Mechanisms of sympathetic restraint in human skeletal muscle during exercise: role of α-adrenergic and nonadrenergic mechanisms.
Adrenergic alpha-Antagonists
/ pharmacology
Adrenergic beta-Antagonists
/ pharmacology
Adult
Blood Pressure
Exercise
Humans
Male
Muscle Contraction
Muscle, Skeletal
/ drug effects
Phentolamine
/ pharmacology
Propranolol
/ pharmacology
Regional Blood Flow
Sympathetic Nervous System
/ drug effects
Vasoconstriction
Vasodilation
cardiovascular reflex
exercise
sympathetic nervous system
α-adrenergic receptors
Journal
American journal of physiology. Heart and circulatory physiology
ISSN: 1522-1539
Titre abrégé: Am J Physiol Heart Circ Physiol
Pays: United States
ID NLM: 100901228
Informations de publication
Date de publication:
01 07 2020
01 07 2020
Historique:
pubmed:
6
6
2020
medline:
7
10
2020
entrez:
6
6
2020
Statut:
ppublish
Résumé
Sympathetic vasoconstriction is mediated by α-adrenergic receptors under resting conditions. During exercise, increased sympathetic nerve activity (SNA) is directed to inactive and active skeletal muscle; however, it is unclear what mechanism(s) are responsible for vasoconstriction during large muscle mass exercise in humans. The aim of this study was to determine the contribution of α-adrenergic receptors to sympathetic restraint of inactive skeletal muscle and active skeletal muscle during cycle exercise in healthy humans. In ten male participants (18-35 yr), mean arterial pressure (intra-arterial catheter) and forearm vascular resistance (FVR) and conductance (FVC) were assessed during cycle exercise (60% total peak workload) alone and during combined cycle exercise + handgrip exercise (HGE) before and after intra-arterial blockade of α- and β-adrenoreceptors via phentolamine and propranolol, respectively. Cycle exercise caused vasoconstriction in the inactive forearm that was attenuated ~80% with adrenoreceptor blockade (%ΔFVR, +81.7 ± 84.6 vs. +9.7 ± 30.7%;
Identifiants
pubmed: 32502375
doi: 10.1152/ajpheart.00208.2020
pmc: PMC7474447
doi:
Substances chimiques
Adrenergic alpha-Antagonists
0
Adrenergic beta-Antagonists
0
Propranolol
9Y8NXQ24VQ
Phentolamine
Z468598HBV
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
H192-H202Subventions
Organisme : HHS | National Institutes of Health (NIH)
ID : NIH 1F32HL1377285-0
Pays : International
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