Impact of intermittent hypoxia on human vascular responses during sleep.

Exp Neurol

University of Calgary, Cumming School of Medicine, Department of Physiology and Pharmacology, 3330 Hospital Drive N.W., Calgary, Alberta T2N 4N1, Canada; Hotchkiss Brain Institute, University of Calgary, Cumming School of Medicine, 3330 Hospital Drive N.W., Calgary, Alberta T2N 4N1, Canada; Libin Cardiovascular Institute of Alberta, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada; Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada; Faculty of Kinesiology, University of Calgary, Calgary, AB, Canada. Electronic address:

Published: January 2022

AI Article Synopsis

  • Intermittent hypoxia (IH) during sleep, often seen in sleep apnea, is hypothesized to increase risks of cerebrovascular and cardiovascular diseases, but previous studies mainly focused on wakefulness.
  • This study aimed to measure the effects of IH during sleep on vascular responses to low oxygen (hypoxia) and high carbon dioxide (hypercapnia) in ten healthy men using two overnight sleep studies.
  • Results showed that while cerebrovascular blood flow was generally reduced during sleep regardless of IH exposure, IH did not significantly change the responses to hypoxia or hypercapnia, although morning heart rates post-IH were higher.

Article Abstract

Exposure to intermittent hypoxia (IH) ≥15 times per hour is believed to be the primary mechanism for the increased risk of cerebrovascular and cardiovascular disease in patients with moderate to severe sleep apnea. Human experimental models of IH used to investigate this link have been predominantly employed during wakefulness, which limits extrapolation of findings to sleep apnea where IH occurs during sleep. Moreover, how IH impacts vascular regulation during sleep has not been measured quantitatively. Therefore, the objective of this study was to assess the impact sleep accompanied by IH on vascular responses to hypoxia and hypercapnia during sleep. Ten males performed two randomly scheduled 6-h overnight sleep studies. One sleep study was performed in room air (normoxia) and the other sleep study was performed during isocapnic IH (60 s hypoxia-60 s normoxia). On each night, cerebrovascular (peak blood velocity through the middle cerebral artery (V¯); transcranial Doppler ultrasound) and cardiovascular (blood pressure, heart rate) responses to hypoxia and hypercapnia were measured before sleep onset (PM-Awake), within the first 2 h of sleep (PM-Asleep), in the 5th (out of 6) hours of sleep (AM-Asleep) and after being awoken in the morning (AM-Awake). Sleep accompanied by IH had no impact on the V¯ and blood pressure responses to hypoxia and hypercapnic at any timepoint (p ≥ 0.103 for all responses). However, the AM-Awake heart rate response to hypoxia was greater following sleep in IH compared to sleep in normoxia. Independent of the sleep environment, the V¯ response to hypoxia and hypercapnia were reduced during sleep. In conclusion, cerebral blood flow responses are reduced during sleep compared to wakefulness, but 6 h of sleep accompanied by IH does not alter cerebrovascular and cardiovascular response to hypoxia and hypercapnia during wakefulness or sleep in healthy young humans. However, it is likely that longer exposure to IH during sleep (i.e., days-to-weeks) is required to better elucidate IH's impact on vascular regulation in humans.

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Source
http://dx.doi.org/10.1016/j.expneurol.2021.113897DOI Listing

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