(761.2) Acute Effect of Intermittent Hypoxia on Peripheral Vascular Function in Young Healthy Adults

Poster Board Number: E505

Sten Stray-Gundersen (Department of Kinesiology and Health Education, University of Texas at Austin), Frank Wojan (Department of Kinesiology and Health Education, University of Texas at Austin), Sahar Massoudian (Department of Kinesiology and Health Education, University of Texas at Austin), Hirofumi Tanaka (Department of Kinesiology and Health Education, University of Texas at Austin), Sophie Lalande (Department of Kinesiology and Health Education, University of Texas at Austin)

Continuous exposure to hypoxia elicits a chemoreceptor-mediated increase in sympathetic nerve activity and a simultaneous peripheral vasodilation due to an increase in nitric oxide production. The aim of the present study was to determine whether short, repeated bouts of hypoxia induce brachial artery vasodilation and acutely improve endothelial function. Ten young healthy adults (4 women, age: 24±3 years, height: 176±9 cm, body weight: 80±13 kg) visited the laboratory on two separate occasions. Endothelium-dependent vasodilation was assessed by brachial artery flow-mediated dilation using a semiautomated diagnostic ultrasound system before and after exposure to either intermittent hypoxia (IH) or intermittent normoxia (IN). Intermittent hypoxia consisted of eight 4-min hypoxic cycles at a targeted arterial oxygen saturation of 80% interspersed with breathing room air to resaturation, and intermittent normoxia consisted of eight 4-min normoxic cycles separated by one minute of breathing room air. Air was made hypoxic by titrating nitrogen into a breathing circuit. Brachial artery diameter was assessed via ultrasound throughout the protocols. Hemodynamics, arterial oxygen saturation, and pulmonary gas exchange were also continuously assessed during the protocols. By design, intermittent hypoxia resulted in an arterial oxygen saturation of 81±2%, corresponding to oxygen levels of 11.9±2.2%. Exposure to intermittent hypoxia, but not intermittent normoxia, elicited a brachial artery vasodilation (IH: 0.38±0.06 to 0.40±0.06 vs. IN: 0.38±0.06 to 0.38±0.06 cm, plt;0.01). However, neither intermittent hypoxia nor intermittent normoxia acutely affected brachial artery flow-mediated dilation (IH: 5.8±1.9 to 5.3±1.6% vs. IN: 6.1±2.4 to 6.5±1.7%, p=0.96). Intermittent hypoxia increased cardiac output (5.2±0.9 to 5.9±1.4 L·min-1, p=0.03) mainly due to an increase in heart rate (57±9 to 68±11 bpm, plt;0.01). In conclusion, exposure to intermittent hypoxia triggered a brachial artery vasodilation but did not affect endothelium-dependent vasodilation in young healthy adults. Multiple sessions of intermittent hypoxia may be necessary to improve nitric oxide synthesis and endothelial function.