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Shafer, Brooke

University of British Columbia

Purpose: In healthy humans, exposure to acute bouts of hypoxia elicits persistent increases in muscle sympathetic nerve activity (MSNA). Long-lasting increases in MSNA may have clinical implications for hypertension development particularly in disorders where hypoxemia is a feature, such as obstructive sleep apnea. Four studies were performed to investigate the neural reflex control of sympathetic activity at rest and in response to arterial blood gases disturbances in healthy males. Methods: Study 1: Sympathetic response to isometric handgrip exercise and metaboreflex activation with post exercise circulatory occlusion was examined before and after 40-minutes of intermittent hypercapnic hypoxia (IHH). Study 2: Baroreflex control and neural recruitment strategies of sympathetic action potential (AP) clusters that mediate sympathetic long-term facilitation (sLTF) following 20-minutes isocapnic hypoxia was investigated. Study 3A: The influence of sympathetic APs on signal-averaged sympathetic transduction of arterial pressure during and after 20-minutes isocapnic hypoxia was quantified. Study 3B: Within-breath modulation of sympathetic transduction of total vascular conductance (TVC) was assessed at rest. Results and Conclusions: Study 1 showed that following IHH, sympathetic responses to exercise and metaboreflex activation were preserved despite overall increases in resting MSNA and arterial pressure. Study 2 demonstrated that hypoxia-induced sLTF is mediated by baroreflex resetting of AP clusters to higher operating points, reduced asynchronous AP firing, and increased contribution from large-amplitude APs. Study 3A revealed that sympathetic transduction of arterial pressure was blunted during hypoxia and remained diminished in early recovery. Furthermore, asynchronous APs attenuate arterial pressure reductions at rest compared with no AP activity. Study 3B showed that TVC reductions were greatest during expiration and low lung volumes. These results advance our fundamental understanding of how neural reflex activation affects sympathetic control of blood pressure and elucidate mechanisms of hypoxia-induced hypertension.

Text

2023-01-27

Attribution-NonCommercial-NoDerivatives 4.0 International

http://hdl.handle.net/2429/83765

Kinesiology

University of British Columbia

UBCO

http://creativecommons.org/licenses/by-nc-nd/4.0/