We studied the effects of sleep fragmentation on arousal and ventilatory responses to hyperoxic hypercapnia, isocapnic hypoxia, and chemical stimulation of the larynx during sleep in 5 dogs. Sleep fragmentation was induced by repeatedly arousing the dogs with acoustic stimuli throughout 2 to 3 consecutive nights. Responses to respiratory stimuli were then studied during a subsequent daytime sleep. Arterial O2 saturation was measured with an ear oximeter, and sleep stage was determined by electroencephalographic and behavioral criteria. Hypercapnic and hypoxic ventilatory responses were unimpaired by sleep fragmentation. In contrast, alveolar PCO2 levels at arousal increased after sleep fragmentation, from a mean +/- SEM of 52.2 +/- 1.4 mm Hg to 55.6 +/- 1.5 mm Hg (p < 0.05) during slow-wave sleep, and from 57.9 +/- 1.5 mm Hg to 61.3 +/- 2.2 mm Hg (p < 0.05) during rapid-eye movement sleep. Similarly, arterial O2 saturation at arousal decreased after sleep fragmentation from 80.1 +/- 1.0% to 70.2 +/- 2.7% (p < 0.05) during slow-wave sleep, and from 66.3 +/- 3.6% to < 55% (p < 0.05) during rapid-eye-movement sleep. Arousal responses to laryngeal stimulation were also impaired after sleep fragmentation. We conclude that arousal responses to respiratory stimuli are decreased by sleep fragmentation.