ScholarWorks@중앙대학교

초록

(Purpose) The present review aimed to clarify the mechanisms by which exercise training modulates the myogenic response of resistance arteries, with particular emphasis on Ca2+-independent signaling pathways and cytoskeletal remodeling that contribute to vascular smooth muscle adaptation to repeated mechanical loading. (Methods) PubMed was comprehensively searched to retrieve studies on the myogenic response and potential effects of exercise. (Results) These mechanisms include Ca2+ sensitization of the contractile apparatus via Rho-associated kinase-dependent inhibition of myosin light chain phosphatase and dynamic cytoskeletal remodeling that facilitates efficient force transmission. Through exercise training, the vascular wall is repeatedly exposed to elevations in intraluminal pressure, circumferential stretch, and shear stress; consequently, mechanosensitive signaling pathways in VSMCs become activated. Exercise training also modulates myogenic responsiveness partly by enhancing Ca2+-independent signaling rather than by altering intracellular Ca2+ dynamics alone. Exercise-induced adaptations in actin polymerization, focal adhesion assembly, and phosphorylation of cytoskeletal regulatory proteins such as heat shock protein 27 possibly augment pressure-induced vasoconstriction by improving mechanical force transmission. (Conclusions) This review suggests that exercise-induced modulation of Ca2+ - independent signaling and cytoskeletal remodeling may represent an important adaptive mechanism underlying improved vascular smooth muscle function. Such mechanisms may have potential implications for developing exercise-based strategies to preserve microvascular function in aging and cardiovascular diseases and for guiding future experimental studies investigating vascular mechanotransduction.

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