Abstract
Purpose: To investigate the physiological mechanisms that explain the end-exercise decrease in oxygen uptake [Formula: see text] during strenuous constant-power exercise, we recruited eleven trained, track cyclists.Methods: On two separated days they performed 1) resting spirometric measures, followed by an incremental test on a cycle ergometer to determine the power output at [Formula: see text] and 2) an exhaustive isokinetic supramaximal cycling exercise (Tlimsupra) at 185 ± 24% of [Formula: see text] (i.e., 640.5 ± 50.8 W). During cycling exercise tests, [Formula: see text], ventilation parameters, stroke volume (SV) and heart rate were continuously recorded. Furthermore, arterialised capillary blood samples were collected to measure blood pH, arterial oxygen saturation, lactate and bicarbonate concentration before and 5 min after Tlimsupra.Results: A > 5% decrease in [Formula: see text] and/or SV was observed in 6 subjects, with 5 out of 6 subjects presenting both phenomena. The magnitude of the [Formula: see text] decrease was correlated with the magnitude of the SV decrease (R = 0.75, P < 0.01), the peak-exercise end-tidal O2 partial pressure (R = 0.80, P < 0.005) and the resting, forced expiratory volume in 1 s (R = 0.72, P < 0.05), but not with any blood variables. The significant post-Tlimsupra decrease in forced vital capacity and forced inspiratory volume corroborate with a possible respiratory muscle fatigue.Conclusion: Based on these findings, we demonstrate that the occurrence of [Formula: see text] decrease in more than half of our subjects, during a strenuous constant-power exercise leading to a mild-acidosis (pH = 7.21 ± 0.04), results mainly from cardio-respiratory factors and not from blood metabolic responses.