Abnormalities of upper airway mechanical properties are a well-recognized and important feature of the pathophysiology of the obstructive sleep apnea hypopnea syndrome (OSAHS). Recently, investigations enhanced our understanding of the factors that promote upper airway obstruction. In patients with OSAHS, anatomic narrowing of the pharyngeal airway, particularly in the lateral dimension with thickening of the lateral pharyngeal walls, is present. In addition, the passive upper airway (absent muscle activity) demonstrates increased collapsibility, which is modulated by caudal tracheal traction, mucosal surface forces, route of breathing, and the balance of intraluminal airway and extraluminal tissue pressures. In patients with OSAHS, pharyngeal dilator muscles (including the genioglossus and soft palate muscles) demonstrate a coordinated pattern of increased muscle activity while awake compared with normals. This is thought to represent a neuromuscular compensatory mechanism for the anatomically narrow, more collapsible upper airway. With the onset of sleep, the reflexes that drive this muscular compensation are diminished, leading to reduced muscle activity and predisposing the OSAHS patient to pharyngeal collapse. Better understanding of the mechanical properties of the upper airway in normals and patients with OSAHS should help in the development of new therapeutic strategies.