Severity of Central Sleep Apnea Does Not Improve Sleeping Oxygen Saturation During Ascent to High Altitude
Authors: Bird Jordan , Kalker A. , Chan J. , Rimke A. , Chan G. , Wilson R. , Brutsaert T. , Jendzjowsky N. , Sherpa M. , Day T. 
Published: April 2020

Central sleep apnea (CSA) is characterized by intermittent periods of apnea (no breathing) and hyperventilation (over breathing) with associated fluctuations in blood oxygen saturation. CSA is universal at high altitude (>3000m), increasing in severity with ascent and/or time spent at high altitude. Although there is a large degree of variability in CSA severity, factors that increase susceptibility to CSA at altitude include: (a) hypoxia, (b) hypoxic ventilatory response‐mediated hypocapnia and (c) increases in chemoreflex responsiveness via ventilatory acclimatization. Whether CSA is adaptive or maladaptive at altitude is unknown. Notwithstanding the brief periods of desaturation associated with apnea, the subsequent relative intermittent hyperventilation may increase oxygen reserves during sleep, protecting overall mean saturation. We hypothesized that CSA protects mean sleeping oxygen saturation during acclimatization to high altitude. In two groups of Diamox‐free native lowlanders, we characterized the effects of increasing CSA severity on night‐time sleeping oxygen saturation during two separate high altitude ascent profiles: (I) incremental ascent to 5160m over 10 days/nights in the Nepal Himalaya (n=21) and (II) rapid ascent to and residing at 3800m over 10 days/nights in the Sierra Nevada mountains, CA, USA (n=21). Using portable polysomnographs and scoring software (ResMed ApneaLink; AASM criteria), we assessed apnea‐hypopnea index (AHI), oxygen desaturation index (ODI), and baseline, mean and nadir oxygen saturation (SpO2) during sleep at each altitude. During sleep across both ascent profiles, AHI and ODI increased in severity, and baseline, mean and nadir SpO2 decreased significantly, suggesting both altitude‐ and sleep apnea‐associated hypoxia. During incremental ascent to 5160m over 10 days/nights (Part I), AHI and ODI increased from 3.9±4.1 and 9.8±7.8 (1045m) to 37.5±32.8 and 54.4±24.8 events/hour, respectively (P<0.001). In addition, baseline, mean and nadir SpO2 decreased from 96.0±2.0, 94.3±1.6 and 87.1±3.7% (1045m) to 78.9±3.6, 73.5±4.2 and 63.7±6.6%, respectively (P<0.0001). After 10 days/nights following rapid ascent to 3800m (Part II), AHI and ODI increased from 3.4±3.5 and 6.8±5.3 (1045m) to 23.2±21.2 and 38.0±24.4 events/hour, respectively (P<0.001). In addition, baseline, mean and nadir SpO2 decreased from 95.3±1.9, 93.7±2.1 and 86.0±5.1% (1045m) to 85.6±1.8, 84.0±2.4 and 74.1±6.2%, respectively (P<0.0001). There were no significant correlations between AHI nor ODI and mean nor nadir SpO2 during sleep at 5160m (night 9/10; Part I; r>−0.35, P>0.2) and 3800m (night 9/10; Part II; r>−0.45, P>0.05). We conclude that the severity of CSA following acclimatization to high altitude does not play a role in improving oxygen saturation. However, the relative hyperventilation between apneas likely protects against the apnea‐mediated oxygen desaturations during sleep at altitude.Support or Funding InformationAlberta Government Student Temporary Employment Program, Alberta Innovates Health Solutions, Natural Sciences and Engineering Research Council of Canada.