RR, you can skip this post, because it isn't brief. Someone else may find something of interest in it, though.
Plasma expansion results in a lower HT, which means a lower oxygen concentration in the blood. The conventional view has been that this means that the V02 max should be reduced. IOW, it is HT, and not Hb mass, which determines oxygen intake and power. If this is the case, then plasma expansion and the accompanying reduction in HT is very relevant to the issue of how much increased oxygen intake there is following an increase in Hb mass by transfusion during a GT.
However—and I didn’t know this before, I find it surprising and unexpected--several studies have shown either no change or even an increase in V02 following plasma expansion, e.g.,
http://jap.physiology.org/content/101/3/707.long
The authors of the linked study (who cite other work consistent with their results) used a plasma volume expander to lower average HT in their subjects from 44 to 41. This means Hb mass remained the same, but in a larger volume. But V02 max actually increased an average of about 5%.
Why? They assumed there had to be a compensatory process that over-rode the lower oxygen concentration, and came to the conclusion that it was probably a larger stroke volume, perhaps because of the reduced viscosity of the blood. Interestingly, in support of this, there are other studies (not noted by these authors, I believe) that show a negative correlation between HT and V02. I.e., individuals with lower HTs tend to have higher V02 maxes (though just to underscore the variable results in this area, an article cited above in this thread reported that individuals with higher V02 maxes tended to benefit less from EP0). While there are many factors that could go into this, it certainly is consistent with the possibility of greater stroke volume.
Thus this and some other studies suggest that plasma expansion might not only not reduce oxygen intake during a GT, but even increase it. IOW, you might get a performance enhancement just by taking saline, and not just to counteract dehydration. However, several caveats:
1) they noted that any compensatory mechanisms are likely to have a limit, and that limit is likely to be breached by a large degree of plasma expansion. Thus they suggested that the compensation might not occur in elite athletes, which AFAIK have not been studied in this manner. As RR noted, plasma expansion can be very large in riders. In fact, they experience a large degree of plasma expansion simply as a result of training, then a further increase if they ride a GT. Thus they might have exceeded the limits of compensatory processes. FWIW, work by Coyle and Coggan suggests that reduction of HT by 5-10% eliminates the increase in V02 seen with a lower reduction of HT, though the above study was conducted with an 8% decrease in HT.
2) Transfusion changes the situation. If a rider transfuses packed cells, the HT increases, which presumably would counteract the effects on stroke volume, IOW reduce the compensatory processes. OTOH, if the rider transfuses whole blood, which has little effect on the HT, there is a further large increase in blood volume, which would further stress any compensatory mechanisms. So it needs to be emphasized that we don’t know what the effect on V02 would be of plasma expansion of elite racers, whether in fact all of any hypothetical 20% increase in Hb mass would translate into increased oxygen intake.
3) An increased V02 does not necessarily translate into more oxygen use by muscles. The authors of the above study cited a much earlier study that showed changes in V02 were paralleled by changes in oxygen getting into the leg muscles, which were measured by comparing the concentration of oxygen in arterial and venous blood. However, even if more oxygen is getting into the muscle, it does not establish that this extra oxygen is actually being used. AFAIK, this has never been established. I raised this point with Andy Coggan in another thread, because Coyle’s conclusion of greater mechanical efficiency rests on this assumption. Everyone in the field seems to assume that V02 is an accurate measurement of oxygen metabolism. That might not always be the case.
Originally Posted by Jonathan Vaughters
Also, an old Finnish study (if you can find it) found that athletes with higher Vo2 maxes benefitted less from EPO use than those who started with lower Vo2 maxes. The more talented athlete were (generally) benefitting less. Another observation of that study was that ectomorphic body types showed less increase than mesomorphic types. So, the variables on the exact advantage are endless and vary person to person (A BIG counterpoint to the argument that just letting everyone dope is fair). I read this study in about 1995 and haven't seen it anywhere since, so i cant find a link, sorry...
Great, a study almost two decades old, can't find the link.
How about
this?
Subjects had an average HT of 42.7% at the outset of the study. After 30 days or less of EPO, they were all over 50% (average of 50.8%). Sounds like LA and Ulle. V02 max increased by an average of 7.5%. Sure, that's a huge increase, definitely helps them win races. But does it suggest the need for added muscle mass? According to the study cited by JV, subjects in this study (who were described as well-trained athletes, but I don't believe were active elite riders) should have benefitted more from EPO than even an average pro, so the 7.5% increase should be an overestimate of the benefit someone like LA or Ulle should get.
Or is your point that adding muscle mass would increase V02 max? Or that there is a correlation between body weight of subject and V02 max increase? That would be very interesting, and would support your hypothesis, but I would like to see a study demonstrating that.
While you're at it, maybe you could explain where the cut-off is. You have strongly implied that less talented riders like (according to you) LA and Ulle could benefit more from the same doping program than more talented riders. Not simply improve more beyond their baseline than the more talented riders could, but shift their baseline from below the baseline of the more talented riders to above it. IOW, clean, LA and Ulle were inferior climbers to certain other riders. On the same doping program (yes, I know, the view is their program was better, but much of your argument implies that it didn't have to be), LA and Ulle were superior to the same climbers, doped to the same degree.
If that's true, where do you draw the line? I mean, I'm inferior naturally to LA and Ulle, does that mean if I doped on the same program as they did, I could beat them? And if not, why not? Because I'm not as muscular? OK, what about some football player who was more muscular than they were? Could he have dominated them climbing just by going on the same doping program? And if not, why not?
The problem with this kind of reasoning--why it leads to conundra like this--is that you aren't merely stating that they improved more than the lighter climbers, but they caught up to them and surpassed them. With that kind of logic, you predict that the worse the athlete is without dope, the better he will be with it.
Another point to add: EPO administration does not increase plasma volume, so any effect of diluting the increase in Hb mass on stroke volume does not occur.