Race Radio said:
....yet you are unable to produce anything to support this theory.
Pot calling the kettle black.
Not surprisingly, this thread has generated into assertions backed by virtually no evidence, from either side. I myself will certainly agree with DQ’s agnostic position. I don’t know if Ulle would have won Tours clean or not. I have no problem with people debating the issue based simply on Ulle’s performances at various stages of his career, but this kind of evidence is never going to be decisive.
I note that on another thread recently, RR made the very provocative statement that Moncoutie was not clean. As another poster, I think it was hrotha, noted, if just about anyone except RR had said that, it would have been regarded as trolling. RR gets a pass on this, and I think reasonably so, because of his credibility on this forum. But last I looked, he hadn’t provided any evidence for that, either.
FWIW, I took this up with Frank Day, who started a physiology thread in another part of this forum. Here is part of his response:
I will take a look at this but I can almost assure you what they are saying is complete BS.
The overall effects of EPO would be related to the amount of exercised muscle mass. But, everyone benefits and it is all relative. There simply is no evidence that drugs like EPO do or might affect different riders differently. To make a claim that this explains Armstrong's or Ulrich's dominance is simply pulling hypotheses out of thin air.
He is not completely correct, of course, when he says that there is no evidence that EPO affects riders differently. Someone called him on this, and he modified his response a little:
Well, the dose response to epo may vary, as would be expected, but the response to changing hct should be exactly the same…Except in certain disease states, we would expect all athletes to respond the same to changing concentrations of RBC's.
What Frank is saying here, I believe, is that if two riders have the same HT, they will have the same amount of oxygen delivered to their muscles. This is because, in his view, delivery results from passive diffusion, a purely physicochemical response that is not going to vary from one individual to another. So if, e.g., you have two riders with 50% HTs, they will have the same amount of oxygen delivered to the muscles. If they have the same natural HT, e.g., 42%, they will get the same benefit from EPO in going to 50%.
Still, training can definitely increase oxygen delivery, by increasing the amount of capillaries in close contact with the muscle:
When we are at rest most of the pre-capillary sphincters are closed, increasing the diffusion distance and keeping oxygen concentration at the capillary where it likes to be. As we exercise, additional capillaries open up, increasing blood flow but, more importantly, decreasing mean diffusion distance, increasing oxygen delivery…The key to increasing oxygen delivery is training that increases capillary density and lowers the mean distance between capillary and mitochondria in the skeletal muscle.
All a drug like EPO does is delay this drop.
So no question that riders adding muscle mass do increase capillaries, through training, but at a given HT, they aren’t going to get any more oxygen to these muscles than another rider with less muscle mass and the same HT gets to his muscles—unless they have trained more. IOW, the benefit from increased muscle mass, is at best, independent of any EPO effect. The increased muscle would allow more power with or without EPO. If the rider with more muscle is not better without EPO, there is no reason to believe, following this line of reasoning, that he's going to be better with EPO. Again, assuming the same rise in HT, and the same amount of training.
And at worst, it might allow less, if the blood supply can’t be maintained:
There is one other thing that interferes with such a simplistic interpretation and that is the energy cost of maintaining body elements. To make muscle mass requires substantial energy cost just as it does to make new capillaries. If one doesn't utilize these elements then they will atrophy. That is why it is so difficult to have lots of muscle mass and lots of aerobic capacity, we only have so much time to train these two completely different elements. That is why strength athletes have large muscles but no aerobic capacity, they only train one aspect. And, it is why marathon runners have small muscles and lots of capillaries, they have no need for a lot of muscle strength. Your body composition is dictated by how you train but everything you do has a maintenance cost. If you don't keep using it then the body will let it atrophy, just ask any astronaut after several months in space what has happened to their abilities.
This is one expert’s view. Take it as you will. I don’t repost it as the final word. He supports a view of V02 max that is not universally held by others in the field, and he makes some other points in this thread I don’t entirely agree with. Most importantly, he doesn't mention some other very relevant research in areas outside his specialization. Several studies suggest that
EPO may increase angiogenesis—the formation of new blood vessels—under some circumstances. It has also been reported to have
negative effects on mitochondrial formation in muscle. These are the kinds of pharmacological effects that one would expect would result in differential responses among individuals. So one could hypothesize, for example, that EPO promotes capillary formation in muscles, and that some riders would develop more capillaries in response to a given dose of EPO (or simply used more of the drug) than others. Or in the case of negative effects, that some riders relatively benefitted from a weaker effect. But even if this were established, and it hasn't been yet, one would still have to show that the kind of body types fitting RR's claim benefitted most. That's a lot to ask.
Another interesting
recent study, conducted in animals only, found that EPO had a performance-enhancing effect that was independent of its effect on HT. This effect is mediated by certain areas in the brain. One would only get this effect if EPO were injected IV, of interest in that it was Ferrari's aim to get a rapid turnover of EPO and avoid a positive test that led to IV injections of this drug by riders. Another pharmacological effect that one would expect might exhibit differential responses.
All of this work underscores the complexity of drug effects, and how very difficult it is to say who benefits the most.
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