运动与衰老骨骼肌线粒体生物合成  

Exercise and Mitochondrial Biogenesis in Aged Skeletal Muscle

作　　者：韩雨梅[1] 刘树森[2] 张勇[3] 

机构地区：[1]山西大学体育学院,太原030006 [2]中科院动物研究所生物膜与膜生物工程国家重点实验室,北京100101 [3]天津体育学院天津市运动生理学与运动医学重点实验室,天津300381

出　　处：《天津体育学院学报》2009年第6期515-517,546,共4页Journal of Tianjin University of Sport

基　　金：国家自然科学基金项目(项目编号:30470837);天津市社会发展重大科技攻关项目(项目编号:05YFGDSF02100)

摘　　要：线粒体生物合成依赖于细胞核与线粒体基因的协同表达。哺乳动物衰老过程中骨骼肌线粒体氧化磷酸化能力下降,其中线粒体数量和/或线粒体功能的缺失是其重要影响因素之一。运动可以诱导骨骼肌线粒体生物合成产生适应性变化,线粒体呼吸链产生的活性氧和自由基参与了线粒体到细胞核的信号传导。综述当前有关运动与线粒体生物合成的分子机理、运动对衰老状态下骨骼肌线粒体生物合成的影响以及在此过程中涉及的信号通路。Mitochondrial biogenesis depends on coordinated expression of genes in the nucleus and mitochondria. A decline in the oxidative phosphorylation capacity of mammalian muscle with age could relate to the absence of the mitochondrial quantity and the function. Exercise can cause adaptive alteration of mitochondrial biogenesis in skeletal muscle. It has been proposed that reactive oxygen species （ROS） and free radicals generated from respiratory chain are involved in the signaling from mitochondria to the nucleus. We reviewed the current molecular mechanism of exercise-induced mitochondrial biogenesis and alterations in the abundance of mitochondria of age-related skeletal muscle in response to exercise and the signaling pathways that are involved.

关 键 词：运动 线粒体生物合成 衰老 氧化应激 

分 类 号：G804.7[文化科学—运动人体科学]