A growing body of literature, particularly over the past ten years, has described the deleterious effects of obstructive breathing during sleep, including repetitive apneas and hypopneas, in the development of erectile dysfunction (ED). The potential mechanisms responsible for triggering or exacerbating ED include not only an intermittent hypoxia, but also the marked fragmentation of sleep architecture that characterizes the obstructive sleep apnea syndrome (OSAS). In addition, OSAS also has known secondary effects that include neurological mechanisms, endothelial dysfunction and alterations in hormonal function which are hypothesized to play a role in ED. Penile erections occur naturally throughout each phase of rapid eye movement (REM) sleep in normal human males, and data are presented to suggest an important role of REM sleep in maintaining normal erectile physiology during wakefulness. REM sleep, also known as paradoxical sleep, is markedly disrupted or diminished in patients with OSAS. Treatment of OSAS with nasal continuous positive airway pressure (CPAP), on the other hand, has been demonstrated to improve daytime erectile function in these patients, potentially not only by re-establishing normal respiratory function during sleep, but also via the consolidation of REM sleep and the resultant increase in REM-related erectile activity. Finally, given the strong association between OSAS an ED, it may be clinically relevant to screen patients with ED for possible OSAS, particularly given data showing that commonly used therapies for ED treatment, such as either phosphodiesterase inhibitors or testosterone replacement, have known exacerbating effects on obstructive breathing during sleep.