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. 2012 Aug 1;6(4):331-346.
doi: 10.1007/s12170-012-0241-5.

Exercise-induced Signals for Vascular Endothelial Adaptations: Implications for Cardiovascular Disease

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Exercise-induced Signals for Vascular Endothelial Adaptations: Implications for Cardiovascular Disease

Nathan T Jenkins et al. Curr Cardiovasc Risk Rep. .

Abstract

This article reviews recent advances in our understanding of hemodynamic signals, external/compressive forces, and circulating factors that mediate exercise training-induced vascular adaptations, with particular attention to the roles of these signals in prevention and treatment of endothelial dysfunction and cardiovascular (CV) diseases.

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Conflict of interest statement

Disclosure: No conflicts of interest relevant to this article were reported.

Figures

Figure 1
Figure 1
Effect of shear (40 dyn/cm2) vs. no shear (0 dyn/cm2) on expression of intercellular adhesion molecule-1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1), E-selectin, and monocyte chemoattractant protein-1 (MCP-1) gene expression in rat carotid arteries. * P < 0.05 vs. no shear.
Figure 2
Figure 2
Proposed “inverted-U” shaped relationship between circulating insulin concentrations and endothelial function.
Figure 3
Figure 3
Summary of hemodynamic signals, compressive forces, and circulating factors involved in exercise training-induced endothelial adaptations, illustrated by contrasting the effect of regular endurance exercise (high mean shear stress and external compression, optimal levels of insulin [see Fig 2], low leptin levels, increased adiponectin levels, and increased number and function of CACs; left side) vs. that of a sedentary lifestyle (for simplicity, depicted as opposite of regular endurance exercise; right side).

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