维生素E对离心运动大鼠骨骼肌超微结构的影响

背景：维生素E作为一种抗氧化剂,具有清除自由基的功效,可减轻运动中抗氧化酶所受的自由基损伤,减缓疲劳出现,从而提高运动能力。 目的：通过维生素E对骨骼肌运动性损伤的干预,探讨其对骨骼肌运动性损伤形态学变化的影响,为骨骼肌运动性损伤的形态学研究和抗损伤机制的探索提供实验依据。 设计、时间及地点：随机分组,动物实验,于2007-05/10在沈阳体育学院国家体育总局重点实验室和中国医科大学电镜中心完成。 材料：雄性SD大鼠16只,随机均分为对照组、运动组、生理盐水组、维生素E组。 方法：维生素E组于实验前1 d腹腔注射维生素E胶丸,注射量为1.0~1.2 mg/kg,总量为4 mL/kg,每8 h注射1次,共4次。生理盐水组以生理盐水为对照,注射方式、注射量及处死时间同维生素E组。运动组只进行运动,不给予药物或生理盐水,对照组仅为常规饲养,无任何干预。采用一次力竭性下坡跑运动建造大鼠损伤模型,运动结束后,取大鼠右侧肱三头肌,制做电镜标本。 主要观察指标：肌原纤维和肌节排列情况;Z线异常变化;细胞膜、细胞核、线粒体、肌浆网、T小管、卫星细胞等形态学改变。 结果：补充维生素E组后,骨骼肌损伤的超微结构改变有明显的改善,虽然肌浆网尚有水肿表现,但肌纤维排列基本整齐,Z线明暗带清晰,细胞核清楚。 结论：补充维生素E可有效地减少离心运动对骨骼肌肌纤维损伤的形态学改变,肌纤维排列更加整齐、肌节更加清晰,其作用可能与维生素E的抗氧化和促进蛋白质的合成功能等因素有关。     

热应激适应与骨骼肌损伤保护

摘要：大强度运动易导致骨骼肌损伤,并且骨骼肌损伤发生的机制比较复杂,涉及许多生理因素。人体在热应激状态下,会发生一定的应激性生理反应,并产生热休克蛋白,热休克蛋白是生物细胞在受到各种理化因素刺激下产生的一类高度保守的蛋白质,作为一种保护性蛋白,在维持细胞的自稳、保护细胞免受各种应激伤害中发挥了重要作用,并在骨骼肌中出现明显的强度依赖性。热应激适应对维持骨骼肌细胞正常功能起重要作用。     

力竭运动大鼠接受复方壮阳中药干预后端脑神经递质的变化

实验观察了以人参、丹参、川芎、五味子、肉桂、鹿茸、巴戟天和蛤蚧为主要成分的复方壮阳中药对力竭运动大鼠4种不同功能状态下端脑单胺和氨基酸类神经递质变化的影响。结果发现,训练服药后大鼠运动1 h后,多巴胺、5-羟吲哚乙酸和γ-氨基丁酸含量明显降低、多巴胺/5羟色胺明显升高,谷氨酸含量和谷氨酸/γ-氨基丁酸极显著升高;力竭即刻,5羟色胺含量和5羟色胺/5-羟吲哚乙酸明显降低,多巴胺/5羟色胺和谷氨酸含量极显著升高;运动力竭恢复12 h后,5羟色胺,5羟色胺/5-羟吲哚乙酸含量仍然极明显下降,多巴胺/5羟色胺,谷氨酸含量和γ-氨基丁酸含量明显升高。证实复方壮阳中药制剂能够改变力竭运动大鼠与恢复过程中端脑枢神经递质含量的变化,改善中枢神经系统的兴奋性。     

运动对骨骼肌脂肪代谢与胰岛素敏感性的影响

随着分子生物学的发展,对胰岛素抵抗机制的认识也在逐渐深入,同时也促进了运动影响胰岛素抵抗的机制研究,文章主要就脂肪酸分解对于胰岛素敏感性的调节作用,运动对于肥胖个体胰岛素敏感性作用,以及运动诱导的肌肉细胞内脂肪酸分解的改变对于胰岛素敏感性的作用等进行探讨,以其为糖尿病和胰岛素抵抗患者的运动处方干预提供理论依据和参考。     

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。     

周围神经损伤大鼠骨骼肌运动终板的变化

本研究观察了周围神经损伤大鼠骨骼肌运动终板的改变,现报告如下. 1 材料与方法 1.1材料(1)动物与分组:24只10周龄SD雄性大鼠,质量220-250 g,常规喂养;随机分为正常对照组、去神经组、制动组,每组8只.     

绿茶多酚的神经保护作用

绿茶多酚多方位的生物学效应包括抗氧化损伤、清除自由基、NAO-B抑制作用、DAT的抑制作用、激活PKC和ERK1/2细胞存活信号转导通路等,提示该类药物在神经保护尤其是治疗帕金森病中具有良好前景。     

离心运动对大鼠骨骼肌细胞增殖和波形蛋白表达的时序性影响

背景：骨骼肌损伤后是通过肌卫星细胞的增殖形成新核来生长和修复的,但关于骨骼肌细胞增殖和波形蛋白表达的关系很少报道。 目的：探讨骨骼肌细胞增殖与波形蛋白表达的关系以及运动性骨骼肌微损伤后修复的机制。 设计、时间和地点：随机对照动物实验,于2007-12/2008-09在湖南师大运动人体科学实验中心完成。 材料：健康成年8周龄雄性SD大鼠50只,随机分成对照组和运动后即刻、运动后3 h、运动后24 h和运动后48 h组,每组10只大鼠。 方法：运动组大鼠进行重复3 d的力竭性离心运动,力竭模型采用跑台运动,速度为16 m/min,坡度为-16°,持续运动至力竭,对照组为正常大鼠,未做运动。 主要观察指标：运动组分别于运动后即刻,3,24,48 h取材,对照组一次性取材,免疫组织化学法检测各组大鼠肱三头肌内侧头不同恢复时相增殖细胞核抗原PCNA的表达和波形蛋白的表达。 结果：骨骼肌细胞增殖出现时序性变化,运动后即刻增殖指数显著大于对照组,运动后24 h达到峰值,运动后48 h增殖指数有所下降。骨骼肌细胞中波形蛋白表达出现时序性,而且其免疫反应分值的时序性与增殖指数出现一致性,但与增殖指数不具有相关性。 结论：3 d重复性力竭离心运动后骨骼肌细胞增殖和波形蛋白的表达出现时序性变化。波形蛋白的表达与肌细胞增殖具有一定的关系,但不是惟一的影响的因素。     

长期耐力运动对大鼠腓肠肌的损伤及一氧化氮的调节作用******☆

背景：长期耐力运动常引起肌肉损伤，但其机制尚不清楚。 目的：观察长期游泳运动对骨骼肌的损伤作用以及内源性一氧化氮的调节作用。 设计、时间及地点：随机对照动物实验，于2006-12/2007-04在江苏大学基础医学与医学技术学院营养科学研究室完成。 材料：健康雌性SD大鼠60只，体质量190~250 g，用于制备大鼠游泳模型；L-NG-硝基精氨酸甲酯(L-NAME)用于抑制大鼠体内一氧化氮的生成。 方法：60只大鼠随机数字表法分为静息组、运动组、静息联合L-NAME组和运动联合L-NAME组，每组15只。在静息联合L-NAME组和运动联合L-NAME组大鼠的饮水中添加一氧化氮合酶拮抗剂L-NAME，1 g/L。运动组和运动联合L-NAME组大鼠游泳5 d/周，2 h/d。 主要观察指标：3个月后取各组大鼠腓肠肌测定氮氧化物(NOx)的含量；苏木精-伊红染色观察腓肠肌的形态变化。 结果：纳入大鼠60只，其中静息联合L-NAME组死亡5只、运动组死亡2只、运动联合L-NAME组死亡6只，死亡原因包括自然死亡、溺水或药物长期作用，进入结果分析47只。①运动组NOx含量高于静息组（P < 0.01）。运动联合L-NAME组NOx含量低于运动组（P < 0.05），但高于静息联合L-NAME组（P < 0.05）。②腓肠肌的肌纤维较细，数量较多，染色较浅，肌纤维结构完整；运动组腓肠肌纤维明显粗大，深染，偶见肌纤维有断裂，少量巨噬细胞浸润；静息联合L-NAME组肌纤维有分支，结缔组织增生；运动联合L-NAME组也可见运动组中的变化，且肌纤维断裂和巨噬细胞浸润现象更明显，还表现为肌纤维坏死溶解，肌纤维有分支。 结论：长期游泳运动造成了骨骼肌纤维的损伤；运动诱导产生的一氧化氮对运动性损伤可能有保护作用。     

骨骼肌细胞中热休克蛋白72表达与运动及肌肉损伤

背景：运动应激诱导的骨骼肌细胞中热休克蛋白72的表达与肌肉损伤程度大小有关。 目的：综述骨骼肌细胞中热休克蛋白72在运动中的表达及其与运动的相互关系,并对其在运动医学领域中潜在的研究价值进行了探讨。 方法：应用计算机检索国家科技文献图书中心1990-01/2009-10的相关文献,检索词“heat shock protein 72, skeletal muscle”,限定文章语言种类为“English”;同时计算机检索万方数据库1994-01/2009-10的相关文献,检索词“热休克蛋白72,骨骼肌”,限定文章语言种类为中文。并通过手工检索相关文献。纳入具有原创性,论点论据可靠,观点明确,分析全面,文献主题内容与此论文联系密切的文章。排除实验设计不合理的文章及观点模糊的综述。 结果与结论：热休克蛋白广泛存在于生物界,对机体具有保护作用。运动应激诱导骨骼肌细胞中热休克蛋白72mRNA 的表达及热休克蛋白72的合成与运动负荷量、运动强度和持续时间密切相关,尤其是运动强度。热休克蛋白72在骨骼肌细胞受到过强应激时,其合成量非但没有减弱相反明显增加。作为肌肉应激指标,热休克蛋白72提供了运动引起的骨骼肌细胞功能变化的重要信息,对预防过度训练和确定随后的训练计划可能是一个很好的量化指标。     

无氧间歇训练对大鼠骨骼肌、心肌、肝脏自由基代谢的影响

背景：无氧间歇训练法是一种被广泛应用的重要训练方法，有关此训练对机体自由基代谢及其抗氧化酶活性影响的系统性研究较少。 目的：观察无氧间歇训练对大鼠体内自由基代谢的影响。 设计、时间及地点：随机对照动物实验，于2008-03/05在徐州师范大学运动生理实验室完成。 材料：健康雄性SD大鼠32只，体质量230~270 g，随机分为安静对照组，间歇训练对照组，间歇运动即刻组，间歇训练即刻组，每组8只。 方法：安静对照组不进行训练，间歇训练对照组和间歇训练即刻组进行跑步运动，以坡度10°，速度26.8 m/min运动1 min，后以坡度为0，速度5 m/min休息3 min，每天连续20次不间断，5 d/周，运动6周。间歇运动即刻组只在第6周最后一天进行一次运动。 主要观察指标：6周运动结束后即刻麻醉下处死各组大鼠，测定其骨骼肌，心肌，肝脏超氧化物歧化化酶，谷胱甘肽过氧化物酶，过氧化氢酶，丙二醛。 结果：①训练组运动后即刻各组织超氧化物歧化酶活性均显著高于间歇运动即刻组(P < 0.05)。②间歇运动即刻组股四头肌、心肌谷胱甘肽过氧化物酶活性显著低于安静对照组(P < 0.05)，丙二醛含量显著高于安静对照组(P < 0.05)，股四头肌和肝脏过氧化氢酶活性显著高于安静对照组(P < 0.05)。③间歇训练即刻组股四头肌、心肌谷胱甘肽过氧化物酶活性显著高于间歇运动即刻组(P < 0.05)，丙二醛含量明显低于间歇运动即刻组(P < 0.05)，股四头肌和心肌过氧化氢酶活性显著高于间歇运动即刻组(P < 0.05)。 结论：无氧间歇训练可以使机体抗氧化酶活性发生适应性变化，自由基清除能力增强。     

Effect of simvastatin on passive strain‐induced skeletal muscle injury in rats

Introduction: HMG‐CoA reductase inhibitors are the most frequently prescribed drugs for treatment of lipid imbalance, but they have side effects, such as myopathy. Our aim was to assess the effect of simvastatin on the inflammatory process induced by skeletal muscle injury. Methods: Rats were divided into experimental groups [control group, simvastatin (20 mg/kg) group, group treated with simvastatin (20 mg/kg) and subjected to injury, and group subjected to injury only]. Histological analysis and analyses of creatine kinase activity and C‐reactive protein were performed. Results: Animals treated with simvastatin exhibited significantly greater morphological and structural skeletal muscle damage in comparison to the control group and injured animals without treatment. Conclusions: Although simvastatin has a small anti‐inflammatory effect in the early stage after a muscle strain injury, the overall picture is negative, as simvastatin increases the extent of damage to muscle morphology. Further studies are needed. Muscle Nerve, 2012     

Preservative solution for skeletal muscle biopsy samples

Context:

Muscle biopsy samples must be frozen with liquid nitrogen immediately after excision and maintained at -80°C until analysis. Because of this requirement for tissue processing, patients with neuromuscular diseases often have to travel to centers with on-site muscle pathology laboratories for muscle biopsy sample excision to ensure that samples are properly preserved.

Aim:

Here, we developed a preservative solution and examined its protectiveness on striated muscle tissues for a minimum of the length of time that would be required to reach a specific muscle pathology laboratory.

Materials and Methods:

A preservative solution called Kurt-Ozcan (KO) solution was prepared. Eight healthy Sprague-Dawley rats were sacrificed; striated muscle tissue samples were collected and divided into six different groups. Muscle tissue samples were separated into groups for morphological, enzyme histochemical, molecular, and biochemical analysis.

Statistical method used:

Chi-square and Kruskal Wallis tests.

Results:

Samples kept in the KO and University of Wisconsin (UW) solutions exhibited very good morphological scores at 3, 6, and 18 hours, but artificial changes were observed at 24 hours. Similar findings were observed for the evaluated enzyme activities. There were no differences between the control group and the samples kept in the KO or UW solution at 3, 6, and 18 hours for morphological, enzyme histochemical, and biochemical features. The messenger ribonucleic acid (mRNA) of β-actin gene was protected up to 6 hours in the KO and UW solutions.

Conclusion:

The KO solution protects the morphological, enzyme histochemical, and biochemical features of striated muscle tissue of healthy rats for 18 hours and preserves the mRNA for 6 hours.     

Electrical stimulation impairs early functional recovery and accentuates skeletal muscle atrophy after sciatic nerve crush injury in rats

Neuromuscular recovery after peripheral nerve lesion depends on the regeneration of severed axons that re‐establish their functional connection with the denervated muscle. The aim of this study was to determine the effects of electrical stimulation (ES) on the neuromuscular recovery after nerve crush injury in rats. Electrical stimulation was carried out on the tibialis anterior (TA) muscle after sciatic nerve crush injury in a rat model. Six ES sessions were administered every other day starting from day 3 postinjury until the end of the experiment (day 14). The sciatic functional index was calculated. Muscle excitability, neural cell adhesion molecule (N‐CAM) expression, and muscle fiber cross‐sectional area (CSA) were accessed from TA muscle. Regenerated sciatic nerves were analyzed by light and confocal microscopy. Both treated (crush+ES) and untreated (crush) groups had their muscle weight and CSA decreased compared with the normal group (P < 0.05). Electrical stimulation accentuated muscle fiber atrophy more in the crush+ES than in the crush group (P < 0.05). N‐CAM expression increased in both crush and crush+ES groups compared with the normal group (P < 0.05). Regenerated nerves revealed no difference between the crush and crush+ES groups. Nevertheless, functional recovery at day 14 post‐injury was significantly lower in crush+ES group compared with the crush group. In addition, the crush+ES group had chronaxie values significantly higher on days 7 and 13 compared with the crush group, which indicates a decrease in muscle excitability in the crush+ES animals. The results of this study do not support a benefit of the tested protocol of ES during the period of motor nerve recovery following injury. Muscle Nerve, 2010     

Localization of protein kinase C in human skeletal muscle.

The immunolocalization of protein kinase C (PKC) isozymes alpha, beta I and beta II, was investigated in human skeletal muscle. All three isozymes were present on the muscle fiber surface membrane and within the muscle fibers. The alpha-isozyme was most clearly delineated on the surface membrane of the muscle fiber and on small blood vessels in the connective tissue. The axons of myelinated intramuscular nerves stained intensely for the beta I isozyme, whereas the endoneurial connective tissue reacted more strongly for the alpha- and beta II-isozymes. PKC isozymes may regulate intracellular signal transduction in human skeletal muscle, as in the other tissues, but their exact role in muscle remains unknown.     

骨骼肌细胞凋亡的影响因素：低氧训练效应

在外界低氧环境的刺激下，骨骼肌细胞易处于缺氧状态，这种缺氧趋势与细胞凋亡存在着某种直接或者间接的联系。在一定强度的运动中，机体的组织和细胞处于一种相对缺血和缺氧的状态，肌肉细胞内氧分压降到很低水平时，在骨骼肌组织中也能检测到细胞凋亡的发生。但有关低氧训练对骨骼肌细胞凋亡的影响目前尚未见报道，低氧训练对骨骼肌细胞凋亡会产生何种影响，骨骼肌细胞凋亡与不同低氧训练刺激时间和方式的关系如何，有必要进行深入研究和探讨。     

Anabolic steroids induce injury and apoptosis of differentiated skeletal muscle

Apoptosis is an active form of cellular death, or suicide, which plays an important physiologic role during organ development and in cellular turnover in differentiated tissues. Apoptosis has also been demonstrated to occur in several organs in response to hypoxic/ischemic, oxidative, or drug-induced injury and is thus involved in disease pathogenesis. However, it is generally assumed that apoptosis does not occur in differentiated skeletal muscle. Apoptosis has been demonstrated in differentiated myocardial muscle, neonatal skeletal muscle, and skeletal myoblasts in response to injury. We therefore studied differentiated murine C2 skeletal muscle cells that have been injured by supraphysiologic doses (>10 μM) of an anabolic steroid, stanozolol. Stanozolol-injured muscle cells exhibited pathologic features suggestive of apoptosis: cytoplasmic shrinkage and chromatin condensation. Muscle cells also showed positive in situ nick-end labeling of nuclear chromatin, indicating DNA strand breakage. Staining with the DNA-binding dye 33342 (bisbenzimide) also showed chromatin changes characteristic of apoptotic nuclei. Total protein levels measured at 4 and 24 hr post-stanozolol injury was not significantly decreased, indicating absence of cell lysis. Cellular ATP levels (nmol ATP/mg protein) of stanozolol-injured muscle cells, measured 4 and 24 hr postinjury, also did not change significantly. In contrast, necrotic muscle cells, injured by the calcium ionophore A23187 (2 μM), showed a progressive decline in total protein and ATP levels. This study supports two other histologic studies that showed evidence of apoptosis in differentiated skeletal muscle fibers. Our data further suggest that during the early stages of apoptosis, but not necrosis, cellular energy metabolism is preserved. J. Neurosci. Res. 47:186–197, 1997. © 1997 Wiley-Liss, Inc.     

机械生长因子对骨骼肌卫星细胞的调控

背景：机械生长因子作为胰岛素样生长因子1的一个亚型,有促进肌卫星细胞增殖,抑制分化的功能,因此利用外源性机械生长因子类物质对卫星细胞进行干预,并对其调控的分子机制进行研究,可以为骨骼肌疾病的临床治疗及组织工程学的研究提供新的思路。 目的：综合分析机械生长因子对骨骼肌卫星细胞的调控及其治疗作用。 方法：采用计算机检索中国期刊全文数据库及PubMed数据库1995/2009相关文献,中文检索词为“机械生长因子,骨骼肌卫星细胞”;英文检索词为“MGF”。纳入标准：具有原创性的研究论文,其研究目的或方法具有代表性。排除标准：重复性研究及与课题相关性较弱的文献。 结果与结论：机械生长因子有激活肌卫星细胞,促进细胞增殖,抑制肌管融合及促进卫星细胞迁移的功能。机械生长因子对骨骼肌损伤修复、神经损伤修复及心肌梗死治疗等方面有积极的临床意义。外源性机械生长因子类物质对肌组织修复、再生方面的作用,有可能为运动损伤的康复治疗开辟新的途径,并且对细胞移植具有一定的临床意义。     

Functional evaluation of acute vincristine toxicity in rat skeletal muscle

Vincristine sulfate (VCR) was administered intravenously to rats at doses of 0.25, 0.5, and 0.75 mg/kg. During the first week following VCR treatment, extensor digitorum longus (EDL) muscle contraction strength and fiber electrophysiologic parameters were measured. At all doses tested, VCR strongly reduced twitch and tetanic tension. EDL fiber resting membrane potential was affected in a dose-dependent manner, and membrane depolarization was associated with the loss of excitability. Local membrane hyperpolarization by intracellular current application restored the capacity to produce action potential (AP). However, to elicit APs with a normal rate of rise, polarizing current had to be maintained for 3-5 minutes, indicating that the removal of Na+ channel inactivation followed a slow kinetics. Minor alterations in spontaneous synaptic transmission and in evoked transmission during high-frequency repetitive stimulation were seen only at the highest dose. It is suggested that VCR impairs skeletal muscle function by affecting primarily the contractile apparatus, whereas sarcolemmal alterations are evident at increased doses of the drug.     

Mass-dependent decline of skeletal muscle function in cancer cachexia

CD2F1 mice were inoculated with C26 adenocarcinoma cells, followed by assessment of ex vivo muscular function. Muscles from tumor-bearing mice had a significantly lower force output during a single maximal contraction and during repeated contractions than control muscles. The relative force output, however, did not differ when corrected for muscle mass. Thus, cachexia significantly reduces absolute skeletal muscle function, but muscle "quality" appears unaltered.