Their arguments against an EPO effect can be summarized as:
1) EPO, by increasing red blood cells and Hb, can increase V02max, but V02max is only one of three key components in performance, and the others—lactate threshold and efficiency—may be more important for elite athletes.
2) Most studies of EPO have not been carried out on elite professional athletes, for obvious reasons
3) Elite athletes spend only a small fraction of the time in most races at high exercise intensity, e.g., in mountain top finishes in GT stages.
Wrt 1), so what? If V02max is increased by EPO without any change in LT or efficiency, then obviously performance will be enhanced. The fact that V02max may not be a great predictor of performance is largely irrelevant. It certainly contributes to performance, and anything that increases it without negatively impacting the other important factors can be expected to be beneficial.
Wrt 2), while it’s true it’s been hard to study EPO effects in elite, currently active professional athletes, the evidence of the 1990s shows very clearly—if not rigorously scientifically—that it does benefit pro cyclists. There have also been some more precise measurements, e.g., note this quote from the book about LA, Cycle of Lies, for which we had a thread several years ago:
Vaughters could raise his hematocrit with EPO to about 52— an improvement of 4 points at most— then he would temporarily lower it for UCI’s health check by infusing a bag of saline into his blood— a common practice among riders manipulating their blood with EPO. After using the drug, Vaughters saw the numbers tick upward on his power meter, the electronic machine affixed to his bike’s handlebars that measured a rider’s power output.
Vaughters noticed that many times EPO would give him a 4 to 6 percent increase in power. That translated into a few percentage points of speed. That translated into better finishes.
viewtopic.php?f=20&t=21959&p=1409456&hilit=Vaughters#p1409456
Wrt 3), yes, GTs usually come down to a relatively small fraction of the total race times, i.e., 20-40 minute climbs at the end of a mountain stage, or an ITT. The fact that EPO wouldn’t benefit riders during most of the rest of the race doesn’t really matter.
There are a lot of irrelevancies discussed here, too, e.g.:
An increase in Hct could lead to an increase in oxygen-carrying capacity, but does this enhance performance? Haematocrit is not a good marker of performance, because endurance athletes usually have lower Hct values than untrained subjects owing to plasma volume expansion [119]. Additionally, it is a very variable measure and is affected by different circumstances [120]. Increases of Hct cause an increase in viscosity of the blood [121, 122], which might hamper performance owing to reductions in blood flow and increased cardiac work. Decreased plasma volume during exercise exaggerates increased Hct [120], as may dehydration, hyperthermia and altitude, so it is not obvious what effects a rise in Hct will have in professional cyclists. The rHuEPO treatment not only increases haemoglobin concentration and Hct, but at the same time decreases plasma volume, thereby resulting in almost no effect on, or a slight decrease in, blood volume [123]. Recombinant human erythropoietin could therefore counteract the plasma volume expansion of endurance training [56].
It’s true plasma expansion decreases HT, but it doesn’t decrease total red blood cell mass or Hb, whereas EPO definitely does increase both of these parameters. So the issue of what the actual HT is is largely irrelevant. With regard to viscosity, studies that I discussed here some years ago showed that viscosity increase accompanying HT increase does not generally become a problem until well over 50% HT.
I understand the authors are trying to address the performance effects of EPO from a rigorous scientific point of view, and I can’t disagree with them that we lack studies doing this, but to imply, as they seem to do at the end, that what we do know isn’t sufficient reason to ban the drug is ludicrous.