"Work-to-Work" exercise slows pulmonary oxygen uptake kinetics, decreases critical power, and increases W' during...

We have previously demonstrated that the phase II time constant of pulmonary oxygen uptake kinetics ( $$ ) is an independent determinant of critical power (CP) when O₂ availability is not limiting, that is, during upright cycle exercise in young, healthy individuals. Whether this causative relationship remains when O₂ availability is impaired remains unknown. During supine exercise, which causes an O₂ availability limitation during the exercise transition, we therefore determined the impact of a raised baseline work rate on $$ and CP. CP, $$ , and muscle oxygenation status (the latter via near-infrared spectroscopy) were determined via four severe-intensity constant-power exercise tests completed in two conditions: (1) with exercise initiated from an unloaded cycling baseline (U→S), and (2) with exercise initiated from a moderate-intensity baseline work rate of 90% of the gas exchange threshold (M→S). In M→S, critical power was lower (U→S = 146 ± 39 W vs. M→S = 132 ± 33 W, P = 0.023) and $$ 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 ([HbO₂  + MbO₂ ]) at baseline or during exercise. The concomitant increase in $$ and reduction in CP during M→S compared to U→S shows for the first time that $$ is an independent determinant of CP in conditions where O₂ availability is limiting.