Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 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

Nathan T Jenkins  1 , Jeffrey S Martin, M Harold Laughlin, Jaume Padilla
Affiliations

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.

PubMed Disclaimer

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).
See this image and copyright information in PMC

References

    1. Blair SN, Kohl HW, 3rd, Paffenbarger RS, Jr, Clark DG, Cooper KH, Gibbons LW. Physical fitness and all-cause mortality. A prospective study of healthy men and women. JAMA. 1989;262:2395–401. - PubMed
    1. Lees SJ, Booth FW. Sedentary death syndrome. Can J Appl Physiol. 2004;29:447. - PubMed
    1. Mora S, Cook N, Buring JE, Ridker PM, Lee IM. Physical Activity and Reduced Risk of Cardiovascular Events: Potential Mediating Mechanisms. Circulation. 2007;116:2110–8. - PMC - PubMed
    1. Green DJ, Walsh JH, Maiorana A, Best MJ, Taylor RR, O’Driscoll JG. Exercise-induced improvement in endothelial dysfunction is not mediated by changes in CV risk factors: pooled analysis of diverse patient populations. Am J Physiol Heart Circ Physiol. 2003;285:H2679–87. - PubMed
    1. Joyner MJ, Green DJ. Exercise protects the cardiovascular system: effects beyond traditional risk factors. J Physiol. 2009;587:5551–8. - PMC - PubMed

LinkOut - more resources