Hyperoxia speeds pulmonary oxygen uptake kinetics and increases critical power during supine cycling

Abstract

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 (τtrueV̇O2). To test whether this relationship is causal, we assessed the impact of hyperoxia on τtrueV̇O2 and critical power during supine cycle exercise. What is the main finding and its importance?The results demonstrate that hyperoxia increased muscle oxygenation, reduced τtrueV̇O2 (i.e. sped up the oxygen uptake kinetics) and, subsequently, increased critical power when compared with normoxia. These results therefore suggest that τtrueV̇O2 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 (τtrueV̇O2) 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, τtrueV̇O2 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 τtrueV̇O2 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 τtrueV̇O2 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, τtrueV̇O2 reduced and CP increased in hyperoxia compared with normoxia, suggesting that τtrueV̇O2 is an independent determinant of CP. The finding that τtrueV̇O2 was related to CP in hyperoxia but not normoxia also supports this notion.

Effect of Hyperoxia on Critical Power and V˙O2 Kinetics during Upright Cycling

“…Furthermore, in a recent study we demonstrated that hyperoxia speeded pulmonary O 2 kinetics and increased CP during supine exercise, but that the change in ! O2 did not correlate linearly with the change in CP (9). Taken together, the relative, independent contributions of !…”

“…[HbO + MbO 2 ] was increased during both moderate (hyperoxia: 74 ± 21 µM, normoxia: ± 18; main effect of condition, P < 0.001, Figure 4A) and severe (hyperoxia: 73 ± 20 µM, normoxia: 66 ± 15; main effect of condition, P = 0.039, Figure 4B) Figure 3A) or severe exercise ( Figure 3B, kinetics increases CP (7,9), and also that a slowing of the O 2 kinetics decreases CP (6,8).…”

“…Specifically, when ! O2 was acutely reduced, CP increased (7,9), whereas when ! O2 was acutely increased, CP correspondingly decreased (6,8).…”

“…However, hyperoxia does not appear to speed the pulmonary O 2 kinetics during upright cycling (13)(14)(15), which is seemingly inconsistent with the putative linkage between ! O2 and CP previously described (6)(7)(8)(9). Nevertheless, Vanhatalo et al (16) previously demonstrated that CP was increased when determined in hyperoxia compared to normoxia, suggesting a central role for O 2 availability per se in determining CP.…”

“…We have recently provided evidence to suggest that ! O2 is an independent determinant of CP (6)(7)(8)(9). Specifically, when !…”