Cardiovascular Adaptations in Spinal Cord-Injured Individuals. Timne course of arterial vascular changes.
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RU Radboud Universiteit Nijmegen, 23 november 2005
Promotor : Bindels, R.J.M. Co-promotor : Hopman, M.T.E.
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SubjectNCEBP 14: Cardiovascular diseases; UMCN 2.2: Vascular medicine and diabetes; UMCN 5.4: Renal disorders
This thesis presents studies on vascular adaptation to physical inactivity and deconditioning. Although it is clear that physical inactivity is an important risk factor for cardiovascular disease, the underlying physiological mechanisms have not yet been elucidated. In contrast to physical inactivity, exercise decreases the risk for cardiovascular disease. This beneficial effect of exercise is partly due to changes in vascular function and structure. However, far less is known about vascular adaptation to physical inactivity. Therefore, structural and functional changes in both the arterial and venous system in response to deconditioning were studied in models of physical inactivity. Unilateral lower limb suspension, bed rest, and spinal cord injury were applied in this thesis as models of deconditioning. Venous capacitance and occasionally venous compliance decreases after deconditioning and via a reduction in preload may contribute to the reduction in exercise capacity after deconditioning. However, changes in the venous system do not play an important role in the development of orthostatic intolerance after bed rest deconditioning. The baseline and maximal diameter of the leg conduit arteries decreased after ULLS and bed rest deconditioning. Therefore, even short-term adaptation in conduit artery diameter probably represents structural changes due to inward remodeling, rather than functional changes in vascular tone. This is clinically relevant, since inward remodeling contributes importantly to blood vessel obstruction in atherosclerotic disease. Since endothelial dysfunction is prognostic for the occurrence of cardiovascular disease and exercise corrects endothelial dysfunction, information on the effect of physical inactivity on endothelial function is important. Deconditioning does not affect baseline endothelial NO production at the arteriolar level. Moreover, deconditioning enhances both endothelium-dependent and endothelium-independent dilatation of conduit arteries. In contrast, exercise enhances baseline endothelial NO production and selectively increases endothelium-dependent dilatation. Therefore, functional arterial adaptations to inactivity are not simply the inverse of adaptations to exercise.
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