基于超声图像的运动肌肉疲劳研究?

分析了运动肌肉疲劳前后肌肉形态结构参数的变化,为运动肌肉疲劳评价提供参考.文中应用B型超声技术,测量9名男性志愿者在递增负荷功率自行车运动疲劳前后下肢肌肉的肌肉厚度、羽状角并对其进行分析.结果表明功率自行车运动疲劳后,不同被测肌肉的肌肉厚度、羽状角较疲劳前显著增加(P0.05),其中大腿股外侧肌、股内侧肌的厚度变化率、羽状角变化率较大.得出了运动肌肉疲劳前后肌肉的肌肉厚度和羽状角发生变化,提示其可结合传统的表面肌电信号评估肌肉疲劳.     

运动性疲劳产生的机制及其消除途径综述

通过文献资料法，从生理生化角度，对运动性疲劳的定义、产生机制及其消除途径进行全方位地阐述。为全面系统地认识运动性疲劳产生的机制提供了有效的途径，同时筛选出一些对消除运动性疲劳较为有效的手段和方法，以供参考讨论。     

运动员运动性疲劳的诊断与恢复措施

无论从事任何一项体育运动训练,都会发生身体不同部位以及不同程度的运动性疲劳。运动性疲劳是由负荷运动引起的机体机能能力或工作效率下降的一种生理现象。本文通过对运动性疲劳的诊断与恢复措施的探讨,意在使从事体育锻炼的读者能够科学的诊断出自己是否处于疲劳阶段及疲劳的程度,并能够学会运用科学的方法去更快,更完全的从疲劳中恢复过来。精力旺盛的投入到训练、学习和工作中去。     

S-nitrosylation of NADPH oxidase regulates cell death in plant immunity

Changes in redox status are a conspicuous feature of immune responses in a variety of eukaryotes, but the associated signalling mechanisms are not well understood. In plants, attempted microbial infection triggers the rapid synthesis of nitric oxide and a parallel accumulation of reactive oxygen intermediates, the latter generated by NADPH oxidases related to those responsible for the pathogen-activated respiratory burst in phagocytes. Both nitric oxide and reactive oxygen intermediates have been implicated in controlling the hypersensitive response, a programmed execution of plant cells at sites of attempted infection. However, the molecular mechanisms that underpin their function and coordinate their synthesis are unknown. Here we show genetic evidence that increases in cysteine thiols modified using nitric oxide, termed S-nitrosothiols, facilitate the hypersensitive response in the absence of the cell death agonist salicylic acid and the synthesis of reactive oxygen intermediates. Surprisingly, when concentrations of S-nitrosothiols were high, nitric oxide function also governed a negative feedback loop limiting the hypersensitive response, mediated by S-nitrosylation of the NADPH oxidase, AtRBOHD, at Cys 890, abolishing its ability to synthesize reactive oxygen intermediates. Accordingly, mutation of Cys 890 compromised S-nitrosothiol-mediated control of AtRBOHD activity, perturbing the magnitude of cell death development. This cysteine is evolutionarily conserved and specifically S-nitrosylated in both human and fly NADPH oxidase, suggesting that this mechanism may govern immune responses in both plants and animals.     

Nitric oxide in female reproductive system

Nitric oxide (NO), synthesized from L-arginine and oxygen by a family of enzymes known as nitric oxide synthase (NOS), is an effective and intercellular signal transduction molecule, and is ubiquitously present in vertebrates. To date, there are three distinct isoforms of NOS: neural NOS (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS). Among them, eNOS and nNOS, also called constitutive isoforms (cNOS), require calcium for activity, and are expressed constitutively in the physiological condition. The third isoforms, iNOS, whose activity is not dependent on calcium, are produced only in response to some stimulus, including cytokines and immune stimulating factors, etc.[1].     

糖原填充对马拉松运动成绩的影响

在马拉松训练与比赛中,肌糖原的耗竭和降低,与运动性疲劳的发生有着密切关系,肌糖原在体内的有氧氧化供能是马拉松训练和竞赛中机体主要的能量来源。赛前糖原填充的方法能够提高运动能力,推迟疲劳来临的时间。对优秀运动员而言,在运动竞赛前36～48小时,通过递减运动量,摄入10～12g/kg/d的糖,以达到赛前糖原填充的要求。运动营养学指出在两次训练间隙,充足糖的摄入,能够有效促进肌糖原的恢复,运动员就可以持续不断的从事训练和得到有效恢复。有人认为机体低糖储备在训练时会产生强烈的应答反应,但事实上低糖饮食对提高马拉松运动成绩不利。有研究表明,长期的低糖饮食对运动能力是有害的,在赛前增加体内糖原的储量,对马拉松运动员来说是十分必要的。     

乳糖对小鼠运动能力的影响研究

以糖作为能量补充的基点,昆明小鼠作为实验对象,将小鼠分为对照组(C)、空白运动组(B)和服用乳糖组(L),研究补充乳糖对减缓昆明小鼠运动性疲劳的作用,以提高小鼠的运动能力.结果表明:(1)在小鼠运动前补充乳糖能减少血液中的乳酸;(2)游泳力竭运动后,空白运动组的小鼠的血糖浓度有一定程度的下降,且下降趋势明显,而服用乳糖组小鼠的血糖浓度下降不大.说明补充乳糖后,可以提高小鼠的运动能力.     

力竭运动对大鼠骨骼肌肌浆网钙转运的影响

采用递增负荷力竭运动方式观察急性运动对肌浆网(SR)钙转运能力的影响,发现运动后股四头肌SR Ca2+-ATPase活性和Ca2+摄取速率均明显下降,表现为SR Ca2+-ATPase活性和Ca2+摄取速率分别下降51.12%(P<0.01)和17.72%(P<0.01);而脂质过氧化物浓度则显著升高,增加48.85%(P<0.01).提示急性运动后SR Ca2+-ATP ase 活性和Ca2+摄取速率下降可能是脂质过氧化增高的结果,而Ca2+摄取功能下降可能与运动性疲劳密切相关.     

肌氧含量的光电无损检测及其在运动训练中的应用

介绍了动脉血氧和肌氧饱和度的概念。从光与组织之间相互作用的内在机理出发，给出了无损光电监测组织中氧含量的基本原理和方法，并推导了计算公式。对运动员在训练过程中肌肉氧代谢能力进行了实时连续无损检测和评估，随着运动状态的改变，明显看到了肌氧含量的变化。测试结果表明，运动员在运动训练过程中及训练后恢复期的氧消耗和恢复与运动强度明显相关。这对于进一步评定训练效果，掌握训练强度，判断疲劳以及运动员选材的深入研究提供了重要的参考价值。     

人参皂甙Rb1和人参总皂甙对运动性疲劳大鼠骨骼肌生化指标的影响

探讨人参皂甙Rb1和人参总皂甙对运动性疲劳大鼠骨骼肌生化指标的影响,将大鼠分为空白组、模型组、人参皂甙Rb1组和人参总皂甙组。采用中等强度的跑台运动建立动物模型,给药后运动连续实验两周后,检测骨骼肌线粒体膜电位、胞内钙离子含量、MDA含量、SOD活性和葡萄糖含量。结果发现人参皂甙Rb1和人参总皂甙都能抑制骨骼肌细胞内钙稳态失衡和线粒体膜电位降低、降低骨骼肌细胞MDA含量、增强SOD活性、增加从血液摄取的葡萄糖含量（均有P〈0.05）,从而抑制运动所致骨骼肌细胞损伤、发挥抗运动性疲劳作用。但在恢复膜电位和降低MDA含量方面,人参总皂甙效果更优;而在恢复线粒体内游离钙含量、提高SOD活性和摄取葡萄糖方面,人参皂甙Rb1的效果更明显。     

一种基于sEMG信号多重分形的肌肉疲劳特征分析方法

针对由表面肌电信号(sEMG)非平稳、非线性、自相似性等复杂特性导致的肌肉疲劳估计不准的问题,提出一种基于sEMG信号多重分形降趋移动平均法(MFDMA)的肌肉疲劳特征分析方法。首先,利用MFDMA方法对采集的sEMG信号、洗牌信号和高斯白噪声信号进行非线性动力学分析;其次,利用MFDMA方法计算sEMG信号的多重分形谱宽度、Hurst指数变化差值、概率测度值和峰值奇异指数4种多重分形特征;最后,利用t-检验法分析肌肉疲劳与非疲劳状态下的多重分形特征的显著差异性。结果表明,MFDMA方法能够描述sEMG信号的多重分形行为,谱宽等多重分形特征在肌肉疲劳与非疲劳状态下具有显著性差异。所提方法能够可靠表征运动性肌肉疲劳,可为肌肉疲劳识别模型建构、康复医学研究提供特征参考。     

析运动性疲劳的预防及其消除

本文运用文献资料法和逻辑分析法,通过对5种具有代表性的运动性疲劳的生理机制的分析,重点论述预防运动性疲劳的方法和消除的措施。     

Localization of the region homologous to the Duchenne muscular dystrophy locus on the mouse X chromosome

Recent progress has resulted in part of the gene mutated in Duchenne and the milder Becker muscular dystrophies being cloned and has suggested that the gene itself extends over 1,000 to 2,000 kilobases (kb). To study how mutations in this gene affect muscle development and integrity, it would be of interest to have available a mouse model of the human disease. The mouse mdx mutation affects muscle and confers a mild dystrophic syndrome, but it is not clear whether this mutation is equivalent to Duchenne/Becker muscular dystrophy in man. Here we describe the use of two sequences from the human Duchenne muscular dystrophy (DMD) gene that cross-hybridize to mouse X-linked sequences to localize the gene homologous to DMD in the mouse. Both sequences map to the region of 10 centimorgan lying between the Tabby (Ta) and St14-1 (DxPas8) loci, close to the phosphorylase b kinase locus (Phk). By analogy with the human X-chromosome, we conclude that the region in the mouse around the G6pd and St14-1 loci may contain two genes corresponding to distinct human myopathies: Emery Dreifuss muscular dystrophy which is known to be closely linked to St14-1 in man and the DMD homologue described here.     

氨基酸代谢、脑神经递质与运动性中枢疲劳

运动性疲劳的机制主要包括存在于大脑的中枢机制和肌肉本身的外周机制两个方面,越来越多的证据表明,氨基酸代谢、脑神经递质与中枢疲劳有着密切关系,对色氨酸、谷氨酸和酷氨酸代谢;脑神经递质;脑神经递质5－羟色胺、r-氨基丁酸和多巴胺及其与运动性中枢疲劳的关系作一简要综述。     

Abnormal expression of inducible nitric oxide synthase in Duchenne muscular dystrophy muscles

Duchenne muscular dystrophy (DMD) is a fatal genetic disease for the youth and children. 8 biopsies of DMD patients were determined and demonstrated that the membrane_binding nitric oxide synthase was enriched in normal skeletal muscles and was little in DMD muscles. The results from Western blot and immunohistochemistry showed that inducible nitric oxide synthase (iNOS) was overexpressed in DMD muscle fibers, while a small amount of highly localized iNOS can be found in normal fibers. Based on these findings, it is proposed that the mechanism of progressive injury in DMD muscle might be associated with the abnormal expression of iNOS.     

热敏灸对运动大鼠运动能力和心肌、骨骼肌细胞线粒体过氧化损伤的影响

目的研究热敏灸对运动大鼠运动能力和心肌、骨骼肌细胞线粒体过氧化损伤的影响。方法将40只大鼠随机分为正常对照组、单纯运动组、运动+普通悬灸组和运动+热敏灸组,采用14 d递增大强度跑台运动训练和生物化学的方法,观察热敏灸对运动大鼠运动能力和心肌、骨骼肌细胞线粒体过氧化损伤的影响。结果运动+热敏灸组大鼠疲劳相关症状显著改善,跑台力竭时间显著高于运动+普通悬灸组和单纯运动组。运动+热敏灸组大鼠心肌、骨骼肌细胞线粒体SOD酶活性高于单纯运动组、运动+普通悬灸组,心肌细胞线粒体SOD酶活性低于正常对照组,但骨骼肌细胞线粒体SOD酶活性与正常对照组比较,差异无显著性;MDA含量低于单纯运动组和运动+普通悬灸组,但高于正常对照组。结论热敏灸足三里穴具有明显的抗运动性疲劳作用,机理与热敏灸降低过度运动大鼠心肌和骨骼肌细胞线粒体过氧化损伤有关。     

S-glutathionylation uncouples eNOS and regulates its cellular and vascular function

Endothelial nitric oxide synthase (eNOS) is critical in the regulation of vascular function, and can generate both nitric oxide (NO) and superoxide (O(2)(?-)), which are key mediators of cellular signalling. In the presence of Ca(2+)/calmodulin, eNOS produces NO, endothelial-derived relaxing factor, from l-arginine (l-Arg) by means of electron transfer from NADPH through a flavin containing reductase domain to oxygen bound at the haem of an oxygenase domain, which also contains binding sites for tetrahydrobiopterin (BH(4)) and l-Arg. In the absence of BH(4), NO synthesis is abrogated and instead O(2)(?-) is generated. While NOS dysfunction occurs in diseases with redox stress, BH(4) repletion only partly restores NOS activity and NOS-dependent vasodilation. This suggests that there is an as yet unidentified redox-regulated mechanism controlling NOS function. Protein thiols can undergo S-glutathionylation, a reversible protein modification involved in cellular signalling and adaptation. Under oxidative stress, S-glutathionylation occurs through thiol-disulphide exchange with oxidized glutathione or reaction of oxidant-induced protein thiyl radicals with reduced glutathione. Cysteine residues are critical for the maintenance of eNOS function; we therefore speculated that oxidative stress could alter eNOS activity through S-glutathionylation. Here we show that S-glutathionylation of eNOS reversibly decreases NOS activity with an increase in O(2)(?-) generation primarily from the reductase, in which two highly conserved cysteine residues are identified as sites of S-glutathionylation and found to be critical for redox-regulation of eNOS function. We show that eNOS S-glutathionylation in endothelial cells, with loss of NO and gain of O(2)(?-) generation, is associated with impaired endothelium-dependent vasodilation. In hypertensive vessels, eNOS S-glutathionylation is increased with impaired endothelium-dependent vasodilation that is restored by thiol-specific reducing agents, which reverse this S-glutathionylation. Thus, S-glutathionylation of eNOS is a pivotal switch providing redox regulation of cellular signalling, endothelial function and vascular tone.     

补充精氨酸与运动能力关系的研究进展

采用文献资料法，论述了运动时精氨酸代谢的影响以及补充精氨酸提高运动能力的机制．在运动应激状态下，机体时精氨酸的需求量明显增加，提供充足的精氨酸能明显减少氮丢失，有益于机体蛋白质合成，促进肌糖原的储备及恢复；同时可增加冠状动脉流量和改善心脏功能，增强和调节机体的免疫功能，因此时延缓疲劳的发生和促进恢复有一定的作用．     

针灸按摩对于运动疲劳及运动损伤后生化指标的影响

目的：探讨中医疗法对于运动性疲劳及损伤后生化指标的影响。方法：运用文献资料法做出运动疲劳及损伤后生化指标的变化分析,同时运用逻辑分析法做出中医诊疗手段对于生化指标的促进恢复作用。结论：中医针灸按摩治疗以活血化瘀、清热解毒、凉血为主,对于运动性疲劳及损伤后生化指标的正常恢复有显著的促进作用。     

Functional improvement of dystrophic muscle by myostatin blockade

Mice and cattle with mutations in the myostatin (GDF8) gene show a marked increase in body weight and muscle mass, indicating that this new member of the TGF-beta superfamily is a negative regulator of skeletal muscle growth. Inhibition of the myostatin gene product is predicted to increase muscle mass and improve the disease phenotype in a variety of primary and secondary myopathies. We tested the ability of inhibition of myostatin in vivo to ameliorate the dystrophic phenotype in the mdx mouse model of Duchenne muscular dystrophy (DMD). Blockade of endogenous myostatin by using intraperitoneal injections of blocking antibodies for three months resulted in an increase in body weight, muscle mass, muscle size and absolute muscle strength in mdx mouse muscle along with a significant decrease in muscle degeneration and concentrations of serum creatine kinase. The functional improvement of dystrophic muscle by myostatin blockade provides a novel, pharmacological strategy for treatment of diseases associated with muscle wasting such as DMD, and circumvents the major problems associated with conventional gene therapy in these disorders.