Of the available data, only two out of 16 data points fall in the claimed five-to-10-percent range in Figure 5. The higher of the points is still only 6.3 percent and comes from the study on junior athletes with no control group. In their discussion, the study authors hypothesized that because the subjects “were elite junior swimmers [they] undoubtedly still had the potential to increase total hemoglobin mass,” in contrast to veteran athletes who may reach a maximum from years of training-induced changes. It is not very strong.
The most credible conclusion is that the strongest data suggests that altitude would result in an increase in Hgb mass between one and five-percent at time points relevant to a grand tour. This is still well short of the five-to-10-percent range that Ferrari claimed.
In a parallel thread, Ferrari asked us to consider that “some elite athletes are used to planning and repeating three-to-four altitude sojourns of training for about two weeks every month, for example, in order to prepare for the [Tour de France]: four periods in the months of March, April, May, and June, about two weeks each time. So a total of six-to-eight weeks, which is about twice as much as proposed in published trials/studies. It is known [Hgb] mass increases by about one percent per week of altitude, both real and simulated (Berglund 1992, Clark 2009). The average life of red blood cells is about 120 days, for which it is logical to expect a sum of increments during a period of about four months.”
The one study that I’ve found that looked directly at cumulative effect similar to what Ferrari proposed followed elite swimmers over the course of multiple coach-prescribed two-week altitude camps alternated with two-week blocks of no altitude (Roberston 2010c). The swimmers showed average gains of 0.9 percent during the camps. However, because of Hgb mass decreases between the camps, there is no measurable difference between starting and finishing mean data in the published figure. The study certainly doesn’t support Ferrari’s proposed cumulative effect. However, since the altitude exposure used was lower than studies finding larger effects, this study does not necessarily end debate on this point.
Red blood cell destruction
Continuing the analysis, working against Ferrari’s hypothesis are two factors related to the fall in natural EPO when altitude exposure is stopped. The first is neocytolysis, which is the destruction of young red blood cells (Rice 2001). The second is suppression of the red blood cell (RBC) production.
Ferrari’s counter-argument held that “neocytolysis, assumed it takes place after a stay at altitude in athletes who continue to train intensely, will be even more present after a transfusion, because it’s stored blood…,” but his statement does not make theoretical sense. Neocytolysis is specifically the destruction of young, not older, RBCs. So, if anything, the older age of stored blood might protect transfused cells from the process of neocytolysis.
Similarly, pointing to the 120-day lifespan of red blood cells is a red herring. The length of time the Hgb mass will stay elevated is determined by the balance between RBC destruction and production. If production is less than normal or destruction is increased, Hgb mass will fall. The rate that it will fall is not determined by the lifespan of an RBC under normal conditions, but the balance between the former and the latter. So, in determining if an accumulation effect is even possible, it is important to look at two things: the Hgb mass at the later time points (not the peak values), and the rate of expected decrease in the Hgb mass.
In response, Ferrari stated, “after altitude training, I am more interested in the ability of performance (increased for more than 16 days since the end of the exposure) rather than the measurement (which is approximate) of [Hgb] mass.”
Again, Ferrari pivoted away from his error.
FILED UNDER: Commentary