Introduction/Purpose Critical power (CP) is a fundamental parameter defining high-intensity exercise tolerance; however, its physiological determinants are incompletely understood. The present study determined the impact of hyperoxia on CP, the time constant of phase II pulmonary oxygen uptake kinetics (tV.O2), and muscle oxygenation (assessed by near-infrared spectroscopy) in nine healthy men performing upright cycle ergometry. Methods Critical power was determined in normoxia and hyperoxia (fraction of inspired O2 = 0.5) via four severe-intensity constant load exercise tests to exhaustion on a cycle ergometer, repeated once in each condition. During each test, tV.O2 and the time constant of muscle deoxyhemoglobin kinetics (t[HHb]), alongside absolute concentrations of muscle oxyhemoglobin ([HbO2]), were determined. Results Critical power was greater (hyperoxia, 216 ± 30 W vs normoxia, 197 ± 29 W; P < 0.001), whereas W' was reduced (hyperoxia, 15.4 ± 5.2 kJ; normoxia, 17.5 ± 4.3 W; P = 0.037) in hyperoxia compared with normoxia. tV?O2 (hyperoxia, 35 ± 12 s vs normoxia, 33 ± 10 s; P = 0.33) and t[HHb] (hyperoxia, 11 ± 5 s vs normoxia, 14 ± 5 s; P = 0.65) were unchanged between conditions, whereas [HbO2] during exercise was greater in hyperoxia compared with normoxia (hyperoxia, 73 ± 20 vs normoxia, 66 ± 15 µM; P < 0.001). Conclusions This study provides novel insights into the physiological determinants of CP and by extension, exercise tolerance. Microvascular oxygenation and CP were improved during exercise in hyperoxia compared with normoxia. Importantly, the improved microvascular oxygenation afforded by hyperoxia did not alter tV.O2, suggesting that microvascular O2 availability is an independent determinant of the upper limit for steady-state exercise, that is, CP.
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