Then why don’t you invite one of them onto the forum to discuss this? I would love to hear what they have to say. Bring it on!
I’m sure they’re not going to admit to helping riders blood dope, but given that three of the main four protagonists we have been discussing here—Riis, Ulle, and LA—have now confessed and/or been sanctioned for doping, you could just ask one of these doctors how, in a dirty peloton where almost everyone had access to EPO and/or transfusions, these relatively large riders were able to climb so well. I assume these doctors must have had a theory of muscle density worked out, else why would they tell their charges to bulk up?
Let me remind everyone why, other things being equal,
the best climbers tend to be small and light:
So the success at climbing of Ulle, LA and certain others does seem odd. Not impossible, but quite unlikely. We’re not talking about one outlier here, but four, who won every TDF but one over a period of fifteen years. Not just by time trialing well, but also by hanging with the competition, if not dominating it, on the climbs. I think RR and others are right to be suspicious of this.
But it's one thing to raise this issue, quite another to provide a coherent explanation for it. Your muscle density claim--as you have expressed it here-- has no apparent support in the scientific literature. It implies an understanding of oxygen transport that, if true, would seem to require a lot of re-writing of physiology textbooks. Blood boosting allows the blood to carry more oxygen, which in turn can be delivered to the muscles. It does not increase alveolar or capillary surface areas, or affect delivery in any other way, that we know of. As I said earlier, it’s possible that EPO, though certainly not transfusions, stimulates angiogenesis, but even if it does, there is no reason to believe it would do so preferentially in densely-muscled individuals.
Moreover, there are known, accepted ways in which some riders can benefit more than others from the same blood boosting program. The most obvious is if they have a lower natural HT. When the 50% limit went into effect, this put a ceiling on HT, so riders with lower HTs could raise theirs to a larger degree. Even before this sanctioned limit, there was a physiological one. When HT goes above the mid-50s, the advantage of more RBCs tends to be cancelled by increased viscosity, hindering blood flow--though the peak HT surely varies from individual to individual, which adds another variable for individual differences.
Another possibility is the relationship between HT and V02. As RR has noted in several of his posts, this differs from rider to rider. There are also differences in how much an increase in V02 a rider achieves with a given increase in HT. So this, too, would benefit certain dopers more than others.
I don't have any problem with explanations like this. What I have a problem with is arguing that the common denominator is muscle density, and that even though this is supposed to be independent of rider size or weight, almost all the riders who benefitted from muscle density just happened to be large ones who would not have been good climbers in a clean peloton.