Preserved ability to blunt sympathetically-mediated vasoconstriction in exercising skeletal muscle of young obese humans.

Kanokwan Bunsawat,Elizabeth C Schroeder,Alexander J Rosenberg,Georgios Grigoriadis,Melissa M Rader,Bo Fernhall,Philip S Clifford,Tracy Baynard,Paul J Fadel

doi:10.14814/phy2.14068

Abstract

Sympathetic vasoconstriction is attenuated in exercising muscles to assist in matching of blood flow with metabolic demand. This “functional sympatholysis” may be impaired in young obese individuals due to greater sympathetic activation and/or reduced local vasodilatory capacity of both small and large arteries, but this remains poorly understood. We tested the hypothesis that functional sympatholysis is impaired in obese individuals compared with normal‐weight counterparts. In 36 obese and normal‐weight young healthy adults (n = 18/group), we measured forearm blood flow and calculated forearm vascular conductance (FVC) responses to reflex increases in sympathetic nerve activity induced by lower body negative pressure (LBNP) at rest and during rhythmic handgrip exercise at 15% and 30% of the maximal voluntary contraction (MVC). FVC was normalized to lean forearm mass. In normal‐weight individuals, LBNP evoked a decrease in FVC (−16.1 ± 5.7%) in the resting forearm, and the reduction in FVC (15%MVC: −8.1 ± 3.3%; 30%MVC: −1.0 ± 4.0%) was blunted during exercise in an intensity‐dependent manner (P < 0.05). Similarly, in obese individuals, LBNP evoked a comparable decrease in FVC (−10.9 ± 5.7%) in the resting forearm, with the reduction in FVC (15%MVC: −9.7 ± 3.3%; 30%MVC: −0.3 ± 4.0%) also blunted during exercise in an intensity‐dependent manner (P < 0.05). The magnitude of sympatholysis was similar between groups (P > 0.05) and was intensity‐dependent (P < 0.05). Our findings suggest that functional sympatholysis is not impaired in young obese individuals without overt cardiovascular diseases.

Highlights

Obesity is an important cardiovascular disease risk factor associated with reduced physical activity levels, coupled with exercise intolerance (Vanhecke et al 2009)
While exercise is often recommended in part to combat obesity (Donnelly et al 2009), our current understanding of how blood flow is controlled in order to meet the metabolic demands associated with exercise in obese individuals is incomplete
LBNP, lower body negative pressure; EX15, exercise at 15% of the maximal voluntary contraction; EX30, exercise at 30% of the maximal voluntary contraction; Forearm blood flow (FBF), forearm blood flow; nFBF, forearm blood flow normalized to lean forearm mass; FVC, forearm vascular conductance; nFVC, forearm vascular conductance normalized to lean forearm mass; AU, arbitrary units. aDifferent than before LBNP stimulation (P < 0.05). #Different from normal-weight participants at this time point (P < 0.05). †Different than rest; ‡Different than EX15 (Exercise Only, Without LBNP) (P < 0.05)

Summary

Introduction

Obesity is an important cardiovascular disease risk factor associated with reduced physical activity levels, coupled with exercise intolerance (Vanhecke et al 2009). One potential mechanism underlying exercise intolerance in obesity is “functional sympatholysis” (Remensnyder et al 1962; Tschakovsky et al 2002). When functional sympatholysis is intact, locally released vasoactive substances within the exercising muscle can effectively attenuate sympatheticallymediated vasoconstriction, contributing to the proper delivery of blood flow, oxygen, and nutrients to contracting skeletal muscles (Remensnyder et al 1962; Tschakovsky et al 2002; Hearon et al 2016). Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.

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