Advancements in the Regulation of Different-Intensity Exercise Interventions on Arterial Endothelial Function

Abstract

Normal-functioning endothelium is crucial to maintaining vascular homeostasis and inhibiting the development and progression of cardiovascular diseases such as atherosclerosis. Exercise training has been proven effective in regulating arterial endothelial function, and the effect of this regulation is closely related to exercise intensity and the status of arterial endothelial function. With this review, we investigated the effects of the exercise of different intensity on the function of arterial endothelium and the underlying molecular biological mechanisms. Existing studies indicate that low-intensity exercise improves arterial endothelial function in individuals who manifest endothelial dysfunction relative to those with normal endothelial function. Most moderate-intensity exercise promotes endothelial function in individuals with both normal and impaired arterial endothelial function. Continuous high-intensity exercise can lead to impaired endothelial function, and high-intensity interval exercise can enhance both normal and impaired endothelial function. In addition, it was demonstrated that the production of vasomotor factors, oxidative stress, and inflammatory response is involved in the regulation of arterial endothelial function under different-intensity exercise interventions. We posit that this synthesis will then provide a theoretical basis for choosing the appropriate exercise intensity and optimize the prescription of clinical exercise for persons with normal and impaired endothelium.

Keywords: arterial endothelial function; cardiovascular diseases; exercise; inflammatory reaction; oxidative stress; vascular diastolic-systolic factors.

Fig. 1.

Potential mechanisms by which exercise of different intensity modulates endothelial function in arteries. eNOS, endothelial nitric oxide synthase; NO, nitric oxide; GPX, glutathione peroxidase; SOD, superoxide dismutase; CRP, c-reactive protein; MCP-1, monocyte chemoattractant protein-1; TNF-$\alpha$, tumor necrosis factor-alpha; ICAM-1, intercellular adhesion molecule 1; VCAM-1, vascular cell adhesion molecule-1;IL-4, interleukin-4; IL-10, interleukin-10; SPRED1, sprouty related EVH1 domain containing 1; VEGF, vascular endothelial-derived growth factor ; ET-1, endothelin-1; UCP2, uncoupling protein 2; AMPK, adenosine monophosphate-activated protein kinase; HIIT, high-intensity interval training; EPCs, endothelial progenitor cells; CTRP9, c1q/tumor necrosis factor-related protein 9; IL-6, interleukin-6; 8-OHdG, 8-hydroxy-2 deoxyguanosine; MDA-LDL, malondialdehyde-low density lipoprotein; PI3K/AKT, phosphatidylinositol 3-kinase/protein kinase B.