Mechanisms of upper airway hypotonia

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, and typically present in snorers and patients with obstructive sleep apnea (OSA)/hypopnea syndrome (1–5). Patients with OSA commonly have structural abnormalities that result in a narrowed upper airway and collapsible pharyngeal walls. During sleep, the airway cross-sectional area decreases considerably and the patients experience repeated, clinically significant, obstructive apneas or hypopneas. However, when OSA patients are awake, their airway remains patent (except during swallowing, speech, etc.). This sleep-wake–state dependence of the disorder points to the involvement of neural mechanisms. The marked increase in resistance is attributed to a sleep-related alteration in the neural control of upper airway striated muscles. In particular, decrements in the activity of upper airway dilator muscles, that is, those that counteract the collapsing force of the negative pressure generated in the airway during inspiration, play a permissive role in sleep-related airway obstructions.