Short-term exercise training augments α2-adrenoreceptor-mediated sympathetic vasoconstriction in resting and contracting skeletal muscle

We hypothesized that exercise training (ET) would alter (2)-adrenoreceptor-mediated sympathetic vasoconstriction. Sprague-Dawley rats (n= 30) were randomized to sedentary (S), mild- (M) or heavy-intensity (H) treadmill ET groups (5 days per week for 4 weeks). Following the ET component of the study, rats were anaesthetized, and instrumented for lumbar sympathetic chain stimulation, triceps surae muscle contraction and measurement of femoral vascular conductance (FVC). The percentage change of FVC in response to sympathetic stimulation was determined at rest and during contraction in control, (2) blockade (yohimbine) and combined (2)+ nitric oxide (NO) synthase (NOS) blockade (N-nitro-l-arginine methyl ester hydrochloride, l-NAME) conditions. ET augmented (P < 0.05) sympathetic vasoconstrictor responses at rest and during contraction. Yohimbine reduced (P < 0.05) the vasoconstrictor response in ET rats at rest (M: 2 Hz: 8 +/- 2%, 5 Hz: 9 +/- 4%; H: 2 Hz: 14 +/- 5%, 5 Hz: 11 +/- 6%) and during contraction (M: 2 Hz: 9 +/- 2%, 5 Hz: 9 +/- 5%; H: 2 Hz: 8 +/- 3%, 5 Hz: 6 +/- 6%) but did not change the response in S rats. The addition of l-NAME caused a larger increase (P < 0.05) in the vasoconstrictor response in ET than in S rats at rest (2 Hz: S: 8 +/- 2%, M: 15 +/- 3%, H: 23 +/- 7%; 5 Hz: S: 8 +/- 5%, M: 15 +/- 3%, H: 17 +/- 5%) and during contraction (2 Hz: S: 9 +/- 3%, M: 18 +/- 3%, H: 22 +/- 6%; 5 Hz: S: 9 +/- 5%, M: 22 +/- 4%, H:26 +/- 9%). Sympatholysis was greater (P < 0.05) in ET than in S rats. Blockade of (2)-adrenoreceptors and NOS reduced (P < 0.05) sympatholysis in ET rats, but had no effect on sympatholysis in S rats. In conclusion, ET increased (2)-mediated vasoconstriction at rest and during contraction.