Chemoreflex modulation of ventilatory dynamics during exercise in humans.

The precision of arterial blood gas homeostasis following a change of work rate depends on the response kinetics of ventilation. The carotid bodies (CB's) have been proposed as modulators of these kinetics. The present investigation was undertaken to determine whether the effect is specific to CB activation or whether other factors that augment the exercise hyperpnea would produce a similar response. We therefore established the effects of increased CB and central (C) chemoreflex activation on the inspired ventilatory (VI) dynamics for moderate-intensity cycling. Work tests were separately performed with air, 12% O2 to increase CB activity, 100% O2 to "abolish" CB activity, and CO2 in O2 to increase C activity. The time constant of the VI response was substantially shortened by hypoxia (40 s) compared with air breathing (58 s) and increased by 100% O2 (92 s) and, even more so, by CO2 in O2 (101 s). We conclude that increased carotid (but not central) chemoreflex responsiveness speeds the kinetics of the exercise hyperpnea by a process that is not merely the consequence of increased ventilatory drive.