Open AccessExercise training and α 1 ‐adrenoreceptor‐mediated sympathetic vasoconstriction in resting and contracting skeletal muscle
Author(s) -
Just Timothy P.,
DeLorey Darren S.
Publication year - 2016
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.12707
Subject(s) - prazosin , vasoconstriction , medicine , endocrinology , stimulation , contraction (grammar) , muscle contraction , receptor , antagonist
Abstract 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.