Obstructive sleep apnea (OSA) is a common disorder with important adverse consequences. This disorder is characterized by repetitive pharyngeal collapse during sleep the etiology of which is likely multifactorial. One important component in apnea pathogenesis is the activity of upper airway dilator muscles and the impact of sleep on these muscles. We plan in the proposal a series of studies assessing how these muscles are controlled. First, we believe there are four primary sources of neural input to these muscles which includes: 1) respiratory premotor neurons; 2) reflex (mechanoreceptor mechanisms; 3) tonic neural input (excluding phasic respiratory influences); and 4) a wakefulness stimulus (could be mediated directly or though 1, 2, and 3 above). Most of the previous work in our laboratory has focused on reflex mechanisms. However, in this proposal, we plan to carefully dissect out the other three sources of neural control to these muscles and determine the effect of sleep on each. Second, we plan a careful assessment of how sleep deprivation influences muscle activation/control both awake and during sleep immediately following such deprivation. Third, early evidence suggests that body position (supine versus lateral) may importantly impact the mechanisms controlling these muscleL We will try to explore this both awake and asleep. Finally, we do not believe that changing pharyngeal muscle activation is the entire explanation for sleep apnea. Decrements in lung volume that occur during sleep may also be important. As a result, we will both measure and influence lung volume during sleep in a group of patients with OSA to delineate the role of changing lung volume in the pharyngeal collapse which characterized this disorder. This series of studies should importantly improve our understanding of the pathophysiology of obstructive sleep apnea.
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