| Popis: |
During sleep, both the tonic and inspiratory-modulated components of upper airway muscle activity are suppressed in parallel with the characteristic postural atonia. In individuals with a constricted upper airway related to anatomical factors such as a large tongue relative to maxilla and mandible (i.e., oropharyngeal crowding), this sleep-related reduction in upper airway muscle activity could precipitate an upper airway occlusion more easily and lead to obstructive sleep apnea. However, in the narrowed upper airway of patients with obstructive sleep apnea, a neuromuscular compensatory mechanism augments the activity of the upper airway dilator muscles in defense of upper airway patency, particularly during inspiration. When the crowded oropharynx is improved by the application of positive airway pressure and/or mandibular advancement, upper airway dilator muscle activity during inspiration is reduced, returning the upper airway toward a normal configuration and pattern of muscle function in patients with obstructive sleep apnea. Accordingly, the upper airway patency in humans is precisely controlled by the close anatomical–functional relationship. |
