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Purpose  To investigate the physiological mechanisms that explain the end-exercise decrease in oxygen uptakeduring 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 atand 2) an exhaustive isokinetic supramaximal cycling exercise (Tlim supra ) at 185 ± 24% of(i.e., 640.5 ± 50.8 W). During cycling exercise tests,, 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 Tlim supra .    Results  A > 5% decrease inand/or SV was observed in 6 subjects, with 5 out of 6 subjects presenting both phenomena. The magnitude of thedecrease was correlated with the magnitude of the SV decrease (R = 0.75, P < 0.01), the peak-exercise end-tidal O 2  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-Tlim supra  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 ofdecrease 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.

Prevalence of cardio-respiratory factors in the occurrence of the decrease in oxygen uptake during supra-maximal, constant-power exercise