Acute changes in forearm vascular compliance during transient sympatho-excitation

Abstract

The study of vascular regulation often omits important information about the elastic properties of arteries under conditions of pulsatile flow. The purpose of this study was to examine the relationship between muscle sympathetic nerve activity (MSNA), vascular bed compliance, and peripheral blood flow responses in humans. We hypothesized that increases in MSNA would correlate with reductions in vascular compliance, and that changes in compliance would correspond with changes in peripheral blood flow during sympatho-excitation. MSNA (microneurography), blood pressure (Finopres), and brachial artery blood flow (Doppler ultrasound), were monitored in six healthy males at baseline and during the last 15 s of voluntary end-inspiratory, expiratory apneas and 5 min of static handgrip exercise (SHG; 20% maximum voluntary contraction) and 3 min of post-exercise circulatory occlusion (SHG + PECO; measured in the non-exercising arm). A lumped Windkessel model was employed to examine vascular bed compliance. During apnea, indices of MSNA were inversely related with vascular compliance, and reductions in compliance correlated with decreased brachial blood flow rate. During SHG, despite increased MSNA, compliance also increased, but was unrelated to increases in blood flow. Neither during SHG nor PECO did indices of MSNA correlate with forearm vascular compliance nor did vascular compliance correlate with brachial flow. However, during PECO, a linear combination of blood pressure and total MSNA was correlated with vascular compliance. These data indicate the elastic components of the forearm vasculature are regulated by adrenergic and myogenic mechanisms during sympatho-excitation, but in a reflex-dependent manner.

Keywords: peripheral blood flow; resistance; sympatho-excitation; vascular compliance.

FIGURE 1

Indices of muscle sympathetic nerve activity (MSNA); (a) burst frequency, (b) burst incidence, (c) normalized burst amplitude and (d) total MSNA, at baseline and during end inspiratory apnea (EIA), end expiratory apnea (EEA), end static handgrip exercise (SHG) and post‐exercise circulatory occlusion (PECO). EIA and EEA data analyzed using a paired, two‐tail t‐test, and SHG + PECO data analyzed using a one‐way repeated measures ANOVA. *, Significantly different from baseline (p < 0.05), X, p = 0.05–0.07 versus baseline. Dotted lines are individual responses (n = 6) and dark, bold lines are mean data

FIGURE 2

Hemodynamics; (a) mean arterial pressure (MAP), (b) brachial artery blood flow (Q), (c) forearm vascular resistance (R) and (d) forearm vascular compliance (C) at baseline and during end inspiratory apnea (EIA), end expiratory apnea (EEA), end static handgrip exercise (SHG) and post‐exercise circulatory occlusion (PECO). EIA and EEA data analyzed using a paired, two‐tail t‐test, and SHG+PECO data analyzed using a one‐way repeated measures ANOVA. *, Significantly different from baseline (p < 0.05), X, p = 0.06 versus baseline. Dotted lines are individual responses (n = 6) and dark, bold lines are mean data

FIGURE 3

Hemodynamic relationships during end inspiratory and expiratory apnea; (a) brachial artery blood flow (Q) plotted against forearm vascular resistance (R), (b) brachial artery Q plotted against forearm vascular compliance (C) during end inspiratory and end expiratory apnea. The R‐flow curve was modeled with a 3rd order polynomial and the C‐flow curve was modeled with a linear regression. Symbols represent individual responses (n = 6)