The pathophysiology of obstructive sleep apnoea syndrome (OSAS) is complex and incompletely understood, but is principally based on an imbalance between the collapsing forces of the upper airway (UA) during inspiration and the counteracting dilating forces of the UA dilating muscles. A narrowed UA is very common among OSAS patients, which is usually due, in adults, to nonspecific factors such as fat deposition in the neck or abnormal bony morphology of the UA. Functional impairment of the UA dilating muscles is particularly important in the development of OSAS, and patients have a reduction in both tonic and phasic contraction of these muscles during sleep when compared to normal subjects. Arousal plays an important role in the termination of each apnoea, but may also contribute to the development of further apnoea because of a reduction in respiratory drive related to the hypocapnia which results from postapnoeic hyperventilation. A cyclical pattern of repetitive obstructive apnoeas may result. A better understanding of the integrated pathophysiology of obstructive sleep apnoea syndrome should help both in the choice of optimum therapy for each individual patient and also in the development of new therapeutic techniques.