Andrew E Beaudin1,2, Xavier Waltz1,2,3, Patrick J Hanly2,4,5, Marc J Poulin1,2,6,7,8. 1. Department of Physiology and Pharmacology, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. 2. Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. 3. Laboratoire HP2, U1042, INSERM, Université Grenoble Alpes, Grenoble, France. 4. Department of Medicine, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. 5. Sleep Centre, Foothills Medical Centre, Calgary, AB, Canada. 6. Libin Cardiovascular Institute of Alberta, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. 7. Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada. 8. Faculty of Kinesiology, University of Calgary, Calgary, AB, Canada.
Abstract
NEW FINDINGS: What is the topic of this review? This review examines the notion that obstructive sleep apnoea (OSA) and intermittent hypoxia (IH) have hormetic effects on vascular health. What advances does it highlight? Clinical (OSA patient) and experimental animal and human models report that IH is detrimental to vascular regulation. However, mild IH and, by extension, mild OSA also have physiological and clinical benefits. This review highlights clinical and experimental animal and human data linking OSA and IH to vascular disease and discusses how hormetic effects of OSA and IH relate to OSA severity, IH intensity and duration, and patient/subject age. Obstructive sleep apnoea (OSA) is associated with increased risk of cardiovascular and cerebrovascular disease, a consequence attributed in part to chronic intermittent hypoxia (IH) resulting from repetitive apnoeas during sleep. Although findings from experimental animal, and human, models have shown that IH is detrimental to vascular regulation, the severity of IH used in many of these animal studies [e.g. inspired fraction of oxygen (FI,O2) = 2-3%; oxygen desaturation index = 120 events h-1 ] is considerably greater than that observed in the majority of patients with OSA. This may also explain disparities between animal and recently developed human models of IH, where IH severity is, by necessity, less severe (e.g. FI,O2 = 10-12%; oxygen desaturation index = 15-30 events h-1 ). In this review, we highlight the current knowledge regarding the impact of OSA and IH on cardiovascular and cerebrovascular regulation. In addition, we critically discuss the recent notion that OSA and IH may have hormetic effects on vascular health depending on conditions such as OSA severity, IH intensity and duration, and age. In general, data support an independent causal link between OSA and vascular disease, particularly for patients with severe OSA. However, the data are equivocal for older OSA patients and patients with mild OSA, because advanced age and short-duration, low-intensity IH have been reported to provide a degree of protection against IH and ischaemic events such as myocardial infarction and stroke, respectively. Overall, additional studies are needed to investigate the beneficial/detrimental effects of mild OSA on the various vascular beds.
NEW FINDINGS: What is the topic of this review? This review examines the notion that obstructive sleep apnoea (OSA) and intermittent hypoxia (IH) have hormetic effects on vascular health. What advances does it highlight? Clinical (OSA patient) and experimental animal and human models report that IH is detrimental to vascular regulation. However, mild IH and, by extension, mild OSA also have physiological and clinical benefits. This review highlights clinical and experimental animal and human data linking OSA and IH to vascular disease and discusses how hormetic effects of OSA and IH relate to OSA severity, IH intensity and duration, and patient/subject age. Obstructive sleep apnoea (OSA) is associated with increased risk of cardiovascular and cerebrovascular disease, a consequence attributed in part to chronic intermittent hypoxia (IH) resulting from repetitive apnoeas during sleep. Although findings from experimental animal, and human, models have shown that IH is detrimental to vascular regulation, the severity of IH used in many of these animal studies [e.g. inspired fraction of oxygen (FI,O2) = 2-3%; oxygen desaturation index = 120 events h-1 ] is considerably greater than that observed in the majority of patients with OSA. This may also explain disparities between animal and recently developed human models of IH, where IH severity is, by necessity, less severe (e.g. FI,O2 = 10-12%; oxygen desaturation index = 15-30 events h-1 ). In this review, we highlight the current knowledge regarding the impact of OSA and IH on cardiovascular and cerebrovascular regulation. In addition, we critically discuss the recent notion that OSA and IH may have hormetic effects on vascular health depending on conditions such as OSA severity, IH intensity and duration, and age. In general, data support an independent causal link between OSA and vascular disease, particularly for patients with severe OSA. However, the data are equivocal for older OSA patients and patients with mild OSA, because advanced age and short-duration, low-intensity IH have been reported to provide a degree of protection against IH and ischaemic events such as myocardial infarction and stroke, respectively. Overall, additional studies are needed to investigate the beneficial/detrimental effects of mild OSA on the various vascular beds.
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