Obstructive sleep apnea (OSA) is characterized by recurrent closure of the pharyngeal airway during sleep. Although risk factors are generally known, the mechanisms remain incompletely understood. There is a widely held view that upper airway (UA) patency is determined by a balance of UA dilating muscle activity versus the collapsing intraluminal pressure generated during inspiration. What is less appreciated is that UA patency may also be influenced by nonneuromuscular factors such as changes in caudal traction, vasomotor tone, and mucosal adhesive forces. To understand the pathogenesis of upper airway obstruction, I first address the determinants of UA patency and the effect of sleep on UA function.