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

Key points Postsynaptic α 1 ‐ and α 2 ‐adrenoreceptors produce tonic vasoconstriction in resting and contracting skeletal muscle. Muscular contraction attenuates sympathetic vasoconstriction (functional sympatholysis). The blunting of sympathetic vasoconstriction during contraction has been mechanistically linked to a reduction in postsynaptic α 1 ‐ and α 2 ‐adrenoreceptor responsiveness and nitric oxide. We recently demonstrated that exercise training augmented sympathetic vasoconstrictor responsiveness and functional sympatholysis. Whether these vascular adaptations were mediated by changes to postsynaptic adrenoreceptors was not investigated. The present findings demonstrate that exercise training augmented α 2 ‐adrenoreceptor‐ mediated vasoconstriction in resting and contracting skeletal muscle. These data indicate that exercise training alters the relative contributions of α‐adrenoreceptors to sympathetic vasoconstriction in resting and contracting skeletal muscle and that the regulation of sympathetic vasoconstriction becomes more complex following exercise training. Abstract We hypothesized that exercise training (ET) would alter α 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, α 2 blockade (yohimbine) and combined α 2 + nitric oxide (NO) synthase (NOS) blockade ( N ω ‐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 α 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 α 2 ‐mediated vasoconstriction at rest and during contraction.