Does upper airway muscle injury trigger a vicious cycle in obstructive sleep apnea? A hypothesis

Abstract

Recent studies have indicated that the level of neural activation of upper airway dilator muscles is abnormally elevated in patients with obstructive sleep apnea (OSA). This is presumed to represent an adaptive mechanism that partially compensates for the anatomically small upper airway found in individuals with OSA. We have reviewed evidence that pharyngeal dilator muscles undergo secondary changes in structure as a direct consequence of their increased activity level in OSA. These alterations have the potential to be both beneficial and harmful with respect to the maintenance of upper airway patency. We propose a model outlining the possible role of activity-induced upper airway muscle remodeling and injury in the pathogenesis of OSA, and discuss potential implications for treatment of the disease.