Carbohydrate metabolism of dog skeletal muscle during immobilization

The effect of immobilization and the following mobilization on muscle carbohydrate metabolism was investigated in dogs. Total carbohydrate and glycogen content of skeletal muscle fell during immobilization. The glycogen-degrading enzyme phosphorylase was activated 1 week after immobilization (a/b ratio 40.6 +/- 7.6 vs. 27.1 +/- 6.5%). Thereafter, the enzyme activity decreased and remained significantly lowered even 2 weeks after the following mobilization. In contrast, muscle glucose and lactate concentration were unchanged. Our data indicates glycogen breakdown of dog skeletal muscle during immobilization. Even after 2 weeks of mobilization muscle glycogen content has not reached glycogen values of the untreated dogs.     

Vascular endothelial growth factor stimulates skeletal muscle regeneration in vivo.

Vascular endothelial growth factor (VEGF) is a major regulator of blood vessel formation during development and in the adult organism. Recent evidence indicates that this factor also plays an important role in sustaining the proliferation and differentiation of different cell types, including progenitor cells of different tissues, including bone marrow, bone, and the central nervous system. Here we show that the delivery of the 165-aa isoform of VEGF-A cDNA using an adeno-associated virus (AAV) vector exerts a powerful effect on skeletal muscle regeneration in vivo. Following ischemia-, glycerol-, or cardiotoxin-induced damage in mouse skeletal muscle, the delivery of AAV-VEGF markedly improved muscle fiber reconstitution with a dose-dependent effect. The expression of both VEGF receptor-1 (VEGFR-1) and VEGFR-2 was upregulated both in the satellite cells of the damaged muscles and during myotube formation in vitro; the VEGF effect was mediated by the VEGFR-2, since the transfer of PlGF, a VEGF family member interacting with the VEGFR-1, was ineffective. These results are consistent with the observation that VEGF promotes the growth of myogenic fibers and protects the myogenic cells from apoptosis in vitro and prompt a therapeutic use for VEGF gene transfer in a variety of muscular disorders.     

Inhibitory effects of salicylate on contractility in skeletal muscle

Salicylate (1-5 mM) had no effect on the peak amplitude (Pt) of twitches elicited at 0.05 to 0.05 Hz, but depressed the Pt in frog and toad "toe" muscles stimulated at 5 to 10 Hz. The maximal tetanic tension (Po) was not reduced significantly by salicylate, but the time to reach Po was increased to several seconds. K-induced contractures were reduced by ca 40 and 50%, respectively, in the presence of 5 and 10 mM salicylate. Pretreatment with salicylate (5 mM) reduced the twitch potentiation by quinine, shortened the duration of twitches in caffeine-treated muscles and inhibited the caffeine- and the quinine-induced contractures. Muscles in contracture because of a previous exposure to quinine relaxed promptly upon addition of salicylate to the bathing medium. The inhibitory effects of salicylate on Pt, on Po and on K- or drug-induced contractures were reversible and were not affected by changes in pH between 7.5 and 6.5. Salicylate depressed the caffeine-rapid cooling contractures (RCC). In toad muscles, this effect was affected markedly by the order in which caffeine and salicylate were applied. Blockade of the caffeine-RCC by salicylate was enhanced by lowering the pH of the medium. Salicylamide (1-5 mM) reproduced the effects of salicylate on the caffeine- and the quinine-induced contractures and the caffeine-RCC. In addition, salicylamide reduced the twitch tension. It is proposed that salicylate and salicylamide affect Casequestration by the sarcoplasmic reticulum.     

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。     

Resistance exercise effects on aging skeletal muscle in rats

The purpose of this study was to determine whether a resistance exercise program could be initiated successfully at progressively older ages in rats. Forty female Sprague-Dawley rats, 7 to 10 in each age group (21, 24, 27, and 30 months, respectively), performed 60 manually resisted chin-ups (three sets of 10 repetitions each twice daily) for three months. Twenty controls, 5 in each age group, were followed for three months but not exercised. Before the experimental period began, the rats' left palmaris longus (PL) muscle was removed, weighed, frozen, sectioned, and stained. After the three-month period, the right PL muscle was removed and the same tissue preparation procedure was followed. Muscle fiber types I and II were identified on photomicrographs, and areas of each fiber type measured. No significant change in muscle wet weight or fiber size occurred in the controls. Significant increases (p less than .01) in type II muscle fiber area occurred for the 21-, 24-, and 30-month-old rats that exercised. No histological evidence of exercise-related harm was observed in tissues from exercised rats. Results indicate that resistance exercise can be introduced successfully to an aging or aged rat without doing harm. Studies are needed to determine whether similar results can be achieved for elderly humans.     

Direct vasodilator effects of physiological hyperinsulin-aemia in human skeletal muscle

Systemic hyperinsulinaemia induces vasodilatation in human skeletal muscle. This effect is gradual in onset, and at low insulin levels not maximal until at least 3 h. To investigate whether the vasodilator response to insulin results from a direct vascular effect, we infused insulin directly into the cannulated brachial artery (perfused forearm technique) in a total of 30 experiments in 20 healthy, lean, normotensive volunteers. Local, intra-arterial, infusion of insulin (180 min, 0.3 mU dL^?1 forearm volume min^?1, n = 15, forearm venous insulin concentration approximately 540 pmol L^?1) induced a gradual increase in forearm blood flow (FBF; venous occlusion plethysmography) from 1.86 ± 0.17 to 3.64 ± 0.64 mL dL^?1 min^?1 after 180 min (anova P < 0.001). Percentage increases in FBF after 60, 120 and 180 min averaged 14.4 ± 5.9, 59.4 ± 25.5 and 124.6 ± 51.2% respectively. Forearm glucose uptake increased from 0.24 ± 0.05 to a maximum of 1.98 ± 0.28 μmol dL^?1 min (P < 0.001). Furthermore, insulin infusion increased forearm lactate release and potassium uptake. In 10 out of these 15 individuals, the forearm glucose uptake was further increased in a second, separate, repeat experiment with concomitant intra-arterial infusion of glucose 5% (0.2 mL dL^?1 min^?1), resulting in forearm venous glucose concentrations of approximately 15 mmol L^?1. This combined infusion achieved a similar vasodilator response to the infusion of insulin alone. The individual vascular responses of the two paired experiments showed a strong correlation (r = 0.87, P < 0.01). In five subjects time and vehicle control experiments were performed, showing no changes in FBF or metabolism during the 180 min. We conclude that the slow vasodilator response to insulin (as observed during systemic infusion) can, at least partly, be explained by a direct vascular effect of insulin. Insulin-mediated skeletal muscle glucose uptake precedes this effect, but seems not to be an important determinant of the vasodilator response to insulin.     

Local and systemic effects of endotoxin in contracting skeletal muscle

This study was performed to determine the direct effect of endotoxin on force generation, O₂ consumption and vascular resistance in contracting skeletal muscle.

We vascularly isolated the gastrocnemius muscle of dogs anesthetized with sodium pentobarbital and mechanically ventilated. The muscle was perfused from a proximal vessel or by a pump that withdrew blood from the contralateral leg. The nerve to the muscle was stimulated with supramaximal voltage 12 tr/min, 15-Hz impulses and a duty cycle of 0.4. Blood flow was measured with an electromagnetic flow probe, and oxygen consumption (VO₂) was calculated from the flow and arterial-venous O₂ content. In Protocol 1 (local infusion), contractions were stimulated for 30 minutes and endotoxin (n = 6) or saline (n = 6) was infused into the vasculature of the isolated gastrocnemius muscle after 10 minutes of contraction and continued for another 20 minutes of contraction. In Protocol 2 (systemic infusion), The normal tension and flow to the gastrocnemius were established and endotoxin (n = 5) or saline (n = 5) infused systemically. One hour later, the flow was set at the control level of contracting muscle, and contractions were stimulated for 30 minutes.

In both groups, endotoxin did not alter the tension VO₂, arterial venous oxygen difference, or vascular resistance at the end of the stimulation period.

Endotoxin must affect muscle force production by acting through intermediates such as cytokines, and the effect is not apparent in the first 60 minutes.     

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.     

骨骼肌缺血再灌注损伤中血管功能障碍与丹参的干预效应

目的:观察骨骼肌缺血再灌注损伤血清一氧化氮、诱导型一氧化氮合酶、内皮素1含量的变化及中药丹参的干预作用。方法:实验于2005-01/12在福建中医学院骨伤系实验室完成。实验分组:选用雄性SD大鼠84只,按随机数字表法分为丹参组、生理盐水组,每组42只,每组又分缺血再灌注10,20,30,40,50,60,90min7个时间点,每个时间点6只。实验方法:①制备大鼠左侧提睾肌缺血再灌注损伤模型。②丹参组于缺血2h时腹腔注射丹参注射液,生理盐水组给予相应剂量生理盐水;分别于缺血再灌注10,20,30,40,50,60,90min抽取腹主动脉血。实验评估:①采用硝酸还原酶法测定血清一氧化氮浓度。②采用比色法测定诱导型一氧化氮合酶活性。③采用放射免疫法测定内皮素1含量。结果:纳入大鼠84只,均进入结果分析。①一氧化氮、诱导型一氧化氮合酶的表达量:缺血再灌注10,20min两组一氧化氮、诱导型一氧化氮合酶的表达量无明显差异(P>0.05);缺血再灌注30,40,50,60,90min丹参组一氧化氮和诱导型一氧化氮合酶的表达量均高于生理盐水组[一氧化氮分别为(70.95±2.10),(68.21±2.23)μmol/L;(77.05±2.28),(72.20±1.56)μmol/L;(81.12±2.74),(74.60±1.90)μmol/L;(68.81±2.32),(62.03±2.80)μmol/L;(57.08±3.02),(46.77±3.01)μmol/L;诱导型一氧化氮合酶分别为(515.17±47.54),(459.78±37.27)μkat/L;(629.46±44.19),(499.37±29.46)μkat/L;(673.73±29.96),(584.77±58.48)μkat/L;(590.62±31.96),(507.78±31.82)μkat/L;(485.33±38.27),(378.64±38.04)μkat/L],差异有非常显著性意义(t=2.238,4.332,4.783,4.569,5.922;2.246,6.000,3.317,4.499,4.843,P<0.05,0.01)。缺血再灌注50min两组一氧化氮、诱导型一氧化氮合酶的表达量均达到最高峰,此后表达量开始下降。②内皮素1的表达量:缺血再灌注40min两组内皮素1的表达量均达到最高峰,此后表达量开始下降;缺血再灌注10min两组间内皮素1的表达量无明显差异(P>0.05),缺血再灌注20,30,40,50,60,90min丹参组内皮素1的表达量低于生理盐水组[分别为(145.77±26.54),(237.76±14.41)ng/L;(197.32±21.80),(258.50±40.20)ng/L;(124.44±6.00),(189.58±7.24)ng/L;(115.88±10.84),(165.93±10.43)ng/L;(103.96±3.84),(158.05±10.62)ng/L;(84.42±6.16),(113.69±10.41)ng/L],差异有非常显著性意义(t=7.462,3.278,16.959,8.149,11.731,5.926,P<0.01)。结论:骨骼肌缺血再灌注损伤导致血清中一氧化氮、诱导型一氧化氮合酶、内皮素1的表达量发生改变,丹参可能通过调整一氧化氮和内皮素1的平衡,改善缺血再灌注损伤造成的血管内皮功能障碍。     

甘丙肽对骨骼肌细胞葡萄糖转运蛋白4的影响

背景：甘丙肽能促进骨骼肌细胞葡萄糖转运蛋白4膜转位和葡萄糖清除,葡萄糖转运蛋白4是运动促进骨骼肌细胞摄取葡萄糖的主要载体,从而增加骨骼肌摄取葡萄糖而降低血糖。目的：探讨甘丙肽与胰岛素联用对糖尿病大鼠骨骼肌细胞葡萄糖转运蛋白4膜位移的作用。方法：由第一作者检索1991年1月2011年12月PubMed数据库（http：//www.ncbi.nlm.nih.gov/PubMed）及万方数据库（http：//www.wanfangdata.com.cn）。英文检索词为＂Galanin;insulin＂,中文检索词为＂甘丙肽;葡萄糖转运蛋白4＂。检索文献量总计143篇,选择甘丙肽与胰岛素在改善骨骼肌摄取葡萄糖的特点及其临床应用方面的文献,排除陈旧及重复实验文章,同一领域文献则选择近期发表或发表在权威杂志的文章,最终纳入37篇符合标准的文献。结果与结论：甘丙肽是一种广泛分布在神经系统的神经肽,具有广泛的神经生物学功能。运动能提高血浆甘丙肽浓度以及甘丙肽对2型糖尿患者的保护机制已经得到认可。甘丙肽及胰岛素都有降低血糖的功效。糖尿病是甘丙肽和胰岛素共同障碍的结果,那么甘丙肽与胰岛素联用的疗效自然成为关注的焦点,即两者联用对糖尿病大鼠骨骼肌细胞葡萄糖转运蛋白4膜位移的作用,是否比单独运用甘丙肽或胰岛素对骨骼肌细胞葡萄糖转运蛋白4膜位移的作用更强是目前研究的趋势。     

Acute effects of functional dry needling on skeletal muscle function

IntroductionFunctional dry needling (FDN) is commonly used to treat soft tissue pain-related conditions. Previous research has demonstrated benefits to chronic resistance training; however, objective physiological measures sensitive to acute exercise have not been found. The purpose of this study was to evaluate the acute effects of FDN on muscle strength and endurance.MethodsTen subjects (height 168 ± 9 cm, mass 68.2 ± 11.3 kg) were tested bilaterally (pre and post) for vastus lateralis (VL) isometric strength, isokinetic fatigue index, muscle electrical activity, and muscle oxygenation. FDN was administered to one leg, while the other served as a control.ResultsLimited acute effects of functional dry needling were observed (p < 0.05).DiscussionFDN does not appear to acutely improve muscle function in healthy young adults. Although there were no improvements in muscle function, there were no adverse effects either, contributing to the safety of FDN healthy populations.ConclusionAcute FDN does not appear to enhance muscle performance in a healthy, non-clinical population. Thus, clinicians should consider the population and desired outcome when applying FDN.     

乌司他丁对大鼠骨骼肌缺血-再灌注损伤的保护作用

目的 探讨乌司他丁对大鼠骨骼肌缺血-再灌注损伤的保护作用.方法 24只健康成年雄性SD大鼠随机分为3组(每组8只):对照组(C组)、缺血.再灌注损伤组(I/R组)、乌司他丁处理组(U组).C组仅麻醉肢体没有缺血操作;I/R组于再灌注前颈外静脉注入生理盐水0.5 ml;U组于再灌注前同法给乌司他丁0.5 ml(5×104 U/kg).以橡皮带环绕结扎大鼠左后肢根部至趾掌无血流信号达4 h后放开橡皮带,再灌注4 h建立大鼠骨骼肌缺血.再灌注损伤模型.再灌注4 h各组处死动物采集标本,采用逆转录-聚合酶链反应(RT-PCR)法测定骨骼肌组织TNF-α mRNA的表达;酶联免疫吸附试验法(ELISA)测定血浆TNF-α水平;比色法检测血浆乳酸脱氢酶(LDH)、肌酸激酶(CK)、丙二醛(MDA)和组织过氧化物酶(MPO)含量,测定湿质量/干质量均(W/D)及光镜、电镜观察骨骼肌组织结构的变化.应用SPSS 10.0统计软件,用单因素方差分析.结果 骨骼肌组织TNF-α mRNA的表达在I/R组明显高于C组(P＜0.05),而U组则低于I/R组(P＜0.01);血浆TNF-α浓度I/R组明显高于C组(P＜0.01),而U组则低于I/R组(P＜0.05);血浆LDH、MDA、CK和组织MDA、MPO水平以及W/D比值I/R组高于C组(P＜0.05),U组则低于L/R组(P＜0.05);骨骼肌组织形态学和超微结构的损伤U组也较I/R组减轻.结论 乌司他丁通过抑制细胞因子的生成、抑制氧自由基代谢产物MDA的产生和减少MPO的活性而对骨骼肌缺血-再灌注起保护作用.     

骨骼肌卫星细胞移植对钝挫伤动物模型的修复作用

目的探讨新生大鼠肌卫星细胞移植修复钝挫伤致动物骨骼肌损伤的作用。 方法取Sprague-Dawley成年大鼠36只,制作右后肢钝挫伤动物模型,随机分为生理盐水对照组和实验组,实验组大鼠左侧末造模正常后肢作为正常对照。用组织块培养法培养肌卫星细胞,免疫荧光抗体细胞染色鉴定后进行荧光标记。用微量注射器抽取肌卫星细胞悬液0.2 ml缓慢注射于实验组右侧小腿腓肠肌的内、外侧头,生理盐水对照组相同部位注射等量的生理盐水。术后第5,10和15天分别测定大鼠肌电图（记录振幅、波宽）、肌湿重恢复比值、HE染色肌纤维横切面积灰度值。所得数据用SPSS 13.0版统计软件进行双因素方差分析。 结果对新生大鼠肌卫星细胞进行分离纯化、鉴定和移植。移植前免疫抗体荧光化学染色鉴定细胞呈鲜红色,荧光标记细胞核为蓝色。术后移植细胞观察发现,随着移植时间延长,荧光细胞荧光度减弱,数目减少,逐渐形成肌管,融入肌组织参与修复;HE染色显示,游离在肌纤维间隙中的细胞核逐渐融入基膜内侧,肌组织轮廓逐渐清晰;肌电图检查结果显示,随着移植时间延长,纤颤电位和正锐波逐渐减少,波形趋于正常;肌电图的振幅及波宽测定结果显示,实验组损伤侧的恢复情况明显优于生理盐水对照组并且接近正常对照侧;HE染色肌纤维横切面积灰度值测定结果显示,移植后第5天,生理盐水对照组和实验组损伤侧灰度值明显低于正常对照侧,术后第10天、第15天观察,实验组损伤侧灰度值明显高于生理盐水对照组,接近于正常对照侧;实验组与生理盐水对照组肌湿重恢复比值结果显示,实验组肌湿重恢复比值≈1,而生理盐水对照组远<1,方差分析结果显示差异有统计学意义（P<0.01）。 结论新生大鼠骨骼肌卫星细胞异体移植对修复损伤肌肉有显著效果。     

Ryanodine: antithetical calcium channel effects in skeletal muscle sarcoplasmic reticulum

The effects of ryanodine, a neutral alkaloid, on the Ca++ uptake and Ca++ release properties of a skeletal muscle isolated sarcoplasmic reticulum (SR) preparation were evaluated. Ryanodine had no effect on the rate of oxalate-facilitated Ca++ uptake in this SR. Ruthenium red, which reportedly blocks Ca++ channels, increased Ca++ uptake by 2-fold in the SR. Although no effect of ryanodine on Ca++ transport by SR was observed, notable effects on Ca++-induced Ca++ release pathways were discovered. Ryanodine acts on the same Ca++ channels that are affected by ruthenium red. When these Ca++ channels were activated by Ca++ to an open state in the presence of ryanodine, then ryanodine maintained the channel in an activated, open state. However, once Ca++ was taken up by the SR, ryanodine tended to lock the channel in a closed state, producing a condition refractory to Ca++-induced Ca++ release. Thus, dual, opposing effects of ryanodine were demonstrated. In a fast-reaction kinetics measurement of Ca++-induced Ca++ release, both rate and amount of Ca++ release were reduced by ryanodine, and Ca++ appeared to act in a noncompetitive, antagonistic mode. These unusual, antithetical effects of ryanodine on the Ca++ efflux pathway are not mechanistically defined by this study, but they reveal the potential value of ryanodine as a probe for exploring Ca++ channel function.