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|Title:||Arousal Intensity is a Distinct Pathophysiological Trait in Obstructive Sleep Apnea.||Austin Authors:||Amatoury, Jason;Azarbarzin, Ali;Younes, Magdy;Jordan, Amy S ;Wellman, Andrew;Eckert, Danny J||Affiliation:||Institute for Breathing and Sleep
Neuroscience Research Australia (NeuRA), University of New South Wales, Sydney, NSW, Australia
YRT Ltd, Winnipeg, Manitoba, Canada
Sleep Disorders Centre, University of Manitoba, Winnipeg, Manitoba, Canada
Division of Sleep Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA.
School of Medical Sciences, University of New South Wales, Sydney, NSW, Australia
Melbourne School of Physiological Sciences, University of Melbourne, Melbourne, Victoria, Australia
|Issue Date:||1-Dec-2016||metadata.dc.date:||2016||Publication information:||Sleep 2016; 39(12): 2091-2100||Abstract:||Arousals from sleep vary in duration and intensity. Accordingly, the physiological consequences of different types of arousals may also vary. Factors that influence arousal intensity are only partly understood. This study aimed to determine if arousal intensity is mediated by the strength of the preceding respiratory stimulus, and investigate other factors mediating arousal intensity and its role on post-arousal ventilatory and pharyngeal muscle responses. Data were acquired in 71 adults (17 controls, 54 obstructive sleep apnea patients) instrumented with polysomnography equipment plus genioglossus and tensor palatini electromyography (EMG), a nasal mask and pneumotachograph, and an epiglottic pressure sensor. Transient reductions in CPAP were delivered during sleep to induce respiratory-related arousals. Arousal intensity was measured using a validated 10-point scale. Average arousal intensity was not related to the magnitude of the preceding respiratory stimuli but was positively associated with arousal duration, time to arousal, rate of change in epiglottic pressure and negatively with BMI (R2 > 0.10, P ≤ 0.006). High (> 5) intensity arousals caused greater ventilatory responses than low (≤ 5) intensity arousals (10.9 [6.8-14.5] vs. 7.8 [4.7-12.9] L/min; P = 0.036) and greater increases in tensor palatini EMG (10 [3-17] vs. 6 [2-11]%max; P = 0.031), with less pronounced increases in genioglossus EMG. Average arousal intensity is independent of the preceding respiratory stimulus. This is consistent with arousal intensity being a distinct trait. Respiratory and pharyngeal muscle responses increase with arousal intensity. Thus, patients with higher arousal intensities may be more prone to respiratory control instability. These findings are important for sleep apnea pathogenesis.||URI:||https://ahro.austin.org.au/austinjspui/handle/1/28178||DOI:||10.5665/sleep.6304||ORCID:||0000-0001-8561-9766||Journal:||Sleep||PubMed URL:||27784404||PubMed URL:||https://pubmed.ncbi.nlm.nih.gov/27784404/||Type:||Journal Article||Subjects:||arousal threshold
|Appears in Collections:||Journal articles|
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