The effect of delayed vagal activity withdrawal on cardiorespiratory responses at an increase in workload was examined. Eleven volunteers (21 ± 3 yr, 66 ± 4 kg) performed cycle ergometer exercise at a work rate corresponding to 80% of ventilatory threshold after 3 min of unloaded cycling. Facial stimulation was given by applying a vinyl bag filled with cold water (3-5°C) to the face 1 min before to 1 min after the increase in workload (S2 trial) or no stimulation was given (Nr trial). Oxygen uptake (O₂), heart rate (HR), and cardiac output () were continuously recorded in four transitions for each trial. Data were averaged for each subject and trial. Mean response time (MRT, sum of delay and time constant) was calculated with a monoexponential fitting. Facial stimulation induced acute bradycardia (10 ± 5 beats/min in S2 trial). The MRT of HR and was significantly longer in the S2 trials (46 ± 35 and 37 ± 23 s) than in the Nr trials (26 ± 18 and 28 ± 19 s, respectively), but no significant change in O₂ MRT was shown (36 ± 7 vs. 38 ± 12 s). These findings suggest that increased vagal activity delays the central circulatory responses, which does not alter the O₂ kinetics at the onset of stepwise increase in workload. The maintenance of O₂ kinetics during acute bradycardia may either reflect the fact that some intramuscular processes (such as oxidative enzyme inertia) limit O₂ kinetics or alternatively that increased sympathetic vasoconstriction at some remote site defends exercising muscle blood flow.