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UBC Theses and Dissertations

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UBC Theses and Dissertations

The effect of acute intermittent hypoxia on sympathetic neurovascular transduction Stuckless, Troy


Obstructive sleep apnea (OSA) patients suffer from intermittent hypoxia (IH) due to repetitive airway obstructions during sleep. IH increases chemoreflex sensitivity, sympathetic vasomotor outflow, and increases blood pressure. The purpose of this study was to determine if acute IH augments sympathetic neurovascular transduction in young healthy men, which could contribute to an increase in blood pressure. It was hypothesized that IH would augment sympathetic neurovascular transduction. Ten healthy males without OSA were exposed to 40 seconds of hypercapnic hypoxia (PETO₂ = 48.1 ± 1 mmHg, PETCO₂: + 4 ± 1 mmHg above baseline) and 20 seconds of normoxia for 40-minutes, mimicking severe OSA. Before and after IH we measured muscle sympathetic nerve activity burst frequency (MSNA BF; peroneal microneurography) and forearm vascular resistance (FVR; brachial artery duplex ultrasound) during rest and three levels of lower body negative pressure (15, 30, and 45 mmHg) while clamping end-tidal gases at baseline values. Sympathetic neurovascular transduction, defined as the slope of the relationship between MSNA BF and FVR, was increased 3-fold immediately following IH (P = 0.015). IH increased minute ventilation (+5 ± 2 l/min, P = 0.025), suggesting long term facilitation of ventilation. Additionally, MSNA BF (+2 ± 1 /min, P = 0.032) and mean arterial pressure (+5 ± 2 mmHg, P = 0.002) were increased following IH. Our results suggest that acute IH increases sympathetic neurovascular transduction and may be an important early mechanism involved in the development of hypertension in OSA.

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