title: Neural control of blood flow during exercise in human metabolic syndrome.
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.
authors.affiliation: School of Education, Department of Kinesiology, University of Wisconsin - Madison, Madison, WI 53706, USA.
authors.forename: Jacqueline K
authors.initials: JK
authors.lastname: Limberg
authors.affiliation: School of Medicine and Public Health, Department of Orthopedics and Rehabilitation, University of Wisconsin - Madison, Madison, WI 53706, USA.
authors.forename: Barbara J
authors.initials: BJ
authors.lastname: Morgan
authors.affiliation: School of Medicine and Public Health, Department of Anesthesiology, University of Wisconsin - Madison, Madison, WI 53792, USA.
authors.forename: Joshua J
authors.initials: JJ
authors.lastname: Sebranek
authors.affiliation: School of Medicine and Public Health, Department of Anesthesiology, University of Wisconsin - Madison, Madison, WI 53792, USA.
authors.forename: Lester T
authors.initials: LT
authors.lastname: Proctor
authors.affiliation: School of Medicine and Public Health, Department of Pediatrics, University of Wisconsin - Madison, Madison, WI 53792, USA.
authors.forename: Marlowe W
authors.initials: MW
authors.lastname: Eldridge
authors.affiliation: School of Education, Department of Kinesiology, University of Wisconsin - Madison, Madison, WI 53706, USA wschrage@education.wisc.edu.
authors.forename: William G
authors.initials: WG
authors.lastname: Schrage
mesh_terms: D000222:Adaptation, Physiological; D000316:Adrenergic alpha-Agonists / Q000008:administration & dosage; D000317:Adrenergic alpha-Antagonists / Q000008:administration & dosage; D000328:Adult; D001783:Blood Flow Velocity; D016022:Case-Control Studies; D015444:Exercise; D005260:Female; D018737:Hand Strength; D006801:Humans; D007261:Infusions, Intra-Arterial; D017078:Laser-Doppler Flowmetry; D008297:Male; D024821:Metabolic Syndrome / Q000175:diagnosis / Q000503:physiopathology*; D009119:Muscle Contraction; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000294:innervation*; D012039:Regional Blood Flow; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D013997:Time Factors; D034941:Upper Extremity; D014661:Vasoconstriction / Q000187:drug effects; D014664:Vasodilation
chemical_list: D000316:Adrenergic alpha-Agonists; D000317:Adrenergic alpha-Antagonists