Recent studies have indicated that the level of neural activation of u
pper airway dilator muscles is abnormally elevated in patients with ob
structive 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 al
terations have the potential to be both beneficial and harmful with re
spect to the maintenance of upper airway patency. We propose a model o
utlining the possible role of activity-induced upper airway muscle rem
odeling and injury in the pathogenesis of OSA, and discuss potential i
mplications for treatment of the disease.