Skeletal Muscle Sympathetic Vasoconstrictor Control Following Short-Term Mild- and Heavy-Intensity Exercise Training

Abstract

The purpose of this thesis was to investigate the effects of short-term endurance exercise training (ET) on sympathetic vasoconstriction in resting and contracting skeletal muscle. To achieve these aims, rats were exercise trained on a motorized treadmill and an anesthetised whole animal in situ vascular preparation was used to investigate the effects of ET on sympathetic vascular control in resting and contracting skeletal muscle. Exercise training augmented resting sympathetic vasoconstrictor responsiveness in a training intensity-dependent manner. Concurrently, endothelium-dependent vasodilation was augmented in a training intensity-dependent manner and significantly correlated to the magnitude of sympathetic vasoconstrictor responsiveness. During acute exercise sympathetic outflow is increased however the vascular response to sympathetic stimulation is diminished and aids in the regulation of skeletal muscle blood flow; a physiologic phenomenon termed functional sympatholysis. The inhibition of sympathetic vasoconstriction during muscular contraction was augmented in a manner influenced by the intensity of ET through a nitric oxide-dependent mechanism. Given the increased resting sympathetic vasoconstrictor responsiveness and enhanced sympatholysis following training, it was hypothesized that ET may mediate these effects, in part, by an altered contribution of post-synaptic α2-adrenergic receptors to the regulation of sympathetic vasoconstriction. Exercise training significantly augmented the contribution of α2-adrenergic receptor to basal sympathetic vasoconstriction. During contraction the α2-adrenergic receptor was relatively resistant to inhibition. The ET induced increase in sympatholysis was mediated, in part, by the inhibition of the α1-adrenergic receptor through a nitric oxide-dependent mechanism. Collectively, these results highlight the integrated nature of ET mediated adaptations to sympathetic regulation of skeletal muscle vascular conductance and the plasticity of sympathetic regulation of skeletal muscle vascular conductance.