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Poor upper airway dilator muscle function may contribute to obstructive sleep apnea (OSA). Sleep deprivation reduces dilator muscle responsiveness, but sleep fragmentation, which is most characteristic of OSA, has not been assessed. This study compared the effects of sleep deprivation and fragmentation on dilator muscle responsiveness during wakefulness. Twenty-four healthy individuals (10 female) participated in two consecutive overnight polysomnography (PSG) sessions. The first was an adaptation PSG of normal sleep. The second was an experimental PSG, where participants were allocated to groups of either normal sleep, no sleep, or fragmented sleep. Inspiratory resistive loading assessment occurred the morning following each PSG. Four 10 cmH2O and four 20 cmH2O loads were presented in random order for 60 seconds while participants were awake and supine. Sleep (electroencephalogram, electrooculogram, electromyogram [EMG]), intramuscular genioglossus activity (EMGGG), and ventilation were measured throughout the loading sessions. Five controls, seven sleep deprivation participants, and seven sleep fragmentation participants provided data. Contrary to expectations, neither EMGGG nor ventilation showed significant interaction effects (group × session × load) during resistive loading. There was a main effect of load, with peak EMGGG (mean % max ± standard error) significantly higher for the 20 cmH2O load (4.1 ± 0.6) than the 10 cmH2O load (3.3 ± 0.6) across both sessions and all groups. Similar results were observed for peak inspiratory flow, duty cycle, and mask pressure. Upper airway function was not affected by 1 night of no sleep or poor-quality sleep. This raises doubt as to whether fragmented sleep in OSA increases disorder severity via reduced upper airway dilator responses. |
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