Ventilatory responses during incremental exercise in men under hyperoxic conditions.

The aim of the present study was to explore the role of the carotid chemoreceptors in the regulation of breathing during incremental ramp exercise. We measured minute ventilation (VE), oxygen uptake (VO2), carbon dioxide output (VCO2), end-tidal PO2 and PCO2 (PETO2 and PETCO2), and heart rate (HR) during incremental exercise in healthy young men breathing air and 50% O2. During incremental exercise (15 W/min, from 0 to 300 W) VCO2 in hyperoxia did not differ from the normoxic response, but VE in hyperoxia increased more linearly with an increasing load in comparison to the curvilinear rise of normoxic VE. The isocapnic buffering of PETCO2 observed in normoxia at the transition from moderate to heavy work did not appear in hyperoxia until a very heavy work load had been attained. This agrees with the observation that normoxic VE/VCO2 that was consistently falling with load and became flat near the isocapnic point and then turned upward with a further increase in work load, while VE/VCO2 in hyperoxia decreased continuously during heavy exercise. These results would suggest the delayed onset of anaerobic metabolism and the depression of VE under hyperoxic conditions. However, we found that VE and HR increased from a specific work rate with a steeper slope during incremental exercise under both normoxic and hyperoxic conditions. There was a significant correlation between the work rates at which the inflection points of the VE and HR slopes were observed. These findings suggest that factors unrelated to peripheral chemoreceptor activity and affecting both the ventilatory and circulatory systems may be responsible for hyperpnea during heavy exercise.