Contribution of peripheral chemoreceptor drive in exercise hyperpnea in humans.

The peripheral chemoreceptors play a dominant role in the respiratory compensation of lactic acidosis during heavy exercise of humans. Our object was to determine the contribution of peripheral chemoreceptors to exercise hyperpnea during mild to moderate and heavy exercise above the anaerobic threshold. We used a hyperoxic suppression test in six normal male subjects. Inspired gas was abruptly changed without the subject's knowledge from air to pure oxygen for 5 to 6 breaths. The maximal ventilatory depression after O2 breathing was 5.5 +/- 1.7 L/min (BTPS) at mild exercise, and the depression increased with increasing exercise intensity up to 12.8 +/- 4.1 L/min (BTPS). The relative contribution of the peripheral chemoreceptors to ventilation in terms of percentage of the maximal ventilatory depression was maintained, being 20% throughout the entire work ranges studied. The contribution of the peripheral chemoreceptors to total ventilation is hardly altered by lactic acidosis caused by heavy exercise above the anaerobic threshold according to our data. These results suggested that the peripheral chemoreceptors may not be solely responsible for excessive hyperventilation, or residual activities of peripheral chemoreceptors still exist after O2 breathing especially during heavy exercise above the anaerobic threshold.