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dc.contributor.authorCori, Jennifer M-
dc.contributor.authorNicholas, Christian L-
dc.contributor.authorAvraam, Joanne-
dc.contributor.authorLee, V Vien-
dc.contributor.authorSchembri, Rachel-
dc.contributor.authorJackson, Melinda L-
dc.contributor.authorJordan, Amy S-
dc.identifier.citationJournal of Clinical Sleep Medicine : JCSM : official publication of the American Academy of Sleep Medicine 2018; 14(5): 715-724en_US
dc.description.abstractPoor 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.en_US
dc.subjectairway dilator musclesen_US
dc.subjectobstructive sleep apneaen_US
dc.subjectsleep deprivationen_US
dc.subjectsleep fragmentationen_US
dc.titleThe Effects of Experimental Sleep Fragmentation and Sleep Deprivation on the Response of the Genioglossus Muscle to Inspiratory Resistive Loads.en_US
dc.typeJournal Articleen_US
dc.identifier.journaltitleJournal of Clinical Sleep Medicine : JCSMen_US
dc.identifier.affiliationInstitute for Breathing and Sleepen_US
dc.identifier.affiliationMelbourne School of Psychological Sciences, University of Melbourne, Parkville, Victoria, Australiaen_US
dc.identifier.affiliationSchool of Health & Biomedical Sciences, RMIT University, Bundoora, Victoria, Australiaen_US
dc.type.austinJournal Article-
dc.type.austinResearch Support, Non-U.S. Gov't-, Joanne
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
item.openairecristype for Breathing and Sleep- and Sleep Medicine- for Breathing and Sleep- for Breathing and Sleep- and Sleep Medicine- for Breathing and Sleep-
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