Proceedings of The Physiological Society

Europhysiology 2018 (London, UK) (2018) Proc Physiol Soc 41, PCA165

Poster Communications

Hyperoxia increases critical power but does not speed pulmonary oxygen uptake kinetics during upright cycling

R. P. Goulding1, S. Marwood1, D. Roche1

1. Health Sciences, Liverpool Hope University, Liverpool, Merseyside, United Kingdom.

We have previously demonstrated that critical power (CP) is mechanistically related to the phase II time constant (τVO2) of oxygen uptake (VO2) kinetics (1). CP is enhanced in hyperoxia compared to normoxia (2), however during upright cycle exercise, pulmonary VO2 kinetics are not normally speeded by hyperoxia (3), which suggests that the improved O2 delivery afforded by hyperoxia should increase CP independently of any changes in τVO2. Hence, whether the enhanced CP in hyperoxia is related to faster VO2 kinetics or improved microvascular O2 delivery per se is presently unclear. We therefore examined the effect of hyperoxia on CP and τVO2 during upright cycle exercise in healthy, recreationally active males (n = 9). CP was determined in normoxia (N) and hyperoxia (H; fraction of inspired O2 = 0.5) via 4 severe-intensity constant load exercise tests to exhaustion on a cycle ergometer, repeated once in each condition. Additionally, 6-minute bouts of exercise were repeated 4 times in each condition at 70% of the gas exchange threshold, in order to characterise τVO2 and the time constant of muscle deoxyhaemoglobin kinetics (τ[HHb]), alongside absolute concentrations of muscle oxy- and total-haemoglobin ([HbO2 ], [THb]) in each condition, the latter measurements via near infrared spectroscopy. Values are means ± SD, compared by paired samples t-test (CP, τVO2) and repeated measures ANOVA (τ[HHb], [HbO2], [THb]). CP was greater in H compared to N (H: 216 ± 30 vs. N: 197 ± 29W; P < 0.001), however τVO2 was unchanged between conditions (H: 25 ± 6 vs N: 24 ± 9 s; P = 0.49). τ[HHb] (H: 11 ± 6 vs. N: 8 ± 6 s; P = 0.93) and [THb] (H: 99 ± 18 vs. N: 99 ± 21 μM; P = 0.98) were unchanged, whereas [HbO2] during exercise was greater in H versus N (H: 74 ± 21 vs. N: 68 ± 18 μM; P < 0.001). In conclusion, this study provides novel insights into the physiological determinants of critical power and by extension, exercise tolerance. Microvascular oxygenation (assessed via NIRS) and CP were improved during exercise in hyperoxia compared with normoxia. Importantly, the improved microvascular oxygenation afforded by hyperoxia did not alter τVO2, suggesting that microvascular O2 delivery is an independent determinant of the upper limit for steady-state exercise, i.e. critical power.

Where applicable, experiments conform with Society ethical requirements