Stimulation of ventilation by normobaric hyperoxia in exercising dogs

In order to describe the factors which, during hyperoxic exercise, can counteract the chemoreceptor-mediated inhibition of ventilation by O₂, minute ventilation (V̇) and the pulmonary gas exchange were studied breath-by-breath in four dogs running on a treadmill (5 km h^-1) for 10 min during and following exposure to O₂ of different durations. We found that a brief inhalation of O₂ applied during the steady state of the V̇ response provoked a reduction in V̇ by 6.5±0.9 l min^-1 whereas hyperoxia applied 2 min before the onset of exercise and maintained for 2.5 min during the running tests had a significantly weaker effect on V̇ (-1.8±0.2 l min^-1, P<0.05). The rise in pulmonary CO₂ output (V̇(CO2)) during the prolonged O₂ exposure was less than in normoxic exercise leading to a deficit of CO₂ eliminated by the lungs of 181 ml. The return to air breathing provoked a rise in V̇, which reached within 73 s a much higher level than the control tests (22.9 ± 3.6 vs. 19.5 ± 2.21 min^-1, P<0.05); V̇ then subsided to control levels with a long exponential decline. The CO₂ deficit during O₂ breathing, was fully compensated after recovery in air within 6 min. No stimulatory effect on ventilation was observed at rest at the cessation of a similar exposure to O₂ despite a higher end-tidal P(CO2) (+4 ± 1 mmHg) than in exercise. In conclusion, the stimulatory effect of O₂ during exercise can be clearly revealed after recovery in air and seems to operate through a more complex mechanism than that thought to be involved at rest. We propose that the changes in CO₂ stores in the exercising muscles could contribute to O₂-induced stimulation during exercise, possibly through stimulation of muscle afferents responding to local circulatory changes. Finally, the observation that during continuous dopamine (DA) infusion (5 μg kg^-1 min^-1) the V(E) response to recovery in air was only a slow decrease, suggests that the arterial chemoreceptors potentiate O₂-induced hyperventilation, or that the vascular actions of DA counteract part of the effects provoked by CO₂ accumulation in the exercising muscles.