Exercise training and α₁ -adrenoreceptor-mediated sympathetic vasoconstriction in resting and contracting skeletal muscle

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 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) 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 α1‐adrenoreceptor blockade. Subsequent NOS inhibition did not alter (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.

Vascular characteristics in young women—Effect of extensive endurance training or a sedentary lifestyle

“…There is some evidence that endurance training may lower muscle sympathetic nerve traffic, but other data argue against this notion . Irrespective of this, it has been shown that aerobic exercise training may modulate sympathetic vasoconstriction in resting skeletal muscle and enhance functional sympatholysis through a nitric oxide‐dependent mechanism . That lower muscle sympathetic vasoconstriction could to some extent explain the lower AI in the physically trained groups is, however, contradicted by the finding that the calculated value of TPR was not significantly different between any of the groups of the present study (Table ).…”

“…41,42 Irrespective of this, it has been shown that aerobic exercise training may modulate sympathetic vasoconstriction in resting skeletal muscle and enhance functional sympatholysis through a nitric oxide-dependent mechanism. 43,44 That lower muscle sympathetic vasoconstriction could to some extent explain the lower AI in the physically trained groups is, however, contradicted by the finding that the calculated value of TPR was not significantly different between any of the groups of the present study (Table 2). Therefore, an alternative and more likely explanation of the detected differences in AI with exercise training or sedentary lifestyle, in spite of the fact that indicators of central arterial distensibility were not different, may be changes in endothelial function as a result of the level of exercise-induced increase in shear stress.…”

Evaluating the NIRS-derived microvascular O2 extraction “reserve” in groups varying in sex and training status using leg blood flow occlusions

“…Second, it could be possible that the magnitude of the O 2 extraction reserve may not only be dependent on the individual maximal O 2 extraction capacity, but also on the amount of oxygenated blood perfusing the area investigated immediately prior to the blood flow occlusion [4]. In this perspective, exercise training adaptations improve the matching of local blood flow with O 2 utilization as well as reduce sympathetically-induced vasoconstriction during exercise [45]. Thus, trained individuals may not necessarily demonstrate a smaller O 2 extraction reserve simply based on a greater oxidative capacity.…”

Sex differences in sympathetic vasoconstrictor responsiveness and sympatholysis

“…Stimulation frequencies of 2 and 5 Hz were selected to reflect levels of sympathetic nerve activity observed at rest and during conditions of elevated nerve activity (such as in response to exercise or physiological stress) and to evoke frequency᎑dependent vasoconstrictor responses in the hindlimb vascular bed at rest and during muscle contraction (1,15,22,30). These frequencies of sympathetic nerve stimulation are routinely used in our laboratory and others to investigate neurovascular control in the skeletal muscle vascular bed (23,33,48). Eight minutes of rhythmic muscle contraction were produced, and lumbar sympathetic chain stimulation at 2 and 5 Hz was delivered 3 and 6 min after the onset of muscle contraction in random order.…”