ABSTRACT
The onset of sleep is associated with a reduction in upper airway patency and an increase in resistance, an effect observed in normal humans and animals, snorers, and patients with obstructive sleep apnea/hypopnea syndrome (OSA) (e.g., Refs. 16; see Refs. 7 and 8 for reviews). Patients with OSA commonly have structural abnormalities that result in a narrowed upper airway and collapsible pharynx; but when they are awake, their airway remains continuously patent (except during swallowing, speech, vomiting, etc.). During sleep, however, the cross-sectional area decreases considerably and they experience repeated, clinically significant, obstructive apneas or hypopneas. This sleep-wake state dependence of the disorder points to the involvement of neural mechanisms. The marked increase in resistance is attributed to a sleeprelated alteration in the neural control of upper airway striated muscles. In particular, decrements in the activity of upper airway dilator muscles, i.e., those that counteract the collapsing force of the negative pressure generated in the airway during inspiration, are believed to play a permissive role in sleep-related airway obstructions.
