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In severe hypoxia, single-leg peak oxygen uptake (VO 2peak ) is reduced mainly due to the inability to increase cardiac output (CO). Whether moderate altitude allows CO to increase during single-leg cycling, thereby restoring VO 2peak , has not been extensively investigated. Five healthy subjects performed an incremental, maximal, two-legged cycle ergometer test, and on separate days a maximal incremental one-leg cycling test in normoxia and in moderate hypoxia (fraction of inspired oxygen (FiO 2 ) = 15%). Oxygen uptake, heart rate, blood pressure responses, power output, and CO (PhysioFlow) were measured during all tests. Moderate hypoxia lowered single-leg peak power output (154 ± 31 vs. 128 ± 26 watts,  p  = 0.03) and oxygen uptake (VO 2 ) (36.8 ± 6.6 vs. 33.9 ± 6.9 mL/min/kg,  p  = 0.04), despite higher peak CO (16.83 ± 3.10 vs. 18.96 ± 3.59 L/min,  p  = 0.04) and systemic oxygen (O 2 ) delivery (3.37 ± 0.84 vs. 3.47 ± 0.89 L/min,  p  = 0.04) in hypoxia compared to normoxia. Arterial–venous O 2  difference (a–vDO 2 ) was lower in hypoxia (137 ± 21 vs. 112 ± 19 mL/l,  p  = 0.03). The increases in peak CO from normoxia to hypoxia were negatively correlated with changes in mean arterial pressure (MABP) ( p  < 0.05). These preliminary data indicate that the rise in CO was not sufficient to prevent single-leg performance loss at moderate altitude and that enhanced baroreceptor activity might limit CO increases in acute hypoxia, likely by reducing sympathetic activation. Since the systemic O 2  delivery was enhanced and the calculated a–vDO 2  reduced in moderate hypoxia, a potential diffusion limitation cannot be excluded.

Acute Moderate Hypoxia Reduces One-Legged Cycling Performance Despite Compensatory Increase in Peak Cardiac Output: A Pilot Study