Jason Amatoury1,2,3, Amy S Jordan4,5, Barbara Toson1, Chinh Nguyen1, Andrew Wellman6, Danny J Eckert1,2. 1. Neuroscience Research Australia (NeuRA), Sydney NSW, Australia. 2. School of Medical Sciences, University of New South Wales, Sydney NSW, Australia. 3. Biomedical Engineering Program, Maroun Semaan Faculty of Engineering and Architecture (MSFEA), American University of Beirut, Beirut, Lebanon. 4. Melbourne School of Physiological Sciences, University of Melbourne, Melbourne, Australia. 5. Institute for Breathing and Sleep, Austin Health, Heidelberg, Victoria, Australia. 6. Division of Sleep Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA.
Abstract
Study Objectives: A negative intrathoracic pressure threshold is one commonly proposed mechanism for triggering respiratory-induced arousals in obstructive sleep apnea (OSA). If so, they should occur during inspiration, shortly after maximal negative pressure swings. Alternatively, respiratory-induced arousals may occur throughout the respiratory cycle if other mechanisms also contribute. However, arousal timing has been minimally investigated. This study aimed to (1) determine the temporal relationship between respiratory-induced arousals and breathing phase and (2) characterize neuromuscular and load compensation responses prior to arousal. Methods: Fifty-one CPAP-treated OSA patients underwent a sleep physiology study with genioglossus and tensor palatini EMG, nasal mask/pneumotachograph, and epiglottic pressure. Transient CPAP reductions were delivered to induce respiratory-related arousals. Results: Of 354 arousals, 65(60-70)%[mean(CI)] occurred during inspiration, 35(30-40)% during expiration. Nadir epiglottic pressure occurred 68(66-69)% into inspiration while inspiratory arousals had a uniform distribution throughout inspiration. Expiratory arousals occurred predominantly in early expiration. CPAP reductions initially reduced minute ventilation by ~2.5 liter/min, which was restored immediately prior to expiratory but not inspiratory arousals. Duty cycle just prior to arousal was greater for inspiratory versus expiratory arousals [0.20(0.18-0.21) vs. 0.13(0.11-0.15)Δbaseline, p = 0.001]. Peak tensor palatini EMG was higher for expiratory versus inspiratory arousals during prearousal breaths [7.6(5.8-9.6) vs. 3.7(3.0-4.5)%Δbaseline, p = 0.001], whereas genioglossus and tonic tensor palatini EMG were similar between arousal types. Conclusions: Over one third of respiratory-induced arousals occur during expiration. These findings highlight the importance of nonpressure threshold mechanisms of respiratory-induced arousals in OSA and suggest that expiratory arousals may be a novel marker of enhanced tensor palatini neuromuscular compensation.
Study Objectives: A negative intrathoracic pressure threshold is one commonly proposed mechanism for triggering respiratory-induced arousals in obstructive sleep apnea (OSA). If so, they should occur during inspiration, shortly after maximal negative pressure swings. Alternatively, respiratory-induced arousals may occur throughout the respiratory cycle if other mechanisms also contribute. However, arousal timing has been minimally investigated. This study aimed to (1) determine the temporal relationship between respiratory-induced arousals and breathing phase and (2) characterize neuromuscular and load compensation responses prior to arousal. Methods: Fifty-one CPAP-treated OSA patients underwent a sleep physiology study with genioglossus and tensor palatini EMG, nasal mask/pneumotachograph, and epiglottic pressure. Transient CPAP reductions were delivered to induce respiratory-related arousals. Results: Of 354 arousals, 65(60-70)%[mean(CI)] occurred during inspiration, 35(30-40)% during expiration. Nadir epiglottic pressure occurred 68(66-69)% into inspiration while inspiratory arousals had a uniform distribution throughout inspiration. Expiratory arousals occurred predominantly in early expiration. CPAP reductions initially reduced minute ventilation by ~2.5 liter/min, which was restored immediately prior to expiratory but not inspiratory arousals. Duty cycle just prior to arousal was greater for inspiratory versus expiratory arousals [0.20(0.18-0.21) vs. 0.13(0.11-0.15)Δbaseline, p = 0.001]. Peak tensor palatini EMG was higher for expiratory versus inspiratory arousals during prearousal breaths [7.6(5.8-9.6) vs. 3.7(3.0-4.5)%Δbaseline, p = 0.001], whereas genioglossus and tonic tensor palatini EMG were similar between arousal types. Conclusions: Over one third of respiratory-induced arousals occur during expiration. These findings highlight the importance of nonpressure threshold mechanisms of respiratory-induced arousals in OSA and suggest that expiratory arousals may be a novel marker of enhanced tensor palatini neuromuscular compensation.
Authors: Amy S Jordan; Danny J Eckert; Andrew Wellman; John A Trinder; Atul Malhotra; David P White Journal: Am J Respir Crit Care Med Date: 2011-08-11 Impact factor: 21.405
Authors: Danny J Eckert; David P White; Amy S Jordan; Atul Malhotra; Andrew Wellman Journal: Am J Respir Crit Care Med Date: 2013-10-15 Impact factor: 21.405
Authors: Joshua Tong; Lauriane Jugé; Peter Gr Burke; Fiona Knapman; Danny J Eckert; Lynne E Bilston; Jason Amatoury Journal: J Appl Physiol (1985) Date: 2019-09-12
Authors: Atul Malhotra; Indu Ayappa; Najib Ayas; Nancy Collop; Douglas Kirsch; Nigel Mcardle; Reena Mehra; Allan I Pack; Naresh Punjabi; David P White; Daniel J Gottlieb Journal: Sleep Date: 2021-07-09 Impact factor: 6.313