“Work‐to‐Work” exercise slows pulmonary oxygen uptake kinetics, decreases critical power, and increases W’ during supine cycling

We have previously demonstrated that the phase II time constant of pulmonary oxygen uptake kinetics ([Formula: see text]) is an independent determinant of critical power (CP) when O(2) availability is not limiting, that is, during upright cycle exercise in young, healthy individuals. Whether this causative relationship remains when O(2) availability is impaired remains unknown. During supine exercise, which causes an O(2) availability limitation during the exercise transition, we therefore determined the impact of a raised baseline work rate on [Formula: see text] and CP. CP, [Formula: see text] , and muscle oxygenation status (the latter via near‐infrared spectroscopy) were determined via four severe‐intensity constant‐power exercise tests completed in two conditions: (1) with exercise initiated from an unloaded cycling baseline (U→S), and (2) with exercise initiated from a moderate‐intensity baseline work rate of 90% of the gas exchange threshold (M→S). In M→S, critical power was lower (U→S = 146 ± 39 W vs. M→S = 132 ± 33 W, P = 0.023) and [Formula: see text] was greater (U→S = 45 ± 16 sec, vs. M→S = 69 ± 129 sec, P = 0.001) when compared to U→S. There was no difference in tissue oxyhemoglobin concentration ([HbO(2) + MbO(2)]) at baseline or during exercise. The concomitant increase in [Formula: see text] and reduction in CP during M→S compared to U→S shows for the first time that [Formula: see text] is an independent determinant of CP in conditions where O(2) availability is limiting.