OSA can be considered to arise as a result of the interaction of sleep-related changes in upper airway muscle function and subtle narrowing of the oropharyngeal lumen. The resulting apnea-induced asphyxia leads to an arousal response that terminates the obstructive event. Recurrent episodes of nocturnal asphyxia and recurrent arousals from sleep induce a series of secondary physiological responses that may eventually produce the clinical cardiovascular, hemodynamic, and neuropsychiatric manifestations of the OSA syndrome. The specific factors responsible for each of the clinical features of OSA are not fully understood. Nevertheless, as reviewed here, many of the mechanisms involved have been defined in recent years. Thus, during the past decade OSA has evolved from a disorder that was virtually unrecognized clinically to one whose pathogenetic and pathophysiological mechanisms are to a large extent well understood.