Acute Intermittent Hypoxia Reduces Endothelial Function in Humans
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Obstructive Sleep Apnea (OSA) is a prevalent and under-diagnosed condition in adults. OSA is characterized by frequent arousals, airway collapse and arterial oxygen desaturation (intermittent hypoxia) during sleep. Epidemiological studies correlate OSA with cardiovascular disease (CVD) as well as endothelial dysfunction; however the specific mechanisms are yet to be determined. Animal models of sleep apnea support an association between intermittent hypoxia and the development of hypertension and CVD. The objective of this study was to assess the effects of acute intermittent hypoxia (60 minutes) on human endothelial function measured by brachial artery flow-mediated dilation (FMD). The effects of acute intermittent hypoxia on hemodynamics and markers of oxidative stress were also measured. FMD was reduced following 60 minutes of acute intermittent hypoxia. Additionally, changes in blood pressure, heart rate, and stroke volume were also observed. There were no changes in markers of oxidative stress. We conclude that 60 minutes of intermittent hypoxia is sufficient to induce endothelial dysfunction. Results from this study support a mechanism linking intermittent hypoxia to CVD in patients with OSA.