Short‐term exercise training shifts the control of sympathetic vasoconstriction in contracting skeletal muscle to the α2‐adrenergic receptor

Abstract

We hypothesized that short‐term mild‐ (M) and heavy‐intensity (H) exercise training (ET) would augment α2‐adrenergic receptor mediated vasoconstriction in skeletal muscle. Sprague‐Dawley rats (n=30) were randomized to sedentary (S), M (20m/min5% grade) or H (40m/min5% grade) ET groups and trained 5d/wk for 4 wks with equal ET volume. Rats were anesthetised and instrumented for lumbar sympathetic chain stimulation and measurement of femoral vascular conductance (FVC). Triceps surae muscles were contracted at 60% of maximal contractile force. The percent decrease in FVC to sympathetic stimulation (2 and 5 Hz) was determined at rest and during contraction before (C) and after α2 blockade (Yohimbine; Y). ET increased (p<0.05) vasoconstrictor responsiveness. Y did not alter (p>;0.05) the decrease in FVC in S rats at rest (C: 2Hz: −22±5% 5Hz: −36±6%; Y: 2Hz: −20±5% 5Hz: −34±6%) or during contraction (C: 2Hz: −6±4% 5Hz: −18±5%; Y: 2Hz: −7±3% 5Hz: −16±5%). In contrast, Y reduced (p<0.05) vasoconstriction in ET rats at rest (M: C: 2Hz: −34±4% 5Hz: −47±7%; Y: 2Hz: −26±5% 5Hz: −38±7%; H: C: 2Hz: −44±5% 5Hz: −57±8%; Y: 2Hz: −30±6% 5Hz: −46±6%) and during contraction (M: C: 2Hz: −12±3% 5Hz: −20±3%; Y: 2Hz: −3±2% 5Hz: −11±5%; H: C: 2Hz: −12±3% 5Hz: −19±7%; Y: 2Hz: −4±3% 5Hz: −12±2%). ET increased α2 mediated constriction and shifted the control of sympathetic vasoconstriction in contracting muscle to the α2 receptor. NSERC, Canada.