Failure of hypoxia to exaggerate the metabolic stress in working muscle following short-term training

Green HJ, Burnett ME, Smith IC, Tupling SM, Ranney DA. Failure of hypoxia to exaggerate the metabolic stress in working muscle following short-term training. Am J Physiol Regul Integr Comp Physiol 297: R593-R604, 2009. First published May 27, 2009; doi: 10.1152/ajpregu.91035.2008.-This study investigated the effects of hypoxia (experiment 1) and the effects of hypoxia following short-term training (experiment 2) on metabolism in working muscle. In experiment 1, eight males with a peak aerobic power ((V) over dot(O2peak)) of 45 +/- 1.7 ml . kg(-1) . min(-1) ((x) over bar +/- SE) cycled for 15 min at 66.1 +/- 2.1% (V) over dot(O2peak) while breathing room air [normoxia (N)] or 14% O(2) [hypoxia (H)]. In experiment 2, nine males with a (V) over dot(O2peak) of 43.3 +/- 1.6 ml . kg(-1) . min(-1) performed a similar protocol at 60.7 +/- 1.4% (V) over dot(O2peak) during N and during H following 5 days of submaximal exercise training (H + T). Tissue samples extracted from the vastus lateralis before exercise and at 1, 3, and 15 min of exercise indicated that compared with N, H resulted in lower (P < 0.05) concentrations (mmol/kg dry wt) of creatine phosphate and higher (P < 0.05) concentrations of creatine, inorganic phosphate, and lactate, regardless of exercise time. When the exercise was performed at H + T and compared with N, no differences were observed in creatine phosphate, creatine, inorganic phosphate, and lactate, regardless of duration. Given the well-documented effects of the short-term training model on elevating (V) over dot(O2) kinetics and attenuating the alterations in high-energy phosphate metabolism and lactate accumulation, it would appear that the mechanism underlying the reversal of these adaptations during H is linked to a more rapid increase in oxidative phosphorylation, mediated by increased oxygen delivery and/or mitochondrial activation.