Critical power (CP) is a fundamental parameter defining high-intensity exercise tolerance and is related to the time constant of phase II pulmonary oxygen uptake kinetics (τV̇O2). To test the hypothesis that this relationship is causal we determined the impact of prior exercise (“priming”) on CP and τV̇O2 in the upright and supine positions. 17 healthy men were assigned to either upright or supine exercise groups, whereby CP, τV̇O2 and muscle deoxyhaemoglobin kinetics (τ[HHb]) were determined via constant-power tests to exhaustion at four work-rates with (primed) and without (control) priming exercise at ∼31%Δ. During supine exercise, priming reduced τV̇O2 (control: 54 ± 18 vs. primed: 39 ± 11 s; P < 0.001), increased τ[HHb] (control: 8 ± 4 vs. primed: 12 ± 4 s; P = 0.003) and increased CP (control: 177 ± 31 vs. primed: 185 ± 30 W, P = 0.006) compared to control. However, priming exercise had no effect on τV̇O2 (control: 37 ± 12 vs. primed: 35 ± 8 s; P = 0.82), τ[HHb] (CON: 10 ± 5 s vs. PRI: 14 ± 10; P = 0.10), or CP (control: 235 ± 42 vs. primed: 232 ± 35 W; P = 0.57) during upright exercise. The concomitant reduction of τV̇O2 and increased CP following priming in the supine group, effects that were absent in the upright group, provides the first experimental evidence that τV̇O2 is mechanistically related to critical power. The increased τ[HHb] suggests that this effect was mediated, at least in part, by improved oxygen availability

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 (τtrueV˙O2). Whether this relationship is causative is presently unclear. This study determined the impact of raised baseline work rate, which increases τtrueV˙O2, on critical power during upright cycle exercise. Critical power was determined via four constant‐power exercise tests to exhaustion in two conditions: (1) with exercise initiated from an unloaded cycling baseline (U→S), and (2) with exercise initiated from a baseline work rate of 90% of the gas exchange threshold (M→S). During these exercise transitions, τtrueV˙O2 and the time constant of muscle deoxyhemoglobin kinetics (τ [HHb + Mb]) (the latter via near‐infrared spectroscopy) were determined. In M→S, critical power was lower (M→S = 203 ± 44 W vs. U→S = 213 ± 45 W, P = 0.011) and τtrueV˙O2 was greater (M→S = 51 ± 14 sec vs. U→S = 34 ± 16 sec, P = 0.002) when compared with U→S. Additionally, τ [HHb + Mb] was greater in M→S compared with U→S (M→S = 28 ± 7 sec vs. U→S = 14 ± 7 sec, P = 0.007). The increase in τtrueV˙O2 and concomitant reduction in critical power in M→S compared with U→S suggests a causal relationship between these two parameters. However, that τ [HHb + Mb] was greater in M→S exculpates reduced oxygen availability as being a confounding factor. These data therefore provide the first experimental evidence that τtrueV˙O2 is an independent determinant of critical power. Keywords critical power, exercise tolerance, oxygen uptake kinetics, power‐duration relationship, muscle deoxyhemoglobin kinetics, work‐to‐work exercise.

We hypothesize that the V˙O2 time constant (τV˙O2) determines exercise tolerance by defining the power output associated with a “critical threshold” of intramuscular metabolite accumulation (e.g., inorganic phosphate), above which muscle fatigue and work inefficiency are apparent. Thereafter, the V˙O2 “slow component” and its consequences (increased pulmonary, circulatory, and neuromuscular demands) determine performance limits.

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.

Introduction/Purpose: Critical power (CP) is a fundamental parameter defining highintensity 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 (! O2), and muscle oxygenation (assessed by near-infrared spectroscopy) in 9 healthy men performing upright cycle ergometry. Methods: CP was determined in normoxia and hyperoxia (fraction of inspired O 2 = 0.5) via 4 severeintensity constant load exercise tests to exhaustion on a cycle ergometer, repeated once in each condition. During each test, ! O2 and the time constant of muscle deoxyhaemoglobin kinetics (τ [HHb]), alongside absolute concentrations of muscle oxyhaemoglobin ([HbO 2 ]), were determined. Results: CP was greater (hyperoxia: 216 ± 30 vs. normoxia: 197 ± 29W; 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 to normoxia. ! O2 (hyperoxia: 35 ± 12 vs normoxia: 33 ± 10 s; P = 0.33) and τ [HHb] (hyperoxia: 11 ± 5 vs. normoxia: 14 ± 5 s; P = 0.65) were unchanged between conditions, whereas [HbO 2 ] during exercise was greater in hyperoxia compared to normoxia (hyperoxia: 73 ± 20 vs. normoxia: 66 ± 15 µM; P = 0.001). Conclusion: 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 ! O2 , suggesting that microvascular O 2 availability is an independent determinant of the upper limit for steady-state exercise, i.e. CP.