To determine whether the carotid chemoreceptors or hyperpnea are required for arousal from sleep by hypoxia, 14 sleep-deprived cats were studied during slow-wave (SWS) and rapid-eye-movement (REM) sleep. Rapid hypoxia was produced by inhalation of 5% O2 in N2 or 6% CO in 40% O2 by intact cats and 5% O2 in N2 after carotid body denervation. Preliminary studies identified a period of SWS unassociated with spontaneous arousals. In 69 studies during SWS unassociated with spontaneous arousals, arterial O2 saturation (SaO2) values at arousal were: 47.1 +/- 1.5% (mean +/- SE) (5% O2, intact); 48.9 +/- 1.4% (6% CO, intact); and 49.9 +/- 2.0% (5% O2, denervated). During SWS associated with spontaneous arousals, SaO2 values at arousal were 71.6 +/- 1.8% (5% O2, intact). Arousal from REM occurred at significantly lower values: 31.7 +/- 3.9% (6% CO, intact) and 43.5 +/- 2.3% (5% O2, intact). During both SWS and REM, inhalation of 5% O2 by intact animals caused a substantial increase in ventilation while 6% CO did not. We conclude that more severe hypoxia is required for arousal from SWS when studies are done in a period unassociated with spontaneous arousals than from SWS associated with spontaneous arousals. Hypoxic arousal does not appear to require activation of the carotid bodies or hyperpnea.