The biological mechanisms of cancer-related skeletal muscle wasting: the role of progressive resistance exercise

Cancer results in perturbations in skeletal muscle protein metabolism leading to muscle wasting. Although severe wasting is seen primarily in persons with advanced malignancies, a number of cancer patients show some degree of wasting at presentation. Although cancer-related skeletal muscle wasting is attributable, in part, to decreased muscle protein synthesis, its primary cause appears to be increased muscle protein degradation. Although several proteolytic systems may be involved, compelling evidence suggests that the major system responsible for skeletal muscle protein degradation in cancer is the ATP-dependent ubiquitin- proteasome system. Other contributing factors include proinflammatory cytokines and the tumor-released proteolysis-inducing factor. Decreased physical activity and decreased nutritional intake may also play a role. Cancer-related skeletal muscle wasting is clinically significant because of its profound effects on functional outcomes and quality of life. Nevertheless, no specific interventions have proved to be effective in preventing or reversing the problem. Interventions such as nutritional supplementation and appetite stimulants are only partially helpful. A nonpharmacologic intervention that may attenuate cancer-related skeletal muscle wasting is progressive resistance exercise training (PRT). PRT is a potent stimulus of growth in muscle mass and strength. PRT may attenuate cancer-related skeletal muscle wasting by downregulating the activity of proinflammatory cytokines and by increasing the phosphorylation of intramuscular amino acid-signaling molecules. This article discusses several cancer-related skeletal muscle wasting mechanisms and proposes how PRT might attenuate muscle wasting by counteracting some of these mechanisms.     

Challenging the role of pH in skeletal muscle fatigue.

Muscle fatigue is frequently defined as a temporary loss in force- or torque-generating ability because of recent, repetitive muscle contraction (1). The development of this temporary loss of force is a complex process and results from the failure of a number of processes, including motor unit recruitment and firing rate, chemical transmission across the neuromuscular junction, propagation of the action potential along the muscle membrane and T tubules, Ca2+ release from the sarcoplasmic reticulum (SR), Ca2+ binding to troponin C, and cross-bridge cycling (for detailed reviews, see Bigland-Ritchie and Woods(1), McLester(2), and Favero(3)). Muscle fatigue may limit the time a person can stand, the distance a person can ambulate, or the number of stairs a person can ascend or descend. In practical terms, however, we cannot know what actually leads to a decline in function for a given patient. For a phenomenon that may have profound clinical implications, muscle fatigue often receives inadequate attention in physiology textbooks, many of which contain a page or less of information on the entire topic (4-8). In addition, many textbooks report that muscle fatigue is mainly the result of a decrease in pH within the muscle cell due to a rise in hydrogen ion concentration ([H+]) resulting from anaerobic metabolism and the accumulation of lactic acid (6-8). Recent literature, however, contradicts this assertion (9-10). The purpose of this update, therefore, is to provide a brief review of the role of pH in the development of muscle fatigue.     

肌肉运动与骨骼肌细胞的凋亡

背景:不少医学研究表明,细胞凋亡能导致大量自由基增多、Ca~(2+)浓度升高、线粒体膜电位下降引起运动能力的下降.因此,研究细胞凋亡与运动训练的关系意义重要.目的:总结与探索关于肌肉运动与骨骼肌细胞凋亡的相关问题.方法:计算机检索中国期刊全文数据(网址http://dlib.cnki.net/kns50/index.aspx)及PubMed数据库(网址http://www.ncbi.nlm.nih.gov/pubmed/)1990-01/2009-06期间的相关文章,检索词为"肌肉运动,骨骼肌细胞凋亡,muscle exercise,apoptosis in the skeletal muscle".纳入与肌肉运动与骨骼肌细胞的凋亡研究现状与发展密切相关.①有关骨骼肌细胞凋亡的研究.②运动与骨骼肌细胞凋亡研究.③运动诱发骨骼肌细胞凋亡的基因调控研究.④骨骼肌细胞凋亡的分子机制研究.⑤同一领域选择近期发表或在权威杂志上发表的文章.排除重复性研究.结果与结论:运动后,正常肌肉中或是病理状态下的肌肉中骨骼肌细胞都会出现凋亡,凋亡的形态学表现与普通凋亡细胞相似,即核固缩、质膜发泡、细胞器紧缩,凋亡小体形成,其凋亡过程大致可分为3个阶段,即启始阶段、效应阶段和降解阶段.骨骼肌细胞凋亡的增加是导致运动性疲劳的重要原因.目前国内外对骨骼肌细胞凋亡的基因调控研究主要是从凋亡调控因子Bcl-2蛋白、肿瘤坏死因子α及死亡蛋白酶半胱氨酸天冬氨酸酶着手.bcl-2基因蛋白的抗凋亡作用主要是通过阻止线粒体通透性转换孔的开放,阻止线粒体释放促凋亡蛋白、防止线粒体膜脂质过氧化以及线粒体基质Ca2+释放实现的.肿瘤坏死因子家族在启动死亡因子及其受体途径中起重要作用,此途径的启动依赖于死亡配体与死亡受体相结合,激活半胱氨酸天冬氨酸酶,导致细胞凋亡.通过研究探索运动强度与骨骼肌细胞凋亡及坏死的界限关系,有利于在运动中认识运动性疲劳产生的机制及有效消除疲劳.     

The potential and the pitfalls of beta-adrenoceptor agonists for the management of skeletal muscle wasting

The beta-adrenergic signaling pathway represents a novel therapeutic target for skeletal muscle wasting and weakness due to its role in the mechanisms controlling protein synthesis and degradation and in modulating fiber type. Stimulation of the pathway with beta-adrenoceptor agonists (beta-agonists) has therapeutic potential for muscle wasting disorders including: sarcopenia, cancer cachexia, disuse and inactivity, unloading or microgravity, sepsis and other metabolic disorders, denervation, burns, HIV-AIDS, chronic kidney or heart failure, and neuromuscular diseases. However, there are also pitfalls associated with beta-agonist administration and clinical applications have so far been limited, largely because of cardiovascular side effects. In rats and mice, newer generation beta-agonists (such as formoterol) can elicit an anabolic response in skeletal muscle even at very low doses, with reduced effects on the heart and cardiovascular system compared with older generation beta-agonists (such as fenoterol and clenbuterol). However, the potentially deleterious cardiovascular side effects of beta-agonists have not been obviated completely and so it is important to refine their development and therapeutic approach in order to overcome these obstacles. This review describes the therapeutic potential of stimulating the beta-adrenergic signaling pathway with beta-agonists, highlighting the beneficial effects on skeletal muscle structure and function and identifying some of the pitfalls associated with short- and long-term beta-agonist administration. The review also identifies some important, but as yet unanswered questions, regarding the importance of beta-adrenoceptor signaling in muscle health and disease and the strategies needed to improve the efficacy and safety of beta-agonists for muscle wasting disorders.     

Muscle-specific expression of IGF-1 blocks angiotensin II-induced skeletal muscle wasting

Advanced congestive heart failure is associated with activation of the renin-angiotensin system and skeletal muscle wasting. We previously showed that angiotensin II infusion in rats produces cachexia secondarily to increased muscle proteolysis and also decreases levels of circulating and skeletal muscle IGF-1. Here we show that angiotensin II markedly downregulates phospho-Akt and activates caspase-3 in skeletal muscle, leading to actin cleavage, an important component of muscle proteolysis, and to increased apoptosis. These changes are blocked by muscle-specific expression of IGF-1, likely via the Akt/mTOR/p70S6K signaling pathway. We also demonstrate that mRNA levels of the ubiquitin ligases atrogin-1 and muscle ring finger-1 are upregulated in angiotensin II-infused WT, but not in IGF-1-transgenic, mice. These findings strongly suggest that angiotensin II downregulation of IGF-1 in skeletal muscle is causally related to angiotensin II-induced wasting. Because the renin-angiotensin system is activated in many catabolic conditions, our findings have broad implications for understanding mechanisms of skeletal muscle wasting and provide a rationale for new therapeutic approaches.     

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。     

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.     

Nonthermal ultrasound and exercise in skeletal muscle regeneration

OBJECTIVE: To determine whether continuous nonthermal therapeutic ultrasound (US) and low-intensity exercise (Ex) influence skeletal muscle regeneration after a standardized contusion injury in an animal model. DESIGN: Randomized controlled trial with blinded comparisons in a 2 x 2 factorial (US by Ex) design. SETTING: Animal care facility and exercise physiology biochemistry laboratory. ANIMALS: Twenty male Wistar rats (age, 8 mo) received a reproducible bilateral contusion injury to the gastrocnemius muscles. Ten gastrocnemius muscles from 5 noninjured, nontreated rats provided baseline control data. INTERVENTIONS: US (continuous duty cycle, 3 MHz; intensity, 0.1 W/cm2 ; transducer, 1cm2 ; duration, 5 min/d; duty cycle, 100%) and exercise (20 min/d of low-intensity treadmill walking at 14 m/min). Gastrocnemius muscles from injured rats received exercise treatment alone (Ex + NoUS), exercise and US treatment (Ex + US), US treatment alone (NoEx + US), and no treatment (NoEx + NoUS). MAIN OUTCOME MEASURES: Ninety-six-hour postinjury muscle mass, contractile protein concentration, fiber cross-sectional area, number of nuclei per fiber, and myonuclear density. RESULTS: Myonuclei per fiber were statistically greater in injured than in noninjured gastrocnemius muscle (P < .05). There were no statistical differences (P > .01) among the 4 injured treatment groups for any of the outcome measures chosen as biomarkers of skeletal muscle regeneration. CONCLUSIONS: There is no evidence that the specific continuous US and Ex protocols investigated enhanced skeletal muscle regeneration after contusion injury.     

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。     

Role of ubiquitin-proteasome pathway in skeletal muscle wasting in rats with endotoxemia

OBJECTIVE: To investigate the mechanism of muscle protein breakdown under endotoxemia condition. DESIGN: Randomized, controlled, animal experiment in a hospital institute. SETTING: Experimental laboratory. INTERVENTION: Either saline or endotoxin (Escherichia coli O(55)B(5), 10 mg/kg) were administered into the peritoneal cavity in rats. MEASUREMENTS AND MAIN RESULTS: The rate of total protein breakdown was increased by 29% and 61% in extensor digitorum longus muscle at 2 hrs and 6 hrs, whereas the myofibrillar proteolytic rate was increased by 155%, 222%, and 40% at 2 hrs, 6 hrs, and 12 hrs, respectively, in the endotoxin treatment group compared with that of the pair-fed normal control group. Meanwhile, compared with the normal control group, the level of 2.4-kilobase (kb) messenger RNA (mRNA) for ubiquitin in extensor digitorum longus muscle in rats was increased by 153% and 470% at 2 hrs and 6 hrs. There were 87% and 117% increases in 1.2-kb mRNA for E2-14K, and 89% and 168% increase in RC2 mRNA expression in extensor digitorum longus muscle in endotoxemic rats than normal control rats at 2 hrs and 6 hrs after injection of endotoxin peritoneally. The tumor necrosis factor-alpha and interleukin-6 concentrations in rat plasma progressively increased after endotoxin treatment, but tumor necrosis factor-alpha peaked at the 2-hr time point, whereas interleukin-6 peaked at 12 hrs. Endotoxin administration resulted in a marked increase in endotoxin level at 2 hrs and 6 hrs. No significant change was observed in soleus muscle after endotoxin injection. A significantly positive correlation was found between the net release of 3-methylhistidine and respective values of endotoxin, intensity of mRNA expression of 2.-kb ubiquitin, 1.2-kb E2-14K, and subunit RC2 in extensor digitorum longus muscle (r =.9882, .9731, .9653, .9814, p <.05). However, no significant correlation was seen between tumor necrosis factor-alpha or interleukin-6 and respective values of 3-methylhistidine, mRNA expression of 2.4-kb ubiquitin, 1.2-kb E2-14K, and subunit RC2 (r =.3580, .4521, .5277, .4931, p >.05; r =.3950, .1767, .2136, .2519, p >.05, respectively.) in soleus muscle. CONCLUSIONS: Endotoxemia can induce enhancement of skeletal muscle protein breakdown, mainly involving myofibrillar protein and white, fast-twitch extensor digitorum longus muscle. Ubiquitin-proteasome proteolytic pathway plays an important and major role in skeletal muscle proteolysis. Endotoxin, tumor necrosis factor-alpha, and interleukin-6 can directly or indirectly regulate muscle protein breakdown.     

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.     

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。     

银杏黄酮对骨骼肌抗疲劳能力的影响

目的:分析银杏黄酮对大鼠背斜方肌微动脉血液循环、腓肠肌收缩能力及小鼠运动能力的影响。方法:实验于2004-02在广西师范大学体育学院完成。银杏黄酮由桂林思特新技术公司天然植物制品厂生产,银杏黄酮含量24%,银杏内酯含量6%,符合国际标准。①大鼠背斜方肌微动脉血液循环的观察:选用SD大鼠40只,随机数字表法分为空白对照组、银杏黄酮2.0,3.0,4.0g/L浓度组,10只/组。各组大鼠均制备游离肌肉标本,游离面固定于特制灌流盒上,用林格氏液灌流,连续观察管径为15～20μm的横向微动脉30min,分别于观察处滴注0.1g/L的去甲肾上腺素障碍液50μL。当血管出现收缩时,银杏黄酮2.0,3.0,4.0g/L浓度组分别滴注对应的银杏黄酮溶液1mL,空白对照组则滴注等量的生理盐水。测量微动脉血管口径的变化以及血管流态的变化。②大鼠腓肠肌肌肉收缩的观察:所选动物的基本情况及分组与背斜方肌微动脉血液循环观察实验相同,共36只大鼠,9只/组。麻醉后于腓肠肌跟腱处结扎剪断,将悬浮电极尖端插入腓肠肌内,通过生理刺激器以1次/s、电压0.8V分别给予各组腓肠肌标本以连续刺激,至肌肉停止收缩时停止刺激,作为肌肉疲劳时间。然后银杏黄酮2.0,3.0,4.0g/L浓度组分别注射相应浓度的银杏黄酮溶液1mL,空白对照组注射等量生理盐水。5min后继续给予刺激,记录肌肉收缩的情况及肌肉疲劳后恢复正常状态的时间。③运动实验:选用健康雄性昆明种小白鼠60只,随机数字表法分为安静对照组、安静服药组、单纯训练组、服药训练组,15只/组。安静服药组、服药训练组每天早晚各灌胃给药1次,剂量为2.4mL/kg体质量;安静对照组、单纯训练组每天灌予等量的白开水。单纯训练组、服药训练组小鼠每天在规格为100cm×50cm×80cm的透明玻璃泳池内进行1次尾部负重游泳训练,30min/次,6d为1个周期,然后休息1d,共训练6周;安静对照组、安静服药组小鼠每天进行15min的无负重游泳适应性训练。各组小鼠第5周进行爬绳实验,测量静止耐力。第6周进行力竭性游泳实验。结果:背斜方肌微动脉血液循环的观察实验选用SD大鼠40只,腓肠肌肌肉收缩的观察实验选用SD大鼠36只,运动实验选用昆明种小白鼠60只,3个实验各自独立,所有动物均进入结果分析。①银杏黄酮对微动脉血管口径的影响:与空白对照组比较,而给药5min后,银杏黄酮各浓度组微动脉血管口径均明显增大(P<0.05或0.01)。②银杏黄酮对微动脉血管流态的影响:与空白对照组比较,银杏黄酮各浓度组微动脉血管流态3级评定、血流停止时间和血流恢复正常条数均有明显差异(P<0.05或0.01)。③银杏黄酮对腓肠肌肉收缩的影响:与空白对照组比较,银杏黄酮各浓度组肌肉疲劳时间无明显变化(P>0.05),但肌肉疲劳恢复时间均明显降低(P<0.05或0.01)。④各组小鼠爬绳及负重游泳能力的比较:安静服药组小鼠的爬绳静止时间明显长于安静对照组(P<0.05),服药训练组小鼠的负重游泳时间显著强于单纯训练组(P<0.01)。结论:银杏黄酮具有促进血液循环、提高新陈代谢速率和缩短肌肉疲劳的恢复等功效,在运动训练的协同作用下,能显著提高小鼠的运动能力,延缓疲劳的发生。     

银杏黄酮对骨骼肌抗疲劳能力的影响

目的：分析银杏黄酮对大鼠背斜方肌微动脉血液循环、腓肠肌收缩能力及小鼠运动能力的影响。方法：实验于2004-02在广西师范大学体育学院完成。银杏黄酮由桂林思特新技术公司天然植物制品厂生产，银杏黄酮含量24％，银杏内酯含量6％，符合国际标准。①大鼠背斜方肌微动脉血液循环的观察：选用SD大鼠40只，随机数字表法分为空白对照组、银杏黄酮2．0．3．0，4．0g／L浓度组，10只／组。各组大鼠均制备游离肌肉标本，游离面固定于特制灌流盒上，用林格氏液灌流，连续观察管径为15-20μm的横向微动脉30min，分别于观察处滴注0．1g/L的去甲肾上腺素障碍液50μL。当血管出现收缩时，银杏黄酮2．0，3．0，4．0g／L浓度组分别滴注对应的银杏黄酮溶液1mL，空白对照组则滴注等量的生理盐水。测量微动脉血管口径的变化以及血管流态的变化。②大鼠腓肠肌肌肉收缩的观察：所选动物的基本情况及分组与背斜方肌微动脉血液循环观察实验相同，共36只大鼠，9只／组。麻醉后于腓肠肌跟腱处结扎剪断，将悬浮电极尖端插入腓肠肌内，通过生理刺激器以1次／s、电压0．8V分别给予各组腓肠肌标本以连续刺激，至肌肉停止收缩时停止刺激，作为肌肉疲劳时间。然后银杏黄酮2．0，3．0，4．0g／L浓度组分别注射相应浓度的银杏黄酮溶液1mL，空白对照组注射等量生理盐水。5min后继续给予刺激，记录肌肉收缩的情况及肌肉疲劳后恢复正常状态的时间。③运动实验：选用健康雄性昆明种小白鼠60只，随机数字表法分为安静对照组、安静服药组、单纯训练组、服药训练组．15只／组。安静服药组、服药训练组每天早晚各灌胃给药1次，剂量为2．4mL／kg体质量；安静对照组、单纯训练组每天灌予等量的白开水。单纯训练组、服药训练组小鼠每天在规格为100cm&;#215;50cm&;#215;80cm的透明玻璃泳池内进行1次尾部负重游泳训练，30min／次，6d为1个周期，然后休息1d，共训练6周；安静对照组、安静服药组小鼠每天进行15min的无负重游泳适应性训练。各组小鼠第5周进行爬绳实验，测量静止耐力。第6周进行力竭性游泳实验。结果：背斜方肌微动脉血液循环的观察实验选用SD大鼠40只，腓肠肌肌肉收缩的观察实验选用SD大鼠36只，运动实验选用昆明种小白鼠60只，3个实验各自独立，所有动物均进入结果分析。①银杏黄酮对微动脉血管口径的影响：与空白对照组比较，而给药5min后，银杏黄酮各浓度组微动脉血管口径均嘎显增大（P〈0．05或0．01）。②银杏黄酮对微动脉血管流态的影响：与空白对照组比较，银杏黄酮各浓度组微动脉血管流态3级评定、血流停止时间和血流恢复正常条数均有明显差异（P〈0．05或0.01）。③银杏黄酮对腓肠肌肉收缩的影响：与空白对照组比较，银杏黄酮各浓度组肌肉疲劳时间无明显变化（P〉0．05），但肌肉疲劳恢复时间均明显降低（P〈0．05或0．01）。④各组小鼠爬绳及负重游泳能力的比较：安静服药组小鼠的爬绳静止时间明显长于安静对照组（P〈0．05），服药训练组小鼠的负重游泳时间显著强于单纯训练组（P〈0．01）。结论：银杏黄酮具有促进血液循环、提高新陈代谢速率和缩短肌肉疲劳的恢复等功效，在运动训练的协同作用下，能显著提高小鼠的运动能力，延缓疲劳的发生。     

The metabolic syndrome: role of skeletal muscle metabolism

Skeletal muscle constitutes the largest insulin-sensitive tissue in the body and is the primary site for insulin-stimulated glucose utilization. Skeletal muscle resistance to insulin is fundamental to the metabolic dysregulation associated with obesity and physical inactivity, and contributes to the development of the metabolic syndrome (MS). The inability to efficiently take up and store fuel, and to transition from fat to glucose as the primary source of fuel during times of caloric abundance (high insulin) or scarcity (low insulin) has been termed metabolic inflexibility which contributes to a whole body metabolic dysregulation and cardiovascular risk. Potential mechanisms contributing to reduced insulin signaling and action in skeletal muscle includes adipose tissue expansion and increased inflammatory adipokines, increased renin-angiotensin-aldosterone system (RAAS) activity, decreases in muscle mitochondrial oxidative capacity, increased intramuscular lipid accumulation, and increased reactive oxygen species. Future research is focused upon understanding these and other potential mechanisms in order to identify therapeutic targets for reducing MS risk. Strategies will include adequate physical activity and maintaining a healthy weight, but may also require specific pharmacologic interventions.     

Consequences of skeletal muscle injury induced by unaccustomed exercise

Unaccustomed exercise is exercise that has never been performed before or has not been performed previously at a certain intensity. Unaccustomed exercise commonly leads to an acute skeletal muscle injury. Several negative consequences develop as a result of this injury and can interfere with daily and recreational physical activities. This article describes what the consequences are, when they occur and recover, and what might cause them to occur. Also, the article discusses the nursing implications of these consequences for healthy young and older individuals and for those individuals who have disuse muscle atrophy.     

运动诱导骨骼肌肥大的信号传导通路

归纳分析运动诱导骨骼肌生理性适应肥大机制,为训练计划设计提供指导性的建议.运动诱导骨骼肌生理性适应肥大机制涉及到多种信号传导途径:①雷帕霉素靶体蛋白(mTOR)信号传导通路刺激骨骼肌生长.②PI3K-mTOR在调节细胞和器官生长中扮演着重要的作用.③mTOR参与肌肉适应性生长的调节.④和肾上腺素能激动剂克伦特罗诱导的肌肉生长通过mTOR和其下游的目标蛋白.⑤mTOR通路参与抗阻力训练诱导肌肉肥大.大量关键蛋白分子和信号传导通路被发现和证实,其中Akt/mTOR信号通路,被认为在参与调节肌肉的生长,增加蛋白的合成方面起到重要的作用.改变运动方式,能够选择性的激活Akt和mTDR的上游的效应分子目前并不清楚,需进一步研究.