Hypoxic environments have repeatedly been observed to depress VO2max during whole-body exercise in humans (Fulco et al., 1998). The mechanisms behind the wide interindividual variability of the reduction of VO2max with hypoxia are largely unknown, especially in a homogenous group of athletes (Lawler et al., 1988; Robergs et al., 1998). The present study investigates the role of cardiac output (Q), arteriovenous oxygen difference (DavO2) and mitochondrial function in the limitation of VO2max with moderate hypoxia (FIO2=14.5 %) in a homogenous group of endurance athletes. Methods 15 endurance trained athletes (normoxic VO2max =58.6±1.7 ml/min/kg) performed maximal cycle incremental tests to assess VO2max, Qmax and DavO2max in normoxia and moderate hypoxia. Muscle biopsies of vastus lateralis were taken one week before the cycling tests to evaluate the maximal muscle oxidative capacity (Vmax) and the sensitivity of mitochondrial respiration to ADP (Km) with and without creatine (Cr) on permeabilized muscle fibers in situ. Results Athletes exhibiting the largest reduction of VO2max in moderate hypoxia (SL group: -18±2%) suffered from both significant reductions in Qmax (-4±1%) and DavO2max (-14±2%). Athletes who tolerated well hypoxia, as attested by a significantly smaller drop of VO2max with hypoxia (ML group: -7±1%), also displayed a blunted Qmax (-9±2%) but, conversely, were able to maintain DavO2max (+1±2%;). Even though Vmax was similar in the two experimental groups, the smallest reduction of VO2max with moderate hypoxia was observed in those athletes presenting the lowest apparent Km for ADP in presence of creatine (Km+Cr). Conclusion In already trained athletes with high muscular oxidative capacities, the qualitative rather than quantitative aspects of the mitochondrial function may constitute a limiting factor to aerobic ATP turnover when exercising in lower oxygen availability, presumably through the functional coupling between the mi-CK and ATP production. This study suggests a potential role for peripheral factors, including intrinsic mitochondrial properties, in determining the tolerance to hypoxia in maximally exercising endurance-trained athletes.
© Copyright 2009 14th annual Congress of the European College of Sport Science, Oslo/Norway, June 24-27, 2009, Book of Abstracts. Veröffentlicht von The Norwegian School of Sport Sciences. Alle Rechte vorbehalten.