Intermittent hypoxia and vascular function: implications for obstructive sleep apnoea
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Updated: Jul 18, 2026

A Model to Simulate Clinically Relevant Hypoxia in Humans
Published on: December 22, 2016
Glen E Foster1, Marc J Poulin, Patrick J Hanly
1Department of Medicine, Faculty of Medicine, University of Calgary, Health Sciences Center, Room 1421, 3330 Hospital Drive NW, Calgary, Alberta, Canada.
Abstract:
Obstructive sleep apnoea (OSA) has been implicated as a risk factor for the development of hypertension, stroke and myocardial infarction. The main cause of cardiovascular and cerebrovascular disease in OSA is thought to be exposure to intermittent hypoxia, which can lead to oxidative stress, inflammation, atherosclerosis, endothelial dysfunction and hypertension. These proposed mechanisms have been drawn from basic research in animal and human models of intermittent hypoxia in addition to clinical investigation of patients with OSA. This review outlines the association between OSA and vascular disease, describes basic mechanisms that may be responsible for this association and compares the results from studies of OSA subjects with those in experimental models of intermittent hypoxia.
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