SKELETAL MUSCLE FATIGUE AND THE CONTRACTILE APPARATUS

骨骼肌疲劳和收缩装置

• 批准号: 2520222
• 负责人: Jay H. Williams
• 金额: $ 1.28万
• 依托单位: VIRGINIA POLYTECHNIC INST AND ST UNIV
• 依托单位国家: 美国
• 财政年份: 1996
• 资助国家: 美国
• 起止时间: 1996-08-15 至 1998-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2520222
• 关键词: Rana; adenosinetriphosphatase; calcium flux; muscle cells; muscle contraction; muscle metabolism; muscle strength; striated muscles

Skeletal muscle fatigue has been defined as the inability of muscle to elicit a desired force output which it is normally capable of producing. The development of muscle fatigue affects a number of everyday activities including decreased exercise performance and worker productivity and is associated with increased susceptibility to orthopedic injury and precipitation of muscle soreness and damage. At present, the mechanisms which cause skeletal muscle fatigue are not fully understood. [It has recently been established that fatigue is associated with diminished maximal Ca2+ activated force and Ca2+ sensitivity of the contractile apparatus. Unfortunately, it is not clear if these changes are the direct result of fatiguing activity or are secondary to the accumulation of metabolic waste products (e.g. H+, P[i] and ADP). In addition, it is not clear if fatigue and/or its byproducts alter the relationship between force and Ca2+ by affecting the transitions of the cross-bridges to and from the force generating state (cross-bridge cycling kinetics) or by modulating cross-bridge recruitment and force generation. The experiments described in this proposal are designed to determine l) if fatigue directly alters maximal force production and Ca2+ sensitivity of the contractile apparatus and 2) if fatigue- and/or metabolite-induced changes in the relationship between force and free Ca2+ are due to altered cross- bridge cycling kinetics or to altered cross-bridge recruitment and/or their average force generation. This will be accomplished by examining cross-bridge recruitment, force generation and cycling kinetics in skinned skeletal muscle fibers taken from rested and fatigued muscles and exposed to incubation media that is formulated to mimic "rested" and "fatigued" intracellular environments. These parameters will be examined using measurements of the rate constant of force redevelopment after a period of isotonic shortening, complemented by measurements of isometric force, ATPase activity and stiffness during isometric contraction at various levels of free Ca2+. In general, the results of the proposed experiments will provide much needed information regarding the mechanisms of skeletal muscle fatigue. These findings should also lead to a better understanding of the fatigue process and provide an experimental basis for developing means of alleviating and avoiding muscle fatigue.]

骨骼肌疲劳被定义为肌肉无力 引起通常能够产生的期望的力输出。 肌肉疲劳的发展会影响许多日常活动 包括运动表现和工人生产力下降 与骨科损伤的易感性增加有关 肌肉酸痛和损伤沉淀。目前，机制 导致骨骼肌疲劳的原因尚不完全清楚。 [它有 最近发现，疲劳与体力下降有关 最大 Ca2+ 激活力和收缩的 Ca2+ 敏感性 设备。不幸的是，目前尚不清楚这些变化是否是直接影响 疲劳活动的结果或继发于累积 代谢废物（例如 H+、P[i] 和 ADP）。此外，它不是 明确疲劳和/或其副产品是否改变了之间的关系 通过影响跨桥到 和 的过渡来施加力和 Ca2+ 从力产生状态（跨桥循环动力学）或通过 调节跨桥招募和部队生成。实验 本提案中描述的目的是确定 l) 是否疲劳 直接改变最大力量产生和 Ca2+ 敏感性 收缩装置和 2) 如果疲劳和/或代谢物引起的变化 力和游离 Ca2+ 之间的关系是由于改变了交叉 桥循环动力学或改变跨桥募集和/或 他们的平均力量产生。这将通过检查来完成 蒙皮中的跨桥募集、力产生和循环动力学 骨骼肌纤维取自休息和疲劳的肌肉并暴露在外 配制为模拟“休息”和“疲劳”的培养介质 细胞内环境。这些参数将使用检查 经过一段时间后力重建速率常数的测量 等张缩短，辅以等长力测量， 各种等长收缩期间的 ATP 酶活性和硬度 游离 Ca2+ 水平。一般来说，所提出的实验的结果 将提供有关骨骼机制的急需信息 肌肉疲劳。这些发现也应该有助于更好地理解 疲劳过程的研究，为开发提供实验基础 缓解和避免肌肉疲劳的方法。]

项目成果

Functional overload attenuates plantaris atrophy in tumor-bearing rats.

• DOI: 10.1186/1471-2407-7-146
• 发表时间: 2007-08-02
• 期刊: BMC CANCER
• 影响因子: 3.8
• 作者: Otis, Jeffrey S.;Lees, Simon J.;Williams, Jay H.
• 通讯作者: Williams, Jay H.

Calcium exchange hypothesis of skeletal muscle fatigue: a brief review.

骨骼肌疲劳的钙交换假说：简要回顾。

• DOI: 10.1002/mus.880180409
• 发表时间: 1995
• 期刊: Muscle & nerve.
• 作者: Williams,JH;Klug,GA
• 通讯作者: Klug,GA

Effects of varied fatigue protocols on sarcoplasmic reticulum calcium uptake and release rates.

不同疲劳方案对肌浆网钙摄取和释放率的影响。

• DOI: 10.1152/ajpregu.1998.275.1.r99
• 发表时间: 1998
• 期刊: The American journal of physiology
• 作者: Ward,CW;Spangenburg,EE;Diss,LM;Williams,JH
• 通讯作者: Williams,JH

Effects of fatigue on depolarization- and caffeine-induced contractures of skinned fibres.

疲劳对去极化和咖啡因引起的带皮纤维挛缩的影响。

• DOI: 10.1046/j.0001-6772.2003.01243.x
• 发表时间: 2004
• 期刊: Acta physiologica Scandinavica.
• 作者: Williams,JH

Glucose 6-phosphate alters rat skeletal muscle contractile apparatus and sarcoplasmic reticulum function.

6-磷酸葡萄糖改变大鼠骨骼肌收缩装置和肌浆网功能。

• DOI: 10.1113/expphysiol.1998.sp004132
• 发表时间: 1998
• 期刊: Experimental physiology
• 影响因子: 2.7
• 作者: Williams,JH;Ward,CW;Spangenburg,EE;Nelson,R;Stavrianeas,S;Klug,GA
• 通讯作者: Klug,GA