运动对心血管系统的影响:分子信号通路和心脏适应

Bauyrzhan Toktarbay, Zaukiya Khamitova, Nurmakhan Zholshybek, Dinara Jumadilova, Yeltay Rakhmanov, Makhabbat Bekbossynova, Abduzhappar Gaipov, Alessandro Salustri
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引用次数: 0

摘要

这篇综述的目的是通过回顾在不同肌肉适应中起关键作用的分子信号通路来描述耐力和力量体育训练对心血管系统的影响,以及在代谢和心脏重构以及血液动力学方面的心脏变化。在耐力运动的反应中,多种信号通路,包括Ca<sup>2+</sup>依赖性通路、活性氧(ROS)、amp依赖性蛋白激酶(AMPK)和丝裂原活化蛋白激酶(p38 MAPK),参与调控过氧化物酶体增殖体活化受体-γ共激活因子-1α (PGC-1α),从而控制线粒体的生物发生。力量训练增加胰岛素样生长因子(IGF-1),启动磷脂酰肌醇3-激酶(PI3-k)-(AKT)-(mTOR)信号级联,导致蛋白质合成和肌肉肥大。除了骨骼肌有充分记录的变化外,运动训练反应的一个关键组成部分是动态心脏重构,根据触发因素分为病理性或生理性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
THE IMPACT OF EXERCISE ON CARDIOVASCULAR SYSTEM: MOLECULAR SIGNALLING PATHWAY AND CARDIAC ADAPTATIONS
The purpose of this review is to describe the impact of endurance and strength physical training on the cardiovascular system by reviewing the molecular signalling pathways, which plays a key role in different muscle adaptations, and the cardiac changes in terms of metabolic and cardiac remodelling, and hemodynamics. In response to endurance-exercise, multiple signalling pathways, including Ca2+-dependent pathways, reactive oxygen species (ROS), AMP-dependent protein kinase (AMPK), and mitogen activated protein kinases (p38 MAPK), are involved in the regulation of peroxisome-proliferator-activated receptor-γ coactivator-1α (PGC-1α), which controls the mitochondrial biogenesis. Strength training increases the insulin-like growth factor (IGF-1) which initiates the phosphatidylinositol 3-kinase (PI3-k)-(AKT)-(mTOR) signalling cascade, resulting in the synthesis of proteins and the muscle hypertrophy. In addition to the well-documented changes in skeletal muscle, a critical component of the response to exercise training is the dynamic cardiac remodelling, which is classified as either pathological or physiological depending on triggers.
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