Arterial Baroreflex Regulation of Sympathetic Discharge During Maximal Voluntary End-Inspiratory Apnea

Abstract

The sympathetic nervous system (SNS) increases sympathetic outflow during physiological stress to maintain blood pressure (BP) homeostasis. The arterial baroreflex represents a critical mechanism regulating sympathetic outflow during rest and physiological stress. Volitional apnea, seen in breath-hold diving, serves as a physiological stressor and a model to increase sympathetic outflow in human neurophysiological research. The study employed a maximal voluntary end-inspiratory apnea to observe simultaneous increases in muscle sympathetic nerve activity (MSNA) and BP. The use of apnea aimed to provide insights into how the maximal voluntary end-inspiratory apneas influence sympathetic action potential (AP) discharge and recruitment patterns in humans, contributing to a better understanding of the mechanisms that regulate MSNA. This study tested two hypotheses. The first hypothesis was that during a maximal voluntary end-inspiratory apnea, the strength (i.e., gain) of arterial baroreflex control of sympathetic AP discharge is preserved at baseline (BSL) levels but reset to higher levels of sympathetic outflow and greater BPs. The second hypothesis was that the relationship between sympathetic discharge and parameters of arterial stiffness will be maintained at BSL levels during maximum voluntary end-inspiratory apnea. A total of six young, healthy, non-smoking, normotensive individuals (3 females; average 22±3, 18-27 years) were included in the current analyses. Each participant completed a 2-minute BSL period and an end-inspiratory apnea of maximal voluntary duration. Consistent with the study’s hypothesis, during apnea, arterial baroreflex control of sympathetic APs was reset upwards to greater firing probabilities and rightwards to higher levels of BP. The gain of baroreflex control of sympathetic AP discharge was preserved at BSL levels. The peripheral component of the arterial baroreflex, as assessed by pulse transit times (PTT), was unchanged with apnea. These findings suggest that during apnea, arterial baroreflex control over sympathetic postganglionic neuronal discharge is reset to greater firing probabilities and higher BPs, but the strength of control is retained at BSL levels. Additionally, the relationship between sympathetic discharge and parameters of arterial stiffness are maintained at BSL levels. These findings advance our understanding of the central and peripheral baroreflex mechanisms governing sympathetic postganglionic discharge towards the human cardiovascular system during apneic stress.