Background and Aims: Arousal induced hypocapnia is thought to predispose to further collapse in obstructive sleep apnea (OSA) by reducing upper airway dilator muscle activity following the return to sleep. Prior research in healthy individuals and treated OSA patients has shown no evidence for reduced dilator muscle activity post-arousal. However, almost all studies assessed arousals that were spontaneous or tone-induced, and often CO2 was not measured. The aim of this study was to determine whether arousals that terminate obstructive events: (1) induce hypocapnia and (2) reduce dilator muscle activity in untreated OSA patients.
Methodology and Key Findings: 31 untreated OSA patients were instrumented with EEG, EMG and EOG, a pneumotachograph, end-tidal CO2 monitoring and intramuscular wires inserted into the genioglossus. CO2 was assessed on the last breath of arousal and compared to each individual’s wakefulness value. 24 participants provided 1137 useable arousals. The mean(SD) CO2 on the last arousal breath was -0.2(2.4) mmHg below wakefulness indicating that hypocapnia typically developed during arousal. CO2 and genioglossus muscle activity were negatively associated such that a 1mmHg reduction in CO2 at end-arousal was associated with a ~2% increase in genioglossus activity on each of the first five breaths of return to sleep immediately following arousal.
Conclusions and Implications: This is the first study to demonstrate that respiratory arousal induces hypocapnia in untreated OSA patients. Contrary to expectations dilator muscle activity was not reduced, rather it was elevated in the presence of pronounced hypocapnia. Therefore post-arousal dilator muscle activity appears to be driven by stimuli other than CO2.These findings suggest that arousal does not predispose to further collapse on the return to sleep at least via reduced dilator muscle activity. Future work should attempt to understand the mechanisms responsible for the elevated activity as they may offer a potential treatment target for OSA.
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Future Directions: Future work should examine whether the elevated dilator muscle activity present post-arousal actually benefits upper airway patency and ventilation in OSA patients following the return to sleep. In addition, future work should attempt to better understand the eliciting stimuli and mechanisms responsible for the elevated dilator muscle activity as they may offer potential treatment targets for OSA or improve current treatments that focus on improving upper airway dilator muscle activation such as hypoglossal nerve stimulation.