Exercise training and α(1)‐adrenoreceptor‐mediated sympathetic vasoconstriction in resting and contracting skeletal muscle

Exercise training (ET) increases sympathetic vasoconstrictor responsiveness and enhances contraction‐mediated inhibition of sympathetic vasoconstriction (i.e., sympatholysis) through a nitric oxide (NO)‐dependent mechanism. Changes in α(2)‐adrenoreceptor vasoconstriction mediate a portion of these training adaptations, however the contribution of other postsynaptic receptors remains to be determined. Therefore, the purpose of this study was to investigate the effect of ET on α(1)‐adrenoreceptor‐mediated vasoconstriction in resting and contracting muscle. It was hypothesized that α(1)‐adrenoreceptor‐mediated sympatholysis would be enhanced following ET. Male Sprague Dawley rats were randomized to sedentary (S; n = 12) or heavy‐intensity treadmill ET (n = 11) groups. Subsequently, rats were anesthetized and instrumented for lumbar sympathetic chain stimulation and measurement of femoral vascular conductance (FVC) at rest and during muscle contraction. The percentage change in FVC in response to sympathetic stimulation was measured in control, α(1)‐adrenoreceptor blockade (Prazosin; 20 μg, IV), and combined α(1) and NO synthase (NOS) blockade (l‐NAME; 5 mg·kg(−1) IV) conditions. Sympathetic vasoconstrictor responsiveness was increased (P < 0.05) in ET compared to S rats at low, but not high (P > 0.05) stimulation frequencies at rest (S: 2 Hz: −25 ± 4%; 5 Hz: −45 ± 5 %; ET: 2 Hz: −35 ± 7%, 5 Hz: −52 ± 7%), whereas sympathetic vasoconstrictor responsiveness was not different (P > 0.05) between groups during contraction (S: 2 Hz: −11 ± 8%; 5 Hz: −26 ± 11%; ET: 2 Hz: −10 ± 7%, 5 Hz: −27 ± 12%). Prazosin blunted (P < 0.05) vasoconstrictor responsiveness in S and ET rats at rest and during contraction, and abolished group differences in vasoconstrictor responsiveness. Subsequent NOS blockade increased vasoconstrictor responses (P < 0.05) in S at rest and during contraction, whereas in ET vasoconstriction was increased (P < 0.05) in response to sympathetic stimulation at 2 Hz at rest and unchanged (P > 0.05) during contraction. ET enhanced (P < 0.05) sympatholysis, however the training‐mediated improvements in sympatholysis were abolished by α(1)‐adrenoreceptor blockade. Subsequent NOS inhibition did not alter (P > 0.05) sympatholysis in S or ET rats. In conclusion, ET augmented α(1)‐adrenoreceptor‐mediated vasoconstriction in resting skeletal muscle and enhanced α(1)‐adrenoreceptor‐mediated sympatholysis. Furthermore, these data suggest that NO is not required to inhibit α(2)‐adrenoreceptor‐ and nonadrenoreceptor‐mediated vasoconstriction during exercise.