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Neural control of blood flow during exercise in human metabolic syndrome
Author(s) -
Limberg Jacqueline K.,
Morgan Barbara J.,
Sebranek Joshua J.,
Proctor Lester T.,
Eldridge Marlowe W.,
Schrage William G.
Publication year - 2014
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2014.078048
Subject(s) - microneurography , vasoconstriction , medicine , endocrinology , clonidine , adrenergic , sympathetic nervous system , blood flow , forearm , vasodilation , phenylephrine , phentolamine , exercise physiology , heart rate , baroreflex , blood pressure , receptor , anatomy
New FindingsWhat is the central question of this study? α‐Adrenergic‐mediated vasoconstriction is greater during simulated exercise in animal models of metabolic syndrome when compared with control animals. Whether such findings can be translated to humans was previously unexamined.What is the main finding and its importance? We observed greater muscle sympathetic nerve activity and clonidine‐mediated vasoconstriction in adults with metabolic syndrome, yet preserved exercise blood flow when compared with age‐matched healthy control subjects. These results suggest that adults with metabolic syndrome exhibit compensatory vascular control mechanisms capable of counteracting altered adrenergic responsiveness, thus preserving blood flow responses to low‐intensity, dynamic hand‐grip exercise.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.