Abstract
We studied the steady state responses of heart rate (HR) to carbon dioxide inhalation under hyperoxic, euoxic, and hypoxic conditions in 9 healthy men. With increasing end-tidal PCO2, HR generally increased slightly. On the other hand, distinct increment in VE in response to step increase in end-tidal PCO2 was observed in all three different conditions. Significant positive correlation between hypercapnic VE and HR responsiveness was found in both hyperoxic and hypoxic conditions, whereas no such tendency was seen in euoxic condition. We suggest that the effect of CO2 inhalation on HR is mainly determined by the pulmonary inflation reflex in hyperoxia, the pulmonary inflation reflex plus peripheral chemoreceptor activity in euoxia, and the additional sympathetic and humoral factors in hypoxia, respectively.
Published Version
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