To investigate the effects of training in normoxia vs. training in normobaric hypoxia (fraction of inspired O2 = 20.9 vs. 13.5%, respectively) on the regulation of Na+-K+-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. Na+-K+-ATPase concentration was 326 ± 17 (SE) pmol/g wet wt before training (Control), increased by 14% with N (371 ± 18 pmol/g wet wt; P < 0.05), and decreased by 14% with H (282 ± 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 ± 0.10 mmol ⋅ h−1 ⋅ g wet wt−1; 70%; P < 0.05) than with N (0.99 ± 0.10 mmol ⋅ h−1 ⋅ g wet wt−1; 51%; P < 0.05) compared with pretraining (0.658 ± 0.09 mmol ⋅ h−1 ⋅ g wet wt−1). 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 Na+-K+-ATPase pump expression. In contrast, normoxic training stimulates increases in both mitochondrial potential and Na+-K+-ATPase concentration.