NEW FINDINGS: What is the central question of this study? Critical power is a fundamental parameter defining high-intensity exercise tolerance and is related to the phase II time constant of pulmonary oxygen uptake kinetics ( τ V ̇ O 2 ). To test whether this relationship is causal, we assessed the impact of hyperoxia on τ V ̇ O 2 and critical power during supine cycle exercise. What is the main finding and its importance? The results demonstrate that hyperoxia increased muscle oxygenation, reduced τ V ̇ O 2 (i.e. sped up the oxygen uptake kinetics) and, subsequently, increased critical power when compared with normoxia. These results therefore suggest that τ V ̇ O 2 is a determinant of the upper limit for steady-state exercise, i.e. critical power. ABSTRACT: The present study determined the impact of hyperoxia on the phase II time constant of pulmonary oxygen uptake kinetics ( τ V ̇ O 2 ) and critical power (CP) during supine cycle exercise. Eight healthy men completed an incremental test to determine maximal oxygen uptake and the gas exchange threshold. Eight separate visits followed, whereby CP, τ V ̇ O 2 and absolute concentrations of oxyhaemoglobin ([HbO2 ]; via near-infrared spectroscopy) were determined via four constant-power tests to exhaustion, each repeated once in normoxia and once in hyperoxia (fraction of inspired O2 = 0.5). A 6 min bout of moderate-intensity exercise (70% of gas exchange threshold) was also undertaken before each severe-intensity bout, in both conditions. Critical power was greater (hyperoxia, 148 ± 29 W versus normoxia, 134 ± 27 W; P = 0.006) and the τ V ̇ O 2 reduced (hyperoxia, 33 ± 12 s versus normoxia, 52 ± 22 s, P = 0.007) during severe exercise in hyperoxia when compared with normoxia. Furthermore, [HbO2 ] was enhanced in hyperoxia compared with normoxia (hyperoxia, 67 ± 10 μm versus normoxia, 63 ± 11 μm; P = 0.020). The τ V ̇ O 2 was significantly related to CP in hyperoxia (R2 = 0.89, P < 0.001), but no relationship was observed in normoxia (r = 0.07, P = 0.68). Muscle oxygenation was increased, τ V ̇ O 2 reduced and CP increased in hyperoxia compared with normoxia, suggesting that τ V ̇ O 2 is an independent determinant of CP. The finding that τ V ̇ O 2 was related to CP in hyperoxia but not normoxia also supports this notion.
NEW FINDINGS: What is the central question of this study? Critical power is a fundamental parameter defining high-intensity exercise tolerance and is related to the phase II time constant of pulmonary oxygen uptake kinetics ( τ V ̇ O 2 ). To test whether this relationship is causal, we assessed the impact of hyperoxia on τ V ̇ O 2 and critical power during supine cycle exercise. What is the main finding and its importance? The results demonstrate that hyperoxia increased muscle oxygenation, reduced τ V ̇ O 2 (i.e. sped up the oxygen uptake kinetics) and, subsequently, increased critical power when compared with normoxia. These results therefore suggest that τ V ̇ O 2 is a determinant of the upper limit for steady-state exercise, i.e. critical power. ABSTRACT: The present study determined the impact of hyperoxia on the phase II time constant of pulmonary oxygen uptake kinetics ( τ V ̇ O 2 ) and critical power (CP) during supine cycle exercise. Eight healthy men completed an incremental test to determine maximal oxygen uptake and the gas exchange threshold. Eight separate visits followed, whereby CP, τ V ̇ O 2 and absolute concentrations of oxyhaemoglobin ([HbO2 ]; via near-infrared spectroscopy) were determined via four constant-power tests to exhaustion, each repeated once in normoxia and once in hyperoxia (fraction of inspired O2 = 0.5). A 6 min bout of moderate-intensity exercise (70% of gas exchange threshold) was also undertaken before each severe-intensity bout, in both conditions. Critical power was greater (hyperoxia, 148 ± 29 W versus normoxia, 134 ± 27 W; P = 0.006) and the τ V ̇ O 2 reduced (hyperoxia, 33 ± 12 s versus normoxia, 52 ± 22 s, P = 0.007) during severe exercise in hyperoxia when compared with normoxia. Furthermore, [HbO2 ] was enhanced in hyperoxia compared with normoxia (hyperoxia, 67 ± 10 μm versus normoxia, 63 ± 11 μm; P = 0.020). The τ V ̇ O 2 was significantly related to CP in hyperoxia (R2 = 0.89, P < 0.001), but no relationship was observed in normoxia (r = 0.07, P = 0.68). Muscle oxygenation was increased, τ V ̇ O 2 reduced and CP increased in hyperoxia compared with normoxia, suggesting that τ V ̇ O 2 is an independent determinant of CP. The finding that τ V ̇ O 2 was related to CP in hyperoxia but not normoxia also supports this notion.
Authors: Richie P Goulding; Dai Okushima; Yoshiyuki Fukuoka; Simon Marwood; Narihiko Kondo; David C Poole; Thomas J Barstow; Shunsaku Koga Journal: Eur J Appl Physiol Date: 2021-02-11 Impact factor: 3.078