共查询到17条相似文献，搜索用时 218 毫秒
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运动训练能促使骨骼肌形态、结构发生适应性的变化，如肌纤维选择性肥大、肌纤维类型转化等。钙调神经磷酸酶的活性与肌纤维选择性肥大、肌纤维类型的表达有着密切的关系，钙调神经磷酸酶信号机制为研究骨骼肌运动适应性变化打开了一扇新的大门。 相似文献
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Akt对骨骼肌质量的作用及运动训练对其影响的分子机制 总被引：2，自引：1，他引：1
Akt,又称蛋白激酶B ( PKB)对骨骼肌的生长和代谢具有举足轻重的地位,与之相关的多种分子信号通路在骨骼肌质量变化过程中扮演十分重要的角色.综述与骨骼肌质量变化相关的两个主要信号通路:一方面是与肌肉萎缩相关的Akt1/FOXOs/MAFbx/MuRF1信号通路;另一方面为与肌肉肥大相关的PI3K/Akt/mTOR/S6K1信号通路,从两方面介绍Akt在骨骼肌质量变化中所处的核心地位.此外,结合以上信号通路的理论基础,进一步解释不同的运动训练方式所导致的肌肉质量变化的分子机制,为运动状态下骨骼肌质量变化的分子机制提供有效的理论依据,从而为治疗与骨骼肌萎缩相关联的疾病提供有效途径. 相似文献
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采用半定量RT-PCR法和透射电镜法,观察大鼠不同运动强度游泳运动后骨骼肌IGF-IEa mRNA和MGF mRNA表达水平的变化以及骨骼肌卫星细胞的形态变化,阐述运动使骨骼肌增生肥大和损伤再修复的机制。 相似文献
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运动防治糖尿病骨骼肌病变的分子机制研究进展 总被引：1，自引：0，他引：1
糖尿病骨骼肌病变分子涉及广泛,包括VEGF和bFGF水平下降、Glut4水平下降、AMPK糖脂代谢途径紊乱、UPS被激活和线粒体形态功能异常、细胞凋亡增加等。运动对于改善血管病理性变化,恢复正常代谢,具有积极意义。本文通过分析运动对糖尿病骨骼肌病变相关分子的影响,探讨糖尿病骨骼肌病变运动防治分子机制,旨在推动糖尿病骨骼肌病变运动疗法的研究。 相似文献
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力量训练与骨骼肌的生理性适应 总被引：1，自引：0，他引：1
骨骼肌质量在维持人类的健康、体力活动和竞技运动成绩等方面起着重要的作用。力量训练显著性生理性适应之一是肌肉肥大。力量训练是提高骨骼肌质量的最有效方法。在分子水平，泛素连接酶MAFbx／atrogin-1和MuRF1可能在力量训练诱导骨骼肌重构机制起着重要的作用。充分认识力量训练诱导骨骼肌实时变化过程，有利于制定力量训练计划。 相似文献
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不同的运动方式诱导骨骼肌产生的适应性改变及分子响应机制不同。抗阻训练诱导骨骼肌发生肥大,其响应分子包括：PI3K、Akt、TSC1/2、mTOR、4EBP1、p70S6K等信号分子;耐力训练诱导骨骼肌的线粒体生物合成,其响应机制与AMPK、p38MAPK、CaMK、PGC-lα、NRF1、MEF2C等信号分子有关。 相似文献
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耐力训练对骨骼肌重量的影响相对较少,而力量训练可显著诱导运动肌发生肥大。不同的训练方式诱导适应的分子机制是不同的,激活和表达各自特异的信号通路和相关的基因。力量和耐力进行组合训练时,在分子水平存在一个干扰现象,不同训练方式可诱导细胞内信号通路产生拮抗,从而抵消骨骼肌对不同运动方式产生特异性适应。当前,一些训练学上的对策已经被证明能够有效降低力量和耐力组合训练产生的干扰。对这一问题的认识有助于我们理解骨骼肌疾病的病因、老龄化时维持其新陈代谢和功能以及运动员的运动训练。 相似文献
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运动能力的下降与骨骼肌中的细胞凋亡有着密切的联系，研究运动训练与细胞凋亡的关系及运动导致骨骼肌细胞凋亡的机制意义重大。运动强度与骨骼肌细胞凋亡及坏死的界限的关系，运动诱发骨骼肌细胞凋亡的基因调控及进一步研究骨骼肌细胞凋亡机制等几个方面都将是运动与细胞凋亡方面的研究热点。 相似文献
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Matthew S. Brook Daniel J. Wilkinson Kenneth Smith Philip J. Atherton 《European Journal of Sport Science》2016,16(6):633-644
Constituting ～40% of body mass, skeletal muscle has essential locomotory and metabolic functions. As such, an insight into the control of muscle mass is of great importance for maintaining health and quality-of-life into older age, under conditions of cachectic disease and with rehabilitation. In healthy weight-bearing individuals, muscle mass is maintained by the equilibrium between muscle protein synthesis (MPS) and muscle protein breakdown; when this balance tips in favour of MPS hypertrophy occurs. Despite considerable research into pharmacological/nutraceutical interventions, resistance exercise training (RE-T) remains the most potent stimulator of MPS and hypertrophy (in the majority of individuals). However, the mechanism(s) and time course of hypertrophic responses to RE-T remain poorly understood. We would suggest that available data are very much in favour of the notion that the majority of hypertrophy occurs in the early phases of RE-T (though still controversial to some) and that, for the most part, continued gains are hard to come by. Whilst the mechanisms of muscle hypertrophy represent the culmination of mechanical, auto/paracrine and endocrine events, the measurement of MPS remains a cornerstone for understanding the control of hypertrophy – mainly because it is the underlying driving force behind skeletal muscle hypertrophy. Development of sophisticated isotopic techniques (i.e. deuterium oxide) that lend to longer term insight into the control of hypertrophy by sustained RE-T will be paramount in providing insights into the metabolic and temporal regulation of hypertrophy. Such technologies will have broad application in muscle mass intervention for both athletes and for mitigating disease/age-related cachexia and sarcopenia, alike. 相似文献
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运动和胰岛素是诱导骨骼肌葡萄糖转运的两种重要生理因素，两者均能通过不同的信号转导通路诱导GLUT4从细胞内转位到细胞膜表面，从而调控骨骼肌的葡萄糖转运。研究表明，TBC1家族结构域家族成员蛋白激酶B蛋白底物160KDa（AS160/TBC1D4）和TBC1D1这两种同源蛋白均可在运动或胰岛素诱导下发生磷酸化，两者可能是运动和胰岛素调控骨骼肌葡萄糖转运信号通路的关键汇聚点。综述AS160与TBC1D1在胰岛素诱导骨骼肌葡萄糖转运中的不同作用以及运动/骨骼肌收缩对其的影响及其机制，以期深入了解运动如何改善胰岛素敏感性、为更科学的运动处方及其他干预措施的研发提供有价值的理论支持。 相似文献
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《运动与健康科学(英文)》2023,12(5):557-567
This review highlights some established and some more contemporary mechanisms responsible for heart failure (HF)-induced skeletal muscle wasting and weakness. We first describe the effects of HF on the relationship between protein synthesis and degradation rates, which determine muscle mass, the involvement of the satellite cells for continual muscle regeneration, and changes in myofiber calcium homeostasis linked to contractile dysfunction. We then highlight key mechanistic effects of both aerobic and resistance exercise training on skeletal muscle in HF and outline its application as a beneficial treatment. Overall, HF causes multiple impairments related to autophagy, anabolic-catabolic signaling, satellite cell proliferation, and calcium homeostasis, which together promote fiber atrophy, contractile dysfunction, and impaired regeneration. Although both wasting and weakness are partly rescued by aerobic and resistance exercise training in HF, the effects of satellite cell dynamics remain poorly explored. 相似文献
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目的:观察长期耐力训练及限食对老龄大鼠骨骼肌线粒体氧化及抗氧化水平的影响,比较其单独及协同作用,为"线粒体衰老"学说提供一定的理论依据。方法:32只17月龄雄性SD大鼠分为4组:安静组(Control,C)、限食组(Caloric-Restricted,CR)、运动组(Exercise,E)和限食加运动组(Caloric-restricted and Exercise,E+CR),训练方式为跑台运动,中等运动强度(64%VO2max,15m/min,60分钟/天,每周5天),限食摄入的标准为正常摄入组的60%,共训练及限食12周,相同月龄对照组正常饲养。12周后于末次训练后取大鼠骨骼肌分别进行线粒体氧化损伤水平及抗氧化水平测定。结果:CR组、E组和CR+E组骨骼肌线粒体丙二醛(malondialdehyde,MDA)含量显著降低,锰超氧化物歧化酶(manganese-containing superoxide dismutase,MnSOD)活性显著增加,谷胱甘肽过氧化物酶(glutathion peroxidase,GSH-PX)活性显著增加;E组和CR+E组骨骼肌线粒体过氧化氢酶(catalase,CAT)活性显著增加。结论:耐力训练提高机体的抗氧化水平,同时使细胞机能节省化,耗氧量相对下降而减少了自由基的产生,限食减弱了机体的氧化应激,减少了自由基的产生,阻止了脂质过氧化,同时限食动员了一系列的适应性的网络防御机制,增加了抗氧化水平,加强了防御。耐力运动在机体抗氧化能力上明显强于限食作用,而耐力运动与限食的协同作用对某些抗氧化酶的影响强于其单独作用的影响。 相似文献
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《运动与健康科学(英文)》2021,10(5):530-536
ObjectiveIn this review, we critically evaluate studies directly comparing the effects of plyometric vs. resistance training on skeletal muscle hypertrophy.MethodsWe conducted electronic searches of PubMed/MEDLINE, Scopus, SPORTDiscus, and Web of Science to find studies that explored the effects of plyometric vs. resistance training on muscle hypertrophy.ResultsEight relevant studies were included in the review. Six studies compared the effects of plyometric vs. resistance training on muscle hypertrophy, while 2 studies explored the effects of combining plyometric and resistance training vs. isolated resistance training on acute anabolic signaling or muscle hypertrophy. Based on the results of these studies, we conclude that plyometric and resistance training may produce similar effects on whole muscle hypertrophy for the muscle groups of the lower extremities. Therefore, it seems that plyometric training has a greater potential for inducing increases in muscle size than previously thought. Despite the findings observed at the whole muscle level, the evidence for the effects of plyometric training on hypertrophy on the muscle fiber level is currently limited for drawing inferences. Compared to isolated resistance training, combining plyometric and resistance exercise does not seem to produce additive effects on anabolic signaling or muscle growth; however, this area requires future study. The limitations of the current body of evidence are that the findings are specific to (a) musculature of the lower extremities, (b) short-term training interventions that lasted up to 12 weeks, and (c) previously untrained or recreationally active participants.ConclusionThis review highlights that plyometric and resistance training interventions may produce similar effects on whole muscle hypertrophy, at least for the muscle groups of the lower extremities, in untrained and recreationally trained individuals, and over short-term (i.e., ≤12 weeks) intervention periods. 相似文献
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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?怂 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. 相似文献