To determine whether change of laryngeal resistance causes shortening of expiratory time (TE) and hence increase of respiratory frequency with CO2 inhalation in conscious humans, 11 fit male subjects with permanent tracheostomies after laryngectomy for cancer (L group) and 8 matched control subjects (C group) inhaled CO2 in mild hyperoxia to produce various levels of steady-state hyperpnea within "nonvagal" range 1. Breathing pattern was averaged at the end of each steady state and behaved similarly in both groups. As end-tidal PCO2 (PACO2) increased, TE significantly shortened in both groups, whereas inspiratory time (TI) remained roughly constant (slightly increasing in the L group), suggesting that the larynx, at least in range 1, has no major role in determining this pattern. Quantitative comparison between the two groups showed that in the L group TE was significantly longer, whereas expiratory flow peaked and declined significantly earlier, resulting in a greater tendency to form end-expiratory pauses. All differences were greatest in eucapnia and decreased as PACO2 increased. Despite matched mean PACO2 values, mean tidal volume (VT) ventilation and mean inspiratory flow (VT/TI) were significantly less in the L group, and the slope of VT/TI vs. PACO2 was significantly depressed.