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. 2014 Sep;99(9):1191-202.
doi: 10.1113/expphysiol.2014.078048. Epub 2014 Mar 21.

Neural control of blood flow during exercise in human metabolic syndrome

Jacqueline K Limberg  1 , Barbara J Morgan  2 , Joshua J Sebranek  3 , Lester T Proctor  3 , Marlowe W Eldridge  4 , William G Schrage  5
Affiliations

Neural control of blood flow during exercise in human metabolic syndrome

Jacqueline K Limberg et al. Exp Physiol. 2014 Sep.

Abstract

α-Adrenergic-mediated vasoconstriction is greater during simulated exercise in animal models of metabolic syndrome (MetSyn) when compared with control animals. In an attempt to translate such findings to humans, we hypothesized that adults with MetSyn (n = 14, 35 ± 3 years old) would exhibit greater α-adrenergic responsiveness during exercise when compared with age-matched healthy control subjects (n = 16, 31 ± 3 years old). We measured muscle sympathetic nerve activity (MSNA; microneurography) and forearm blood flow (Doppler ultrasound) during dynamic forearm exercise (15% of maximal voluntary contraction). α-Adrenergic agonists (phenylephrine and clonidine) and an antagonist (phentolamine) were infused intra-arterially to assess α-adrenergic receptor responsiveness and restraint, respectively. Resting MSNA was ∼35% higher in adults with MetSyn (P < 0.05), but did not change in either group with dynamic exercise. Clonidine-mediated vasoconstriction was greater in adults with MetSyn (P < 0.01). Group differences in vascular responses to phenylephrine and phentolamine were not detected (P > 0.05). Interestingly, exercise-mediated vasodilatation was greater in MetSyn (P < 0.05). Adults with MetSyn exhibit greater resting MSNA and clonidine-mediated vasoconstriction, yet preserved functional sympatholysis and higher exercise blood flow during low-intensity hand-grip exercise when compared with age-matched healthy control subjects. These results suggest that adults with MetSyn exhibit compensatory vascular control mechanisms capable of preserving blood flow responses to exercise in the face of augmented sympathetic adrenergic activity.

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Figures

Figure 1
Figure 1. Study time line
All trials were separated by a minimum of 10 min of quiet rest. Trials 2–5 were randomized and counterbalanced. Abbreviations: CL, clonidine; PE, phenylephrine; and PH, phentolamine.
Figure 2
Figure 2. Muscle sympathetic nerve activity (MSNA) at rest and during exercise
Control n = 12, metabolic syndrome (MetSyn) n = 9. A and B, representative neurogram from a single subject with MetSyn showing that MSNA levels are maintained during dynamic exercise. C and D, MSNA (burst frequency and burst incidence) is greater in adults with MetSyn (*P < 0.05 versus Control) and did not increase during dynamic exercise in either group (P > 0.05). Repeated measures ANOVA.
Figure 3
Figure 3. Phenylephrine-mediated vasoconstriction
Control n = 16, MetSyn n = 13. Phenylephrine-mediated vasoconstriction was blunted from resting levels with exercise (main effect of condition, †P < 0.01 versus Rest). The level of phenylephrine-mediated vasoconstriction was not different between groups (main effect of group, P = 0.11). Repeated measures ANOVA.
Figure 4
Figure 4. Clonidine-mediated vasoconstriction
Control n = 16, MetSyn n = 14. Clonidine-mediated vasoconstriction was blunted from resting levels with exercise (main effect of condition, †P < 0.01 versus Rest). The level of clonidine-mediated vasoconstriction was greater in adults with MetSyn when compared with healthy control subjects (interaction effect of group and condition, *P < 0.01). Repeated measures ANOVA.
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References

    1. Agapitov AV, Correia ML, Sinkey CA, Haynes WG. Dissociation between sympathetic nerve traffic and sympathetically mediated vascular tone in normotensive human obesity. Hypertension. 2008;52:687–695. - PMC - PubMed
    1. Alberti KG, Eckel RH, Grundy SM, Zimmet PZ, Cleeman JI, Donato KA, Fruchart JC, James WP, Loria CM, Smith SC., Jr Harmonizing the metabolic syndrome: a joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity. Circulation. 2009;120:1640–1645. - PubMed
    1. Ardévol A, Adán C, Remesar X, Alemany M, Fernández-López JA. Muscle blood flow during intense exercise in the obese rat. Arch Physiol Biochem. 1996;104:337–343. - PubMed
    1. Beltowski J. Leptin and the regulation of endothelial function in physiological and pathological conditions. Clin Exp Pharmacol Physiol. 2012;39:168–178. - PubMed
    1. Bristow MR, Ginsburg R, Minobe W, Cubicciotti RS, Sageman WS, Lurie K, Billingham ME, Harrison DC, Stinson EB. Decreased catecholamine sensitivity and β-adrenergic-receptor density in failing human hearts. N Engl J Med. 1982;307:205–211. - PubMed

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