运动对骨骼肌肌球蛋白重链的影响

肌球蛋白重链(MHC)是骨骼肌收缩蛋白的重要组成成分，运动对骨骼肌MHC的影响是目前研究的热点之一。大量文献报道运动的影响主要表现在MHC各亚型之间的相互转化上，转化方向大致如下：Ⅰ←→Ⅱa←→Ⅱx←→Ⅱb。关于MHC基因表达的调控，目前认为运动等的影响主要作用于转录水平上，具体机制有待于进一步研究。     

运动对骨骼肌肌球蛋白重链基因表达的影响

骨骼肌是人体重要的运动器官。无论是在结构还是在功能上,骨骼肌都表现出多样性的特点,具有很好的可塑性,这使得骨骼肌对外界环境的变化具有极强的适应能力。肌球蛋白是肌肉中重要的结构和功能型蛋白,其结构中的重链(MyosinHeavy Chain MHC)有多种同功异构型,已有的研究显示,肌     

运动性骨骼肌损伤后不同时刻大鼠肱三头肌超微结构及肌酸激酶的变化

通过建立大鼠下坡跑运动损伤模型,研究运动损伤后骨骼肌超微损伤和恢复发生的机制。主要结果:运动后大鼠肱三头肌超微结构发生改变,电镜下可见肌纤维排列紊乱,Z线异常(包括Z线流、Z线模糊、Z线扭曲和Z线消失),肌细胞膜模糊、溶解,线粒体肿胀、空泡样改变等。这些现象随运动时间的不同而发生改变。运动后24 h表现最为明显,而后逐渐恢复;运动后72 h恢复明显,但没有完全恢复。运动后即刻血清CK活性(2035.42±426.49)U/L与对照组血清CK活性(293.66±76.07)U/L相比,非常显著增高(P<0.01),达到了峰值,而后逐渐恢复。运动后72h组血清CK活性(425.51±143.34)U/L与即刻组血清CK活性相比已显著恢复(P<0.01)。结论:运动后24h骨骼肌的损伤程度最为严重,72 h后可明显恢复;大强度运动对CK的活性具有非常显著的影响,血清CK活性的变化能够反映运动后骨骼肌超微结构损伤的状况。     

运动性骨骼肌损伤机制的研究进展

从损伤机制和检测指标两个方面对运动性骨骼肌损伤的研究进展进行综述,结果表明:运动性骨骼肌损伤主要原因为机械外力导致骨骼肌的肌膜完整性、流动性和通透性受损,进而导致骨骼肌细胞内钙离子超载,细胞膜的脂质过氧化,一些蛋白如Caveolin-3、Calpains和Ubiquitin的表达改变可能参与了细胞内的钙超载调控,机械性外力作用和代谢性刺激综合作用可以诱发、加重骨骼肌微结构的损伤.     

细胞骨架及运动性骨骼肌微损伤研究进展

综述了细胞骨架的结构和功能的研究进展,分析了骨骼肌细胞骨架在维持骨骼肌肌小节的正常结构和功能中的重要性。重点叙述了骨骼肌细胞骨架蛋白desmin、dystrophins、arcoglycant、itin和nebulin在运动中的变化,对细胞骨架蛋白在运动性骨骼肌微损伤中的作用进行了讨论。     

运动性骨骼肌微损伤机制的研究进展

综述运动性骨骼肌微损伤机制的研究进展,将其归纳为机械损伤学说、代谢学说(包括能量代谢紊乱学说、细胞内钙稳态失调学说和自由基学说等)、炎症反应学说等不同假说。认为:运动性骨骼肌微损伤的机制仍处于探索之中,应综合机械损伤和化学损伤等假说解释运动性骨骼肌微损伤。     

冷冻疗法干预运动性骨骼肌损伤的研究进展

运动性骨骼肌损伤是指高强度离心收缩或不习惯运动引起的肌肉结构、肌膜和细胞外基质的破坏,通常表现为延迟性肌肉酸痛、肌力下降等.冷冻疗法是指将人体暴露在超低温下进行治疗的一种康复手段.本文初步研究了冷冻疗法对运动性骨骼肌损伤的干预效果.冷冻疗法对机体的氧化应激、延迟性肌肉酸痛和炎症均有一定的治疗效果,但对于肌肉力量的恢复效...     

一次力竭性离心运动后大鼠骨骼肌MHC基因表达及针刺对其影响

为了研究一次力竭性离心运动后大鼠骨骼肌肌球蛋白重链(MHC)基因表达及针刺对其影响,将130只成年SD大鼠随机分为安静对照组和运动实验组.运动实验组又分为非针刺组和针刺组.将非针刺组和针刺组根据运动后的不同的取样时间分别分为运动后即刻组、6 h组、12 h组、24 h组、48 h组和72 h组.运动组大鼠动物在跑台上以16 m/min的速度进行持续性下坡跑至力竭(跑台坡度为-16°).运动时间为3.5-4.5 h,平均4 h.在一次力竭性离心运动后即刻,对针刺组大鼠进行针刺.安静对照组和非针刺组不进行针刺处理.分别在运动后即刻、6、12、24、48、72 h取肌肉样品.利用定量反转录聚合酶链式反应(QRT-PCR)法测定MHC基因表达.本研究发现,一次力竭性离心运动后大鼠骨骼肌总MHC基因表达在运动后6～12 h低于安静对照组,运动后48 h出现延迟性超量基因表达.运动后针刺组总MHC基因表达的变化曲线与非针刺组相似,但针刺组恢复时限提前,超量基因表达提前,而且超量基因表达的幅度大于非针刺组.说明针刺可以促进大负荷运动后骨骼肌MHC基因表达的恢复.     

骨骼肌运动性疲劳乳酸机制研究进展

目前在生物化学、运动生理学的教科书中依然把乳酸作为代谢性酸中毒的原因,但许多科学家认为用乳酸中毒来解释代谢性酸中毒是没 有研究基础支持的。有实验表明,乳酸的产生并没有完全使肌肉收缩力量下降,酸性化缓和了因细胞外[K+]升高而导致的骨骼肌疲劳。乳酸可以 通过改变氯离子通道活性从而促进动作电位的产生,使骨骼肌在开始疲劳时仍可以保护兴奋的传播。乳酸通过膜屏障在细胞间和细胞内穿梭是 靠单羧酸转运蛋白推动的,它协同转运乳酸和氢离子。其中慢肌纤维中MCT1 含量最高,有利于摄取乳酸使进入细胞,而快肌中MCT4 含量较高, 有利于把乳酸送出。     

血清肌酸激酶与骨骼肌损伤关系的探讨

研究目的在于对血清肌酸激酶与骨骼肌损伤之间的关系进行探讨。采用跑台一次性离心运动至力竭的动物模型,48只7周龄雌性大鼠随机分为安静对照组和运动后即刻、1、2、4和7天组,测定血清肌酸激酶活性,同时通过HE染色分析骨骼肌形态学损伤变化。结果显示血清肌酸激酶活性峰值出现在运动后即刻,运动后1天迅速下降。HE染色结果则表明离心运动后骨骼肌损伤呈现延迟性时相特点,在运动后第2天骨骼肌损伤范围达到最大。本实验表明血清肌酸激酶与骨骼肌损伤的变化趋势并不一致,血清肌酸激酶水平不能反映骨骼肌损伤。     

运动性骨骼肌损伤的内稳态研究综述

从功能内稳态(function-specific homeostasis,FSH)角度分析EIMD/DOMS过程影响运动成绩的正常发挥,而防治措施又大多无效这一现象,结果发现力竭运动所致的EIMD/DOMS,骨骼肌蛋白质代谢远离了蛋白质代谢内稳态(protein metabolite specific homeostasis,PmSH),EIMD/DOMS康复延迟,外源性有利因素干预可促进EIMD/DOMS康复;非力竭运动所致的EIMD/DOMS,蛋白质代谢处于PmSH,EIMD/DOMS正常康复,外源性因素对EIMD/DOMS无明显影响作用。     

Effects of roller massager on muscle recovery after exercise-induced muscle damage

Two experiments (n = 10) were conducted to determine the effects of roller massager (RM) on ankle plantar flexor muscle recovery after exercise-induced muscle damage (EIMD). Experiment 1 examined both functional [i.e., ankle plantar flexion maximal isometric contraction and submaximal (30%) sustained force; ankle dorsiflexion maximal range of motion and resistance to stretch; and medial gastrocnemius pain pressure threshold] and morphological [cross-sectional area, thickness, fascicle length, and fascicle angle] variables, before and immediately, 1, 24, 48, and 72 h after an EIMD stimulus. Experiment 2 examined medial gastrocnemius deoxyhaemoglobin concentration kinetics before and 48 h after EIMD. Participants performed both experiments twice: with (RM) and without (no-roller massager; NRM) the application of a RM (6 × 45 s; 20-s rest between sets). RM intervention did not alter the functional impairment after EIMD, as well as the medial gastrocnemius morphology and oxygenation kinetics (P > 0.05). Although, an acute increase of ipsilateral (RM = + 19%, NRM = ?5%, P = 0.032) and a strong tendency for contralateral (P = 0.095) medial gastrocnemius pain pressure threshold were observed. The present results suggest that a RM has no effect on plantar flexors performance, morphology, and oxygenation recovery after EIMD, except for muscle pain pressure threshold (i.e., a soreness).     

Influence of vitamin D mushroom powder supplementation on exercise-induced muscle damage in vitamin D insufficient high school athletes

Abstract

Incidence of vitamin D deficiency is increasing worldwide. The purpose of this study was to determine if supplementation with vitamin D₂ from Portobello mushroom powder would enhance skeletal muscle function and attenuate exercise-induced muscle damage in low vitamin D status high school athletes. Participants were randomised to Portobello mushroom powder (600 IU/d vitamin D₂) or placebo for 6 weeks. Participants then completed a 1.5-h exercise session designed to induce skeletal muscle damage. Blood samples and measures of skeletal muscle function were taken pre-supplementation, post-supplementation/pre-exercise and post-exercise. Six weeks supplementation with vitamin D₂ increased serum 25(OH)D₂ by 9.9-fold and decreased serum 25(OH)D₃ by 28%. Changes in skeletal muscle function and circulating markers of skeletal muscle damage did not differ between groups. In conclusion, 600 IU/d vitamin D₂ increased 25(OH)D₂ with a concomitant decrease in 25(OD)D₃, with no effect on muscular function or exercise-induced muscle damage in high school athletes.     

Evidence of exercise-induced muscle damage following a simulated rugby league match

Abstract

This study investigated symptoms of exercise-induced muscle damage following a simulated rugby league game. Ten male participants were assessed before, immediately after (0 h), and 24 and 48 h after the simulated game. Perceived muscle soreness was higher at all time points (P=0.001) and creatine kinase values were increased at 24 h following the simulated game (P=0.001). Peak knee extensor torque at 60 deg · s^?1 was reduced up to 48 h (P =0.04) but was unchanged at 240 deg · s^?1. Similarly, peak knee flexor torque at 60 deg · s^?1 was lower than baseline up to 24 h, while at 240 deg · s^?1 it was reduced at 24 h only (P=0.045). Correlations between changes in strength loss of the knee extensors and fat mass to fat-free mass ratio reveleaved no significant relationship between variables (P >0.05). In addition, countermovement jump performance was reduced at 0 and 24 h following the simulated game (P=0.008). Our results suggest that symptoms of exercise-induced muscle damage occur up to 48 h following a simulated rugby league match. Coaches should be cognisant of the large increases in muscle soreness and reductions in slow velocity force generation, and should adapt training accordingly in the 48 h period following a game.     

骨骼肌衰老的研究进展

骨骼肌是人体最重要的运动器官，在衰老过程中骨骼肌机能的下降是衰老的重要标志。伴随着衰老研究的进展，对于骨骼肌衰老的研究不断深入到基因水平，研究已经试图从衰老个体中分离出骨骼肌的“衰老因子”。就骨骼肌衰老的表现和可能机制进行了综述，以期为运动员提高骨骼肌的机能提供理论依据。     

运动与肌球蛋白重链研究综述

肌球蛋白作为骨骼肌纤维内主要的收缩蛋白和调节蛋白,对于骨骼肌纤维的收缩特性起重要作用,肌球蛋白重链是肌球蛋白重要组成,它有多种亚型表达,不同亚型收缩特性存在显著差异,研究发现,当外界刺激条件变化时,骨骼肌纤维肌球蛋白重链亚型组成可以改变,骨骼肌纤维收缩特性在肌球蛋白重链组成改变时发生显著变化,因此,研究不同运动条件下骨骼肌纤维肌球蛋白重链组成的变化对于深刻理解运动影响骨骼肌收缩性能具有重要意义。     

Angle-specific impairment of elbow flexors strength after isometric exercise at long muscle length

Abstract

In this study, we examined the long-term reductions in maximal isometric force (MIF) caused by a protocol of repeated maximal isometric contractions at long muscle length. Furthermore, we wished to ascertain whether the reductions in MIF are dependent on muscle length — that is, are the reductions in MIF more pronounced when the muscle contracts at a short length. The MIF of the elbow flexors of seven young male volunteers was measured at five different elbow angles between 50° and 160°. On a separate day, the participants performed 50 maximal voluntary isometric muscle contractions with the elbow flexors at a lengthened positions that is, with the shoulder hyperextended at 45° and the elbow joint fixed at 140°. Following this exercise, the MIF at the five elbow angles, range of motion, muscle soreness and plasma creatine kinase activity were measured at 24 h intervals for 4 days. On day 1, the decline in MIF was higher at the more acute elbow angles of 50° (42±8%) and 70° (39±8%; both P<0.01) than at 90° (26±4%) and 140° (16±3%; both P<0.01). No significant reduction in MIF was evident at an elbow angle of 160°. Maximal isometric force at an elbow angle of 140° was fully restored on day 3, whereas at an angle of 50° it remained depressed for the 4 day observation period. Restoration of MIF was a function of the elbow angle, with force recovery being less at the smaller angles. The range of motion was decreased by 14±2° on day 1 (P<0.01) and did not return to baseline values by day 4. Muscle soreness ratings remained significantly elevated for the 4 day period. Serum creatine kinase peaked on day 1 (522±129 IU, P<0.01) and decreased thereafter. We conclude that the disproportionate decrease in MIF at the small elbow angles and the length-specific recovery in MIF after repeated maximal isometric contractions at long muscle length may be explained by the presence of overstretched sarcomeres that increased in series compliance of the muscle, therefore causing a rightward shift of the force-length relationship.     

重复运动对骨骼肌超微结构变化的实验研究

目的:探讨重复运动后大鼠骨骼肌超微结构的改变。方法:雄性SD大鼠72只随机分为对照组、1次离心运动组和连续1周重复运动训练组。1次离心运动组进行1次下坡跑运动,重复运动组按照同样的强度进行连续7天的下坡跑训练。分别在1次离心运动即刻、24h、48 h、72 h、120 h、168 h和第7天末次训练后即刻24 h、48 h、72 h、120 h、168 h取股四头肌。结果:1次离心运动后即刻和24 h、48 h,股四头肌超微结构的损伤性变化呈现渐进性加重,运动后第168 h基本上可恢复到运动前水平;7次离心训练后即刻和24 h股四头肌超微结构的损伤性变化也具有相似的趋势,但训练后168 h后仍未完全恢复;且在各个时段,7天离心训练组股四头肌的损伤性变化均比一次离心运动组更加严重。结论:重复运动所致的骨骼肌损伤具有一定的延迟现象,在1次离心运动后即刻,骨骼肌损伤从整体看并不严重,但在运动后24h出现明显的损伤性变化;48 h达到高点,而运动后7天骨骼肌损伤基本上可以恢复。连续的重复运动可能导致骨骼肌纤维的损伤产生一定的累加作用。     

The efficacy of cooling with phase change material for the treatment of exercise-induced muscle damage: pilot study

Post-exercise cryotherapy treatments are typically short duration interventions. This study examined the efficacy of prolonged cooling using phase change material (PCM) on strength loss and pain after eccentric exercise. Eight adults performed 120 bilateral eccentric quadriceps contractions (90% MVC). Immediately afterwards, frozen PCM packs (15°C) were placed over the quadriceps, with room temperature PCM packs on the contralateral quadriceps. Skin temperature was recorded continually (6 h PCM application). Isometric quadriceps strength and soreness were assessed before, 24, 48, 72 and 96 h post-exercise. The protocol was repeated 5 months later, with room temperature PCM applied to both legs. There were three treatments: legs treated with 15°C PCM packs (direct cooling), legs treated with room temperature PCM packs contralateral to the 15°C PCM packs (systemic cooling), and legs tested 5 months later both treated with room temperature PCM packs (control). Skin temperature was 9°C–10°C lower with direct cooling versus systemic cooling and control (P < 0.01). Strength loss and soreness were less (P < 0.05) with direct cooling versus systemic cooling and control (strength 101%, 94%, 93%, respectively; pain 1.0, 2.3, 2.7, respectively). Six hours of PCM cooling was well tolerated and reduced strength loss and pain after damaging exercise.     

Protection against muscle damage in competitive sports players: the effect of the immunomodulator AM3

Strenuous physical exercise of the limb muscles commonly results in damage, especially when that exercise is intense, prolonged and includes eccentric contractions. Many factors contribute to exercise-induced muscle injury and the mechanism is likely to differ with the type of exercise. Competitive sports players are highly susceptible to this type of injury. AM3 is an orally administered immunomodulator that reduces the synthesis of proinflammatory cytokines and normalizes defective cellular immune fractions. The ability of AM3 to prevent chronic muscle injury following strenuous exercise characterized by eccentric muscle contraction was evaluated in a double-blind and randomized pilot study. Fourteen professional male volleyball players from the First Division of the Spanish Volleyball League volunteered to take part. The participants were randomized to receive either placebo (n?=?7) or AM3 (n?=?7). The physical characteristics (mean±s) of the placebo group were as follows: age 25.7±2.1 years, body mass 87.2±4.1?kg, height 1.89±0.07?m, maximal oxygen uptake 65.3±4.2?ml?·?kg^?1?·?min^?1. Those of the AM3 group were as follows: age 26.1±1.9 years, body mass 85.8±6.1?kg, height 1.91±0.07?m, maximal oxygen uptake 64.6±4.5?ml?·?kg^?1?·?min^?1. All participants were evaluated for biochemical indices of muscle damage, including concentrations of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, creatine kinase (CK) and its MB fraction (CK-MB), myoglobin, lactate dehydrogenase, urea, creatinine and γ-glutamyltranspeptidase, both before and 30 days after treatment (over the peak of the competitive season). In the placebo group, competitive exercise (i.e. volleyball) was accompanied by significant increases in creatine kinase (494±51 to 560±53?IU?·?l^?1, P?<?0.05) and myoglobin (76.8±2.9 to 83.9±3.1?μg?·?l^?1, P?<?0.05); aspartate aminotransferase (30.8±3.0 to 31.1±2.9?IU?·?l^?1) and lactate dehydrogenase (380±31 to 376±29?IU?·?l^?1) were relatively unchanged after the 30 days maximum effort. AM3 not only inhibited these changes, it led to a decrease from baseline serum concentrations of creatine kinase (503±49 to 316±37?IU?·?l^?1, P?<?0.05) and myoglobin (80.1±3.2 to 44.1±2.6?IU?·?l^?1, P?<?0.05), as well as aspartate aminotransferase (31.1±3.3 to 26.1±2.7?IU?·?l^?1, P?<?0.05) and lactate dehydrogenase (368±34 to 310±3?IU?·?l^?1, P?<?0.05). The concentration of CK-MB was also significantly decreased from baseline with AM3 treatment (11.6±1.2 to 5.0±0.7?IU?·?l^?1, P?<?0.05), but not with placebo (11.4±1.1 to 10.8±1.4?IU?·?l^?1). In conclusion, the use of immunomodulators, such as AM3, by elite sportspersons during competition significantly reduces serum concentrations of proteins associated with muscle damage.