We tested whether the leftward shift of the oxygen dissociation curve of hemoglobin with hyperpnea delays the oxygen uptake (VO(2)) response to the onset of exercise. Six male subjects performed cycle ergometer exercise at a work rate corresponding to 80% of the ventilatory threshold (VT) VO(2) of each individual after 3 min of 20-W cycling under eupnea [control (Con) trial]. A hyperpnea procedure (minute ventilation = 60 l/min) was undertaken for 2 min before and during 80% VT exercise in hypocapnia (Hypo) and normocapnia (Normo) trials. In the Normo trial, the inspired CO(2) fraction was 3% to prevent hypocapnia. The subjects completed two repetitions of each trial. To determine the kinetic variables of VO(2) and heart rate (HR) at the onset of exercise, a nonlinear least-squares fitting was applied to the data averaged from two repetitions by a monoexponential model. The end-tidal CO(2) partial pressure before the onset of exercise was significantly lower in the Hypo trial than in the Con and Normo trials (22 +/- 1 vs. 38 +/- 3 and 36 +/- 1 mmHg, respectively, P < 0.05). The time constant of VO(2) and HR was significantly longer in the Normo trial (28 +/- 7 and 39 +/- 18 s, respectively) than in the Con trial (21 +/- 7, 34 +/- 16 s, respectively, P < 0.05). The VO(2) time constant of the Hypo trial (37 +/- 12 s) was significantly longer than that of the Normo trial, although no significant difference in the HR time constant was seen (Hypo, 41 +/- 28 s). These findings suggested that respiratory alkalosis delayed the kinetics of oxygen diffusion in active muscle as a result of the leftward shift of the oxygen dissociation curve of hemoglobin. This supports an important role for hemoglobin-O(2) offloading in setting the VO(2) kinetics at exercise onset.

We examined whether the diving reflex without breath-holding (face immersion alone) increases vagal activity, as determined by heart rate variability. A group of 15 men [mean age 20 (SD 3) years, height 172 (SD 5) cm, body mass 68 (SD 9) kg] performed 12 trials at various breathing frequencies (5, 10, 15, 20, 30 breaths x min(-1) and uncontrolled breath) with or without face immersion. The R-R intervals of the ECG and gas exchange variables were recorded during the 2 min of each trial. The subjects immersed their faces in 8 10 degrees C water while breathing through a short snorkel. The subject sat in the same position either with or without face immersion. The mean R-R interval (RRmean), standard deviations (SD[RR]) and coefficient of variance (CV[RR]) of the R-R interval were calculated from the R-R intervals during 30-120 s. The face immersion significantly increased SD(RR) and CV(RR) (P < 0.05), and increased RRmean (P < 0.05) at 20 breaths x min(-1). Face immersion itself had no effect on oxygen uptake, tidal volume, end-tidal O2 and CO2 partial pressures. The diving reflex without breath-holding increased the heart rate variability, indicating that face immersion alone increases vagal activity.

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 (V˙o 2), heart rate (HR), and cardiac output (Q˙) 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 Q˙ 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 inV˙o 2 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 V˙o 2 kinetics at the onset of stepwise increase in workload. The maintenance ofV˙o 2 kinetics during acute bradycardia may either reflect the fact that some intramuscular processes (such as oxidative enzyme inertia) limitV˙o 2 kinetics or alternatively that increased sympathetic vasoconstriction at some remote site defends exercising muscle blood flow.