Downregulation of Na1-K1-ATPase pumps in skeletal muscle with training in normobaric hypoxia

Green, H., J. MacDougall, M. Tarnopolsky, and N. L. Melissa. Downregulation of Na1-K1-ATPase pumps in skeletal muscle with training in normobaric hypoxia. J. Appl. Physiol. 86(5): 1745–1748, 1999.—To investigate the effects of training in normoxia vs. training in normobaric hypoxia (fraction of inspired O2 5 20.9 vs. 13.5%, respectively) on the regulation of Na1-K1-ATPase pump concentration in skeletal muscle (vastus lateralis), 9 untrained men, ranging in age from 19 to 25 yr, underwent 8 wk of cycle training. The training consisted of both prolonged and intermittent single leg exercise for both normoxia (N) and hypoxia (H) during a single session (a similar work output for each leg) and was performed 3 times/wk. Na1-K1-ATPase concentration was 326 6 17 (SE) pmol/g wet wt before training (Control), increased by 14% with N (371 6 18 pmol/g wet wt; P , 0.05), and decreased by 14% with H (282 6 20 pmol/g wet wt; P , 0.05). The maximal activity of citrate synthase, selected as a measure of mitochondrial potential, showed greater increases (P , 0.05) with H (1.22 6 0.10 mmol·h21 ·g wet wt21; 70%; P , 0.05) than with N (0.99 6 0.10 mmol·h21 ·g wet wt21; 51%; P , 0.05) compared with pretraining (0.658 6 0.09 mmol·h21·g wet wt21). These results demonstrate that normobaric hypoxia induced during exercise training represents a potent stimulus for the upregulation in mitochondrial potential while at the same time promoting a downregulation in Na1-K1-ATPase pump expression. In contrast, normoxic training stimulates increases in both mitochondrial potential and Na1-K1-ATPase concentration.