I get what he’s saying, but this is not explained very well.
First he notes a decrease in both Hb and retics:
The following graphic indicates a fairly regular and normal pattern of Hemoglobin (Hb) values until a significant drop on May 5, 2009, four days before the start of the Giro d'Italia(the Tour of Italy which was contested from May 9-31, 2009 and where Armstrong placed 21st)… The decrease in Hemoglobin from April 30, 2009 to May 31, 2009 (149 – 130) in samples 10 to 13 is 15% however there is no expected increase in reticulocytes. In fact from October 16, 2008 the average reticulocyte levels are 1.1 but from May 18, 2009 the average reticulocyte levels are 0.6.
What is the reason for the drop in Hb? Parisotto says there should have been an “expected increase” in retics. By this he presumably means that a drop in Hb triggers a feedback mechanism that results in increased retic synthesis. However, one can imagine “natural” causes that would result in reduced retic synthesis, and the immediate effect of this would be to result in reduced Hb. In fact, if the latter samples in this group were taken during the Giro (?), one would indeed expect such a drop. Eventually, if Hb continued to fall, one would expect an increase in retics, but since no samples were taken for a couple of weeks after this, we can’t evaluate this. A drop in Hb could have resulted from a withdrawal of blood, but (beyond the fact that LA would most certainly not be withdrawing blood during or even right before the Giro) in this case it definitely should have been associated with an increase in retics, and this was not observed. So it’s difficult to make a very good case that this particular trend is suspicious; if I have my dates straight here, it seems to be a result of riding in a GT.
Then Parisotto notes a large increase in Hb in the samples taken in the middle of June:
The sudden increase in Hb from sample May 31, 2009 to June 16, 2009 (130 – 160) in samples 13 to 15 is 23%, however the response in reticulocytes is again not consistent with normal physiology. Such a scenario is consistent with a deceleration in red blood cell production following auto-bleed and re-infusion(i.e. removal of blood to store for later re-infusion, otherwise know as blood doping).
Parisotto is correct that an increase in Hb along with a decrease in retics is not consistent with normal physiology. It is not particularly consistent with a withdrawal followed by a transfusion, either, however, unless the amount transfused was significantly greater than the amount withdrawn. If the two amounts were roughly equal, one would expect to see little change in either parameter. It would be consistent with a transfusion not preceded by a withdrawal, but only if one assumes LA was not knowledgable enough to follow the transfusion with saline to dilute Hb concentration. Keep in mind that a typical transfusion would not raise Hb concentration by more than 10% at the most, even without saline dilution. In fact, if we assume the large decrease in May resulted from riding in the Giro, and that his Hb levels recovered to normal (150) before the June sample were taken, the increase is about 6-7% over the earlier, stable Hb levels. This is certainly consistent with blood doping, but the problem is that natural increases of this order can’t be easily ruled out, either.
The subsequent low reticulocyte values are consistent with re-infusion of blood and continued micro-doses of rhuEPO (recombinant erythropoietin) to ‘stabilize’ and therefore mask the expected response in reticulocytes.
This would be correct, expect we don’t see a strong sign of stabilization in the right time frame. The Hb increase is in samples 14 and 15. Retics drop in sample 14, and though they are slightly higher in sample 15, they are still down considerably from sample 13 (and most previous samples). They are seen to stabilize after that, but Hb levels are also much lower then. So this relationship is consistent with normal physiology.
Bottom line: Certainly this could be the result of blood manipulation, but I don’t see the conclusion as definitive as Parisotto makes out. Perhaps, as someone who studies this phenomenon, he has seen other samples of known blood doping that reflect the same relationships, but taken in isolation, these data lend themselves to alternative explanations.