AROUSAL DOES NOT LEAD TO REDUCED DILATOR MUSCLE ACTIVITY IN THE HEALTHY Arousal from Sleep Does Not Lead to Reduced Dilator Muscle Activity or Elevated Upper Airway Resistance on Return to Sleep in Healthy Individuals

53 Airway Physiology Following Arousal—Jordan et al. INTRODUCTION The pathogenesis of obstructive sleep apnea (OSA) is only partially understood; in particular, the potential role of arousals from sleep in destabilizing upper airway function is controversial.1 Arousals from sleep commonly occur at the termination of respiratory events in OSA2,3 and have been suggested by some authors to predispose to further upper airway collapse on the return to sleep.2 The adverse effect of arousal on airway function has been proposed because the brief period of hyperventilation which accompanies arousal lowers the partial pressure of endtidal CO2 (PETCO2). As upper airway dilator muscles such as the genioglossus are known to vary their activity in response to both chemical and mechanical drives,4,5 the arousal-induced hypocapnia could lower airway dilator muscle activity on the return to sleep, predisposing to upper airway collapse. Despite this commonly described sequence of events and evidence indicating hypocapnia can lead to dilator muscle hypotonia6 and increased airways resistance6–8 during stable sleep in susceptible AROUSAL DOES NOT LEAD TO REDUCED DILATOR MUSCLE ACTIVITY IN THE HEALTHY