|Authors||Cori, J. M.|
O'Donoghue, F. J.
Rochford, P. D.
White, D. P.
Jordan, A. S.
|Type||Journal Article (Original Research)|
|Year of Publication||2017|
|Download||zsx057.pdf (1.1 MB)|
To determine whether arousals that terminate obstructive events in obstructive sleep apnea (OSA) (1) induce hypocapnia and (2) subsequently reduce genioglossus muscle activity following the return to sleep.
Thirty-one untreated patients with OSA slept instrumented with sleep staging electrodes, nasal mask and pneumotachograph, end-tidal CO2 monitoring, and intramuscular genioglossus electrodes. End-tidal CO2 was monitored, and respiratory arousals were assigned an end-arousal CO2 change value (PETCO2 on the last arousal breath minus each individual's wakefulness PETCO2). This change value, in conjunction with the normal sleep related increase in PETCO2, was used to determine whether arousals induced hypocapnia and whether the end-arousal CO2 change was associated with genioglossus muscle activity on the breaths following the return to sleep.
Twenty-four participants provided 1137 usable arousals. Mean ± SD end-arousal CO2 change was −0.2 ± 2.4 mm Hg (below wakefulness) indicating hypocapnia typically developed during arousal. Following the return to sleep, genioglossus muscle activity did not fall below prearousal levels and was elevated for the first two breaths. End-arousal CO2 change and genioglossus muscle activity were negatively associated such that a 1 mm Hg decrease in end-arousal CO2 was associated with an ~2% increase in peak and tonic genioglossus muscle activity on the breaths following the return to sleep.
Arousal-induced hypocapnia did not result in reduced dilator muscle activity following return to sleep, and thus hypocapnia may not contribute to further obstructions via this mechanism. Elevated dilator muscle activity postarousal is likely driven by non-CO2-related stimuli.
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