J Appl Physiol 99: 2057-a, 2005;
doi:10.1152/japplphysiol.00956.2005
8750-7587/05 $8.00
POINT-COUNTERPOINT
REBUTTAL FROM DRS. LEVINE AND STRAY-GUNDERSEN
The discussion of measurement error by Gore and Hopkins, although erudite, is not germane to this debate. Their own meta-analysis (3) demonstrated that the error of measurement for Hbmass by CO rebreathing (30 days) was 4%, with confidence intervals that overlapped with Evans blue dye-based erythrocyte volume. Indeed, measurements of RCV made in our studies had among the lowest error reported by any laboratory and were consistent with Hbmass errors (3). When blood volume was measured by both our laboratories simultaneously, before and after hypobaric hypoxia (4), the results were virtually identical (slope = 1.0, r2 = 0.85). Finally, when all the athletes in our studies who have spent at least 1 mo living (>20 h/day) at 2,500 m are considered together (n = 74), the P value for the increase in RCV is 0.0007—even Dr. Hopkins would consider this level of probability "very likely" real and not random measurement error (5).
In contrast, an improvement in economy has not been consistently reported, even by Gore and colleagues. Thus from the same laboratory, some studies have shown an improvement in economy (2, 7), whereas others have not (1, 10). This lack of consistency argues against changes in economy being the primary mechanism of improvement after LHTL. On the contrary, even in some of our studies in which RCV was not measured, accelerated erythropoiesis was confirmed by an increase in soluble transferrin receptor (8)—measurements that were made by Dr. Gore’s laboratory at the Australian Institute for Sport! We also presented supporting evidence that increased RCV improved O2 delivery; during race pace speeds on the treadmill, cardiac output was decreased in the athletes who lived at altitude, suggesting increased oxygen transport reserve (6).
Finally, we would suggest caution against using simple linear correlations to "prove" or "disprove" cause and effect. Performance in sport is dependant on many factors, the interactions among which may be decidedly nonlinear. In fact, even a clear increase in 
O2max may not improve track performance, as seen in our athletes who lived and trained at altitude in whom the increase in RCV and O2max was offset by muscle deconditioning (6, 9). Moreover, contrary to the contention by our opponents, we did report the sustainable fraction of O2max, as assessed from the ventilatory/lactate threshold (6). Indeed, we found that only the LHTL athletes had an increase in the O2 at ventilatory/lactate threshold (and velocity at O2max), which contributed to the improved performance. This low-altitude training effect is critical to the success of the LHTL paradigm.
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Highlights from the Literature
Physiology,
February 1, 2006;
21(1):
3 - 5.
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