Age‐ and fitness‐related alterations in vascular sympathetic control

Abstract

In the current study we explored (1) if there were differences in sympathetic activity and baroreflex function by age, sex, or physical activity status, (2) if any aspect of baroreflex function related to differences in resting sympathetic activity, and (3) if mechanical and/or neural baroreflex components related to differences in integrated baroreflex gain. Electrocardiogram, blood pressure, carotid diameter and muscle sympathetic nerve activity were recorded continuously at rest and during sequential bolus injections of sodium nitroprusside and phenylephrine in 22 young, 21 older sedentary and 10 older trained individuals. Analyses of co-variance were used to examine age, sex and training status differences and to explore the explanatory power of integrated baroreflex gain and its mechanical and neural components. Training status and sex influenced neither resting sympathetic outflow nor sympathetic baroreflex gain components. Older subjects had a smaller mechanical component and a strong tendency towards a greater neural component of the sympathetic baroreflex during both pressure falls and pressure rises. Opposing age-related changes in mechanical and neural components resulted in a smaller integrated gain during pressure falls, but a greater integrated gain during pressure rises in older subjects. Thus, in older individuals, compromised sympathetic activation to pressure falls was owing to the stiffening of barosensory vessels, whereas the more sensitive sympathoinhibition to pressure rise was due to an increased neural control. Enhanced neural control with age, however, did not contribute the increased resting sympathetic outflow, which indicates that these two changes are probably driven by distinct neural mechanisms.

Carotid baroreflex control of arterial blood pressure at rest and during dynamic exercise in aging humans

“…This possibility is in accordance with recent work demonstrating greater ABR-mediated sympatho-inhibition in older subjects in response to pharmacological increases in BP at rest (46). However, whether an enhanced ability to inhibit sympathetic outflow persists during dynamic exercise in older subjects remains to be determined.…”

“…Shi et al (41) also reported that the resting sensitivity of the carotid-BP stimulus response curves were similar in young and older subjects; however, the location of the operating point on the reflex function curve was not examined. Moreover, Studinger et al (46) demonstrated that age-related differences in ABRmediated responses of SNA to rises and falls in BP were not evident when the responses were combined; that is, the gain of the integrated ABR control of SNA was not different between the young and older groups. However, sympathetic responses to reductions in BP were clearly attenuated in older subjects, while greater sympatho-inhibition to pharmacologically induced hypertension was also present.…”

“…cardiovascular control; autonomic nervous system; baroreflex sensitivity; arterial baroreceptors; total vascular conductance THE ARTERIAL BAROREFLEX (ABR) plays a critical role in the moment-to-moment regulation of arterial blood pressure (BP) via modulation of autonomic neural activity to the heart and vasculature. Although a wealth of data has indicated that aging is associated with impairments in resting cardiac baroreflex function (3,14,19,29), studies examining ABR control of muscle sympathetic nerve activity (SNA) have reported equivocal results demonstrating impaired, preserved, or augmented responsiveness in older healthy adults (11,14,24,29,30,46). Moreover, regarding overall ABR regulation of BP and aging, limited studies have been performed suggesting either reduced (24, 27) or unchanged (4, 41) control with advanced age.…”

14 nights of intermittent hypoxia elevate daytime blood pressure and sympathetic activity in healthy humans

“…To make the analysis objective and, therefore, independent of investigator bias, we analysed the data via a piecewise linear regression that required at least five data points to define the presence of threshold and/or saturation (if any). Arterial baroreflex control of MSNA was derived from the method developed by STUDINGER et al [32]. Briefly, this technique excludes all data 2 mmHg above the greatest pressure associated with a sympathetic burst and weights all cardiac cycles associated with zero sympathetic activity.…”

The Role of Ultrasonography in the Assessment of Arterial Baroreflex Function

“…To account for this error, cardiac cycles can be weighted according to the presence or absence of observable sympathetic bursts. For example, cardiac cycles with zero's below the lowest pressure associated with a sympathetic burst are assigned a weight of 0 ('false' zero) whereas zeros above the highest pressure associated with a sympathetic burst were assigned a weight of 1 ('true' zero) 30 . Some groups employ data binning (e.g.…”