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| Eero Antero Mantyranta in Innsbruck 1964. Source: https://upload.wikimedia.org/wikipedia/ commons/6/6e/EeroMantyranta-Innsbruck1964.jpg |
Some of you will probably stop reading after seeing “Olympic champion” and “hormone” in one sentence.
Don’t be discouraged so easily, I promise doping isn’t the linking word.
Eero Antero Mäntyranta wasn’t just a reglar Finnish skier. He was awfully successful Finnish skier, one of the most successful Finland has ever produced. Eero competed in four Winter Olympics (1960.-72. – or for history nerds, Squaw Valley, Innsbruck, Grenoble, Sapporo). At three of those he won 7 medals. You gotta be a bit impressed by now.
So, you get it, he was ultra successful skier, but he was also important “substrate” for exercise physiology lesson. Why?
Now the EPO thing comes in play.
EPO or erythropoietin is the glycosylated protein that controls the red blood cell production in our body. When you consider that red blood cells carry oxygen around, delivering it to your muscles (when you are, let’s say cycling) enabling them to turn energetic substrates into ATP, ultimate cellular energetic money, you can conclude that red blood cell production is pretty important for guys who want to run around the woods on their skis for an hour and a half.
A lot of other coaches, athletes and doctors concluded just the same thing (and not only for cross-country skiing) and that is basically how the blood doping and EPO doping were born.
But our Finnish guy Eero did not dope. There was something different and that’s what makes this case so valuable for anyone that enjoys a bit of biology, sport science, pathophysiology and even sport ethics and future of doping.
Endurance traits are
of course – polygenic, meaning that you have to be really lucky to get the
right cards (genetic cards it is) to play with.
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| Picture 1: EPO, EPO-R magic and my paint skills all in one picture |
However, there are exceptions to every rule. EPOR (EPO receptor) is one of our famous “polygenic endurance traits” exceptions meaning that if there is a very rare DNA sequence variation in your EPOR code, single mutation could result in big phenotypic difference. One little specific DNA segment could make you much more happy while running a marathon against your peers with boring normal DNA. Our famous Finnish skier was one of those people. To be extra creepy I would now like to share with you ultimate private information you all desperately want to know. To be as happy as Eero in terms of endurance sports you have to have your big G (guanine) switched for adenine in the 6002. position of your EPOR gene. This kind of mutation will result in creation of so called “STOP codon”. STOP codon, as you might have guessed, means that transcription has to stop and that you will get shortened EPOR mRNA and finally - shortened receptor. Usually, incompletely transcribed proteins are degraded or function less, but in this case, erythropoietin receptor becomes hyperactive. You can explain this easily by assuming that the last bit of the EPOR protein (when you have it) inhibits EPOR activity. When you lose it, your EPOR gets out of control. Hyperactive EPO gives you ultra high haematocrit and haemaglobin. High haematocrit and haemaglobin results in increased VO2max. VO2max... oh you know how it goes.
To continue in creepy but scientifically satisfying tone, haemoglobin concentrations in Eero Mäntyranta and other affected males from his family were between very high 183 and ultra high 231 g/L 1.
Prof. Wackerhage and prof. Roth highlight one interesting fact right next to this skyrocketing haemoglobin values: cycling world governing body has stated that haematocrit >50% and >170g/L haemoglobin are defined as abnormal levels (usually this means administration of exogenous EPO or blood doping). Athlete who exceeds this threshold will be declared temporarily unfit for at least 15 days.
This gives rise to one important conclusion and one important question. “Union Cycliste Internationale” are not naive and banning this sky-high haemoglobin numbers means this is indeed one of the limiting factor in human performance ( I should add here “human on a bike and 3500km of challenge in front of him” kind of performance just to be sure those of you that are all into 100m dash don’t turn their hopes for upcoming Rio Olympics to the almighty haemoglobin).
So much for the conclusion. The question on the other hand is a bit more ethically oriented. If Mr. Mäntyranta was a cyclist today, should he be banned from competing as his haematocrit is too high? If it is so, should we look for another important mutations that can have great impact on endurance performance and ban them also? And if so, should we treat polygenetic traits equally. E.g. if there are 10 genes involved in endurance, should we allow just five “good” genes. Or seven?
Literature:
1. De la Chapelle, A., Träskelin, A. L. & Juvonen, E. Truncated erythropoietin receptor causes dominantly inherited benign human erythrocytosis. Proc. Natl. Acad. Sci. U. S. A. 90, 4495–9 (1993).
2. Cooper C. Run,swim,throw,cheat. New York: Oxford University Press, 2013.
3. Henning Wackerhage et al.Molecular Exercise Physiology. Abingdon: Routledge, 2014.
4. https://en.wikipedia.org/wiki/Eero_M%C3%A4ntyranta
1. De la Chapelle, A., Träskelin, A. L. & Juvonen, E. Truncated erythropoietin receptor causes dominantly inherited benign human erythrocytosis. Proc. Natl. Acad. Sci. U. S. A. 90, 4495–9 (1993).
2. Cooper C. Run,swim,throw,cheat. New York: Oxford University Press, 2013.
3. Henning Wackerhage et al.Molecular Exercise Physiology. Abingdon: Routledge, 2014.
4. https://en.wikipedia.org/wiki/Eero_M%C3%A4ntyranta
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