RESPONSES TO HYPOXIA ARE LIKELY TO BE PERIPHERALLY INFLUENCED
Ponsot, E., Dufour, S. P., Doutreleau, S., Lonsdorfer-Wolf, E., Lampert, E., Piquard, F., Geny, B., Mettauer, B., Ventura-Clapier, R., & Richard, R. (2009). Do skeletal muscle mitochondria play a role in the reduction of VO2max with moderate hypoxia in endurance athletes? A paper presented at the 14th Annual Congress of the European College of Sport Science, Oslo, Norway, June 24-27.
This study investigated 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 (N = 15). Ss performed maximal cycle incremental tests to assess VO2max, Qmax and DaVO2max in normoxia and moderate hypoxia. Muscle biopsies of the 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.
Ss exhibiting the largest reduction of VO2max in moderate hypoxia suffered from both significant reductions in Qmax and DaVO2max. Athletes who tolerated hypoxia well, as attested by a significantly smaller drop of VO2max with hypoxia, also displayed a blunted Qmax but, conversely, were able to maintain DaVO2max. Although maximal muscle oxidative capacity 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).
Implication. 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 mitochondrial-CK and ATP production. This study suggests the potential role for peripheral factors, including intrinsic mitochondrial properties, in determining the tolerance to hypoxia in maximally exercising endurance-trained athletes.
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