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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 (τVO2). To test the hypothesis that this relationship is causal we determined the impact of prior exercise (“priming”) on CP and τVO2 in the upright and supine positions. 17 healthy men were assigned to either upright or supine exercise groups, whereby CP, τVO2 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 τVO2 (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 τVO2 (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 τVO2 and increased CP following priming in the supine group, effects that were absent in the upright group, provides the first experimental evidence that τVO2 is mechanistically related to critical power. The increased τ[HHb] suggests that this effect was mediated, at least in part, by improved oxygen availability.

What is the central question of this study? Critical power (CP) represents the highest work rate for which a metabolic steady state is attainable. The physiological determinants of CP are unclear, but research suggests that CP might be related to the time constant of phase II oxygen uptake kinetics (τV̇O2). What is the main finding and its importance? We provide the first evidence that τV̇O2 is mechanistically related to CP. A reduction of τV̇O2 in the supine position was observed alongside a concomitant increase in CP. This effect may be contingent on measures of oxygen availability derived from near-infrared spectroscopy. 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. Seventeen healthy men were assigned to either upright or supine exercise groups, whereby CP, τV̇O2 and muscle deoxyhaemoglobin kinetics (τ