Exercise training augmented α1-adrenoreceptor-mediated vasoconstriction in resting skeletal muscle and enhanced α1-adrenoreceptor-mediated sympatholysis (P<0.05).
23 male Sprague Dawley rats randomized to sedentary or heavy-intensity treadmill exercise training.
Heavy-intensity treadmill exercise training vs Sedentary
Percentage change in femoral vascular conductance (FVC) in response to sympathetic stimulation, p=<0.05
p-value: p=<0.05
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 α2-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 α1-adrenoreceptor-mediated vasoconstriction in resting and contracting muscle. It was hypothesized that α1-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, α1-adrenoreceptor blockade (Prazosin; 20 μg, IV), and combined α1 and NO synthase (NOS) blockade (l-NAME; 5 mg·kg(-1) IV) conditions. Sympathetic vasoconstrictor responsiveness was increased (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) during contraction. ET enhanced (P 0.05) sympatholysis in S or ET rats. In conclusion, ET augmented α1-adrenoreceptor-mediated vasoconstriction in resting skeletal muscle and enhanced α1-adrenoreceptor-mediated sympatholysis. Furthermore, these data suggest that NO is not required to inhibit α2-adrenoreceptor- and nonadrenoreceptor-mediated vasoconstriction during exercise.
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Timothy P. Just
University of Alberta
Darren S. DeLorey
University of Alberta
Physiological Reports
University of Alberta
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Just et al. (Mon,) reported a other. Heavy-intensity treadmill exercise training vs. Sedentary was evaluated on Percentage change in femoral vascular conductance (FVC) in response to sympathetic stimulation (p=<0.05). Exercise training augmented α1-adrenoreceptor-mediated vasoconstriction in resting skeletal muscle and enhanced α1-adrenoreceptor-mediated sympatholysis (P<0.05).
synapsesocial.com/papers/6a2263394f82ab017db6f594 — DOI: https://doi.org/10.14814/phy2.12707