OSA syndrome is characterized by recurring episodes of upper airway (UA) obstruction during sleep. The UA is subjected to collapse when the negative airway pressure generated by inspiratory activity of the diaphragm and intercostal muscles exceeds the force produced by the UA dilating muscles. Factors that reduce UA calibre lead to increased UA resistance with the generation of a more negative pharyngeal pressure during inspiration, and thereby predispose to UA occlusion during sleep. As a consequence, UA dilating muscles must contract more forcefully to maintain a patent UA, which may predispose to fatigue. Nasal CPAP counteracts these collapsing forces and is associated with resting of the UA muscles. The more recent development of auto-adjusting CPAP (APAP) is a reflection of the understanding that the pressure required to prevent UA collapse fluctuates throughout the night and results in a lower mean pressure that may be more comfortable for some patients. The predominant morbidity of the OSA syndrome is cardiovascular and there is growing understanding of the basic mechanisms involved. Intermittent hypoxia appears to play a central role by activating transcription factors that predispose to atherogenesis, particularly NFkappaB. Sympathetic overactivity also appears to play an important role but the mechanisms involved are unclear.