The purpose of this research program is to understand the vascular adaptation that occurs within skeletal muscle in response to chronic to exercise. The investigators have demonstrated that exercise training produces an increase in the capacity of skeletal muscle vascular beds to transport nutrients to muscle. Data suggest that this increase is most evident in muscle tissue with the greatest relative increase in activity during training sessions. Experiments outlined for aim 1 will test the hypothesis that exercise training increases microvascular permeability and alters the control of permeability by altering endothelium-dependent regulation of permeation in skeletal muscle vascular beds. Transcapillary exchange will be examined in situ with single vessel perfusion techniques.
Aim 2 will determine whether angiogenesis of arterioles and venules is stimulated by exercise training. The investigators' hypothesis is that angiogenic changes in pre- and post-capillary networks are coupled so that the pre- to post- capillary resistance ratio is maintained. Morphometric indices of structural vascular adaptation and biochemical estimates of oxidative capacity will be obtained to elucidate interactions of exercise, vascular function, and skeletal muscle biochemistry after training.
Aims 3 and 4 are focused on the hypothesis that exercise training alters intrinsic, hemodynamic control mechanisms in skeletal muscle vascular beds.
Aim 3 will examine blood flow control in in situ, contracting rat hind limb muscles and in conscious rats during locomotory exercise. The investigators' hypothesis is that training causes alterations in intrinsic control mechanisms of microcirculatory beds of skeletal muscle and that these changes are focused in the muscle tissue with the greatest relative increase in activity during training sessions. The investigators will assess skeletal muscle vascular function with measurements of total and regional blood flow.
Aim 4 will examine isolated arterial resistance vessels in vitro to test the hypothesis that training alters intrinsic control mechanisms of both vascular smooth muscle and endothelium of skeletal muscle resistance vessels. Preliminary results indicate that the most exciting training-induced changes involve enhancement of endothelium-mediated vasodilator mechanisms in the skeletal muscle microcirculation.
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