In order to assess the role of hypoxemia in the sleep disruption of patients with COPD, we studied patients breathing air and oxygen during sleep. In 24 patients with COPD, we determined the 95% confidence bands for arterial O2 saturation (SaO2) in the various sleep stages. The lowest mean SaO2 was during REM sleep. Patients spent 22.4% of the night desaturated (SaO2 more than 5% below awake SaO2). Apneic episodes were uncommon and occurred in only 2 patients. When compared with established age-matched normal subjects from another center, poor sleep quality was indicated by reduced sleep time, increased sleep stage changes, and increased arousal frequency. Oxygen therapy had no apparent effect on sleep quality. Arousal frequency was independent of measurements of awake pulmonary function or chemical control of breathing. During room air breathing, arousals were strongly associated with periods of arterial oxygen desaturation. However, relief of the hypoxemia with supplemental oxygen had no effect on arousal frequency. This suggests that it is not hypoxemia per se, but an associated phenomenon such as hypercapnia that causes the arousals.