The upper airway is the primary conduit for passage of air into the lungs. Its physiology has been the subject of intensive study: both passive mechanical and active neural influences contribute to its patency and collapsibility. Different models can be used to explain behavior of the upper airway, including the "balance of forces" (airway suction pressure during inspiration versus upper airway dilator tone) and the Starling resistor mechanical model. As sleep is the primary state change responsible for sleep disordered breathing (SDB) and the obstructive apnea/hypopnea syndrome (OSAHS), understanding its effects on the upper airway is critical. These include changes in upper airway muscle dilator activity and associated changes in mechanics and reflex activity of the muscles. Currently SDB is thought to result from a combination of anatomical upper airway predisposition and changes in neural activation mechanisms intrinsic to sleep. Detection of SDB is based on identifying abnormal (high resistance) breaths and events, but the clinical tools used to detect these events and an understanding of their impact on symptoms is still evolving. Outcomes research to define which events are most important, and a better understanding of how events lead to physiologic consequences of the syndrome, including excessive daytime somnolence (EDS), will allow physiologic testing to objectively differentiate between "normal" subjects and those with disease.