired Finnish steeplechaser Mikko Ala-Leppilampi told publicly his story in the Finnish media. (Wessman, 1981) The athlete that had ended his career pretty much after he didn’t make it to the 1976 Olympic team not only revealed having used method as early as in 1972, but he also was under the impression that he was left out of the ”inner circle” of blood dopers a year earlier when he was 5th at the European championships in 3000m steeplechase. He was heavily under the impression that at least some Finnish athletes had benefitted from the method a year earlier and that the method was widely used by the Finnish runners mentioning even Juha Väätäinen and Lasse Viren by name and emphasizing that a non-blood doped Finnish runner was actually an exception – not the other way around. Finnish MDs had maintained that the operations couldn’t have been carried out because there were no freezing technologies and there was then and is today debate about how applicable autotransfusions with refrigerated blood are from doping viewpoint. “In fact, blood-boosting is out if the question in Finland”, had sports MD Pekka Peltokallio and a friend of Lasse Viren claimed shortly after the 1976 Olympics. ”We haven’t got the special facilities for properly preserving the blood. The nearest facilities are in Stockholm and in Holland”. (Raevuori & Haikkola, 1978) Ala-Leppilampi revealed one answer to this mystery – almost all the transfusions used by the Finnish athletes were from the abundant supplies of the Red Cross blood bank. He still mentioned almost in passing that autotransfusion had been used, but in order to avoid the anemia recovery problem, the blood was stored after high altitude training when hemoglobin concentration was high in order to make the relative anemia less severe. His own initiation came in 1972 on the eve of the summer Olympics, when the Finnish Olympic team gathered for a dinner in a conference center in Finland. Dr. Pekka Peltokallio – the accredited team doctor – discussed with the athletes one-by-one, and when it came Ala-Leppilampi’s turn, the doctor asked whether he’d be interested in taking advantage of ”medical aids”. ”OK, let’s use transfusion”, the runner replied. Peltokallio wasn’t that talkative about the topic, but he admitted that the 1972 incident took place even when he denied that other Finns had taken advantage of the method. ”I don’t feel obliged to tell where and how the operation was conducted”, he stressed. (Forss, 1981) Regardless of the alleged benefits, he wasn’t that convinced about its efficacy and referred to the study with cross-country skiers showing no benefits. “For most people, the method is of no use, even when it is beneficial for anemic people”. (Tulusto, 1982) When Björn Ekblom commented on the issue in Swedish media, he revealed that he happened to know about the case of Ala-Leppilampi already beforehand not wanting to reveal what he knew about the other Finnish runners. Steeplechaser Anders Gärderud who had told having some interest in the method a decade earlier denied having never used it, but still clearly didn’t find the issue worth all the media fuss. ”This is in no way prohibited?”, speculated Gärderud the ethical implications of the confession of Ala-Leppilampi. ”Unesthetic? Well, we need to make a clear difference between the risk-free fitness and the sport, at which level we are. This is bloody serious and everyone uses the methods that they have faith in”. (Byström & Loren, 1981)* *Viren has always denied blood doping and no solid evidence has emerged about his having used the method even when the claim is today almost ”common knowledge” and some of his comments were equivocal. Of the GIH-researchers, Peo AÅãstrand told having followed the issue closely but hadn’t heard of the method been applied. ”Therefore I don’t believe that Lasse Viren or any other international star would’ve taken the change or risks”, AÅãstrand stated. (Lehman, 1981) Ekblom wrote also diplomatically in 1982 that ”by looking at [Viren’s] performance and his training background, it has been suggested that his results can be explained by other means”.(Ekblom, 1982) Ekblom’s colleague Kenneth Lundmark of the GIH has since stated that the Finnish runners were the ”most known examples” of blood dopers and stated that Viren more-or-less confessed having blood doped. (Stenberg, 2000) If it isn’t known how prevalent world doping was, the practice spread when denying its efficacy became an untenable position, and Kaarlo Maaninka wasn’t the only blood doper of the 1980 games, because some Italian athletes had also used the method and Soviet runner Aleksandras Antipovas admitted some ten years later having blood doped in 1980. Melvin H. Williams on his part told The New York Times in 1982 that he was approached regularly by athletes and coaches who would like information and assistance to use the method. ”All I predict is that with the 1984 Olympics getting closer and closer, more athletes will try to use it”, he correctly speculated (Rogers, 1982). Williams also recalled three decades later that one group of the 1984 blood dopers were interested in the technical details: In the early 1980’s I was at a sports medicine conference in Colorado, and gave a presentation on blood doping. Some advisors to the American Olympic team questioned me in detail about the procedure and its effects. When discussing the case of Mikko Ala-Leppilampi in media, Ekblom stressed that the method was banned under the IOC’s general clause even when it wasn’t specifically listed as a banned method by the rules. There was a new line of discussion whether the method should be banned or not and even whether it already was banned or not now that it was shown definitely that it worked. The issue was a complex one with various opinions and even definitions, for instance on what constituted a ”doped” hemoglobin value or whether it was fair that rich countries could have enough resources to send their athletes to altitude training whereas poor countries didn’t. But that is another story for another day altogether. This is part four of a multi-part series titled “Limiting Factors – A Genesis of Blood Doping”. The full bibliography for this research can be found at the end of Limiting Factors – A Genesis of Blood Doping (part one). This is part three of a multi-part series titled “Limiting Factors – A Genesis of Blood Doping”. It comes to FasterSkier from Sammy Izdatyev. You can read part one here, and part two here. Sammy Izdatyev is the pen name of a Finnish sports enthusiast and unaffiliated amateur historian, who has been interested in endurance sports since the turn of the millennium. He hopes that his pro bono – research can provide more information into the body of literature of earlier underresearched areas of the history of sports. Part IV: “The Breakthrough” (1969-) The functional importance of the heart in the performance context was illustrated as early as 1897 when famous Swedish doctor Salomon Henschen estimated in one canonical study the heart sizes of ski racers before races using rather primitive techniques. When he compared the findings to the race results, they correlated strikingly well. Henschen thus concluded that “skiing causes an enlargement of the heart and that this enlarged heart can perform more work than the normal heart. There is, therefore, a physiological enlargement of the heart due to athletic activity: the athlete’s heart.” (Astrand, 1991) Henschen had only speculated about athletes’ hearts being affected by training, but more than three decades later in the 1930s, it was observed that regular training lowered heart rate at a fixed work rate. That indicated that the amount of blood pumped and oxygen delivered with each heartbeat was larger, and correspondingly, a lower heart rate could keep the oxygen demand sufficient. And the implication was that there were extra reserves to be utilized when heart put ”all-in” when compared to the pre-trained level. (Saltin & Strange, 1992) The México Olympics went well compared to the preceding panic about the possible health hazards and when endurance running events were dominated by African runners, one of the triumphant endurance athletes was cyclist Gösta Pettersson, who had been tested by Ekblom and his Norwegian co-author Lars Hermansen at the GIH. Whereas maximal oxygen uptake tests had been conducted on elite-level athletes, their cardiovascular system had remained a mystery until researchers began investigating the magnitude of how these athletes’ hearts adapted to training. The results were surprising. (Ekblom & Hermansen, 1968) The first discovery was that the athletes’ hemoglobin concentrations were borderline anemic compared to “normal” clinical reference values. Gösta Pettersson’s hemoglobin concentration was only 13.4 g/dl, and one male orienteer had an even lower number, 12.8 g/dl, which equaled hematocrit values around 40 percent and 38 percent, respectively. The strangest part was that their maximal oxygen uptakes were still very high and this was explained by the enormous amount of blood their heart pumped every minute. The highest figures Ekblom and Hermansen measured were so high that they re-tested the athlete to make sure they hadn’t made an error. The figures came back the same, but the highest cardiac-output figure was still too high to be believed by Ekblom’s colleagues. “They thought it was wrong, that we had measured it wrong in some way,” he reflected. “It was impossible for the heart to beat three times a second and put out some 200 to 220 milliliters per stroke.” The research emphasized the importance of cardiovascular adaptation and tilted heavily to the validity of the “central” theory. When one Swedish journalist visited the GIH in 1969 to write about the laboratory, Ekblom mentioned the low hemoglobin concentration as an interesting phenomenon. The journalist speculated that it might be explained by iron deficiency, but Ekblom had a different opinion. “Even though the values are clearly lower than usual for healthy people in their 20’s, I do not think these athletes suffer from iron deficiency,” he said, explaining that lower hemoglobin concentrations can be considered a normal adaptation mechanism of the well-trained body rather than anemia. (Olson, 1969) In the midst of the blood-reinfusion studies, Ekblom obtained data that the human body aims to dilute the blood and that some well-trained athletes can have borderline anemic hemoglobin concentrations. He didn’t consider this any “real” form of anemia, but rather a natural and possibly a beneficial reaction to regular training. Ekblom still considered the theory behind the blood doping to be sound since earlier research had given some positive results. One item from unpublished blood-doping research found its way into this paper, as Ekblom and Hermansen noted former’s “unpublished observations” on cardiac output being elevated after blood donation, when the amount of blood was recovered but diluted. That is to say, the heart partially compensates for the loss of blood-oxygen carrying capacity by increasing blood flow above a normal level. The observations were made during one inconclusive blood-doping experiment. Nothing had yet been published about blood doping, and if a sharp-eyed reader of theJournal of Applied Physiologywondered why Ekblom had removed the blood of his subjects, he or she would find the answer a few years later from pages of the same peer-reviewed journal. A new attempt After a few dead-end blood doping attempts with inconclusive results, in 1970, Ekblom took another attempt on the subject in 1970 coauthoring another paper on the subject with Dr. Alberto N. Goldbarg, who was an MD and on leave from the Department of Medicine (cardiology) of the University of Chicago. (Ekblom et al, 1972a) While most people today, doping specialists included, are unaware of the preceding attempts to test the blood-doping hypothesis from the 1960s, there is a great deal of data available about this study since the detailed report was published in a prestigious journal. Blood infusion was now tested with two experimental groups, with significantly higher amounts of blood than was earlier used. Group I donated 800 milliliters blood that was reinfused 28 days later, whereas Group II donated 400 milliliters of blood three times at four-day intervals, totaling 1200 milliliters, and had the blood reinfused 32 days after the first donation. Ekblom said there hadn’t been a complex thought process regarding the storage period and amount reinfused, and by chance, they ended up with this protocol. Various blood and endurance parameters were monitored during the research. The key endurance test was the time to exhaustion, requiring the subjects to run as long as they could, and maximal oxygen uptake was also measured. As expected, both maximal oxygen uptake and maximal working time both fell significantly after blood donation. Hemoglobin concentration decreased by about 13 percent in Group I and 18 percent in Group II, and their treadmill-running endurance also collectively decreased by a third. Bone marrow quickly began increasing red-blood-cell production, and when the blood stored at 4 degrees Celsius was infused four weeks later, there was an “overnight” improvement both in endurance time and in VO2max in the Group I. The authors noted the participants’ sudden 9 percent increase in VO2max and ability to run 23 percent longer on a treadmill. This is the blood-doping effect that shocked the world. Actual day-to-day competition remained vastly different than time-to-exhaustion while running, and it should be emphasized that the 23 percent improvement in the maximal working time in that treadmill test describes how much longer an athlete could run at given speed, rather than how much their speed could be increased at a given distance. The improvement in speed wouldn’t be of the same magnitude, and Ekblom himself told the Swedish media that steeplechaser Anders Gärderud could theoretically improve his 3000-meter steeplechase record by 10 seconds, and because his personal best (and the Swedish national record) at that time was 8:28.4, the “real” improvement in direct speed would be “only” 2 percent. Even when 2-percent improvement in speed, as well as improvement in VO2max figures, sound tolerable, they would have a serious impact on performance for reasons Ekblom would describe a decade later. “Firstly, it should be borne in mind that in sport the difference in performance between first and last, in a top-level event, may be only measurable in parts of a percent, which means that even very small changes in the different factors contributoryto physical performance may be of vital importance,” Ekblom wrote in 1982 when putting the performance improvements in “real” context. “Secondly, increasing gross maximal aerobic power by 5 percent in an already well-trained athlete may be almost impossible, at least over a year or so.” (Ekblom, 1982) One can deduct that researchers thought there would be other studies to follow and thus didn’t keep overly detailed data on the aforementioned study. There was also a chance the results wouldn’t be published at all. Even when one of the assumptions was to research the effect of elevating hemoglobin concentration on the other links, cardiac output wasn’t measured even when Ekblom was familiar with the procedure, having studied the cardiac systems of athletes a few years earlier with the Norwegian exercise physiologist Lars Hermansen. Yet at the time, Ekblom and Goldbarg were involved in other research projects regarding other links of the oxygen transport chain and in any case, their research lab resources were finite.* Later, Ekblom went on to republish the data and figures on the 800 ml group, but the authors seemed unconvinced about the improvements in the 3×400 ml group, even when the improvement in the working time was similar. This led to a situation where there were only three subjects in the “main group”, which led to some anomalies. Goldbarg and Ekblom were surprised that maximal oxygen uptake had returned to the original level in 14 days, while hemoglobin concentration had barely risen from low “anemic” values and maximal work time was below the original level and hadn’t fully recovered even after 27 days just before the reinfusion. They had no explanation. Another interesting observation was that submaximal heart rate wasn’t lower after blood reinfusion, even when oxygen flow should have been sufficient at lower blood flow, i.e., lower heart rate. There had also been no increase in VO2max in “Group 2”, where the reinfused amount was 3×400 ml of blood, even when total hemoglobin had been increased by some 10 percent. While the researchers concluded that the results were generally similar among the groups, that incremental protocol was rarely used again in testing. Additionally, when Ekblom described the research in detail in an article he wrote for the Swedish sports journal Svensk Idrottin 1972, he didn’t bother to mention the incremental group but focused solely on the 800 ml group and all the three subjects of this group also recalled their ”blood doping” research experiments later in various media outlets. While now there was a blood reinfusion study with improvement, the study was heavily prone to criticism for a variety of reasons and not alone for the reason that there were very only a handful of subjects. The most pertinent problem was that there was no ”real” control group because all the changes in the data were compared to earlier baseline values of the same people, which would lead to two types of future criticism. The first criticism was the placebo effect, when the participants might have known what the research was about and known not giving full effort after blood donation and perhaps an extra boost when they knew about the benefits of the extra red blood cells. It has also been suggested that some training effect might have taken place, as the subjects gave their maximal effort on a treadmill on several occasions and their regular training protocol wasn’t monitored. Correspondingly it was possible that some changes in VO2max could have been explained simply by natural training adaptation and not in the change of hemoglobin concentration or total hemoglobin. Another criticism was how well the results could be extrapolated to elite-level athletes, an item that Ekblom recalled the media being more interested in than the scientific community: You just take out some blood and give it back thirty days later that gives performance enhancement going from the last place in the race to the first. That has an enormous sport effect. That’s why the reinfusion of blood became so interesting in the media. That was not that much discussed in the scientific world as in the media. The effect of sports performance was, of course, something that the journalists found very interesting. While the subjects of Ekblom and Goldbarg were fit medical students with relative VO2max figures ranging from 54.9 to 71.4 ml/kg/min, there was always doubt whether the method would work on international-level athletes who were following rigorous professional type training programs and had reached the natural limits of their VO2max. It might’ve also been that the actual ”limitation” in the oxygen delivery chain might be different than that of even national-level athletes. While both Ekblom and Åstrand voiced concerns about the doping aspect publicly in the 1970s, considering it very likely that the method would also benefit elite-level athletes, they didn’t specifically touch the issue in their papers. “Research surrounded by secrecy” In September 1971, some Swedish newspapers got tipped off about the ongoing research and contacted Ekblom and Åstrand for comments. (Carlsson, 1971a) Åstrand declined to comment, and Ekblom wasn’t that talkative and told the media that “it will be just a lot of sensational writing” because “it is a matter of medical expertise that really understands what we do” and therefore there was “nothing for sports journalist”. That prompted a sports journalist from Aftonbladetto write that their research was “surrounded by a lot of secrecy”. That journalist knew also that there were two attempts, of which only one gave clear benefits and the other was more inconclusive. He also knew that there were two physiologists involved, but his assumption that Ekblom’s coauthor was Åstrand indicated that he wasn’t that fully aware of the details. Goldbarg wasn’t mentioned in the news despite being the coauthor of perhaps the most significant blood-doping research paper, which confirmed that the research wasn’t Swedish “inside business”. In fact, foreigners coauthored even unpublished research. To this day, Ekblom refutes the secrecy claim as he discussed some items in his lectures, even when the material wasn’t published anywhere: A lot of people knew about it. There were roughly 25 students in two parallels each year, so fifty per year, if the were on the lectures, of course. We have had so many subjects also, they knew the effect. In the late 1968 or 1969, I had lectures at the GIH for the students and I presented them some of the results before we had published anything in the publication.* *A Swedish correspondent of Track and Field News also easily found a Swedish student who was familiar with the research and knew it in detail and gave some comments on the subject matter. (Track and Field News, 1971) While the researchers didn’t comment on the subject publicly while the research was ongoing, it wasn’t necessarily a secret considering the first attempt was revealed at the 1966 meeting of the Scandinavian Physiological Society in with a brief mention in its journal Acta Physiologica Scandinavica. Additionally, the prestigious peer-reviewed Journal of Applied Physiologyhad accepted the manuscript for publication two months earlier, therefore the “secrecy” would have been unsealed relatively quickly, in some 10 to 11 months. Ekblom nevertheless gave a more detailed account to journalist Omar Magnergård of the large newspaper Svenska Dagbladet, whom he was in friendly terms with, and the resulting article was a deep look into the subject headlined: “perfect doping”. Ekblom described the key technical details of the research, such as the time between blood removal and reinfusion, the amount of blood reinfused, as well as the performance enhancement. He also stated that the test subjects were GIH student-athletes, including some football and basketball players and even one of Ekblom’s orienteering teammates. (Magnergård, 1971) Magnergård observed that there had been no control group, but it didn’t automatically invalidate the results, far from it. “Critical voices can disagree, that psychological or other factors have been played and partly caused the increase. Björn Ekblom agrees with this reasoning.”, noticed the journalist correctly one possible criticism of the findings. “However, no such a thing can affect the oxygen uptake capacity. And it increased by nine percent!”. (Magnergård, 1971) Additionally, Ekblom emphasized that the participants didn’t know the goal of the research, only that they would run on a treadmill and have blood removed and reinfused, a view confirmed by one of the participants some 40 years later. ”It was very secretive,” Bengt Fredenlund – a national-level basketball player and one of the seven participants (all of which were GIH students) – also recalled. ”We didn’t know what we said yes to.” (Hansson, 2009) One should also keep in mind that in 1970 there was no term blood doping and nobody knew how it would affect performance. It means also that it isn’t certain that the placebo effect existed that much when the subjects didn’t read too much into its known benefits, because there existed no known benefits, no literature, no sensational headlines, no succesful blood dopers to refer to. While Ekblom and the journalists were concerned that the practice would spread into sports, Ekblom was also interested in whether the method could be used to treat other medical conditions in more ordinary health care. He wasn’t able to determine that, but said he felt he contributed a “small piece” to the puzzle of understanding the premises that have significance on the mechanisms of the human body. Still, the sports issue troubled Ekblom very much, and he expressed that it would be undetectable. “To detect this type of doping is almost impossible,” he wrote in 1972 in an article titled, “Does blood doping become a sports problem?”. “Theoretically there would exist some possibilities for this, but it is not realistic in practical terms.” (Ekblom, 1972) He also states in the same article that blood doping would without doubt fit the definition of doping. Worldwide interest Blood doping was reported worldwide in various media outlets and some sports journals, such as Track & Field News, became interested in the topic and inquired the opinions of specialists on the subject matter. (Track and Field News, 1971) Dr. Ernst Jokl of the University of Kentucky had five years earlier told about South African runners who resided at the altitudes of Cape Town to gain more red blood cells with benefits. ”There has accumulated a great deal of evidence to show that considerable advantage results from living and training at an altitude of 6,000 feet, and if they wish to set new records, they go back to sea level to compete”, Jokl described the benefits of this technique in one Mexico-related international symposium in 1966. (Bynum, 1967) Against this background, Jokl was surprisingly not convinced about blood doping hypothesis. ”It is probably worthless but it may be appropriate to inquire from Prof. P.O. Astrand what all the noise is about”, Jokl told the T&F News correspondent.* *Historian John Gleaves writes in his essay about the cycling blood doping scandal of the 1984 summer olympics that this article ”brought the scientific debate over the benefits of blood transfusions to a North American audience of athlete and coaches interested in improving running performances” (Gleaves, 2015). Ekblom’s view was that the issue became ”of worldwide interest” only some five years later after the 1976 Summer Olympics (Ekblom 1982). Gleaves doesn’t find that much blood doping-related media material preceding the 1976. Not all were as dismissive as Jokl was. “The Swedes are perhaps the most advanced nation in the study of exercise physiology,” commented Olympic running coach Jack Daniels, who studied in Sweden and knew the GIH researchers. “If Ekblom actually did the work, I have no reason to doubt the results – if reported correctly.” Ekblom clarified his research to Daniels in a letter quoted by T&F News, clarifying the purpose of the research pointing out that the goal ”was not to find a perfect way of doping athletes but to study the different parameters that will influence the oxygen transport system chain and general physical performance” even when ”the study has become of greatest interest to coaches and trainers all over the world”. While some sports people contacted him, Ekblom recalls that there were surprisingly few exercise physiologists who contacted him directly and more (but not much) interest came from people who wanted to take advantage of his method: One of the first questions I had was that if this type of manipulation could be done on race horses and dogs, which is strange that it was not the sport people that called. Ekblom revealed to the American journal that he was offered 100,000 Swedish Krona ($20,000 U.S. dollars) for the exact method, an offer he refused. One journalist later claimed that this offer was made by a professional cycling team in order to help them with the procedure. (Byström, 1981) ”That is right and as a poor father of two children it would’ve been tempting, but I understood the consequences – I would’ve lost my credibility in the future”, Ekblom recalls today. While the few opinions about the validity of Ekblom’s research were diverging within the community of exercise physiologists, still one specialist of his own arena thought he knew better: There was a professor of cardiology who said: ‘You must have made something wrong; this is not possible. The viscosity will increase and you will have reduced circulatory performance during heavy exercise’. That sentence would set the tone of the discussion for the next decade to come. *** Meanwhile, research on manipulation of the other links continued, and two additional studies coauthored by Ekblom were published in 1972. One dealt with “blocking” a portion of hemoglobin by inhaling carbon monoxide, which had higher affinity to hemoglobin than oxygen. Unsurprisingly VO2max and performance fell significantly when a large amount of RBCs were rendered unusable. Another interesting venue was limiting maximal heart rate by administering two beta blocker – substances: atropine and propranolol to hinder heart function and to keep hear rate artificially low. When the body couldn’t increase oxygen flow to muscles by increasing heart rate even when muscles had a high demand for oxygen, there were two compensatory mechanisms. The body increased the stroke volume above earlier presumed “maximal” levels and it also increased the relative amount of oxygen used by the muscles. Correspondingly, maximal oxygen uptake was lowered by just 6 percent, which was statistically negligible. One could deduct that this showed the body’s enormous capabilities when it adapted if one link was manipulated down. Another plausible scenario was that central circulation wasn’t the key limiting factor or at least not the end of the story about what limits Vo2Max. Part V: “Too simple trick” The media interest in the autumn of 1971 triggered more than just public discussion and ranging opinions. Some interested parties attempted to replicate the findings before they were published in full detail in August 1972, using bits and pieces of what they could extract from news reports.At least two attempts took place before the study was published. The first published attempt took place in late autumn of 1971, a few months before the 1972 Sapporo Winter Olympics, when a doctor with the Finnish Ski Federation and future member of the International Ski Federation (FIS) Medical Committee, Tapio Videman, and his colleague Tapio Rytömaa tried to determine whether blood doping enhanced performance by testing reinfusion on 10 recreational-level cross-country skiers (Videman was one of them) taking out between 400 and 600 millilitres of blood and reinfusing it back 14-21 days later. The only performance-related item measured was submaximal heart rate, and while Videman and Rytömaa observed some benefits in performance after reinfusion (slightly lower submaximal heart rate), the enhancement wasn’t statistically significant and could have been explained by training effect. (Videman & Rytömaa, 1977) In light of the later revelations about the blood-doping use in the ’70s, it is interesting that this finding was reported to the Finnish Olympic Committee and some MDs later recalled having participated in a meeting where blood doping was discussed and shown to have been ineffective. The Videman-Rytömaa research paper was published only in 1977, over six years after the research.* *After blood doping was debated in the Finnish television in November 1972 –, shortly after the ’72 Olympic games – and concerned doctors claimed that the use was rampant, this study was mentioned in passing when the officials denied the efficacy of the method. ”Recently a known blood specialist Tapio RytoÅNmaa gave a statement in a meeting of sports MDs and coaches telling that transfusion has no benefit for a normal person or an athlete”, the training chief of the Finnish Olympic Committee told in one interview. ”Why on earth would transfusions be used in sports, if they are of no benefit whatsoever?” (Vaasa, 1972) Only a few months later, exercise-physiology student Jerald Bocrie at Old Dominion University in Virginia showed professor Melvin H. Williams the Track & Field Newsarticle about the blood-doping research. Williams was heavily interested in physiology being the head coach of the cross-country team of the university and Bocrie was the assistant coach. He also deeply respected the Swedes and felt their reinfusion-hypothesis was intuitively logical knowing also that the GIH had a good reputation, considering Åstrand coauthored the famous Textbook of Work Physiologywith Kaare Rodahl: Sweden was the place to study, and many of the top exercise physiologists in the United States did so. I admired Dr. Åstrand, and used his textbook to teach my graduate exercise physiology class. I met him at several American College of Sports Medicine meetings over the years. He was the pioneer of exercise physiology. I would have liked to have studied in Sweden after my doctorate, but was not aware of their program at the time.* *Some remarks made by Melvin H. Williams (1938-2016) with no reference are based on our email-correspondence that took place in 2014. Williams and the student decided to conduct a study to find out whether the theory worked by using runners from a local club as their subjects teaming up with two other researchers to solve the mystery of blood doping. They placed the runners into four groups, where each component of blood was tested in isolation. Knowing that exercise increased the amount of plasma, Williams and the studentwere interested in how exercise would be affected when only plasma was infused, without the red blood cells. (Williams et al, 1973) They measured submaximal heart rates and time to exhaustion and observed minor but mostly inconsistent declines in heart rates in every group, an effect that was most evident in the “whole blood” group. Still, their statistical analysis revealed no differences between the four groups, and correspondingly, Williams and his coauthors concluded that with the limitations of the study, blood doping didn’t work. Thus the first two published attempts taking place outside Sweden to test the underlying theory behind the Swedish researchers’ blood-doping hypothesis failed. Ekblom continued to focus mostly on his own work and avoided confrontation in dealing with skepticism. Still a decade later he wrote that “some very serious mistakes occurred in these studies”, (Ekblom, 1982) and if he had seen the test protocols beforehand, he likely would have predicted the outcome since he had firsthand information about similar mistakes made a few years earlier. “We had done exactly the same mistakes in our own pilot studies in the late 1960s”, he thinks about the obvious similarities. In addition to using only half the amount of blood and reinfusing it back in only 21 days, a week earlier than Ekblom and Goldbarg had, one of the mistakes was that the authors of the Williams et al study didn’t gather any hematological data, so in hindsight it isn’t certain that there was an increase in hemoglobin concentration at all. Still, Williams and his co-authors appear to have been sincere and honestly confused and surprised about the findings spending a full third of the research paper on various possible reasons to explain why the method didn’t work. They notice a similarity between high altitude studies with inconclusive results. ”These findings may be analogous to studies which have shown that polycythemia associated with training at altitude exerts no beneficial effect on maximal oxygen uptake or performance on subsequent return to sea level”. The Finnish findings can also be explained by the same problem because the amount of blood reinfused in the Finnish research was only 400-600 milliliters – only half of what Ekblom and Goldbard had used – and the research paper is strikingly similar with the earliest inconclusive tests. The authors didn’t find significant performance enhancement even when they concluded correctly that the ”prerequisite for a possible benefit from autotransfusion is that hemoglobin level and [hematocrit] recover sufficiently within 2 to 3 weeks”. Their study didn’t meet this condition and the volunteers were clearly anemic when the reinfusion took place, hematocrit being almost the same before blood removal (42.2 %) and after reinfusion (43.3 %). Melvin Williams met Åstrand in many conferences and Tapio Videman visited the GIH at least once (in March 1973) with the best Finnish cross-country skiers, when the 6”5 skier Juha Mieto broke the absolute Vo2Max world record with gigantic his oxygen engine of 7.40 l/min when he was tested by Bengt Saltin. Unfortunately, Ekblom can’t recall what types of discussions took place about the subject-of-the day. “Whether Melvin – whom I knew well – or Videman discussed the matter with us when they visited the GIH, I don’t remember, but it is likely that we did, particularly when it was P-O Åstrand who initiated visits and discussions on various subjects”, Ekblom recalls. While the published blood doping research was scarce in number in the years following immediately the 1972 study, Ekblom believes that people started to make their own ”underground” experiments with blood reinfusion almost right after his study was published. As one interesting anecdote, Björn Ekblom recalls how a member of the Soviet embassy in Sweden contacted his lab and wanted to see the testing premises and discuss the matter. Afterward,d it didn’t seem so good idea even when he told him everything that he had told everybody else interested in the matter. After the fall of the Soviet Union, it was revealed that blood reinfusion research started in the country in the mid-1970s. (Kalinski, 2003) In any case, the research was available for everyone interested and who bothered to visit the nearest university library to pick up a copy of the journal and read it for themselves.* *Track and Field News affiliate quarterly journal Track Technique also published a detailed account of the 1972 study in 1973 titled ”Blood Boosting: Its effects on Exercise”. (Track Technique, 1973) Fundamental vs. practical research If many of the so-called ”real” physiologists and medical doctors had looked down on exercise physiologists and the research undertaken at the GIH because they didn’t do ”real” worthwhile science, the opposition that came from within sport circles was of an almost totally different type of nature. When the cooperation between the Swedish Ski Federation and GIH started in the mid-1950’s, some skiers felt that they didn’t want to be subjected to ”scientific” training. Two Swedish historians wrote that ”many of the skiers were hesitant or even hostile to this scientific turn. They felt that their own expertise was undermined, that they were reduced to guinea pigs in the lab and that they did not get sufficient explanation of the test procedures, results and how to use them in their own training”. (Svensson & Sörlin, 2018) Björn Ekblom also noticed two decades later that the attitude of coaches wasn’t that better when with Per-Olof Åstrand he explained the research conducted at the GIH to one journalist who was visiting the institute. “There does exist an aversion of many sports bosses and coaches to physiologists. We are often accused of being only theorist. Therefore, I think it’s good that we have this contact with the actual sport. In addition, what we are dealing with here at the institution is in large part applicable directly to sports”, he explained. (Almgren, 1970) The key area of improvement would be individual training programs and Ekblom considered the ”one-size-fits-all” training papers worthless and while a football enthusiast and a coach himself, he even preferred individual exercise to a large extent as time-saving when compared to group training that took up to three hours at a time. Perhaps a clear majority of the research conducted at the GIH was still the so-called fundamental type of research which was barely comprehensible for sport enthusiasts even with above average knowledge on physiology in which the connection between research and application was everything but obvious. While blood doping was in its core fundamental type of research, it still was in the gray area of research, because the blood doping research was quickly dubbed simply ”GIH-method” when everyone understood right away that implications of the knowledge it provided and wondered how much this ”in large part applicable” blood doping know-how had been offered to the Swedish athletes. And how come the Journal of Applied Physiology that published the research has the name ”applied” in its name?* *Finnish steeplechaser Jouko Kuha most likely wasn’t alone with his reading of the implications of the study with his 1971 remarks. ”The information from Sweden was so unbelievable thing that it made me laugh even a long time after I’d read it”, the earlier world record holder commented. ”If it was true that results would be bettered that much, you wouldn’t tell it publicly but you would take advantage of the method in secret”. (Raevuori, 1971) An R&D research center of blood dopers? In 1971, the Belgian cycling superstar Eddy Merckx was at the height of his career but skipped that year’s edition of the Tour of Italy. The Tour was subsequently won by Gösta Pettersson, who had been tested by Björn Ekblom and a participant of his study from the late 1960s that measured cardiac outputs. The physiologist commented on Pettersson’s physiology in the media when the cyclist had managed to become one of the few Swedes to compete at the international elite level in cycling. Pettersson complained regularly in 1970-1971 about his anemia and was infused with sugar solution and iron shots by the Italian team doctor of his Ferretti team, even when Ekblom hadn’t been that worried about the low hemoglobin concentrations as such of athletes with superior hearts. One can only speculate what kind of thought went through the minds of his competitors when the existence of blood doping was revealed only a few months after his Tour of Italy win, but we do know that some French cyclists did ask Ekblom for assistance with the blood doping process and Pettersson’s main rival Eddy Merckx has later revealed that the Belgian was offered a possibility to use transfusion when the attempted to break the hour record in 1972. What we do know is that later triumphant athletes from the Nordic countries wouldn’t be so lucky and the first ”real” target of blood doping accusations was found only shortly thereafter. Only shortly after blood doping became known as a method in fall of 1971, it was reported that 23-year old cross-country Sven-Åke Lundbäck recorded the highest relative oxygen uptake ever at the GIH laboratory, 87 ml/kg/min. Lundbäck would be triumphant at the Sapporo Winter Olympics only months later by winning a gold medal in the 15-kilometer race by a 32-second margin, one of the largest in the history of Olympics and never surpassed since. Björn Ekblom commented about Lundbäck in various media outlets and the collaboration between the two was widely known and referred to in daily newspapers. Blood doping was also known as a method, and unsurprisingly a Swiss team doctor Hans Howald and the Norwegian team doctor Kjell Öystein Rökke recalled only a few years after the games that there were rumors about participants from the Nordic countries having taken advantage of transfusions (Howald, 1975; Dagbladet, 1978). The allegations remained still mostly unpublished until a Finnish biographer of endurance runner Lasse Viren claimed years later that many Finnish skiers were convinced that Lundbäck had indeed blood doped, complaining to their Finnish MDs and coaches that they wanted also access to the same arsenal of methods that the Swedes had. (Saari, 1979)* *Dagens Nyheter journalist Bobby BystroÅNm questioned the claim about LundbaÅNck on the grounds there was no reason for LundbaÅNck not to triumph in the preceding major competitions (1974, 1976) if blood doping was a ”guaranteed way to medals” (BystroÅNm, 1980). The Finnish biographer of Viren also don’t believe in the LundbaÅNck-gossip in the actual book but considered that ”miracle method that everyone else certainly used” was only an easy way to explain one’s own bad success. The discussion was very heated also in Sweden and already in 1971 steeplechaser Anders Gärderud mentioned in passing being interested in testing the method when the issue was the first time a news item. (Carlsson, 1971b) At the same time one journalist recalled hearing rumours that Swedish athletes had taken blood transfusion for the Mexico pre -Olympics (Olofsson, 1971) and a year later wrestler Pelle Svensson (world champion) named in his provocative book Öppet Brev Till Sveriges Idrottspampar in 1972 one Swedish swimmer by name as a ”guinea pig” of blood reinfusion experiments. (Svensson, 1973) Some media outlets claimed that the alleged physiologist of the latter experiment was none-other-than Bengt Saltin, and interestingly Svensson had been a participant of the Saltin’s 1965 high-altitude expedition (with some ten other athletes, among them cyclist Gösta ”Fåglum” Pettersson and steeplechaser Anders Gärderud) where Saltin had made some remarks about the use of blood transfusion as one option, so the people involved could’ve heard at least some speculation about the method. The allegations were denied and after the issue had been debated in Swedish national television in 1973, Per-Olof Åstrand wrote even an open letter denying the allegations and specifically mentioned that the claim about Saltin was totally untrue, (Aslund, 1973) and the swimmer also denied later the claim. ”I never have doped, I trained hard”, he commented over two decades later the matter. (Bergfeldt, 1995). Pentathlete Björn Ferm – a participant of the pre-Olympics – also denied having ever heard that transfusions had taken place in Mexico, and Ekblom from his part denied that the method had been used at the 1968Olympicss. ”Overall the whole thing has been overblown”, he also commented how media got the research totally wrong. ”Some folks have deliberately misunderstood and distorted this topic. The method hasn’t been invented in order for athletes to enhance their performance”. (Olofsson, 1971) Nevertheless, if the Swedes had a secret weapon, they had been unsurprisingly unsuccessful at the endurance events at the 1972 Summer Olympics. The development had been totally different in Finland, where there was a triumph after triumph that had started in 1968 when endurance runner Jouko Kuha broke the 3000m steeplechase world record after three mediocre decades. The success continued and three years later in 1971, Juha Väätäinen won both the 5000m and 10000m events at the European Championships in August 1971 and the success at the 1972 Summer Olympics was unbelievable with four medals – Lasse Viren (two golds), Pekka Vasala (gold) and Tapio Kantanen (bronze). When blood doping was mentioned as a research topic in September 1971 – only a month after the triumph of Väätäinen – Risto Taimi, the editor-in-chief of the largest Finnish sports journal Suomen Urheilulehti, wasn’t that certain that Ekblom had invented something totally new. ”This published research most likely isn’t a novelty inside the sports medicine circles of the world even when people haven’t kept that much noise about the topic”, he wrote, adding also that ”one can find clear evidence about the beneficial effects of this type of treatment, also from Finland”. (Taimi, 1971) When blood doping was mentioned as a research topic in September 1971 – only a month after the triumph of VaÅNaÅNtaÅNinen – Risto Taimi, the editor-in-chief of the largest Finnish sports journal Suomen Urheilulehti, wasn’t that certain that Ekblom had invented something totally new. ”This published research most likely isn’t a novelty inside the sports medicine circles of the world even when people haven’t kept that much noise about the topic”, he wrote, adding also that ”one can find clear evidence about the beneficial effects of this type of treatment, also from Finland”. (Taimi, 1971) When the editor-in-chief was asked about details by well-known journalist Antero Raevuori, he revealed that a competitor of Jouko Kuha had revealed to him that Kuha had been treated with a transfusion in 1968 for the world record run. The other incident he knew took place in 1970 when a well-known unnamed Finnish MD had told Risto Taimi that Juha Väätäinen had been also treated with a transfusion before he broke the 10,000m national record. (Raevuori, 1971) While the alleged incident took place a year before the 1971 games, a year after the games one Finnish doctor affiliated with the sports circles told knowing for certain that a number of Finnish runners had taken advantages of transfusion already for the 1971 European Championships, and Track & Field News correspondent Cordner Nelson recalled also having heard whispering about double gold medallist Väätäinen having used blood transfusions. (Nelson, 1972) Väätäinen wasn’t available for the comments, but he was later dismissive about the benefits of blood doping and always maintained that ”naturally” obtained altitude red blood cells were the safest and best ones. While Jouko Kuha specifically denied the allegation, he mentioned having been familiar with the procedure and some other athletes, coaches physiologists told also that they knew that transfusions had taken place in Finland. MD Kaarlo Hartiala, the future Finnish member of the International Olympic Committee Medical Commission also told that the issue wasn’t totally new.” On a theoretical level, the subject has been known for a long time”, he remarked mysteriously. (Raevuori, 1971) Interestingly Tapio Videman – who had conducted the first known attempt outside GIH to research blood doping – also later recalled having heard ”amazingly sounding” rumors about athletes taking transfusions in the late 1960s. (Siukonen, 2001) With all this evidence, there is an apparent mystery there – how could the method that was revealed in September 1971 be in use first time up to three years before that and how come the Finnish sports circles were aware of the method beforehand? There are many possible answers to this question. Aside of the possibility that the Finns had invented the method on their own, they could’ve built upon the Swedish research having heard about the line of research, because dozens of Finnish exercise physiologists and sports MDs participated in the 1966 conference held in Finland where the first inconclusive results of Ekblom and Åstrand were discussed. Kaarlo Hartiala – who was the 1968 chief doctor of the Finnish summer Olympic team – also participated in the conference and was very well connected with the Swedish researchers relating to the high altitude adaptation research. He was also the Finnish doctor of the 1965 expedition at the Mexico pre-Olympics with Bengt Saltin, so with his particular comments, he could’ve referred also to this line of research if the ways to take a shortcut to elevate hematocrit was discussed among the Nordic researchers. The third possibility was that his comments or the Finnish transfusions weren’t carried out at all to ”blood dope” but to treat relative anemia, a condition very common among the Finnish athletes. This was actually the consensus view of the rationale as told by the Finnish sportspeople who commented on the topic in 1971. In fact, Finnish athletes had been regularly complaining about their low hemoglobin counts and many had received iron shots with more-or-less success.* *Finns also noticed the anemia recovery problem quite early on, already before the 1972 study was published. Dr. Pekeltokallio – a respected sports MD – speculated whether the body could’ve recovered ”via normal ways” from anemia in a month when the donated blood had to be reinfused (Raevuori, 1971) and Juha VaÅNaÅNtaÅNinen had a lot of substance in his comments. ”If one uses one’s own blood that has been stored earlier, the beneficial effect is questionable”, the European Champion commented the matter in November 1971. ”Human blood is a living substance, and today it isn’t possible to store it for a long time without some blood destruction taking place. After the blood has been stored for three weeks, some 30 % of the red blood cells. If the storage period is shorter, the human body hasn’t recovered the balance, ie. the amount of blood. Therefore one can’t gain anything by reinfusing the blood”. (Telaranta, 1971) About what took place in Sweden, Björn Ekblom insists to this day that blood doping didn’t take place at GIH and that he wasn’t pressured to blood dope Swedish athletes, even when he doesn’t have a full picture about the prevalence of blood doping use at that time: After my own experience [with blood reinfusion], I understood that this would be doping – no doubt about it. But how much this was used during the 60’s and early 70’s I do not know. How the accusations fell out during that time I do not remember – just that I denied all allegations that I and others Peo would’ve been involved in the matter. He still revealed in an interview in 1975 to a Dagens Nyheter journalist that he had heard that a West German swimmer had broken the national record with the help of blood transfusion and he had information from his ”research colleagues” that the method had been used at a national level competition in a country he didn’t want them to reveal (Loren, 1975). Ekblom heard about the latter incident by an accident: In one conversation I got confidential information – ‘ He went to a hospital to treat his anemia, but one doesn’t get three blood bags to treat anemia of a well-trained athlete’. The same argument has been used when athletes develop so-called ‘sports anemia’ and it must be taken care that he must have blood. After these newspaper comments I actually got some threats both from those who thought who he was and from those who had some questions to answer for. The newspapers had called blood doping ”perfect doping” only a few years earlier, and Ekblom himself had been very skeptical about its detection possibilities, in fact, there had only been some speculation that elevated blood pressure might reveal blood dopers, but that the method was very insensitive because the normal range was so large. In this 1975 interview, Ekblom revealed that some thought process had still been going on also in this arena. ”The blood has an age range that can reveal if transfusion has occurred”, Ekblom speculated one possible method. ”When the blood is stored outside the body, the blood cells age at a different rate than those in the body” (Loren, 1975). While he described surprisingly accurately the future detection developments, he laments that very little was done in this area in the 1970s: Our impression was that we could see the difference between frozen and fresh blood in the size of red blood cells, their age and perhaps from something else. We got the tip from a hematologist but didn’t proceed with this thing – pretty stupid from our part. No Swedish athlete has ever admitted using ”old school” blood doping and Björn Ekblom has always consistently denied his own participation in blood doping. It still wasn’t listed as a banned method by the official rules and Ekblom recalls having heard complains inside Sweden that their athletes should have access to the same arsenal of methods as their foreign competitors: I certainly think that some people had the interpretation that the method was unethical but unfortunately allowed because it wasn’t banned – mostly to give the Swede the same preconditions that the athletes from the other countries had. I can certainly hear the same interpretation yet today about many things – high altitude housing, pressure dressing during exerciseetc. The researchers of the GIH also inquired Swedish blood banks whether they had offered their services for athletes and every blood bank answered in negative except Karolinska Institutet, the institution that had assisted the GIH researchers in the research process. Based on this information, there was no reason for Ekblom to believe that that blood doping was in widespread use in Sweden.* *Dr. Hans Howald also reported from a 1977 conference where doping methods were discussed that ”[a]ccording to the information received by Dr. Ekblom, blood transfusions have not yet been carried out, at least in Scandinavia, on top level athletes for the purpose of improving performance during important competitions (this is true above all as regards Lasse Viren and Anders GaÅNrderud)”. (Howald, 1978) Gossip is always gossip, but perhaps more damning accusation has labeled directly again Ekblom by 1964 Olympic gold medalist speed skater Jonny Nilsson, who has claimed on a few occasions that the physiologist asked him to become a subject of the blood reinfusion tests in early 1966, only shortly before the FIS Nordic World Ski Championships in February. The offer that Nilsson refused took place during a training camp at Davos, Switzerland. (Wikström, 1999)* *Finnish historian Erkki Vettenniemi claims in his book about Finnish skiing doping history that Jonny Nilsson told publicly about the blood doping ”offer” almost right after the blood doping research was revealed in 1971. (Vettenniemi, 2017a) Ekblom – who had become a coach of the Swedish Speed Skating Union in 1964 and researched the physiology of that sport extensively – recalls having been at the Davos camp and that many blood samples were indeed drawn as the effect of altitude was researched and he also later has recalled having discussed about ongoing blood reinfusion research with Nilsson during the late 1960s. ”I know that I brought a bicycle ergometer with me to Davos and we did lactic acid test”, he recalled the training camp over thirty years after the incident. ”Perhaps we did blood volume tests to Jonny Nilsson”. Even when their recollections about what happened in the late 1960s diverge, Nilsson has wanted to emphasize that it was it wasn’t doping but a research project, nothing else. ”Björn is not a wrongdoer”, he wanted specifically emphasize regarding the Davos-incident in 1999. Ekblom reveals that he has discussed the subject matter with Nilsson and they have no disagreement anymore about what happened. There was a misunderstanding which could’ve been because it is true that they did discuss the ongoing blood doping research regularly during the late 1960s when Ekblom spent time with the speed skaters. While Ekblom has emphasized in media that blood doping ”didn’t even exist in 1966”, it is possible that they did discuss about the item already in January-February 1966 as a research topic, because if Ekblom and Åstrand presented their first results in August 1966, the idea of blood doping research must’ve started to materialize around the time when Nilsson recalls the ”offer” being made.* *Ekblom traces back his reluctance to participate in doping being heavily influenced by his experiment in a one-night orienteering race when he had a magnificent race almost until the end, but he took an illegal choice of route and should’ve been disqualified. ”Nobody asked about the thing, but cheating it certainly was”, Ekblom recalls the incident today. ”I felt so ashamed about the second place in the competition that I decided never to cheat again”. Not only being an eminent physiologist, Ekblom was also an accomplished orienteerer and the Swedish champion of night-orienteering in 1964. The peripheral counterattack Whereas the research trends and results of the 1960s stressed the importance of the ”central” factors in limiting maximal oxygen uptake, there was another line of research that started to gain momentum around the time when the blood doping research started. “Until quite recently it was generally believed that the improvement in exercise capacity that occurs in response to regularly performed endurance exercise is due to increased delivery of blood and oxygen to the working muscle cells made possible by exercise-induced cardiovascular adaptation. Endurance training was equated with training the ‘oxygen transporting system’”, wrote one John O. Holloszy in 1973, only a year after the first blood doping study was published. ”However, within the past six years, evidence has accumulated which shows that, in addition to the cardiovascular adaptations, major adaptations also occur in the skeletal muscles which result in an increase in the capacity for aerobic metabolism”. (Holloszy, 1973) John Holloszy was an eminent physiologist and very modestly leaves out that the ”accumulation” started in 1967 when his outstanding research paper was published by the Journal of Biological Chemistry shows that there was enormous adaptability at the muscle level associated with endurance exercise, of which the most eminent was a huge increase the in the mitochondrial content of the trained muscle. (Holloszy, 1967) Mitochondria are the sites that ”consume” the oxygen, so theoretically doubling the amount could double the oxygen consumption capacity of muscles at least at the peripheral level. While at first look this doesn’t look such a big deal, the implications were clear. If the vulgar and simplistic version of the central limitation theory went that Vo2Max was related only to the amount of oxygen delivered by heart, why was there any kind of adaptation at the peripheral level at all? Why indeed? While the possibility of peripheral limitation was seriously considered as the key limiting factor in the oxygen delivery chain quite early on, the muscle itself had been very understudied area before the late 1960s at least from the endurance type of activity viewpoint. Now the research wasn’t just a few random studies, but there emerged an enormous body of literature, of which most was apparently in contradiction with the ”central” theories focusing on oxygen delivery as the key limiting factor. Even some blood reinfusion researchers considered this as a possibility when the reinfusion just didn’t seem to increase performance and when Melvin H. Williams and his coauthors speculate about why their experiment failed, they have one 1972 lecture by Holloszy in their references. (Williams et al, 1973) ”Within some few years in the early 1970s, a wealth of data appeared in the literature, all pointing at the enormous adaptability of the skeletal muscle in response to aerobic training”, could Bengt Saltin and his coauthor Sören Strange write later about this line of research, pointing to research on elevated mitochondrial and capillaries levels in the aerobically trained muscles that was conducted during this time period. ”Without a doubt, the oxygen extracting and utilizing the capacity of skeletal muscle came into focus in the mid-1970s as the key to the understanding of what caused maximal oxygen uptake to vary between individuals and with physical activity level”. (Saltin & Strange, 1992) To add validity to the importance of the peripheral factors as a possible key limitation of Vo2Max, Lennart Kaijser from the Department of Clinical Physiology of the Karolinska Institutet took an attempt to modify the amount of oxygen delivered to the muscles and conducting various types of performance tests on his subjects for his doctoral thesis published in 1970. Unlike some researchers who had used different mixtures of oxygen and air, Kaijser used high air pressure generated in a hyperbaric chamber, where oxygen availability to the muscles should’ve been higher. Whereas breathing of oxygen ”enriched” air had increased Vo2Max pretty consistently in research papers since the 1920s, this didn’t take place this time with higher air pressure and unlike expected, the data didn’t support the theory that the muscles could use the extra oxygen offered. Even when the subject of ”enriched air” had given consistent results in the past, many blood doping skeptics and proponents of the peripheral theories would cite Kaijser’s conclusion that the capacity of the cardiovascular system was limited to the capability of muscles to use the ”offered” oxygen. One Finnish hematologist influenced by Kaijser’s research also draws blood doping-related implications from this material when lecturing about the blood doping literature in 1976. ”It is pointless to try to enhance the oxygen delivery through transfusion, because it doesn’t cause a change in the oxygen utilization by the muscle. The amount of oxygen offered could be increased, but the muscle isn’t capable to utilize more oxygen than that it has adapted to use through an earlier exercise regimen”. (Remes, 1976) Whereas Kaijser’s work dealt with acute manipulation of the system, of Ekblom’s closest colleagues particularly Bengt Saltin was very interested in what types of changes endurance training caused in muscle and in the mid-1970s he coauthored the famous experiment when the scientists tested how weeks of endurance training using only one leg cycling affected Vo2Max figure of both the trained and the untrained leg. The maximal oxygen uptake increased by 23 % when work was performed only by using the trained leg, but only 7 % in the non-trained leg. The question then was the obvious one. If the ”central” factors were most important for oxygen uptake, why didn’t the Vo2Max figure of both legs improve in tandem? (Saltin et al, 1976) ”The present results suggest that the local adaptation of skeletal muscle to training is of primary importance for enhancing work capacity and oxygen uptake”, Saltin summed up the paper shortly later. (Saltin, 1977)* *Saltin and his coauthors also wrote in the paper that the findings ”focuses attention on peripheral factors as being at least as essential for the cardiovascular performance during exercise as any central factors”, adding that German researcher named Muller came to the similar conclusion ”already in 1942”. Saltin would later write many chapters on books and papers on the history of thought of exercise physiology. While this research raised questions about the importance of cardiovascular system as a determinant of Vo2Max, it wasn’t in contradiction with the ”central theory”, because the limiting factor of oxygen uptake could’ve been different with different types of work, a point emphasized by Ekblom some a quarter of a century after Bengt Saltin and his coauthors had published their interesting paper. ”Whether or not `peripheral’ factors such as capillary density, enzyme concentrations, and muscle mass limit oxygen consumption during heavy exercise has been a matter of controversy for many years”, Ekblom wrote in 2000 in a review on what was known then about blood doping. ”However, it depends on the type of exercise carried out. During exercise using small muscle groups such as during isolated dynamic arm work these `peripheral’ factors are of the utmost importance for, and do limit, the aerobic energy turn-over and endurance”. (Ekblom, 2000) Ekblom’s view today is that there could be a difference in different types of sports such as cycling vs. running, where, in cycling the peripheral factors and muscle level adaptation can play a relatively more important role. “It deals with the question of P50 and mitochondrial capacity and function”, Ekblom said of what he sees as the most pertinent peripheral issues today. ”Everything is not clear”. The question was of importance to him even in the 1970s when he tested how various combinations of limbs affected Vo2Max and there was even discussion in the decade about a paper on how blood doping affected the performance of isolated limbs, but as time was a scarce resource, the study never materialized. But one test was conducted using only arm work after reinfusion. While there was no increase in Vo2Max, time to exhaustion did increase. One muscle-related finding was also that when it was known that there were different types of muscle fibers (fast vs. slow), the muscle theories as a key limiting factor of Vo2Max gained some extra momentum when it was also noticed that there was a correlation between the amount of endurance type ”slow” type I muscle fibers and maximal oxygen uptake. (Bergh et al, 1978) Ekblom’s blood doping research is barely mentioned in this research on the peripheral limitation theories, but his other research was of great interest to the scientists interested in the muscle adaptation to aerobic exercise. It didn’t go unnoticed that Ekblom himself had observed that Vo2Max barely fell even after cardiac output had been reduced by some 12 % in the 1972 beta-blockade experiment when maximal heart rate was reduced by some 30-40 beats. Holloszy also found it most relevant that in many longitudinal training studies the increased stroke volume of heart accounted only roughly half of the increased Vo2Max whereas the other half was that muscles could use more of the oxygen of every given unit of blood leaving left ventricle. (Holloszy 1973) Holloszy concluded that oxygen consumption wasn’t only about oxygen delivery but that other factors were equally important. One of the materials referenced by Holloszy was Björn Ekblom’s thesis published in 1968 under the title Effect of physical training on the oxygen transport system in man. (Ekblom, 1968) If it wasn’t clear what to make about this material in the 1970s and how to contrast it with the emerging blood reinfusion research, the muscle itself became a real research topic from endurance viewpoint and there evidently happened a lot at the peripheral level. This is part three of a multi-part series titled “Limiting Factors – A Genesis of Blood Doping”. The full bibliography for this research can be found at the end of Limiting Factors – A Genesis of Blood Doping (part one). This is part two of a multi-part series titled “Limiting Factors – A Genesis of Blood Doping”. It comes to FasterSkier from Sammy Izdatyev. You can read part one here. Sammy Izdatyev is the pen name of a Finnish sports enthusiast and unaffiliated amateur historian, who has been interested in endurance sports since the turn of the millennium. He hopes that his pro bono – research can provide more information into the body of literature of earlier underresearched areas of the history of sports. PART II: Can blood doping work? Can blood doping work? Is hemoglobin concentration such a bottleneck in the oxygen-transport chain that elevating it above normal level increases maximal oxygen uptake and performance? For a modern reader, the answer to these questions is so obvious that the questions are no-brainers and one can easily imagine that this was how the issue was viewed some 50 years ago. But if this was common knowledge already in the ’60s, then the reader is left with a logical problem – the technological know-how to “blood dope” had been available since the first blood transfusion took place in the 19th century, so why did it take until the mid-’60s for the subject to be researched and why was the reception so negative and dismissive, not only on ethics but also on physiological grounds as well? The simple answer is that not that many people considered that method would “work” in the sense that hemoglobin concentration limited maximal oxygen uptake as an independent factor. As Ekblom recalls, the main opposition wasn’t ethical problems with the doping outcome, but that the entire premise was considered strange. Indeed, if the idea of blood doping is to assume that elevating hemoglobin concentrations artificially above the normal “healthy” range is beneficial from a performance standpoint, various observations, theories, and logical conclusions refute this hypothesis. Some of these ideas were publicized after the first blood doping research was published in the early ’70s, but it is equally likely that these same reasons prevented the research taking place in the first earlier because the efficacy sounded unlikely from a performance viewpoint. “Blood doping can’t work, because natural is optimal” The first reason to dismiss the idea behind blood doping was related to viscosity and to the observation that when particles are added to a solution, it makes the solution flow more slowly, in this case, with blood. While an increase in hemoglobin concentration does increase the relative amount of oxygen carriers per given unit of blood, it simultaneously makes the blood more sluggish. Correspondingly when red blood cells are added to blood, the marginal gain is lower with each extra red blood cell, because the velocity of the blood is diminished. With very low hemoglobin concentrations, the increase of oxygen carriers is beneficial from an oxygen-transport viewpoint, but relatively quickly the marginal gains will become minuscule, and at some point, there is a point after which the added oxygen has only negative effects. Because the properties of red blood cells and plasma are quite similar among different individuals, this phenomenon logically leads to the idea of “optimal” hematocrit, which should be roughly the same for every person. It has been assumed that the oxygen transport was highest around 45 percent, which was coincidentally also roughly the mean resting hematocrit of men residing at sea level. The interesting part of the theory is that it doesn’t even “care” whether the red blood cells are “natural” or “blood doped”, but the optimal value should be the same regardless. While some athletes in the ’60s occasionally complained about their low hemoglobin concentrations, contrary to the theory, exercise physiologists and sports doctors working with athletes and measuring their blood counts didn’t notice that high hemoglobin was associated with lowered maximal oxygen uptake as the theory would dictate. Even the sports hematologists seem not to have fully believed the theory, because while it was referred to widely even decades later by various experts, there hasn’t been one documented case that a doctor recommended elevating performance via blood donation if the hematocrit was above 45 percent. While there was clearly a discussion about the viscosity problem among exercise physiologists, Ekblom recalls that most of the viscosity discussion was driven by cardiologists, and his own data gave was no indication of any “optimal” hematocrit level: You can just look at the data you have in front of you, that all these important tests you’ve done on skiers, cyclists, runners, the peak variation in hemoglobin and hematocrit at the highest level of performance at that time. I could not find that there was an optimal hemoglobin concentration. You must just look at the papers and see that some guys had higher hemoglobin and hematocrit than the so-called ‘optimal’ and still they were Swedish champions. So I couldn’t find the discussion about ‘optimal’ hematocrit as scientifically proven. Interestingly when Åstrand and Rodahl wrote about viscosity in the first edition of their “Textbook of Work Physiology” published in 1970, they have a few paragraphs on the issue, but took a different approach on “optimal hematocrit”. They were also dismissive on whether the viscosity theories could be applied to the human system, writing that blood has “anomalous” viscosity which leads to “a lower viscosity of the blood than expected”. (Åstrand & Rodahl, 1970) *Åãstrand and Rodahl also write about the FaÅãhraeus-Lindqvist effect which leads “reducing the load on the heart”, particularly blood associated phenomenon where viscosity decreases with the decrease in the diameter of the tube the implication being that blood most likely flowed at a better rate than expected through the smallest capillaries. The “viscosity problem” still made enough sense that many blood-doping researchers conducting blood reinfusions have referred to it regularly. Those who didn’t find any benefit with elevated hemoglobin concentrations found it explained the absence of benefit, and many of those who noticed benefits assumed that the 45-percent figure vouched for by hematologists and cardiologists was, for some reason, too low, even when the premise was sound. An equally plausible theory against the benefits of blood doping was that human circulatory system was always best adapted to the specific conditions, and if the human body regulated the number of oxygen carriers to a certain value after a rigorous exercise training program, it indicated that it was also the most optimal for the given condition and individual. While regular exercise increased the total amount of oxygen-carrying red blood cells, it simultaneously increased the amount of plasma and correspondingly, the total blood volume. The blood didn’t become thicker, but on the contrary, it was regularly seen that the amount of plasma increased more than the number of red blood cells and the blood actually became diluted and hemoglobin concentration fell slightly. Even when there was debate how much this “anemia” was natural adaptation and what was caused by iron deficiency, overtraining or red blood cells being destroyed during training (by causes such as the so-called “foot strike anemia”), the best athletes didn’t have to have high hematocrits, and mediocre athletes who took the training seriously didn’t necessarily elevate their hematocrits by an iota even if their performance increased significantly. If “blood doped” high hematocrits carried more oxygen, it was equally counterintuitive why there would be no correlation between hematocrit and performance, but on the contrary, an athlete whose hematocrit was only 36 percent could and occasionally did win a race against someone whose figure was as high as 52 percent. As an illustration of this, many Finnish sports MDs were aware how cross-country skier Veikko Hakulinen had the lowest hemoglobin concentration of the 1956 Finnish Olympic team, but still went on the be the second best skier of the Olympics with one gold and two silver medals.* *When blood doping was the ”hot” topic in 1977, Finnish hematologist Kari Remes who was closely affiliated with the sports circles also observed in his lecture that ”hemoglobin concentration isn’t as important for an athlete that has been widely assumed, because the range of normalcy is very large” and correspondingly ”world records have been broken with as values as low as 117 g/l and on the other hand with values as high as 220 g/l”. (Remes, 1977) The third item for skepticism was related to the relative complexity of the oxygen delivery/utilization system, because, as we have seen, red blood cells don’t take oxygen from the air and “consume” it, producing a watt output, but there is a chain of oxygen delivery from air to the mitochondria. One prevalent view of during the early ’60s was that all the links of the chain were fully utilized and so heavily interdependent that artificial manipulation of any link wouldn’t change the total quantity of oxygen delivered and used. As previously explained, regular exercise increased the capacity of the links, so it didn’t make much sense to have extra “reserve” in any of the links just sitting idle. While Ekblom’s mentor Åstrand took part into the blood-doping research process from very early on, Ekblom’s recollection was that he and the majority of physiologists were skeptical about the prospects of artificial elevation of hemoglobin concentration precisely on the premise that the oxygen transport/utilization was in full use and each link was highly limited: If we go back to 1965-1966, Alf Holmgren and Per-Olof Åstrand had a paper stating that all these links in the oxygen transport chain stay in some rough relation to each other and that was the view that most people had, that the links were so closely linked together that it is no gain to increase one because that should not have any positive effects if the other links were so used to 100 percent. Mitochondria weren’t measured, but there were high correlations between Vo2Max and all the variables – total hemoglobin, lung capacity etc. (Holmgren & Åstrand, 1966) This didn’t preclude the possibility that if one link was manipulated down, such as at high altitude when there was shortage of oxygen in the lungs, or in anemia, when the number of oxygen carriers are well below normal, the other links couldn’t compensate for the shortage and there was a decline in VO2max, and in performance: If a link is decreased, that is another thing. If you take away blood, then of course the other links can not work. But if you increase the blood volume or hemoglobin concentration then there will only be some kind of resistance in the other links that would not let the oxygen uptake go up. In relation to this downward manipulation, the fourth item against the blood doping was that the human body had enormous adaptive capabilities, and it wasn’t certain that manipulating the links had conclusively negative effects on performance. Whereas the disconnect between hemoglobin concentration and Vo2Max observed by Ekblom raised suspicions about the viscosity theories, the material also raised questions about the importance of Hb concentration because human system seemed to be capable to give similar Vo2Max values with so different concentrations. When the literature also gave no answer to the question of how elevating hematocrit above normal levels affected maximal oxygen uptake and performance, there was surprisingly little research on how lowering hematocrit affected those variables. While Björn Ekblom and his coauthors concluded about the preceding blood donation research in 1972 that “most investigators agree that after blood loss there is a deterioration of physical performance”, the research was far from consistent and VO2max was almost never measured in this context. In addition, the fall in hemoglobin isn’t the only outcome of blood donation and there is also a temporary fall in blood volume which might have a detrimental effect on performance independent of the number of oxygen carriers when there wasn’t just enough fluid to fill the vessels.* *The paper that went furthest in this regard went on to claim that it was BjoÅNrn Ekblom who first observed the significant fall in Vo2Max after blood donation. “Only Ekblom et al have shown major changes in Vo2Max with phlebotomy”, wrote a team of US Army Research Institute of Environmental Medicine researchers in their 1974 paper. (Horstman et al, 1974) There was literature stating that while it took up to several weeks for the body to replace the “shortage” of red blood cells caused by blood donation, performance capacity or Vo2Max recovered significantly faster and in some research papers work capacity not only fully recovered in a few days but even surpassed the initial level when the number of oxygen carriers was still comparatively low. (e.g. Gullbring et al, 1960) One of the exercise physiologists who had measured the effect of blood loss on maximal oxygen uptake was Loring B. Rowell of the University of Minnesota, who published his thesis in 1962. One item he researched was how removing a relatively large amount of 700-1000 milliliters of blood affected VO2max and the results weren’t favorable for the blood-doping hypothesis. After blood removal, there was a fall of hemoglobin concentration from 15.7 g/dl to 13.5 g/dl, and even when the number of oxygen carriers fell by 14 percent, there was only 4 percent decrease in maximal oxygen uptake, which seems contrary to the later research and must have raised questions about the importance of hemoglobin concentration in the oxygen delivery chain. If lowering had a surprisingly inconsistent effect that the body could almost fully overcome, why did increasing above the normal level bring the presumed benefits? (Rowell et al, 1964) Rowell’s work was published also in the Journal of Applied Physiology in which most of Ekblom’s research on link manipulation appeared. When Ekblom described the roots of the blood-doping research in 1982, he acknowledged knowing “that some groups had done some minor experiments” and listed Rowell’s thesis among them, so he was at least aware of the anomalous finding. (Ekblom, 1982) …Or can it work? Still, there were cases more-or-less known within the sports world that indicated blood doping might be beneficial. There was also a chance that one or more of these observations had attracted enough interest that someone else would have invented the blood doping independently of the research carried out in Sweden. Blood doping has been often compared to high-altitude training because both techniques elicit similar types of responses (higher hemoglobin level), even when high-altitude adaptation takes time — weeks and months and the effect of altitude training isn’t usually of the same magnitude as with blood doping. Even when the benefits are debated even today, high-altitude training was a scientific area that got attention in the 1960s partly because native high athletes residents started to break their way into elite levels of endurance running, partly because many countries researched the question because of the 1968 summer Olympics in México City at 7000 feet (2200 m) altitude. When scientists from various countries presented their altitude training findings in March 1966 symposium titled The Effects of Altitude on Physical Performance, Dr. Bruno Balke summed up the material presented and noticing many positive effects. ”The majority of investigators observed an improvement of maximum aerobic capacity or, at least, an improvement of performances soon after return from altitude to sea level”, he concluded. ”The athletes, in many instances, had reached a consistent level of physical condition prior to the altitude training and it appeared most unlikely that a continuation of training at sea level, instead of at altitude would have resulted in identical improvement”. It still should be noted that any absence of a consistent increase in maximal oxygen uptake led Balke still to speculate about some other mechanism than elevated Vo2Max. (Balke, 1967) Internationally it also didn’t go unnoticed that native altitude residents such Kipchoge Keino and Naftali Temu were extremely successful at sea level, and Keino was even tested by Åstrand and Saltin in 1965, when tests showed that his relative VO2max was very high (82.0 ml/kg/min), indeed highest of the few runners. While Ekblom conducted relatively little researched on the topic of altitude-adaptation, his recollection is that it wasn’t a uniform view that these ”high-altitude” blood values were the primary reason for their success: One should remember that there was some experiment done at that time that showed that if you look at VO2max in well-trained athletes, there was no relation between VO2max and hemoglobin even in well-trained athletes and that is why the high values of Kip Keino and other people was only that they were one of those guys who had higher values more-or-less by natural cause. Swedish cross-country skiers still regularly trained at altitude in the 1960s for short periods before many Winter Olympics in order to elevate their hemoglobin count, assuming that high hemoglobin was beneficial even at much much lower altitudes, where most of the competition venues were located. The academic scientific research about altitude gave still very inconsistent results and would do so until our days. One of the scientists who at least considered seriously the idea that high hemoglobin induced by altitude training could be beneficial was Ekblom’s colleague Bengt Saltin, who tested the adaptation capabilities of a group of athletes at altitude in the mid-60s. While the experiment was a failure from the adaptation viewpoint (performance was below that of sea level after several weeks), the authors were interested in the possible benefits with “thicker blood”. “Adaptation to high altitude theoretically could increase maximal Vo2 on return to sea level owing to the greater oxygen-carrying capacity of the blood,” the scientists wrote in the research paper published in 1968. ”However, following 3 weeks at 3,100 m, four of five young athletes had a lower maximal Vo2 when they returned to low altitude, and when top Swedish athletes spent 3 weeks at 2,300 m, five of seven had a reduction in maximal Vo2 on return to sea level.” (Saltin et al, 1968) More detrimental to the higher RBC-count related benefits of high altitude training, all except one of this 1965 group that spent three weeks at high altitude had higher total hemoglobin mass (up to 10 %) when they returned to sea level. (Saltin, 1966; Saltin, 1967a) One possible clue of the benefits of high hemoglobin counts was that aside from altitude residents, there were other high-performers with high hemoglobin counts. While there was no correlation between hemoglobin concentration and Vo2Max when men were researched as a group, it was well-known that men tended to have both higher hemoglobin concentration and higher oxygen uptake than women had. The Swedish researchers – among then Åstrand – also concluded that the difference between the Vo2Max figures was explained by the difference in the oxygen carrying capacity of blood. “When exercising the lower concentration of hemoglobin for women is no doubt a handicap from a circulatory viewpoint,” Åstrand and his coauthors wrote as early as 1964. (Astrand et al, 1964)* *The viscosity theory of hematocrit 45 % (Hb c:a 15 g/dl) being the ”optimal” is very “male-centric” theory because close to 98-99 % of females would find the method beneficial having their natural values well below that. When Finnish sports MDs of the Unit for Sports and Exercise Medicine (University of Helsinki) published the monitored blood values of athletes they tested between 1974 and 1986, the average for males was 14.92 g/dl, but the highest value of the 97 females was only 15.2 g/dl with the mean of 13.61 g/dl. (Kujala et al, 2000) One good case study for the benefit of high hemoglobin concentration was also the mysterious case of the Finnish cross-country skier Eero Mäntyranta, who won two gold medals at the 1964 Olympics in Innsbruck, Austria. His high hemoglobin concentration was occasionally referenced in the media in the 1960s and he wrote in his memoirs (published in 1968, before blood doping was “invented”) that his fellow cross-country skiers were surprised about his blood values as early as the ’50s and attributed it to his success. “[In 1957] I was a subject of a lot of wondering because of my blood,” he wrote. “It was a starting point to a myth that if a man has hemoglobin values that high, he will become a master skier and it takes nothing else.” A few paragraphs later, Mäntyranta explained he was unsure whether he benefited from his atypical blood. “Just recently the science has reached the right conclusion that hemoglobin value has no meaning as such. Everyone has his own normal hemoglobin value. If it falls, he has anemia,” he continued, explaining that he had ”anemia” in December 1967, shortly before the 1968 Olympics when his hemoglobin concentration fell to 20 g/dl. He lamented that he wasn’t informed about this “anemia” until after the Olympics. (Vuorio & Mäntyranta, 1968) In the 1960s, people took notice of his above-average hemoglobin values, but when genealogists and hematologists looked into his case in the late 1980s, Mäntyranta’s blood values turned out to be almost unbelievably high, when his hemoglobin concentration was measured at 23.1-23.6 g/dl and correspondingly his hematocrit was 68 percent, higher than any measured ever even from any confirmed blood doper of whom the highest known is the alleged figure of 64 % from the Danish cyclist Bjarne Riis who won the 1996 edition of the Tour de France.The amount of red blood cells in his body was around 4.8 liters, which was twice the normal amount of men of his size who had that amount of blood in their circulation of which less than half was constituted of red blood cells. He had been described as almost unbeatable, but even when he was named “Mr. Seefeld” for his success at the 1964 Innsbruck Games, it is arguable whether he was necessarily the world’s best cross-country skier of the ’60s when considering all his major-competition results between 1960 and 1968. Even if one didn’t see him then or today as a super athlete, there was one part of his case that should have raised eyebrows of the hematologists and should have given blood-doping skeptics within the community of exercise physiologists a moment of pause. If the viscosity theory was sound and the optimal hematocrit for oxygen delivery was the earlier presumed 45 percent, the Finn shouldn’t have had any advantage over his competitors. On the contrary, his VO2max should’ve been unbelievably low, comparable to someone clinically anemic. In addition to this, his relatively slow blood flow would have many other detrimental effects when blood flow was needed to carry hormones and to thermoregulate. As an illustration of how other athletes’ suspicions have often preceded the underlying science, it is also interesting that Mäntyranta’steammates might have been on the right track about the link between his blood values and his performance. Total hemoglobin Then there is the correlation between total hemoglobin and maximal oxygen uptake, an item that had been of interest to Per-Olof Åstrand since the early 1950s. While many blood-doping researchers have focused on hematocrits and hemoglobin concentrations because they are so easy to measure in a single test, one definition of blood doping is the artificial elevation of the total amount of hemoglobin (i.e. hemoglobin mass), the total sum of hemoglobin molecules circulating in the bloodstream. If someone’s hemoglobin concentration is 150 g/l and he has 5 liters of blood, his total hemoglobin is 750 grams (ie. 5 x 150) and someone with 120 g/l and 7 liters of blood has 840 grams (7 x 120) and so forth. While hemoglobin concentration is easier to measure regardless of the blood-doping method used, the goal of blood dopers is to actually increase the amount of total hemoglobin. In this light, it is interesting that while physiologists of the ’60s noticed no correlation between hemoglobin concentration and maximal oxygen uptake, a very strong correlation between total hemoglobin and maximal oxygen uptake had been proven in the ’50s. (Åstrand, 1952) This was seen in comparisons between individuals; both also at least tended to rise and fall after training and detraining. That is to say, simply by knowing that Person A had twice the amount of total hemoglobin than Person B, it was very likely the maximal oxygen uptake of A was also twice as high. It was also known that total hemoglobin was correlated with performance because data published in 1949 by Swedish researchers clearly showed a linear correlation between total hemoglobin and the watt output at a fixed heart rate between individuals. For example, if someone has 500-600 grams of total hemoglobin in his/her system, that person can produce power output of some 100-160 watts at heart rate of 170, whereas individuals whose total hemoglobin is double (1000-1200 g), their watt output at the same heart rate is also double (200-350 watts). (Kjellberg et al, 1949) Why did blood doping even have to be invented if the idea was inherently there? More hemoglobin equals bigger oxygen engine and better performance, right? While Ekblom acknowledged that modern readers with access to the latest information might interpret the material in this manner, that’s not how the matter was viewed in the ’60s: “I don’t remember anyone saying that if you go along the line of hemoglobin, you will have higher VO2max,” Ekblom recalls how this material was read when the idea of blood doping research started to materialize. First of all, while the connection between the two exists, at the same time, all the criticism against the efficacy of meddling with the ”natural” system still exists and the linear correlation doesn’t debunk these theories per se, because the hemoglobin values and the cardiovascular system of these people were still “natural” adapted values (with hemoglobin concentrations most likely in the normal range). The nature of the connection is alsopeculiar because it isn’t a direct connection between total hemoglobin as such and maximal oxygen uptake. When physiologist R.J. Shephard briefly discussed this correlation in his 1971 book “Endurance Fitness”, he wrote that “stroke volume is influenced by the availability of blood for pumping”, that the causal connection is actually between blood volume and VO2max, and the correlation between total hemoglobin and VO2max is just more a statistical anomaly because blood does contain the hemoglobin. Shephard even pointed out that some researchers found this very indirect connection between hemoglobin and maximal oxygen uptake arbitrary because absolute VO2max correlates also heavily with absolute body dimensions and larger people tend to have larger oxygen engine. Almost certainly a 6-foot-3-inch person would have a higher total amount of hemoglobin and a larger oxygen engine than someone who is 5’1”. (Shephard, 1971) To illustrate how researchers were very unsure whether hemoglobin concentration as independent variable “caused” higher VO2max, it is telling that when Åstrand’s friend Alf Holmgren discussed the correlation during a conference in 1965, the following dialogue took place: Q: Dr. Holmgren, did the data which you showed mean that big people have big total hemoglobins and big maximum oxygen uptakes, or can you say that in the same person, increasing the total hemoglobin is an effective way to increase maximum oxygen uptake? A: If you relate total hemoglobin to body size, athletes have higher total hemoglobins than non-athletes. (Holmgren et al, 1966) No conclusion there that infusing red blood cells into the bloodstream increased VO2max, and Holmgren wasn’t convinced that altitude training or other methods primarily targeted at increasing total hemoglobin in turn “naturally” increased performance. Even Holmgren – who knew well the hemoglobin/Vo2Max-correlation material having gathered a large portion of it and some with Peo Åstrand – was reluctant to acknowledge the link in such a straightforward manner.* *Dr. Wilhelm von DoÅNbeln – the physiologist who invented bicycle ergometer – researched the same issue in 1956 and comparing Vo2Max both to total hemoglobin and to fat-free body mass. Because von DoÅNbeln found a higher correlation between body mass and Vo2Max he finally concluded that ”the main reason for the correlation between total hemoglobin and maximal oxygen uptake is that the total amount of hemoglobin is related to body size.” (von DoÅNbeln, 1956) It is still telling that Ekblom and his coauthors referred to this “correlation” in their published “breakthrough” research paper of the early 1970s and even in the opening sentence: “It is well established that the total amount of circulating hemoglobin (total Hb) is well correlated with maximal oxygen uptake (VO2max)”. (Ekblom et al, 1972a) Even when Ekblom muddled this repeatedly, the connection is ex-post fact so obvious. Then there were those who claimed that the efficacy of blood doping was self-evident in the mid-’60s for totally another reason: that blood doping had already been invented twenty years earlier. Efficacy of blood doping dates back to the 1940s? As stated in Part I, there was some existing blood-infusion material that, at least retrospectively, proves some benefits associated with artificially elevating blood volume/hemoglobin concentration. When looking back at these first studies with more recent knowledge on blood doping, certain researchers and historians flirt heavily with the idea that blood doping was actually invented before the ’60s, possibly as early as in 1945. The most interesting of these experiments is the research conducted at the Bethesda military hospital at the end of World War II, which was published as a preliminary report in 1945 in Science (Pace et al, 1945) and two years later in American Journal of Physiology. (Pace et al, 1947) The report is of great interest for mainly one thing: it showed that transfusion of red blood cells elevated performance at high altitude and more importantly, that transfusion increased performance also at sea level. Its researchers conducted treadmill tests over several days at different simulated altitudes, and the test subjects inhaled different mixtures of nitrogen and oxygen. While their main interest was to combat altitude-induced hypoxia, once they conducted tests on sea-level performance, the results came back quite similar. “Even at sea level, where the blood is nearly saturated, the exercise pulse rate of the transfused groups showed a significant reduction following transfusion,” the report stated. Retrospectively it appeared that higher oxygen flow to the muscles and correspondingly lower heart rate can suffice the oxygen demand. So did this prove the efficacy of blood doping? Yes and no. Their experiment showed that some endurance-related parameters were increased even at sea level, and the research was quite sophisticated because it circumvented some of the later pitfalls. There was a control group, and participants didn’t know whether they received red blood cells or saline, and the amount of blood transfused was very large: 2000 milliliters. Correspondingly, the mean hematocrit of the group increased from 46.2 percent to 58.3 percent. On the other hand, this was not a study on exercise physiology per se, but an attempt to research how human body adapted to different conditions, in this case, to different altitudes and the researchers concluded that one could circumvent the time-consuming acclimatization process by elevating blood red cell count by a simple transfusion. The sea-level-related performance enhancements were simply coincidental and not even mentioned in the 1945 preliminary report published in Science nor in the “summary and conclusions”-section of the actual full research paper published two years later in American Journal of Physiology. Even the extrapolation of the performance enhancement would have been difficult because the finding was that heart rate was somewhat lower when the participants walked at a very modest speed (4 miles per hour) on a treadmill at zero incline. That was the only endurance item measured; there were no attempts to run until exhaustion and no maximal oxygen uptake tests. Also of interest, a reinfusion study conducted in the late 1950s and with the findings delivered in a lecture in 1958 and the report published two years later. (Gullbring et al, 1960) It is interesting because one of its authors, blood specialist Bengt Gullbring, participated in the blood collection, storage and reinfusion logistics of the later blood doping research at the GIH. The research protocol was very simple. There were six participants, of whom all donated roughly 10 percent of blood that would be reinfused later, and there were various tests conducted at various points of the study. While it is usually listed vaguely under the category of “blood-doping studies” in some literature reviews, it wasn’t a blood-doping study as such, because its main focus was to see how body reacted to differences in blood volume. Even when there was even a roughly 10 % increase in performance, hemoglobin level never went above normal the initial level because the blood was reinfused only seven days after removal. Correspondingly the mechanism had pretty much nothing to do with how artificial surplus of red blood cells affected performance and also questioned the importance of changes in hemoglobin concentration on work capacity. Ekblom recalls that this paper wasn’t even discussed with Gullbring in relation to the blood doping research. “It is interesting that because Gullbring was a coauthor in the first performance paper and he didn’t mention that when we were working with him on the [late 1960s blood reinfusion] papers”, he recalls. There is a third paper of interest, and Ekblom wrote in the early 1970s that artificial elevation of blood volume had been researched before his own work and it as such has very little on performance, (Ekblom, 1972) referring most likely to the research published in 1966 by a group of researchers conducting their research at the National Heart Institute, Bethesda, Maryland, in which the researchers tested how elevating blood volume acutely affected Vo2Max and cardiac output. (Robinson et al, 1966) The research is interesting because even when total hemoglobin mass must’ve been elevated after 1000-1200 ml of blood was infused, the researchers observed an only negligible increase in Vo2Max because hematocrit remained mostly stable and the amount of blood pumped wasn’t elevated. While the authors of this researched slightly different thing than Ekblom focused on, the conclusion would later be referred to in the blood doping literature as a study where a large blood reinfusion barely enhanced performance. *** If there is one conclusion to be drawn about the material presented above, it’s this: the issue was very nuanced. Even when the concept of VO2max had been known for almost half a century, it was only researched more systematically for roughly a decade, so the opinions were not concrete and much confusion still existed. The transfusion research preceding the Swedish experiments can be particularly confusing, because when compiling the reviews of existing blood-doping studies in the ’70s and later, many authors lump them all under the vague category of “blood-doping studies”, and one may view the research from the 1940s in the same continuum as the experiments conducted forty years later. While eminent exercise physiologist and MD James Stray-Gundersen wrote plausibly in 1988 about this pre-1970s material that “there were some interesting data suggesting a minor improvement in endurance performance with transfusion but nothing particularly compelling,” concluding that “the methods used by all groups can be said to have prevented the actual effects from being elucidated”. (Stray-Gundersen, 1988) There is nothing wrong in this reading of the material, but it should be remembered that these earlier researchers did find actual effects of what they were researching being elucidated, but none of them considered researching whether elevating hemoglobin concentration would increase maximal oxygen uptake and performance at sea level. While it is easy to see that in these early transfusions studies there were some random items tilting towards the direction that blood doping “worked” particularly with the modern knowledge, it is far from clear what lessons were drawn from the material at the time when they were conducted. It is more than telling that when the first studies about the efficacy of blood doping emerged in the 1970s and the earlier material was also reviewed with the “real” blood doping studies, the case wasn’t closed for the efficacy, far from it. If the quasi-blood doping material + the GIH-research far from shifted the consensus, it is unlikely that this earlier material alonewould’ve convinced anyone if there was even that much attention paid to it at all. Part III: Dead ends (1966-1968) “Blood reinfusion research almost from ex nihilo” In summary, with the knowledge of the mid-1960s, it was far from evident that blood doping increased maximal oxygen uptake. If that was an open question, an equally not-too evident question of how the increase in hemoglobin concentration should be brought upon and what limitations the reinfusion techniques had. “To our knowledge there has been no report on any complication in connection with reinfusion using autologous whole blood or packed [red blood cells] when this has been carried out for scientific purposes,” Ekblom stated in one of his essays at the turn of the millennium, after some 35 years of ongoing blood-doping research. (Ekblom, 2000) That was somewhat surprising considering there had been warnings since the ’70s about the increased risk of blood clots and heart failure with blood doping. In fact, dozens of blood-infusion studies had been conducted involving non-anemic participants since the ’60s, with some protocols involving removing and reinfusing more than two liters of blood, consisting over a third of normal blood volume and, in some instances, elevating hematocrit levels to nearly 60 percent. But none of this information was available to researchers in the ’60s who were attempting to elevate hemoglobin concentrations. There was not much data on how the body tolerated the infusion of extra blood and no information on how much time there should be between blood donation and reinfusion, leaving the researchers to rely on practical knowledge of blood banks and legal limitations of which Bengt Gullbring from the blood bank consulted them on. And the problem was also a downside because when Gullbring was coauthoring a different blood-reinfusion research paper almost a decade earlier, one participant almost fainted during an exercise performed right after blood donation. One doesn’t necessarily have to elevate hemoglobin concentration through blood infusion, and as early as the 1960s there was published literature about other ways to elevate hematocrit levels, such as living at high altitude and inhaling small amounts of carbon monoxide. One doping method used today that was invented before WWII was the administration of cobalt, which was shown to stimulate the natural red blood cell production by bone marrow. Ekblom couldn’t recall who came up with the idea of using blood reinfusion in the research, but it is interesting that Åstrand was a close friend and an occasional co-author with Holmgren, who had was one of the authors of the aforementioned blood-reinfusion research paper published in 1960. In any case, the GIH-researchers had also some interest in the acute anemia and these other methods don’t elicit changes acutely, but gradually, so perhaps transfusion was the obvious answer to the research question. Irma Ryhming, who, with her future husband Peo Åstrand, developed the nomogram to measure VO2max indirectly, had left the GIH several years later to finish her studies in medicine. Yet she gave the researchers at least one tip: that they shouldn’t take too much blood at the first experiment, but proceed slowly with the experiments. Even when this very risk-averse approach would have its downside, it was, in essence, a sound one. The researchers also were unsure if they needed to infuse saline to replace the shortage of blood after blood donation. Had Ekblom and his coauthors been aware of the earlier blood transfusion research of the Bethesda military hospital when they started their own reinfusion studies, they might have used directly higher amounts of blood: I wasn’t then aware of the 1945 research, but was notified about it quite late by Bengt Saltin. I think that he was somewhat happy about this earlier research that showed that I wasn’t the first one the publish [about blood doping]. Even when we were good friends, he presented the data to me with a little ‘smile’. Gullbring from the blood bank consulted on the technical issues, and the Swedish researchers of the team were Ekblom and Åstrand. In addition, there were two foreign researchers involved – Mike Rapport from the United States and Henryk Kirschner from Poland. While the research has been for many reasons described as Swedish research, Ekblom’s opinion is that this isn’t the whole story: We were very open, it was Peo Åstrand’s personality. He brought foreign people here and they had the same values as me and the other people.* *AÅãstrand was also very optimistic about the openness of the discipline in general. ”It is very promising that the physiology of performance, including competitive sports, is international in its true sense, without any barriers and ‘we keep it secret’ tendencies due to nationalism”, he told in 1973 during one conference. ”There is, in other words, an absolutely open discussion on training methods, ways of improving performance and avoiding injuries, treatment of injuries, etc.” (AÅãstrand et al, 1973) He was perhaps slightly too optimistic because one of his fellow lecturers was N.I. Volkov, who would be the brain behind the secret Soviet blood doping program (Kalinski, 2003)] The first test – is reinfusing one’s own blood easy? The protocol of the first test that took place in the spring of 1966 was simple. There were five subjects, and each of donated 500 milliliters of blood, or about 10 percent of their total blood volume. The blood would be reinfused three weeks later, and during each phase, multiple tests would be conducted. In addition to VO2max, various other items were also measured, among them heart function, saturation and whether there was an effect on performance at conditions simulating high altitude. (Acta Phys Scand Suppl, 1966) The altitude line of blood reinfusion research at the GIH was dropped after the ‘68 México games. Very little is known about this first attempt, but it is certain that it didn’t show blood doping to be beneficial, at least not when the data was subjected to statistical analysis. Ekblom himself was the first subject of this early research, and his personal experience still was that there was a performance enhancing effect when he tested his capabilities in a popular Stockholm park. I had my run at Lill-Jansskogen and broke my personal best by 15 seconds to about 13 minutes. And I felt how the slopes felt light and above all the recovery after the slope became all the easier. My opinion is that this sensation can’t be placebo. Yes, a critic could say that after this I could have made my research so that it would give a certain outcome. But the following research showed that this wasn’t the case. This first attempt illustrated the problem that would plague the blood-doping research particularly over the next fifteen years, the ”anemia recovery problem”. While the reinfusion of one’s own blood sounds easy when it is described in the popular literature, it is surprisingly difficult task, because it isn’t just the case that doctor only takes a given amount of athlete’s blood (for instance 10 %) and then reinfuses it later and then the athlete has the given amount of extra red blood cells (110 % of the original). This is because when blood is removed for later infusion and refrigerated at 4 degrees Celsius, the scientists are unable to wait until the hemoglobin concentration is fully recovered before reinfusing the blood, because the quality of the stored blood falls each day and there have been even legal limitations on how long blood could be stored for later use, both in blood banks and in scientific research. Even when the body tends to speed up the production of new red blood cells after blood donation, there is a huge variation in how fast people recover from the relative anemia. Correspondingly, the increase in hemoglobin concentration following blood reinfusion is always somewhat unpredictable. Even reinfusing larger blood volumes do not automatically mean that hemoglobin concentrations rise more than with lower volumes because blood withdrawal simultaneously causes a more severe shortage of red blood cells for the body to recover from in the weeks preceding the reinfusion This phenomenon had implications when Ekblom and Åstrand started their reinfusion research and it would have strong implications in the ’70s when many international research teams started to find out whether the reports about blood doping were sound or if they should conduct their own research. If the rise in total hemoglobin was somewhat unpredictable, there were other phenomena that would plague the research, one example is that there was never clear 1-to-1 correlation between the different measurable variables even when one might assume that if total amount of hemoglobin is increased by a given amount after blood reinfusion, hemoglobin concentration, maximal oxygen uptake, and performance will rise in tandem with almost 1-to-1 correlation. However, this is not the case – far from it. It was not uncommon that blood volume remained slightly elevated after reinfusion and correspondingly there was very little increase in hemoglobin concentration even there were more red blood cells and hemoglobin flowing in the vessels and oxygen engine was higher. The bigger problem from the statistical analysis was that there were also differences in how each body utilized these extra oxygen carriers, and increases in maximal oxygen uptake didn’t correlate well with increases in the amount of red blood cells between different individuals. As previously mentioned, VO2max wasn’t the sole predictor of performance, so even this increase in VO2max didn’t correlate strikingly well with different types of performance tests. To add further noise into the data, blood removal causes always some detraining effect when athlete have lower watt output or just didn’t feel good and can’t give the normal effort during exercise, a phenomenon that would plague also the altitude training research. Correspondingly there is also a tendency for performance to be below normal level after blood donation even when blood values had fully recovered.* *This detraining has occasionally large impact on the results. When Swedish blood doping researcher Christer Malm and his team researched blood reinfusion in the 2010s, even four months wasn’t enough for performance and the Vo2Max to fully recover for all subjects to the initial level after 900 ml blood removal ”testifying the hardship with training after a donation of two units of blood”. (Malm et al, 2016) This ”noise” here and there in the data would not have been such a problem if the increases in total hemoglobin and other parameters were high, but researchers all over the world (also Ekblom and Åstrand in the first attempts) regularly used such little amounts of blood and too short storage times that the increases in total hemoglobin masses of their subjects were regularly far less than 5 percent, which rendered the results very often inconclusive when changes in performance and Vo2Max were even less than that, only barely above zero with a large variance. Even if mean values showed something interesting when the data were analyzed with the statistical tools, it was very often the case that is was very difficult to distinguish the blood doping-induced ”boost” from the natural day-to-day variation, measurement errors, etc. *** These initial findings were presented and discussed at the XII meeting of The Scandinavian Physiological Society in Finland in 1966. While there was very little breakthrough material to publish at the time, the first research was also discussed and three papers authored by Ekblom were presented at the meeting (although he can’t recall for sure whether he was present), which included more than 200 physiologists. (Acta Phys Scand Suppl, 1966) Ekblom recalled other blood reinfusion attempts in addition to his 1966 experiment with five subjects. “I would say that we had at least two attempts in which we didn’t really succeed in,” Ekblom recalls this unpublished research. “When we took out blood we infused saline or plasma and we had a too short period between withdrawal and reinfusion.”** **When the issue was fresh in Ekblom’s mind in 1972, he wrote that “circa 14” people were subjected to the blood reinfusion studies of whom 7 were part of the 1972 study. (Ekblom, 1972). Correspondingly there most likely was some but not much research in addition to the 1966 experiment. While he has since recalled that some results showing performance benefit were in seen in the ’60s and he casually stated three decades later that “1968 was the first time when we could show one could become better with this type of manipulation,”almost no word of this earlier material found its way into academic journals. (Wikström, 1999) In addition to the dead-end research, one problem of the ’60s was that exercise physiology was not established science. Correspondingly the attitudes of “clinical people” at the Karolinska Institutet (the largest hospital university in Sweden) toward “exercise people” generally ranged from negative to skeptical. Ekblom recalled that the atmosphere was “really bad” around the 1960s. “We were not regarded as real medical people, so these hematologists and internal medicine professors looked down on us,” Ekblom said, referring to himself and his colleagues, including Åstrand and Saltin. “The head of the physiological department in Karolinska Hospital was a very strong opponent of Peo and Irma Åstrand, so Irma could not have her Ph.D. dissertation in Stockholm and she had to go to Gothenburg.” Even when Ekblom collaborated with the hospital’s medical department, the atmosphere was tense, but recalls his coauthors at the institute, including blood specialist Bengt Gullbring, being always cooperative. In the time preceding the obesity epidemic and its byproducts, such as coronary heart disease and Type II diabetes, Ekblom recalled that the “real” physiologists found very little health benefits associated with regular exercise: “The effect of exercise is that you are clean after shower, that is the only positive effect,” was the general consensus or at least not far from it. Mexico City, 1968: Blood doping connection? As described in Part I, the roots of the “Swedish” blood-doping research originates in 1962 are related in understanding the links in the chain of oxygen delivery, how their manipulation affects other links, and the maximal oxygen delivery/utilization system. Still, there was another line of research that dealt with elevating hemoglobin concentration and performance that coincided chronologically and possibly geographically with the GIH research. This was a result of the decision by the International Olympic Committee (IOC) in 1963 for the 1968 Summer Olympics to be hosted in México City at some 7000 feet (2300 meters) above sea level, where it was known that performance would be impaired due to lower availability of oxygen. Contrary the popular belief, the México Games were the first Summer Olympics at altitude because there had been some Winter Games at slightly lower elevations, most notably in 1956 and specifically in 1960, of which the effects of altitude were illustrated in the cross-country skiing men’s relay. Sweden had been leading the race after the first leg, but its second skier, Janne Stefansson, hit the wall while Finland’s second man, 22-year old Eero Mäntyranta, broke through to help Finland win gold. In his memoirs, Mäntyranta later wrote that they skied together until the last two kilometers or so until Stefansson collapsed and tagged off more than two minutes later. Mäntyranta was also convinced that the Soviet team suffered from the thin air. “The shortage of oxygen had also overcome the first dangerous rival and a defender of Olympic gold medal,” he wrote. “Soviet Anatoly Shelyukhin hit the wall during his starting leg and reached the goal only seventh, over two minutes after the fastest skiers.” (Vuorio & Mäntyranta, 1968) “In almost every team including the Swedish one, athletes collapsed during competition in Squaw Valley [1960 Games]”, told Per-Olof Åstrand in one of his lectures when the acclimatization problem was discussed in 1965 in relation to the forthcoming summer Olympics. “It was not the not unusual exhaustion but something they and we had not experienced before”. (Åstrand, 1967) The problem was evident also in 1968 and because “thick-blooded” Africans were victorious in México and because many countries tried to elevate the hematocrit levels of their athletes by various means, many academic researchers, including Randy Eichner, Chris Cooper, and Jakob Morkeberg, later have assumed that the altitude games actually sparked interest into the blood-doping research. “Interest in blood doping soared after the 1968 Mexico City Olympics (7300 feet), where most winners of endurance footraces hailed from the highlands”, writes physiologist E. Randy Eichner in one of his often-referred essays. “The premise that drove the ensuing research on blood doping was that athletes from altitude had ‘thick blood’ that helped them win in ‘thin air’”. (Eichner, 1992) The first blood doping attempts were taken well before the 1968 games and whereas native high altitude residents were very triumphant in Mexico, it was also far from certain that they would have similar future success. In fact, they were expected to triumph at those Olympics since precisely because they had adapted to altitude since their birth, yet it was equally likely that they would not have an advantage and the playing field would be even again when the Games returned to sea level. When physiologist R.J. Shephard wrote about high-altitude training in one his 1974 essays, he concluded that while the performances of some native altitude residents “far exceeded that of the other contestants” in México, in his opinion “it seemed but a small leap of faith to suggest that if living at altitude was good for competition at altitude, it was even better as a preparation for sea level competition”. (Shephard, 1974) Shephard came to this conclusion after the countries with athletes from high-altitude regions failed to repeat their 1968 domination four years later at the 1972 Summer Olympics in Munich, Germany. Shephard would later co-edit the book “Endurance in Sport” with Åstrand. As expected, there is still more than a grain of truth about the connection between Mexico and blood-doping research, but this connection is more in the years preceding the 1968 games, when the connection between hematocrit level and performance gained extra boost when the brightest researchers all over the world sought out ways to elevate hematocrit to better adapt to altitude and discussed the matter in different international meetings. Part of the discussion was only observational items about the severity of the fall in performance and Vo2Max at altitude, but an equally interesting question was how to manage the problem, ie. how many weeks it took for the body to increase the number of RBCs to compensate the detrimental effect of “thin air”. When going through the material about who exactly took part in this academic discussion, two names catch the attention immediately. The first one is Henryk Kirschner from the Warsaw University, who wrote in the late 1960s about how high altitude had a detrimental effect on performance. (Kirschner, 1968) Interestingly he had participated in the 1966 blood reinfusion research with Ekblom and Åstrand and while the results of those experiments were inconclusive at best, he had first-hand knowledge of the blood doping research by the 1968 Olympics. In one of his papers, he published a chart showing the performance of five subjects at a simulated altitude of 4000m. The material most likely originated from the first reinfusion research where the subjects breathed air with lower oxygen content in some tests. Another name of interest is Frank Consolazio of US Army Medical Research and Nutrition Laboratory, Colorado, because he was a coauthor of the Bethesda military hospital experiment conducted in 1945, some two decades earlier. As we have seen, the authors concluded that the time-consuming acclimatization in “thin air” that took up to months could be circumvented by a simple RBC infusion in a few hours concluding that “the polycythemia induced artificially in this [transfusion] experiment and the polycythemia which occurs during acclimatization to high altitudes are very similar”. (Pace et al, 1947) Particularly Consolazio took part in many conferences and when the dozens if not hundreds of scientists discussed the problem of the 1968 Mexico Games worldwide with the intention of elevating hematocrit level and one could come up with the idea independently, it should be obvious that using transfusion to speed up the adaptation came up during the discussions. And indeed someone come up with the idea either on his own or through the pre-existing knowledge, someone very close to Björn Ekblom. When Bengt Saltin researched the adaptation process in the field in October 1965 by bringing Swedish elite level athletes into altitude for the 1965 pre-Olympics in a joint Nordic venture, he discussed the method as more than theoretical alternative publicly. “This is no joke, and I seriously mean it”, he is quoted having said by the Swedish daily Expressen. He also describes how endurance performance capacity falls at altitude by “5-10-15 percent” and because of the shortage of oxygen, some “become blue” and athletes collapse (such as the Swede at the 1960 games) and can risk their health and in extreme cases, there is even the risk of death. (Nilson, 1965) He continues that fortunately through adaptation processes at altitude, the body increases red blood volume by up to nine decilitres to function better, but Saltin had even a better and a more straightforward idea. “But why should we wait for these regenerations [of performance capacity]”, Bengt Saltin put it bluntly. “You can, in a transfusion, get fresh blood before the departure to Mexico City, thus minimizing the adaptation problems”. He also describes having discussed the matter with medical experts and the general view was that even when this type of intervention would be conducted on healthy people, it didn’t violate medical ethics because it was beneficial from medical viewpoint to overrun the “fatigue syndrome”. “I can without doubt say that we will test the method”, he also told the reporter. “And if it shows to be effective – as one can imagine – there is no reason whatsoever why we wouldn’t use it in 1968”. Whereas The Swedish paper titled the article “Horrifying picture”, the Norwegian daily Verdens Gang titled it more modestly “Blood transfusion can make the transition easier” when re-publishing the article and it is interesting the handful of news items treated the issue more as a problem of medicalization of the sports than as anything against “fair play”. When Saltin gave a lecture about his observations in Symposium on Sports in Medium Altitude organized on December 15-19 in Switzerland, the published manuscript doesn’t mention transfusion idea, but instead he writes that for pre-emptive adaptation before the Olympics “[o]ne possibility for a country such as Sweden with no suitable altitudes may be to have its competitors training and perhaps living in a low-pressure chamber”. (Saltin, 1967b) The method is similar to the one used today by the athletes to mimic low-oxygen environment, whereas today the preferred and simpler method is to “enrich” the air with nitrogen in order to lower the oxygen content. While Björn Ekblom referred to the Bethesda research in some of his research papers from the 1970s, he recalled that it was Saltin who brought the research into his attention in the first place, so the older colleague was familiar with the research. While it is far from certain if Saltin ever conducted the altitude transfusion experiment, altitude adaptation through needle found its way into academic publications. Two West German researchers took a group to high altitude and injected them intravenously daily with an extract made from the blood of calves. They did this for a few weeks and noticed that the group performed better at altitude than the placebo group. While the researchers weren’t that interested in this the sea level performance, the charts of the paper also reveal a tendency for performance to be higher after returning to sea level, but the difference wasn’t statistically significant. (Albrecht & Albrecht, 1969) Shortly after the Olympics, Argentinian hematologist Enrique Rewald from the Fundacion Mar de Plata took a cohort of tennis players to altitude and infused half of them with 1200 milliliters of blood and conducting exercise test on them. He noticed that “subjective tolerance of exertion was almost similar to that at sea level” and compared to the control group, they had a “clear-cut advantage” and their exercise heart rates were also significantly lower than those of the placebo group when walking at speed of 4 mph. The research is very much related to blood doping and was published in The Journal of Sports Medicine and Physical Fitnessin 1970. (Rewald, 1970) As a result, there were research papers with transfusion elements focusing on performance around the time when the blood-doping research was conducted in Sweden. When Ekblom described the blood-doping research for the first time with Swedish media in 1971, he speculated that someone else might’ve invented the method recalling that “some East Germans” had told him they’d heard something similar in a conference in Mexico but were unable to provide references. (Magnergård, 1971) It is very likely that this something similar might’ve related to the altitude adaptation problem and not directly to his research problem he had been working on. It should be emphasized that while the blood transfusion research (and possible application) surrounding the 1968 Olympics was conducted in order to elevate performance, it tilted more towards “restoring” the exercise capacity to that of sea level and it wasn’t taken as given that elevated hematocrit increased Vo2Max and performance universally, so the Swedish “real” blood doping research and this research were two different subjects and even if competitors at the México Games were transfused, it doesn’t automatically follow that blood doping was “invented”, even if transfusions were carried out in practice. In any case, transfusion research in the sports context was getting more and more momentum internationally. This is part two of a multi-part series titled “Limiting Factors – A Genesis of Blood Doping”. (The bibliography listed below presents the full list of resources used in gathering information for the series.) If you find yourself this morning in a part of the world where it’s truly cold, we feel for you. If you get outside and ski today, say in the Midwest (we’re thinking of you Duluth), the snow might be sandpaper slow, but the upside, there will be no snow melt. The trail conditions will hold until the next banana belt puff of air blows through. Here at FasterSkier, we scanned the archives to bring you some cold-related resources. This may not be the type of Wednesday Workout you expected. If it’s not: be careful in the sub-arctic cold, but by all means, head out and kill the 30 x 30’s or the pre-Birkie 4 x 4 threshold efforts. By the way, not so fast Houghton. By comparison, maybe it’s time for beach towels in the UP. Duluth’s cold is real-deal-cold at -22 Fahrenheit at the time we pressed “publish”. First on the resource list is this brief piece on cold-related injuries. This comes complete with grim photos to deter those from heading out with improper protection. For those of you keen on reading up on respiratory issues and the cold, here’s an interview written by Chelsea Little. The article below features Michael Kennedy, PhD Associate Professor of Kinesiology, Sport, and Recreation at the University of Alberta. If you’re looking to log a rest day, and have already written the following into the notes section of your log, “Too Cold to Exercise”, the New York Times (NYT) published a piece back in 2008 that still resonates. And the title of the article may have you rummaging for those hand and toe warmers, face tape, and respiratory heat exchanger. Don’t leave the NYT so fast. Knowing much of the country would be blanketed in frigid air today, they published a short resource for combating cabin fever. Yes, we agree, it is downright cold out there. We’d say under a certain temperature, cold is simply cold, no matter what the thermometer reads. Editors at Scientific American ran a piece yesterday titled, “The Coldest Place on Earth”. They may disagree with the assertion that under a certain benchmark (its personal for each skier) cold is cold. They aptly end yesterday’s piece with this sentence: “So take heart if you’re experiencing a polar cold, it will get warmer again, and it could be much worse.” One of the biggest public health challenges worldwide is physical inactivity. As the World Health Organization reported in August, the number of obese children and teenagers has grown by ten times in the last 40 years, and in five more years there may be more obese children than underweight children in the world. As a result, there’s a lot of interest in how to motivate people to take part in physical activity. As we wrote about earlier this fall, that includes a study of American Birkebeiner participants which found that participating in group-based exercise provided an important extra bit of motivation even for people who were quite self-motivated to exercise or train. Another piece of the picture was examined in Finland. There, researchers had the opportunity to use a study of twins to disentangle the genetic and environmental contributions to people’s motivation to do physical activity in their “leisure time.” “In classical twin studies, we compare a resemblance within pairs of identical twins to the resemblance within pairs of fraternal twins,” Dr. Sari Aaltonen, the lead author on the study which was recently published in the Scandinavian Journal of Medicine & Science in Sports (but is behind a paywall), wrote in an email. “For instance, if identical twins are more similar than fraternal twins, then genes significantly influence that trait. If the correlations for fraternal twins are equal to those for identical twins, then shared environmental influences (e.g., childhood home environment, if the children were raised together) are indicated to have influence that trait.” Using this framework, Aaltonen and colleagues in Helsinki and Jyvaskyla, Finland, and in Amsterdam, the Netherlands, worked with 1,271 pairs of twins in their early and mid 30’s. They gave each twin a survey to assess how much each of eight different dimensions of motivation contributed to the reasons they exercise. In that part of the study, three of these dimensions turned out to be most highly rated by the twins as reasons why they exercise. One was physical fitness, the next psychological state, and the third enjoyment of sport. Then using genetic twin modeling, the researchers inferred how “heritable” each of these different types of motivation was. Heritability is an estimate of the proportion of variation in trait, in this case the source of motivation, which is controlled by genetic variation. In a perfectly heritable trait, 100% of the variation is controlled by genes inherited from the parents. In a completely non-heritable trait, genes have no influence and instead the environment or other factors control how the trait is expressed. “In general, we know that the most of human phenotypic traits are complex traits; both genetic and environmental factors influence them,” Aaltonen wrote. “Our heritability estimates of the motives for physical activity have ranged between 13% and 53%.” That’s a wide range. The paper gets into which sources of motivation are more heritable than others. For example, “others’ expectations”, “mastery” (improving one’s skills or abilities), “competition/ego”, and “physical fitness” were all highly influenced by environment. For these dimensions of motivation, around 80 percent of the variation in people’s assesment of their importance was driven by environment, rather than genetics. Even for the more heritable dimensions of motivation, environmental factors were still clearly important. In the most highly heritable source of motivation, “enjoyment”, with 33 percent of the variation in men and 53 percent of the variation in women being explained by genetics influences. “Enjoyment is a strong intrinsic motive, which means that a person is motivated to be physically active because she or he finds it pleasant, fun and/or satisfying,” Aaltonen wrote. “When people are intrinsically motivated, they follow their innate needs and interests. Therefore, it may not be surprising that ‘enjoyment’ was found to be the most heritable motive dimension in our study.” Similarly, in a study in the Netherlands, lack of enjoyment was found to be moderately heritable in men – that is to say, for those who really hated exercise, environment didn’t do much to affect that. “Previous animal studies (mainly in rodents) and human studies suggest that there may be a biological regulation in terms of the motives for physical activity,” Aaltonen added. The next most heritable source of motivation was “affiliation”, defined as “be with friends and/or do activity with others,” with 39 percent of the variation in men and 35 percent of the variation in women being explained by genetic influences. How can heritability be different between men and women – aren’t genes passed on in the same way? Aaltonen explained. “Generally, the heritability estimate is always time-, age-, population specific and, above all, it is an estimate of the genetic influences to individual differences on a population level, not an estimate pertaining to a single individual,” she wrote, explaining that all the variation can be partitioned into either genetic or environmental sources, so a high heritability estimate can simply mean that environmental influences exist, but that they are not so important in terms of determining the trait. “The high heritability estimate for enjoyment in women, for example, means that women’s enjoyment as a motive factor for leisure-time physical activity is less affected by environmental influences.” “Why environmental factors are less important for women’s, but more important for men’s enjoyment to exercise in Finnish adults in their mid-thirties?” she mused. “Right now, I don’t have an answer for that. Based on our quantitative genetic results, we are not even able to reveal what the specific genes or environmental factors are that cause the difference between men and women. In terms of clinical implications, physical activity-promoting measures that try to motivate people to exercise may be even more important for men than for women, because of the greater role of environmental influences in men.” That was just one of the insights that the researchers gained about how public health efforts could be targeted for success in motivating people for physical activity. For example, physical fitness and enjoyment were both highly-ranked sources of motivation, but the former was determined more by environmental factors – and thus may be easier to affect by intervention – while the other was fairly heritable, controlled by genetics rather than a person’s surroundings or interactions. “Several studies have suggested that extrinsic motives (for example, you want to be fitter than others, you exercise only because someone told you to do so, etc.) could be dominant during the early stages of exercise adoption, but that intrinsic motives (enjoyment and the satisfaction of exercise) would be more important for progression to and long-term maintenance of activity,” Aaltonen explained. “In other words, it may not be that difficult to get people to be motivated to exercise, but a challenge is to get them continue the activity habit. It helps if you enjoy it.” “Due to this, a key issue may be to find a physical activity habit that is the most enjoyable for you,” she continued. “Then, you may better be able to stick to your activity routines also when you have a lack of motivation.” At the same time, recreational athletes using heart rate monitors during their training will sometimes see numbers go up as high as 220 or 225 beats per minute (bpm). Such racing heartbeats are called tachycardia, and some of the possible underlying causes can be life-threatening. But does a high heart rate reading on a heart rate monitor equate to this dangerous condition? That’s what Polish doctor Robert Gajda and colleagues set out to investigate. They suspected that the super-high heart rate readings were errors, but knew that they did cause anxiety for some of the athletes in question. Even if a reading seems crazy, it can sow a seed of doubt about an athlete’s health. And that makes them important. “I assure you, we do not get seriously sick during training and not notice it,” Gajda wrote in an email. “More than the [heart rate monitor] indications, clinical symptoms are important and should worry us … we need to inform people about the occurrence of artifacts in heart rate monitor readings, instead of sending them for senseless diagnostic procedures or abstaining from physical activity.” They also had a second question. Regardless of whether the high readings were correct, if athletes had any other kind of heart arrhythmia, would an off-the-shelf heart rate monitor detect it and thus provide them information they could use to protect themselves? In a paper recently accepted by the Scandinavian Journal of Medicine and Science in Sports, Gajda worked with 142 runners and cyclists who came to his Center for Sports Cardiology because they were suspected to have heart arrhythmias. All of the athletes had seen sudden, large increases in the heart rate readings on their monitors while exercising. Under the researchers’ watchful eyes, the athletes tried to replicate these readings, this time wearing not only a heart rate monitor but also a Holter Electrocardiogram (ECG). This small device uses electrodes and provides a detailed picture of electrical signals. “The Holter ECG is a professional device recognized worldwide by doctors as the gold standard for assessing arrhythmias in patients,” Gajda explained. “It accurately records the heart rate at a given moment of measurement, the average value of the whole record, as well as its minimum and maximum value … we see not only the heart rate but also its possible abnormalities, such as extra ventricular and supraventricular beats.” A heart rate monitor, on the other hand, simply “detects the main electrical field produced by the heart muscle.” Instead of seeing the whole heartbeat as one would on an electrocardiogram performed at a hospital, or from a Holter ECG, a heart rate monitor simply counts what it detects as heart beats and displays that as an average rate. “Some [heart rate monitors] with ‘beat-to-beat’ measurements and data storage capabilities do permit accurate heart rhythm analyses,” Gajda wrote. “However, these devices are also prone to artifacts that are often similar to a ‘beat’… we still do not know whether we observed the R-R distance (QRS to QRS) or only the ‘artifact peak to artifact peak’.” (The QRS is a phase of the heartbeat when the ventricles are depolarized before contraction, and the R wave – the middle of the QRS – is the biggest wave or peak on an electrocardiogram, as seen in the diagram at right.) Wearing both their own normal heart rate monitors – such as the Suunto Ambit3 or a wide variety of Garmin Forerunner models – and the Holter ECG’s, the athletes were told to head out on their usual training for about an hour. Of the group, 39 percent failed to replicate the earlier high readings. Neither their heart rate monitors nor the Holter ECG’s picked up anything abnormal, and there was also no difference between the readings provided by the two instruments in terms of average, maximum, or minimum heart rate. A second group of athletes, about 15 percent of the total pool of subjects, picked up signs of arrhythmias on the Holter ECG but not on their heart rate monitor. These were single ventricular or supraventricular heartbeats, and, in the absence of other symptoms, don’t really indicate major heart problems. “Every healthy person has supraventricular and ventricular beats during the Holter ECG record,” Gajda explained. “Arrhythmias have been observed in athletes with ‘healthy hearts,’ but it is not a negative prognostic factor and does not constitute grounds for abstaining from sporting activities … athletes in this group should not be concerned about these irregular beats, especially if there are no other connected clinical symptoms, for example chest pains.” If there are those other symptoms, then it’s another story. Most off-the-shelf heart rate monitors do not detect such single beats, because they “average out the rhythm” by counting electrical stimuli. So if an athlete has some indication that they should worry about heart disease and wears a heart rate monitor, they will not find out about these extra beats. An actual ECG would be needed. “The value of [heart rate monitors] for detecting arrhythmias in runners and cyclists is not supported by the results of this study,” the authors wrote in the paper. Finally, for 45 percent of athletes, an arrhythmia was indicated by the heart rate monitor: on average, a reading of 199 bpm for roughly a minute, but in the most extreme case a reading of 236 bpm for three minutes. In only one athlete was this reading accompanied by the detection of an arrhythmia on the Holter ECG. For that athlete, it was quite clear that something serious was happening as the heart rate rose from 167 bpm to 227 bpm. “The athlete was forced to cease training due to clinical symptoms and the sudden decrease in exercise capacity,” Gajda explained. After resting, the rhythm went back to normal. For the other 64 athletes, the high reading on their heart rate monitors was not accompanied by either clinical symptoms or high readings on the Holter ECG. Those athletes were not having arrhythmias. The readings were just errors. “It is not possible to have a HR of 200-220 bpm and feel good,” Gajda wrote. “Such arrhythmia ‘cuts off’ the athlete suddenly, and even if he or she does not lose consciousness, they cannot continue to exert at the same level of intensity. Such tachyarrhythmia forces you to stop. You can’t catch your breath. You think about the worst. This is the feeling of person with severe tachyarrhythmia. You can’t miss it.” The fact that so many athletes can encounter these faulty readings, Gajda believes, is something of a public health issue. The numbers are alarming and cause some athletes to dial back, either in that particular exercise session or in terms of how much they exercise at all. “A physically active lifestyle is widely promoted for healthy individuals and large groups of patients,” Gajda wrote. “Millions of physically active individuals worldwide use heart rate monitors to control exercise intensity. False ‘arrhythmias’ or surprisingly high bursts of heart rate during exercise can induce fear in physically active individuals and might cause them to reduce or even abstain from training, or to seek unnecessary, time-consuming, and costly medical diagnostics. So we can say: this is a public health issue.” The reason such anomalous readings are generated has to do with electricity. Heart rate monitors are just meant to pick up the electrical field of the heart, but many of these “artifacts” come from other electrical signals. “Sometimes it is enough to change the position of the belt and the pulse values will return to normal,” Gajda explained. “Sometimes we run alongside the high-voltage line and the heart rate monitor goes ‘crazy’. A few meters further it returns to normal.” A few other factors can lead to more frequent errors in the readings. For example, carrying a cellphone with you training provides additional electromagnetic waves that can disrupt transmission from the chest strap to the watch. Sometimes other athletes’ heart rate monitors create interference and errors as well. Another source of artifacts is additional clothing either around the chest strap or the watch. For winter sports athletes, this could be a particular issue. “There is no doubt that thicker winter clothing is conducive to the development of more artifacts,” Gajda wrote. “A thick glove on the ‘watch,’ too. Sometimes this occurs in the form of a complete disappearance of the connection between the belt and the watch … It is likely that synthetic materials that are easier to electrify may produce more distortions.” And women, wearing sports bras, have an extra layer they have to worry about. “The idea is for the chest strap to stick well to the body,” Gajda wrote. “This problem is beginning to be noticed by manufacturers of heart rate monitors. Today there are already some on the market that use a sports bra or shirt as the strap of a heart rate monitor (equipped with integrated electrodes). I think further development in this area will solve this problem completely.” Then, there’s simple body movement. There are fewer artifacts in heart rate monitor data for cyclists than for runners, indicating that having a steady upper body position reduces the error rate. Gajda wasn’t sure what the cross-country skiing motion would mean in terms of these erroneous readings. If an athlete carefully adjusts for all these factors – repositioning the chest strap, wetting the sensors so they stick to the skin better, re-arranging clothes, replacing batteries and other parts, and avoiding other sources of electrical interference – but the high readings keep coming, then they should seek out a physician even if they don’t have other symptoms, Gajda and his colleagues suggested in their paper. But overall, his message is clear. Heart rate monitors are valuable for monitoring and controlling the intensity of training, but for detecting arrhythmias, they aren’t as great. Very high heart rate readings shouldn’t alarm athletes in the absence of any other symptoms of discomfort. The way to check whether the number is real, Gajda reminded, was to stop what you’re doing for a minute and take your pulse. The biggest problem with anomalous readings from heart rate monitors is one of annoyance, he posits, because such artifacts make it harder to accurately track the intensity of exercise. Sure, your heart rate isn’t actually 220, which is a relief – but what is it? “We should be upset that you do not record the training in accordance with its actual reality,” Gajda wrote. “For me, still an active runner, it is an extremely important part of the training, which informs me not only about the quality of the effort but also my form – overtraining or lack of training.” Robert Gajda, MD, PhD, director and owner of Center for Sports Cardiology (CSC) at the Gajda-Med Medical Center in Pułtusk/Poland, is a cardiologist and sports medicine physician. His main area of research interest is physiological adaptation to endurance training as well as to extreme endurance efforts. He cooperates with Polish scientific institutes in this field. Dr Gajda is an active runner and the record holder of Polish doctors in the marathon. Biathlon is a notoriously variable sport: besides skiing, there’s the shooting aspect which can ruin a race in a matter of seconds. Sometimes an athlete like Lowell Bailey wins a World Championship for the first time after 15 seasons competing; sometimes the most reliable guy in the sport, Martin Fourcade, finishes 46th. It’s a wild world. Norwegian PhD student Øyvind Skattebo set out to quantify just how variable the sport is, and what amount of improvement is needed to make the signal of better performance come through that noise and lead to more medals. “The trend is for more athletes on the podium in biathlon compared with cross-country skiing,” Skattebo, who recently published one of his studies with Thomas Losnegard at the Norwegian School of Sports Science in the International Journal of Sports Physiology and Performance, wrote in an email. (The paper is available for free/open-access here.) “The reason for this is not that it’s a ‘tougher’ field than in cross-country skiing,” he explained. “If anything, there is less spread between the best athletes in cross-country skiing than in biathlon. However, the biathletes vary more in performance from race to race due to the combination of several components: skiing, shooting time, and shooting result.” Skattebo reviewed data from World Cup sprint competitions from 2005 to 2015, making up 109 races for women and 110 races for men. That represented more than 10,000 performance observations, and more than 1,000 observations of athletes who were ranked in the top 10 during a World Cup season. Looking at the variability of performance within and between individual athletes, he could find some interesting patterns. For instance, men were no more consistent than women, but the top athletes were better matched in terms of ski speed. Another finding was that while shooting times are highly variable between athletes, in terms of statistical significance, the magnitude of this variation didn’t have much effect on the final result of a sprint competition. Athletes spend much more time skiing than shooting, and missing a shot has a greater effect than simply shooting slower than the next athlete on the range. “There has been a great development in shooting time the last 10-15 years, and I believe a further reduction in shooting time (for the best athletes in the field) is more or less a waste of training time,” Skattebo asserted. “They have more to gain by getting more accurate or skiing faster. Understand me right, there are still a lot of senior competitors out there that can improve performance by reducing shooting time, but I think more or less that the best athletes don’t have anything to gain.” It’s possible that shooting speed would have a bigger effect on total race time in head-to-head competitions like pursuits and mass starts, but Skattebo didn’t look at these results because sprints are much more straightforward to analyze – and there are more of them on the World Cup schedule, too. “Maybe if we had looked at the last shooting in mass start or pursuit, where a quick shooting with several competitors entering the shooting range at the same time can definitely give an advantage on the last lap, [there would have been something],” he wrote. Meanwhile, in terms of total race time, there was more variability in athletes’ overall performance than in either skiing or shooting separately. “The shooting and skiing performance varies moderately and accumulates into a large variability in overall performance,” Skattebo explained. Strategies to try to make teams and athletes more competitive should, at an organizational level, take this into account. In biathlon, having a solid, but not star, athlete — one ranked between 10th and 20th, for example — can lead to medals, but not reliably. “The annual top ten cross-country skiers vary 1.8% in performance from race to race (in a 15 k skate race), compared with 2.5% for the same standard of biathletes,” Skattebo wrote. “Therefore, at one biathlon event the apparently best athlete can miss the top-10, and if several of the best performers fail a normally ~15th-ranked athlete can win. The biathletes are generally less reliable in performance than athletes in several other endurance sports and, therefore, it is less easy to predict the winner.” In some ways, that’s a selling point of biathlon: the excitement of a race, the anything-could-happen feeling in a mass start, the lead changes and penalty loops. “This makes it more exciting to watch,” Skattebo wrote. “Of course, [I’m being] completely objective since this is coming from a former biathlete.” To get reliable medals instead of waiting for a chance for that 15th-ranked athlete to seize the day requires a targeted approach to improvement. Skattebo applied a calculation used in other sports to try to find the minimal “worthwhile improvement” needed for an top-10 athlete to get one more medal out of every ten sprint starts. The strategy is to take the variability in performance of the top-10 athletes – and in this case, take the standard deviation as the measure of variability – and multiply it by 0.3. “Previous statistical analysis of performance times and data simulations have shown that a performance improvement of 0.3-0.4 times an athlete’s SD will lead to about one more podium placement per ten competitions, for an elite athlete normally finishing among top 10,” Skattebo explained. “These analyses and simulations were originally conducted in track and field, but the derived thresholds have later been checked and used for other sports, such as rowing, swimming, orienteering, cycling, and cross-country skiing.” For a biathlon sprint, that measure corresponds to about 12 seconds for both men and women if the athlete is already in the top 10. In other words, that variability in performance will always be there for each athlete. But if one of them improves their performance on average by 12 seconds – skiing 1.2 seconds faster per kilometer for me, or hitting one more shot every other race, perhaps – then the best end of that variability will be medal-worthy 10% more of the time. For athletes ranked further down the standings, bigger gains would need to be made. “An improvement corresponding to 0.3 x an athlete’s SD that normally finishes 30th place would not get him/her to the podium,” Skattebo wrote. “This since the 30th-place male on average finishes ~96 seconds behind the winner, and an improvement of 12 seconds would ‘only’ get him to 24th place, on average. An improvement of six ranks is substantial, and would of course be meaningful for the athlete. But not enough to aim for the medals. So, even though the thresholds are calculated to evaluate how much a top-10 athlete need to improve to be at the podium more often, an athlete in the middle of the field would definitely benefit from a similar improvement.” But for a top-10 athlete where 12 seconds will make a big difference, the next question is where those 12 seconds will come from. One interesting result that Skattebo saw was that simply targeting greater resources for championship events — where medals matter the most — might not cut it. Although such a strategy might raise the performance of a team’s athletes, performance actually improves substantially across the board, so it might not be enough. And showing up at the Olympics and turning in simply an average performance from the rest of the season will not lead to impressive results. “It looks like all the athletes (on average) improve 2-3% towards championships compared to their mean performance at the World Cup,” Skattebo said. “So, to even finish equally as [they would at] World Cup they need to improve. And to improve their rank they need to improve their performance even more.” To take a top-10 World Cup athlete and make an improvement worthy of an Olympic medal, then, Skattebo suggested that a 3-percent improvement would be needed — more like 45 seconds compared to the athlete’s standard previous World Cup time. A number of strategies are possible to try to get to such a level, and probably they should all be pursued. “I believe it is not a single explanation, but a combination of … better prepared skis and physiological peaking by the athletes,” Skattebo wrote. What are the physiological capacities of nordic-combined athletes and can laboratory tests predict performance capabilities on the World Cup? Those are the questions that a team of Norwegian researchers set out to answer by testing 12 competitors from eight different countries before a 2015 World Cup competition in Trondheim, Norway. The study, led by Vegard Rasdal of the Norwegian University of Science and Technology and the Norwegian Olympic Sports Center, was recently published in the academic journal Plos One. It is an open-access journal, so you can read the paper here. “The sport is always evolving,” Rasdal wrote in an email to FasterSkier about the results. “Today it is no longer enough to be ‘just’ a strong ski jumper or cross-country skier, you really have to excel in both in order to be successful in terms of podiums. Johannes Rydzek and Eric Frenzel, the two most successful athletes last season, were not only two of the best jumpers last season but also the fastest skiers.” Indeed, they found that the best skiers in the nordic combined field have VO2Max capacities close to those of the best cross-country skiers, period – and even higher than those of Olympic medalist sprinters. Furthermore, this was a good predictor of World Cup results in the Trondheim competition. Variability in Abilities and Physiology There have been plenty of physiological studies on top cross-country skiers and some on ski jumpers, but the fascinating aspect of nordic combined is that two very different sports are combined. That creates uncertainty about what the ideal physiology for a competitor might actually be. Should they be light and explosive, for jumping? Strong and enduring, for skiing? And do nordic-combined atheltes have as much explosive power as ‘special jumpers’, or as high aerobic capacities as cross-country skiers? “As with most endurance sports, you will find a strong association between VO2Max and performance when the study group is heterogeneous, as e.g. a study group of 200 college students,” Rasdal explained. “Overall, VO2max is widely accepted as the most important factor for endurance performance. However, in a more homogenous study group, such as elite cross-country skiers, all athletes may have a ‘high enough’ VO2max to perform well at an elite level. Thus, other factors such as skiing efficiency becomes a stronger determining factor.” Rasdal and his co-authors wondered whether nordic-combined athletes fell into the first group, with moderately variable VO2Max, or the second group, where all had such high capacity that they had to be distinguished by some other characteristics. Because some athletes get their start in ski jumping, and all must also train for jumping, the athlete selection process and training background from young ages is different than for cross-country skiers and could lead to more variability among individuals. “It is not given that all nordic combined athletes have a ‘high enough’ VO2max or vertical jump capacity,” Rasdal wrote. “The shortcomings in one may to some degree be compensated with higher level in the other.” To address that question, the research team partnered with the International Ski Federation (FIS) to conduct laboratory tests on athletes the day before a World Cup competition. “FIS was responsible for the invitation of athletes, and each nation in the World Cup was invited and encouraged to participate with two athletes to be tested,” Rasdal explained. “To collect data on the very best athletes in the world is always a challenge, especially so close to an important international competition. We as a research group are extremely grateful that so many World Cup athletes chose to participate in the data collection.” The athletes ran the gamut from being ranked second to 66th in the previous season’s overall World Cup standings, and included the eighth-best skier and second-best ski jumper. About Endurance Capacity, and World Cup Success The hypothesis that nordic-combined athletes were more variable in their physiology compared to single-sport specialists was largely upheld. “Among the athletes we studied, a VO2peak range of 66.9-80.8 could be found, which does illustrate the heterogeneity in nordic combined,” Rasdal wrote. “This may make subordinate factors such as skiing efficiency relatively less important (although still important) than VO2peak.” The upper measurements of VO2Max among the 12 athletes are close to those of cross-country skiers. Furthermore, it was clear that the athletes on the lower end of the VO2Max spectrum were somewhat less successful on the World Cup. At least at this World Cup event, the overall ranking at the end of the day was strongly correlated to an athlete’s VO2Max and ski performance. “This study together with the study by Tønnessen et al. may indicate that a body-mass normalized VO2Max in the region of 75 ml/kg/min is a sufficient capacity for a strong cross-country performance in Nordic Combined, whereas 80 is at very highest percentile,” Rasdal explained. However, the Trondheim World Cup course is not necessarily representative of all World Cup venues. And poor cross-country skiing could have been penalized even more at this venue than usual. “Trondheim is a special arena compared with other courses in the World Cup, with many steep uphills and fast downhill terrain,” Rasdal wrote. “In addition, 2015 was a bad winter in Trondheim, and the course was salted and ice hard. This made the event well suited for technical good skiers with strong upper-body capacity. It is therefore necessary to investigate the impact of ski jumping versus cross-country skiing on overall performance, as well as the associations to laboratory capacities, also at other venues and conditions.” And About Those Jumps The implication is that perhaps at a different competition, the association between ski jumping performance and overall competition ranking might be stronger. “Unpublished data does show that [across a whole season], the regression line for ski jumping to overall performance is similar to that of cross-country and the correlation coefficients are similar,” Rasdal explained. When it came to benchmarking, the researchers also identified laboratory measurements that could predict ski jumping performance by nordic-combined athletes. They tried two measurements: a straight, simple squat-jump, and an “imitation jump” where the athletes were asked to start in the same position they would on a ski jump ramp. The jumping style and technique varied from athlete to athlete. While it seems logical that these would be good predictors of ski jumping performance, it actually wasn’t a trivial matter. Such measurements have mainly been validated on straight ski jumpers, and because of their different body mass and physiology the relationship between squat jumping and performance, for example, could very well have been different among nordic-combined athletes. “The time available at the take-off in the [ski jump] hill may present a greater challenge for NC athletes than specialist ski jumpers as two-thirds of the NC athletes’ annual training consists of endurance training,” the authors wrote in the paper. “This does not only leave less time available for power and [jumping-] specific training compared to the specialists, but endurance training may lead to negative effects on muscle strength and power.” But in the end, the same measurements did predict ski jump performance. “The jump capacity in the sport-specific imitation jump distinguished performance level better than the general jump capacity in squat jump,” Rasdal wrote. “That supported the argument for sport-specific testing at an elite level.” Still, the imitation jump wasn’t perfect at predicting actual ski jump performance. “The upper range of the lowest ranked performance group touches the lower range of the highest ranked performance group,” Rasdal said of the imitation jump measurements. “There is not necessarily a continuous linear relationship with performance. At some level, the ability to utilize the capacity in the field as well as other factors become more determining for performance, e.g. body mass, transition to flight (minimize the loss of speed), flight performance, etc… Ski jumping is an extremely challenging technical task to be performed in less than 0.35 seconds, and where a well execution may compensate more for a lack of physical capacity.” And then there’s money. “In ski jumping the equipment plays an important role, and the nations with the highest budgets may for instance have better suits which makes them jump farther,” Rasdal said of other potentially confounding factors in predicting jump performance. What to Shoot For At the end of the paper, the authors summarized the ideal characteristics of a nordic-combined athlete: high VO2Max, a strong upper body, a good vertical jump, and low body mass. Hitting all those different metrics at the same time is a tough calculus, but it’s what is required to be a champion these days. “Although the relative importance of ski jumping to overall performance has varied in the sport over time, the pendulum today appears to lean more towards ski jumping,” Rasdal noted. “That’s both as a result of regulations (e.g. increase of meter-value in large hills in 2015), and also an increase in overall performance level where the best ski jumpers also ski fast.” When I heard that there was a new book coming out about heart arrhythmias in endurance athletes, I was interested. Several years ago, I read some of the research papers that the book’s authors refer to. One was a cohort study on participants in the Vasaloppet, the 90-kilometer ski marathon in Sweden. Those researchers found that skiers who competed in more Vasaloppets had more heart arrhythmias – as did those who finished the race the fastest. I wrote a piece about the findings at the time. The FasterSkier commenting system has changed, so original comments no longer appear at the bottom of the article, but I remember them clearly. Multiple commenters found the study hard to believe. One commenter was so sure that the findings were impossible that he wrote multiple angry comments arguing that exercise is good for you, so it couldn’t possibly cause heart problems. As a scientist, I was flabbergasted. There are a lot of crappy studies out there in sports science — and science in general, but I’m used to reading sports science papers with sample sizes of eight athletes. It’s hard to defend a lot of conclusions made from such studies. But this one? The researchers had following thousands and thousands of individuals and, well, numbers are numbers. An individual is either diagnosed with an arrhythmia or they aren’t. This was pretty straightforward. Scientists go out and measure a phenomenon, and then we present numbers as an estimation of the world. There are many legitimate reasons to question the data or interpretation, and this is actually built into the scientific process. Before publication, other scientists will rip a a study apart as part of “peer review”, suggesting ways to make it better or even recommending it not be published. That doesn’t mean that all published research is perfect. After publication, scientists continue to raise important points about whether the data collected represents reality (due to potential flaws like bias or study design), whether the statistical techniques are appropriate and correctly performed, whether alternative mechanisms could explain the patterns shown, and more. The public should absolutely engage in this process — and scientists should do better about engaging with the public. Anyone outside the study itself can ask questions that the researchers might not have seen, illuminating important aspects and leading to new research questions or repeating the study in a different way. In the end, this leads to gradually more and more accuracy in that estimation of the world. Asking good questions is different than arguing that data is wrong simply because of a gut feeling or belief. The reaction to the Vasaloppet article was a frustrating moment for me but, I would come to realize, not an unusual one. When presented with facts that do not support our worldview, we tend to just discount them. It’s human nature. All of which is to say that I was very interested to read The Haywire Heart by Chris Case, John Mandrola and Lennard Zinn. First, I wanted to get more background on the topic, and I wanted it to be explained to me in clear, straightforward language instead of the scientific jargon of research papers. Second, I wondered if the book would get the same reaction as my old writeup of the Vasaloppet study. And third, I was interested to see whether, when presented with some scary narratives, I had the same reaction as those few FasterSkier commenters. After all, as much as I tout that I’m a scientist, I, too, have knee-jerk reactions — and I spend a lot of time exercising. I guessed that I might find the conclusions of the book plenty threatening. The book opens with the story of Zinn, who is a former national team cyclist and a staff writer for VeloNews. Zinn is riding his bike outside of Boulder, Colo. He feels his heart skip a beat, and his heart rate “had jumped from 155 to 218 beats per minute (bpm), and stayed elevated.” Zinn initially takes some rest and dials his training back, but ultimately he tries to keep riding and training. The incidents become more and more frequent until his heart actually stops at one point. After that, Zinn radically changes his lifestyle. He does no hard efforts and much less training volume, period. Because of that, he’s still around to write the book today. His life is richer now, he writes (although it sometimes sounds like he is trying to convince himself as much as the reader). He has developed more different hobbies and can spend more time with his family. But it took him a long time to come to that understanding. It’s a transfixing story about what can happen to a seemingly fit, healthy person. Because Zinn is an author on the book, you know that he will make it out alive. But how far will he go before he stops training? What will happen to him? Could that happen to me? As we say in research, the plural of anecdote is not data. While the authors include “case studies” at the end of every chapter (several of which feature cross-country skiers who nearly died on the side of Colorado ski trails), they also bring the data. The book presents a compelling argument that we should be thinking more about our hearts – and particularly, the heart’s “electrical system,” as the authors call it. Endurance exercise doesn’t seem to increase the prevalence of problems with the “plumbing system,” or how the blood is pumped. That’s not to say that athletes don’t have heart attacks (or, more accurately, myocardial infarctions). Risk factors are risk factors, and don’t completely disappear with exercise. High blood pressure, high cholesterol, a family history of heart disease, being male rather than female – these increase the risk of a myocardial infarction. In particular, athletes who came to endurance sports later in life and previously smoked or were overweight still carry those risks with them. But the unique risk associated with long and intense bouts of exercise seems to be in the electrical system. Studies across multiple sports and countries, as well as in animal models like mice, rats and goats, have shown that the electrical impulses that keep the heart in rhythm can be made, well, haywire, by a lifetime of endurance training. There’s a wealth of observational, epidemiological data suggesting that a long-term habit of endurance exercise can cause atrial fibrilliation, a rapid and irregular heartbeat originating in the atria. (Atrial fibrillation was the type of arrhythmia mentioned in the Vasaloppet study.) Other arrhythmias seem to occur more frequently in athletes, too, like ventricular fibrillation. Premature ventricular contractions are common in trained athletes and don’t necessarily lead to bad outcomes; complex ventricular arrhythmias are also common, and can lead to cardiac arrest. Exercise can also make genetic diseases like arrhythmogenic right ventricular cardiomyopathy (ARVC) more dangerous, and can lead to the disease even in the absence of genetic markers. Some causes are straightforward. One symptom of “athlete’s heart,” as it is called, is enlarged chambers in the heart. And this is associated with atrial fibrillation: patients with atrial fibrillation tend to have larger left atria than those without. Exercise also leads to inflammation of muscles. The heart is a muscle; inflammation can lead to scarring, which can then disrupt the transmission of electrical signals across cells. The logic and evidence go on and on. The authors explain all of this much better than I can, even when paraphrasing. I’ll let you read the book and just say: it’s convincing. And if you haven’t studied human anatomy since high school, don’t worry. It’s clear and well-explained. As to the second question, the authors tackle that, too. Mandrola, a doctor, notes that when many athletes receive a diagnosis of a heart problem, they go into denial. Many decide not to change their behavior. There’s a sort of cognitive dissonance to being told that something you have always believed is healthy is actually putting you at eventual risk of death. “It is completely natural to go into denial for a while,” Zinn writes. “I don’t know of any masters athletes diagnosed with non-life-threatening arrhythmias who didn’t go back to pushing it hard in training or racing in hopes that the incident that sent them to a cardiologist was just a fluke.” If you do have a problem with heart rhythm, the authors provide several chapters as a guide for when to go to the doctor, what to ask and tell them, and what treatment options might be available. Getting a correct diagnosis is key, and as cross-country skiers, that is not a trivial ask. “Even doctors who run marathons don’t quite get the intensity thing,” Mandrola writes. “Marathons are a different sort of affair. There is no question that they are hard, but they generally have an even pace and don’t involve the competitive crises that flare up repeatedly in a bicycle race or a cross-country ski race or triathlon.” Women, too, are often misdiagnosed. The authors explain that women are more likely to be assessed as having an anxiety disorder than men, even when suffering from the same underlying heart problems: “Women younger than 55 were seven times more likely to be misdiagnosed and turned away from the ER than their male counterparts.” But the main advice, when confronted with a heart arrhythmia, is first to go to the doctor, and second to back off of training. It might save your life – and it might also make the problem disappear. That doesn’t necessarily mean stopping completely, but it might mean going slower and for shorter sessions. “Detraining” is a good therapy for several diagnoses. “In the end, I believe that all that denial and continued racing and training hard with the hopes of retaining some portion of my former life either damaged my heart or trained it so that it now goes into arrhythmia more easily,” Zinn writes of his own situation. Detraining might seem horrible, like an unacceptable lifestyle adjustment. But as the authors point out, once you know the other options – medications with scary side effects, procedures with non-trivial rates of complications, death – training a bit less might seem like a much better option. As for me? I definitely reacted to the book, but not by going into denial. Instead, I was scared. “The day before he died, he had gone for a six-hour run,” the authors wrote of Micah True, a barefoot- and distance-running legend. I read that the day after I had done a four-hour overdistance running workout. It hit home: none of us are invincible. That said, the one thing I found missing from the book was a real estimate of the prevalence of these heart problems. I could easily follow why they would develop, based on the physiology of the heart and what we do to it. And I found the research cited credible. But how many people does this happen to? Just what is the risk, statistically? One reason the answer might be lacking is simply that it’s hard to do comprehensive research on such a topic. As the authors point out, you can’t really do a randomized, controlled, double-blind trial – the gold standard for scientific studies – about the effects of lifelong exercise. Nevertheless, it’s clear that such health issues are common enough to give one pause. I’m just 30 years old, and I am probably not going to change my exercise habits after having read this book. But it reinforced a lot of peripheral behaviors that I should know are important anyway. For instance, in some patients, arrhythmias pop up only when they are stressed. Leading a high-stress life and sleeping too little are major risk factors. Burning the wick at both ends: that’s the sort of life I lead – and the sort of thing I always know I should work to address, but here’s another good reason to do so. Likewise, making sure to get enough electrolytes when training, to avoid dehydration, to get good rest and recovery, and to listen to your body – these are important. “You have probably been training for many years, if not most of your life,” Mandrola writes in one chapter. “Those years of training have given you a good sense of what ‘normal’ feels like. What you are looking for is anything that falls outside the boundaries of normal.” If I do ever feel a flutter in my chest, I’ll now know not to ignore it. “I think if you’re a nordic skier in New England, you should definitely be alarmed.” “That’s one of the main take-homes: skiing is not going to disappear completely, but it will generally be higher [in elevation].” So says Cameron Wobus, a Bowdoin ski team alumnus and a researcher at Abt Associates, a global research firm. Wobus and colleagues based in Boulder, Colo., and Washington, D.C., recently published a study in Global Environmental Change assessing the impact of projected climate change on the ski industry. (The article is available free of charge here.) Their results: by 2090, many cross-country ski areas across the U.S. are likely to see 50-100 percent reductions in season length. That could translate to more than a million fewer visits by skiers, and millions of dollars of losses in trail-pass revenue. A lucky few ski areas could see only minor impacts, but a lot of that depends on greenhouse-gas emissions scenarios – basically, what the world does to curb the release of carbon dioxide and other greenhouse gases between now and then. “I think a main finding is that elevation is your friend, which isn’t surprising,” Wobus said in a phone interview from Boulder last week. “If you’re a ski area in the Rockies and your base elevation is 10,000 feet, you’re obviously in better shape than if you’re a ski area in central Vermont and your base elevation is 500 feet.” The Nerdy Part of Prediction A previous report by Protect Our Winters and the Natural Resources Defense Council took a more detailed look at the economics of the winter sports industry under projected climate change. What Wobus and his colleagues wanted to do rather than to get bogged down in predicting how interest and tourism for winter sports would change in a warmer world, was to make the best possible predictions of how snowpack and season length would be affected at ski areas. “We wanted to do was a more detailed analysis of the physical snowpack modeling,” Wobus explained. To get to their conclusions, the research team modeled snowpack at 247 alpine and nordic ski areas by combining historical datasets, climate change models, and greenhouse gas emissions scenarios. As a starting point, they used North American Land Data Assimilation System meteorological forcing data, which has been recorded at a fine scale since 1979. They then put this meteorological data into the Utah Energy Balance model to derive snowpack at ski areas, based on what comes out of the sky and landscape factors that would determine how long snow stays on the ground. When the researchers compared this derived snowpack estimate to actual measurements of winter season length collected for the Snow Data Assimilation System – a framework that combines satellite data, airborne measurements, and on-the-ground observations – the match was solid. “We did a reasonably good job,” Wobus said. “Not surprisingly, it’s a little bit messy … but on a region-by-region basis, the only thing we need to get out of the physical model is the season length. So with the exception of the Pacific Southwest, we are generally capturing trends in season length from region to region.” With that information about winter season length in different parts of the U.S. in hand, the researchers applied different climate change models to predict the magnitude of reduction in season length. “We applied a simple delta from what all the climate models were telling us, to say, okay, we aren’t going to rely on the climate models to tell us what the weather is doing,” Wobus said. “We’re going to use a 30-year historical time series to look at natural month-to-month and year-to-year variation in weather. But then we’re going to superimpose on that weather, a climate change signal that is a change in monthly average temperature and monthly average precipitation, coming out of different climate models and different emissions scenarios.” The climate models used, known as General Circulation Models, or GCMs, are mathematical representations of the physical processes happening on and around the earth. “[GCMs], representing physical processes in the atmosphere, ocean, cryosphere and land surface, are the most advanced tools currently available for simulating the response of the global climate system to increasing greenhouse gas concentrations,” the Intergovernmental Panel on Climate Change writes on its website. “GCMs depict the climate using a three-dimensional grid over the globe, typically having a horizontal resolution of between 250 and 600 km, 10 to 20 vertical layers in the atmosphere and sometimes as many as 30 layers in the oceans.” There are many different GCMs – and while they are pretty good at predicting temperature, their predictions about precipitation vary widely. “The precipitation predictions tend to be all over the map,” Wobus said. “We tried to beat it down to the extent that we could by using as many different climate models as we could, given the constraints of our budget. And by modeling as many years as we would, again, given the constraints of how much time we have to do the modeling.” In the end, that meant using five different GCMs. And additionally, the team put all of those models through two different greenhouse gas emissions scenarios. The Findings Especially under the high-emissions scenario, a lot of the differences between predictions made from the different GCMs disappeared by 2090. The authors demonstrated this in a graph of predicted season length for the Bretton Woods cross-country ski area in northern New Hampshire. They showed the predictions for all five GCMs under both emissions scenarios, compared to the baseline season length at present (68 days, with a range of up to 150 days). By 2050 under a lower emissions scenario, mean season length dropped precipitously to roughly 12-33 days, but the range of possible season lengths is quite wide for some of the GCMs. “All these different GCMs have different parameterizations of precipitation, and so they are all going to do slightly different things,” Wobus said. By 2090 under a high-emissions scenario, though, the model predictions all converge between two and 13 days, and the current average season length is not even in the range of possible predictions for any of the models. “By 2090, it’s pretty clear that your distribution of season lengths is very different from baseline to future,” Wobus explained. “That’s kind of regardless of which [emissions scenario] you pick, but RCP 8.5 [the higher emissions scenario] is worse. “That’s one of the main takeaways from the paper,” he continued. “Climate change isn’t good for skiing in the future, but a greenhouse-gas mitigation scenario looks better than a no-mitigation scenario, pretty much across the board.” Why is that? Despite the variability in the precipitation predicted by the models, temperature increases would be so great by 2090 that precipitation largely wouldn’t matter. “You’re looking at close to 10 degrees Fahrenheit of warming,” Wobus said, discussing predictions for the Midwest. “It doesn’t necessarily protect you to be way up north or to be really frigid now. There’s obviously a latitudinal dependence on where things are worse, along with elevation. So maybe if you’re up in northern Michigan with [the higher-emissions scenario] you might still have half your ski season, but it’s certainly going to be shorter than you’re used to.” Part of this prediction arises from the fact that the team assumed that cross-country ski areas don’t use snowmaking. Wobus said that he knows some nordic areas are investing heavily into snowmaking (or snow storage), but in general, not enough currently use it to build into their projects as they did for alpine ski areas. But even if ski areas were to rely on snowmaking, they might be in trouble. For instance, under a high low emissions scenario, just 23 percent of alpine ski areas would have accumulated enough hours of snowmaking in 2090 to open by Dec. 15. As most of the cross-country ski areas are restricted to lower-elevation areas at the bottom of mountains, they would not be in better shape. Without snowmaking, a high-emissions scenario would lead to roughly 87,000 fewer visits to cross-country ski areas by 2050 and 1.1 million fewer visits in 2090 – equivalent, by that point, to $10.2 million less in trail passes sold. Are We Listening? The idea for this piece of research came while spitballing. “We’ve been doing work for ten years around impact of climate change on various sectors of the economy,” Wobus said. “I’ve published papers on the impacts of ocean acidification and ocean warming on coral reefs and linking that to a recreational use model. I did one on inland flooding and monetary damages from flooding. We’ve done all these different sectoral analyses for different economic impacts of climate change.” Living in Boulder and being skiers, the team thought – why not look at that? “We were basically pitching ideas, and we were like, skiing is a pretty important industry in certain parts of the country and it probably has a serious economic impact … so we did it,” Wobus laughed. But the findings have made a splash. “People seem to have been noticing,” Wobus said. “I actually credit Global Environmental Change for having a Twitter feed, of all things. Protect Our Winters picked it up, and Powder Magazine picked it up. … Most times people don’t pay any attention to my research. So it’s kind of cool to have something that’s a little more out there.”