骨骼肌的运动适应机制

背景：骨骼肌运动适应机制的研究对提高运动成绩,预防和治疗一些代谢紊乱性疾病具有重要意义。 目的：探讨骨骼肌运动适应的机制。 方法：应用计算机检索PubMed数据库和中文期刊全文数据库2011-03前发表的相关文章,检索词分别为“skeletal muscle, exercise, adaptation, cytoskeleton, dystrophin”和“骨骼肌,运动,适应,骨架蛋白,肌营养不良蛋白”,共检索到56篇文献,纳入所述内容与骨骼肌运动适应机制相关的文献,排除重复性研究,保留31篇进行综述。 结果与结论：激烈的运动使肌肉结构和细胞代谢产生应激反应,包括肌肉损伤和氧化应激反应。高强度的离心运动可造成肌肉超微结构损伤,但运动性肌损伤后存在肌肉再重建反应。运动训练可促进健康的个体对一氧化氮系统产生各种各样的适应,通过各种机制增强骨骼肌的生物学有效性,这些适应性变化可有效增加运动能力,对心血管系统具有保护作用。目前,大多数人类骨骼肌运动适应机制还没有被发现。     

运动对骨骼肌卫星细胞的影响及作用机制

骨骼肌卫星细胞在骨骼肌生长发育、损伤修复以及骨骼肌重塑等生理病理过程中具有重要的作用。适宜的运动训练可活化卫星细胞,促进卫星细胞增殖并向成肌细胞分化。本文就骨骼肌卫星细胞的起源、形态特征和特异性的标记以及运动训练调控骨骼肌卫星细胞活化、增殖、分化的作用机制进行综述。     

运动训练中骨骼肌细胞凋亡的研究进展

细胞凋亡是程序化细胞死亡过程 ,是受一系列基因控制的生理性细胞死亡方式。细胞凋亡是广泛存在于组织细胞的基本生物学现象 ,是细胞应答不同有害刺激或疾病而发生的一种特殊的细胞自杀行为。通过这种细胞自杀行为 ,机体消除损伤、衰老、突变的细胞 ,以维持生理平衡。这是完全不同于坏死的一种死亡途径 ,通常对机体是有利的。细胞凋亡存在于发育、成熟和衰老过程之中 ,同时也存在于多种现代疾病中 ,细胞凋亡异常与多种肌细胞疾病的发生机制有关。探讨肌细胞凋亡的机制对预防和处理运动导致的骨骼肌损伤 ,以及某些骨骼肌疾病的运动保健与功能…     

抗阻运动对骨骼肌肥厚的影响

背景：抗阻运动能促进骨骼肌生长,导致骨骼肌肥厚。 目的：对目前采用细胞生物学及分子生物学方法观察抗阻运动对骨骼肌影响的文献进行综述。 方法：检索PubMed数据库中1999/2011-05收录的与抗阻运动后骨骼肌肥厚相关的文章,经筛选共纳入45篇文献,通过PubMed获得文献摘要及部分文献原文,如果没有全文通过Springer或Sciencedirect数据库或其他原文传递方式获得全文,分析抗阻运动对骨骼肌肥厚的研究进展。 结果与结论：抗阻运动后循环同化激素包括生长激素、胰岛素样生长因子1和睾酮发生应答性变化,对骨骼肌肥厚产生影响。抗阻运动对骨骼肌细胞生物学影响的研究主要集中在雷帕霉素靶蛋白介导骨骼肌蛋白合成途径,前列腺素、肿瘤坏死因子α介导的炎性机制与增肌关系和张力感受器在信号改变后对增肌的影响3个方面。     

衰老骨骼肌蛋白质的合成与抵抗**

背景：老年人随增龄出现的骨骼肌丢失现象称为骨骼肌衰老,通常表现为骨骼肌质量的丢失和力量的下降。其主要原因是衰老骨骼肌对骨骼肌蛋白合成刺激(补充蛋白质和运动)的敏感性下降,也即衰老出现了“蛋白质合成抵抗”现象。 目的：从概念、可能机制和干预手段等方面对衰老骨骼肌蛋白质合成抵抗进行综述,为探究营养和运动等干预手段来预防和延缓骨骼肌衰老提供理论依据。 方法：应用计算机检索Pubmed数据库和中国期刊网2000年1月至2011年12月相关文献。英文检索词为“skeletal muscle, aging,resistance training,protein”;中文检索词为“骨骼肌衰老,抗阻运动,蛋白质”。纳入标准：①观点明确,论点论据可靠的实验性文章。②与骨骼肌衰老以及相关内容的文章。排除标准：①与文章目的无关的内容。②重复性研究。 结果与结论：随着年龄的增长,老年人骨骼肌对较低浓度的氨基酸敏感性下降,蛋白质合成速率减弱,即出现“蛋白质合成抵抗”。研究表明蛋白质补充及抗阻运动可促进老年人骨骼肌蛋白质合成。而抗阻运动并结合蛋白质补充对老年人骨骼肌蛋白质合成的影响更加明显。但是老年人补充蛋白质的量,抗阻运动的强度以及何时补充蛋白质仍需做进一步的研究。     

运动诱导的骨骼肌信号机制

背景：运动可通过增强骨骼肌葡萄糖转运及胰岛素活动,来调节葡萄糖内环境。明确这些复杂过程的分子机制将无疑为治疗提供更多的靶向,也为认识这些复杂的生理过程提供最基本的知识。 目的：综述运动诱导骨骼肌葡萄糖转运的分子信号机制。 方法：以“骨骼肌,运动,腺苷酸活化蛋白激酶,葡萄糖摄取,葡萄糖运载体4”为中文检索词,以“skeletal muscle, exercise, AMPK, glucose uptake, GLUT4”为英文检索词。应用计算机检索PubMed数据库和中文期刊全文数据库2011年11月前发表有关运动诱导骨骼肌信号机制的研究文献,排除重复性研究及Meta分析类文章。共保留39篇文献进行综述。 结果与结论：运动/收缩和胰岛素是骨骼肌葡萄糖转运的最有效的和生理相关的刺激,运动诱导的信号机制代表着糖尿病治疗药物学靶点发展的一个重要步骤。运动是通过增加骨骼肌葡萄糖摄取来改善葡萄糖内环境的,而运动诱导的葡萄糖摄取是有多种信号途径来介导的,包括腺苷酸活化蛋白激酶、非典型蛋白激酶C、钙调节依赖蛋白激酶及相对分子质量为160 000的Akt底物等。这些骨骼肌信号机制通过刺激葡萄糖运载体4活动增加来调节葡萄糖的转运。     

骨骼肌卫星细胞生长因子与运动训练的关系

背景：大运动量训练可以导致骨骼肌组织微细结构的损伤性变化, 而骨骼肌卫星细胞的激活、增殖与分化和肌肉组织损伤的修复有密切关系。 目的：文章从训练导致肌肉组织结构性损伤需要修复的客观实际出发,提出运动后骨骼肌结构的修复与骨骼肌卫星细胞生长因子之间存在某种依赖关系。 方法：由第一作者通过计算机网络检索中国期刊全文数据库(CNKI)和Medline数据库(2000/2010),检索词分别为“骨骼肌卫星细胞,生长因子,运动训练,骨骼肌超微结构”和“Skeletal muscle satellite cells,exercise,growth factor”。 共检索到97篇文章,按纳入和排除标准对文献进行筛选,共纳入23篇文章。从运动后骨骼肌组织修复与骨骼肌卫星细胞生长因子的激活作用机制进行总结,对两者间的联系进行分析。 结果与结论：大强度训练可以导致骨骼肌组织的损伤,而卫星细胞是运动后恢复期骨骼肌修复的关键,其生长因子也与训练方式等因素有关。目前在骨骼肌卫星细胞的生长因子与运动训练之间的联系还缺乏足够的认识与研究。     

循环miRNAs作为骨骼肌对运动反应与适应的生物标志物的可能性

背景：运动对机体产生刺激反应和生物学适应,对骨骼肌和心肌中的mi RNAs表达水平产生影响。不同运动方式能诱导不同的生物适应,比较而言离心收缩运动相对于向心收缩运动对肌肉刺激更大、生物学效应更积极。mi RNAs是短的非编码RNA,通过调节转录后的基因表达来影响生物过程。在大多数体液中有稳定存在的循环mi RNAs,对运动类型和强度有高度敏感性和特异性。目的：综述不同运动类型对循环mi RNAs表达水平的影响,分析了循环mi RNAs作为骨骼肌对运动反应与适应的生物标志物的可能性,以期为运动训练和运动促进健康过程中的干预提供参考。方法：检索有关骨骼肌mi RNAs、循环mi RNAs、运动对mi RNAs影响的文献,以“exercise;myomi RNAs;ci-mi RNAs;HIIT;biomarker”为关键词,在Pub Med、Web of Science等数据库进行检索;以“运动、mi RNAs、myomi RNAs、ci-mi RNAs、反应、生物标志物”为关键词,在CNKI、万方、维普等数据库进行检索。对检索获得的全部文献阅读、分析、判断,最终纳入符合标准的86篇文献进...     

骨骼肌减少症与运动训练对肌卫星细胞影响的研究现状及展望

BACKGROUND: The phenomenon of atrophy or reduction of muscle, causing degenerative changes of muscle functions, appears along with age. Sports training, in which muscle satellite cells are of great importance, is beneficial to increase in muscle mass and improvement of muscle function.  OBJECTIVE:To summarize regulatory mechanism of satellite cells in skeletal muscle mass; changes of satellite muscle cells in the degenerative process of muscle mass and strength; declining and reverse effects of sports training intervention; situations and problems of current research and prospective of the future.  METHODS: A computer-based online search was conducted in PubMed database by using the key words of “sarcopenia, skeletal muscle, satellite cells” from 1986 to 2015. The language was limited to English. The eligible papers were further analyzed and reviewed. RESULTS AND CONCLUSION: A total of 168 papers were screened. Finally, 39 papers were selected according to the titles and objectives. Skeletal muscle atrophy is shown as II type muscle fiber atrophy, and the II type muscle fiber satellite cell content decreases simultaneously. Exercise is beneficial to increase muscle mass and improve muscle function in older people. Both resistance and endurance trainings can increase the skeletal muscle, especially the II muscle fiber satellite cell content with a further increase in the satellite cell activation and proliferation. The number and activation degree of satellite cells are related to muscle aging, and satellite cells and proliferation factors regulate muscle cell formation. Therefore, future researches should not only focus on the increase of satellite cell bank, but also explore effective ways to promote the activation of satellite cells, such as exercise training, nutrition and drugs. 中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程     

运动重置骨骼肌生物钟调控线粒体质量控制的研究进展

<正>昼夜节律是指生物体的行为、生理和生化反应呈现出近24 h的节律活动,这些节律受生物钟系统控制调节。流行病学调查表明,长时间的光照或轮班工作扰乱了生物钟系统,导致生物钟基因节律性表达出现紊乱,不仅增加了罹患肿瘤^[1]、心血管疾病^[2]、糖尿病及肥胖等代谢系统疾病^[3]的风险,也可能造成骨骼肌质量^[4]及运动能力下降^[5]。     

Coordinate regulation of ribosome biogenesis and function by the ribosomal protein S6 kinase,a key mediator of mTOR function

Current understanding of the mechanisms by which cell growth is regulated lags significantly behind our knowledge of the complex processes controlling cell cycle progression. Recent studies suggest that the mammalian target of rapamycin (mTOR) pathway is a key regulator of cell growth via the regulation of protein synthesis. The key mTOR effectors of cell growth are eukaryotic initiation factor 4E-binding protein 1 (4EBP-1) and the ribosomal protein S6 kinase (S6K). Here we will review the current models for mTOR dependent regulation of ribosome function and biogenesis as well as its role in coordinating growth factor and nutrient signaling to facilitate homeostasis of cell growth and proliferation. We will place particular emphasis on the role of S6K1 signaling and will highlight the points of cross talk with other key growth control pathways. Finally, we will discuss the impact of S6K signaling and the consequent feedback regulation of the PI3K/Akt pathway on disease processes including cancer.     

运动激活骨骼肌卫星细胞:增龄性肌衰减症及肌肉损伤修复的运动预防和治疗

背景:骨骼肌是维持人体健康的主要组织,其衰减症会影响人们的健康和生活质量.肌卫星细胞是骨骼肌干细胞,受到运动刺激时激活增殖与分化,促进肌肉肥大,延缓肌衰减症的发生.目的:为增龄性肌衰减症、肌肉萎缩及肌肉损伤修复提供运动预防和治疗指导,同时为后续研究提供理论支撑.方法:在知网、PubMed、Web of Science等...     

Extracellular matrix adaptation of tendon and skeletal muscle to exercise

The extracellular matrix (ECM) of connective tissues enables linking to other tissues, and plays a key role in force transmission and tissue structure maintenance in tendons, ligaments, bone and muscle. ECM turnover is influenced by physical activity, and both collagen synthesis and metalloprotease activity increase with mechanical loading. This can be shown by determining propeptide and proteinase activity by microdialysis, as well as by verifying the incorporation of infused stable isotope amino acids in biopsies. Local tissue expression and release of growth factors for ECM such as IGF-1, TGF-beta and IL-6 is enhanced following exercise. For tendons, metabolic activity (e.g. detected by positron emission tomography scanning), circulatory responses (e.g. as measured by near-infrared spectroscopy and dye dilution) and collagen turnover are markedly increased after exercise. Tendon blood flow is regulated by cyclooxygenase-2 (COX-2)-mediated pathways, and glucose uptake is regulated by specific pathways in tendons that differ from those in skeletal muscle. Chronic loading in the form of physical training leads both to increased collagen turnover as well as to some degree of net collagen synthesis. These changes modify the mechanical properties and the viscoelastic characteristics of the tissue, decrease its stress-susceptibility and probably make it more load-resistant. The mechanical properties of tendon fascicles vary within a given human tendon, and even show gender differences. The latter is supported by findings of gender-related differences in the activation of collagen synthesis with exercise. These findings may provide the basis for understanding tissue overloading and injury in both tendons and skeletal muscle.     

Acute resistance exercise increases skeletal muscle angiogenic growth factor expression

AIMS: Both aerobic and resistance exercise training promote skeletal muscle angiogenesis. Acute aerobic exercise increases several pro-angiogenic pathways, the best characterized being increases in vascular endothelial growth factor (VEGF). We hypothesized that acute resistance exercise also increases skeletal muscle angiogenic growth factor [VEGF and angiopoietin (Ang)] expression. METHODS: Seven young, sedentary individuals had vastus lateralis muscle biopsies and blood drawn prior to and at 0, 2 and 4 h post-resistance exercise for the measurement of VEGF; VEGF receptor [KDR, Flt-1 and neuropilin 1 (Nrp1)]; Ang1 and Ang2; and the angiopoietin receptor--Tie2 expression. Resistance exercise consisted of progressive knee extensor (KE) exercise to determine one repetition maximum (1-RM) followed by three sets of 10 repetitions (3 x 10) of KE exercise at 60-80% of 1-RM. RESULTS: Resistance exercise significantly increased skeletal muscle VEGF mRNA and protein and plasma VEGF protein at 2 and 4 h. Resistance exercise increased KDR mRNA and Tie2 mRNA at 4 h and Nrp1 mRNA at 2 and 4 h. Skeletal muscle Flt-1, Ang1, Ang2 and Ang2/Ang1 ratio mRNA were not altered by resistance exercise. CONCLUSIONS: These findings suggest that acute resistance exercise increases skeletal muscle VEGF, VEGF receptor and angiopoietin receptor expression. The increases in muscle angiogenic growth factor expression in response to acute resistance exercise are similar in timing and magnitude with responses to acute aerobic exercise and are consistent with resistance exercise promoting muscle angiogenesis.     

Dynamic intravoxel incoherent motion imaging of skeletal muscle at rest and after exercise

The purpose of this work was to demonstrate the feasibility of intravoxel incoherent motion imaging (IVIM) for non‐invasive quantification of perfusion and diffusion effects in skeletal muscle at rest and following exercise. After IRB approval, eight healthy volunteers underwent diffusion‐weighted MRI of the forearm at 3 T and eight different b values between 0 and 500 s/mm² with a temporal resolution of 57 s per dataset. Dynamic images were acquired before and after a standardized handgrip exercise. Diffusion (D) and pseudodiffusion (D*) coefficients as well as the perfusion fraction (F_P) were measured in regions of interest in the flexor digitorum superficialis and profundus (FDS/FDP), brachioradialis, and extensor carpi radialis longus and brevis muscles by using a multi‐step bi‐exponential analysis in MATLAB. Parametrical maps were calculated voxel‐wise. Differences in D, D*, and F_P between muscle groups and between time points were calculated using a repeated measures analysis of variance with post hoc Bonferroni tests. Mean values and standard deviations at rest were the following: D*, 28.5 ± 11.4 × 10^?3 mm²/s; F_P, 0.03 ± 0.01; D, 1.45 ± 0.09 × 10^?3 mm²/s. Changes of IVIM parameters were clearly visible on the parametrical maps. In the FDS/FDP, D* increased by 289 ± 236% (p < 0.029), F_P by 138 ± 58% (p < 0.01), and D by 17 ± 9% (p < 0.01). A significant increase of IVIM parameters could also be detected in the brachioradialis muscle, which however was significantly lower than in the FDS/FDP. After 20 min, all parameters were still significantly elevated in the FDS/FDP but not in the brachioradialis muscle compared with the resting state. The IVIM approach allows simultaneous quantification of muscle perfusion and diffusion effects at rest and following exercise. It may thus provide a useful alternative to other non‐invasive methods such as arterial spin labeling. Possible fields of interest for this technique include perfusion‐related muscle diseases, such as peripheral arterial occlusive disease. Copyright © 2014 John Wiley & Sons, Ltd.     

Hsp70 expression in human skeletal muscle after exercise

Prolonged exercise of a sufficiently high intensity is thought to create physiological stress and to disturb cellular homeostasis, ultimately inducing cellular adaptations which enable the organism to better deal with any future exercise challenge. Heat shock proteins (hsp) are expressed when cells are exposed to different types of stress. In this study, we have investigated whether the expression of the heat inducible form of hsp70 is increased in human skeletal muscle cells after a single bout of exercise. Five untrained subjects performed an exercise bout at their individual anaerobic threshold for 30 min on a treadmill. Hsp70 mRNA concentration was significantly increased by a factor of four at 4 min post-exercise. Similarly high levels were also observed 30 min and 3 h after the end of exercise. Hsp70 protein concentration, on the contrary, did not change within 3 h after cessation of exercise. Thus, a single exercise bout in humans is able to increase the steady state concentration of hsp70 mRNA, but is probably not sufficient to have an effect on the already high basal level of its protein. The analysis of hsp70 mRNA is potentially useful as a method to detect stress in tissues with a high basal level of heat shock proteins.     

运动诱导骨骼肌线粒体生成中沉默信息调节因子1的作用

BACKGROUND:Silent information regulator factor-1 is an energy metabolism regulator newly received attention in sports science, which playing roles in skeletal exercise-induced muscle mitochondrial biogenesis with other regulatory factors. OBJECTIVE:To review the effect and mechanism of silent information regulator factor-1 on skeletal muscle mitochondrial biogenesis in exercise. METHODS: The PubMed database and Highwire database were retrieved with computer for the articles on exercise, silent information regulator factor-1 and skeletal muscle mitochondrial biogenesis from January 2000 to January 2013 with the key words of “SIRT1, AMPK, PGC-1α, mitochondrial biogenesis, skeletal muscle, exercise” in English. After primary search, the articles about the association between silent information regulator factor-1 and skeletal muscle mitochondrial biogenesis in exercise were selected. Articles on repeated experiment were excluded. RESULTS AND CONCLUSION:Totally 165 relevant articles were selected, and articles on repetitive research were excluded, so finaly 62 articles were included. As a NAD+-depended deacetylase, silent information regulator factor-1 induced skeletal muscle mitochondrial biogenesis by up-regulated peroxisome proliferator-activated receptor coactivator after activated during exercise. The molecular mechanism involved adenosine monophosphate-activated protein kinase and hypoxia-inducible factor 2α. In recent years, the effect of silent information regulator factor-1 on skeletal muscle mitochondrial biogenesis was doubt, the researchers though that silent information regulator factor-1 was not required for exercise-induced muscle mitochondrial biogenesis.Silent information regulator factor-1 plays an important role in exercise-induced muscle mitochondrial biogenesis. But protein and activity detection methods are different in experimental results.