Lindsey F Berthelsen1, Sean van Diepen2, Andrew R Steele1, Emily R Vanden Berg1, Jordan Bird3, Scott Thrall1,3, Alexandra Skalk3, Britta Byman3, Brandon Pentz3, Richard J A Wilson4, Nicholas G Jendzjowsky5, Trevor A Day3, Craig D Steinback6. 1. Neurovascular Health Lab, Faculty of Kinesiology, Sport, and Recreation, University of Alberta, 1-059A Li Ka Shing Centre for Health Research Innovation, 8602-112 St, Edmonton, AB, T6G 2E1, Canada. 2. Faculty of Medicine and Dentistry, Department of Critical Care and Division of Cardiology, Department of Medicine, University of Alberta, Edmonton, AB, Canada. 3. Department of Biology, Faculty of Science and Technology, Mount Royal University, Calgary, AB, Canada. 4. Department of Physiology and Pharmacology, University of Calgary, Calgary, AB, Canada. 5. The Lundquist Institute for Biomedical Innovation at Harbor, UCLA Medical Center, Torrance, CA, USA. 6. Neurovascular Health Lab, Faculty of Kinesiology, Sport, and Recreation, University of Alberta, 1-059A Li Ka Shing Centre for Health Research Innovation, 8602-112 St, Edmonton, AB, T6G 2E1, Canada. craig.steinback@ualberta.ca.
Abstract
PURPOSE: Autonomic control of the heart is balanced by sympathetic and parasympathetic inputs. Excitation of both sympathetic and parasympathetic systems occurs concurrently during certain perturbations such as hypoxia, which stimulate carotid chemoreflex to drive ventilation. It is well established that the chemoreflex becomes sensitized throughout hypoxic exposure; however, whether progressive sensitization alters cardiac autonomic activity remains unknown. We sought to determine the duration of hypoxic exposure at high altitude necessary to unmask cardiac arrhythmias during instances of voluntary apnea. METHODS: Measurements of steady-state chemoreflex drive (SS-CD), continuous electrocardiogram (ECG) and SpO2 (pulse oximetry) were collected in 22 participants on 1 day at low altitude (1045 m) and over eight consecutive days at high-altitude (3800 m). SS-CD was quantified as ventilation (L/min) over stimulus index (PETCO2/SpO2). RESULTS: Bradycardia during apnea was greater at high altitude compared to low altitude for all days (p < 0.001). Cardiac arrhythmias occurred during apnea each day but became most prevalent (> 50%) following Day 5 at high altitude. Changes in saturation during apnea and apnea duration did not affect the magnitude of bradycardia during apnea (ANCOVA; saturation, p = 0.15 and apnea duration, p = 0.988). Interestingly, the magnitude of bradycardia was correlated with the incidence of arrhythmia per day (r = 0.8; p = 0.004). CONCLUSION: Our findings suggest that persistent hypoxia gradually increases vagal tone with time, indicated by augmented bradycardia during apnea and progressively increased the incidence of arrhythmia at high altitude.
PURPOSE: Autonomic control of the heart is balanced by sympathetic and parasympathetic inputs. Excitation of both sympathetic and parasympathetic systems occurs concurrently during certain perturbations such as hypoxia, which stimulate carotid chemoreflex to drive ventilation. It is well established that the chemoreflex becomes sensitized throughout hypoxic exposure; however, whether progressive sensitization alters cardiac autonomic activity remains unknown. We sought to determine the duration of hypoxic exposure at high altitude necessary to unmask cardiac arrhythmias during instances of voluntary apnea. METHODS: Measurements of steady-state chemoreflex drive (SS-CD), continuous electrocardiogram (ECG) and SpO2 (pulse oximetry) were collected in 22 participants on 1 day at low altitude (1045 m) and over eight consecutive days at high-altitude (3800 m). SS-CD was quantified as ventilation (L/min) over stimulus index (PETCO2/SpO2). RESULTS: Bradycardia during apnea was greater at high altitude compared to low altitude for all days (p < 0.001). Cardiac arrhythmias occurred during apnea each day but became most prevalent (> 50%) following Day 5 at high altitude. Changes in saturation during apnea and apnea duration did not affect the magnitude of bradycardia during apnea (ANCOVA; saturation, p = 0.15 and apnea duration, p = 0.988). Interestingly, the magnitude of bradycardia was correlated with the incidence of arrhythmia per day (r = 0.8; p = 0.004). CONCLUSION: Our findings suggest that persistent hypoxia gradually increases vagal tone with time, indicated by augmented bradycardia during apnea and progressively increased the incidence of arrhythmia at high altitude.
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Authors: Christopher John Boos; David A Holdsworth; David Richard Woods; John O'Hara; Naomi Brooks; Lee Macconnachie; Josh Bakker-Dyos; John Paisey; Adrian Mellor Journal: Circulation Date: 2017-02-21 Impact factor: 29.690
Authors: Stephen A Busch; Sean van Diepen; Andrew R Steele; Victoria L Meah; Lydia L Simpson; Rómulo J Figueroa-Mujíca; Gustavo Vizcardo-Galindo; Francisco C Villafuerte; Michael M Tymko; Philip N Ainslie; Jonathan P Moore; Mike Stembridge; Craig D Steinback Journal: Front Physiol Date: 2020-01-22 Impact factor: 4.566
Authors: Stephen A Busch; Sean van Diepen; Richard Roberts; Andrew R Steele; Lindsey F Berthelsen; Megan P Smorschok; Cody Bourgoin; Craig D Steinback Journal: Physiol Rep Date: 2021-01