SKELETAL MUSCLE FATIGUE AND THE CONTRACTILE APPARATUS

骨骼肌疲劳和收缩装置

• 批准号: 2376660
• 负责人: Jay H. Williams
• 金额: $ 7.85万
• 依托单位: VIRGINIA POLYTECHNIC INST AND ST UNIV
• 依托单位国家: 美国
• 财政年份: 1994
• 资助国家: 美国
• 起止时间: 1994-03-01 至 1998-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2376660
• 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， 引出其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， 与骨科损伤易感性增加相关， 沉淀肌肉酸痛和损伤。目前，机制 引起骨骼肌疲劳的原因还不完全清楚。[It具有 最近已经确定，疲劳与减少 收缩肌的最大Ca ~（2+）激活力和Ca ~（2+）敏感性 设备.不幸的是，目前尚不清楚这些变化是否是直接的 疲劳活动的结果或继发于 代谢废物（如H+、P[i]和ADP）。此外， 明确疲劳和/或其副产品是否会改变 力和Ca 2+通过影响过渡的跨桥和 从力产生状态（跨桥循环动力学）或通过 调整跨桥招募和部队组建。实验 本提案中描述的设计旨在确定l）是否疲劳 直接改变最大力的产生和Ca 2+的敏感性， 收缩器和2）如果疲劳和/或代谢诱导的变化 力与自由Ca 2+之间的关系是由于交叉改变所致 桥循环动力学或改变的跨桥募集和/或 平均发电量。这将通过检查 跨桥招募，力的产生和循环动力学在皮肤 骨骼肌纤维取自休息和疲劳的肌肉， 培养介质被配制成模拟“休息”和“疲劳” 细胞内环境这些参数将使用 测量一段时间后的力再发展的速率常数， 等张缩短，辅以等长力测量， 等长收缩过程中ATP酶活性和刚度的变化 游离Ca 2+水平。总的来说，所提出的实验的结果 将提供有关骨骼肌损伤机制的急需信息， 肌肉疲劳这些发现也应该能让我们更好地理解 并为开发新的疲劳试验方法提供了实验依据 缓解和避免肌肉疲劳的方法。