MECHANISMS OF SKELETAL MUSCLE FATIGUE

骨骼肌疲劳的机制

• 批准号: 6171281
• 负责人: Jay H. Williams
• 金额: $ 19.09万
• 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 2002-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6171281
• 关键词: calcium flux; carbohydrate metabolism; fatigue; glycogen; laboratory rat; muscle contraction; muscle metabolism; muscle strength; sarcoplasmic reticulum; striated muscles

DESCRIPTION (Adapted from the applicant's abstract): Acute skeletal muscle activity often leads to the development of fatigue. The effects of fatigue are most often seen in venues such as the athletic arena, work site and rehabilitation clinic. In most instances, skeletal muscle fatigue results in decreased athletic performance and work productivity. However, in a number of cases, fatigue can increase ones susceptibility to orthopedic and musculo-tendinous injury and may lead to the development of muscle soreness. Although these consequences and the personal and financial costs of fatigue are well known, the mechanisms meditating this phenomenon are not completely understood. If means are to developed to prevent and alleviate both fatigue and its end results, then it is imperative that the fatigue process be fully understood. The overall objective of the proposed research is to gain insight into the mechanisms which mediate skeletal muscle fatigue. Fatigue appears to result from alterations in the excitation -contraction coupling process secondary to changes in the functional properties of the sarcoplasmic reticulum and the contractile apparatus or in the communication between the transverse tubule and SR. For years, it has been known that the onset of fatigue is associated with a reduction in the level of muscle glycogen and an accumulation of lactate. In addition, other glycolytic metabolites are elevated within the muscle fiber. This suggests that some aspect of carbohydrate metabolism influences skeletal muscle force output, possibly the depletion of glycogen or the accumulation of metabolites. Accordingly, the specific aims of this proposal are as follows. First, to determine if glycogen metabolites alter CA and SR function as well as TT-SR communication. Second, to determine if glycogen extraction, in vitro, alters CA and SR function as well as TT-SR communication. Third, to determine if glycogen depletion in skeletal muscle, in vivo, alters CA and SR function as well as TT-SR communication. The results of the proposed experiments will provide much needed information regarding the mechanisms which mediate skeletal muscle fatigue. In addition, it will attempt to identify direct links between muscle glycogen levels, CHO metabolism and the fatigue process.

描述（改编自申请人的摘要）：急性骨骼肌 活动通常导致疲劳的发展。疲劳的影响是 最常在体育舞台，工作地点和 康复诊所。在大多数情况下，骨骼肌疲劳会导致 降低运动表现和工作生产力。但是，许多 情况，疲劳会增加对骨科的敏感性和 肌肉紧张损伤，可能导致肌肉酸痛的发展。 尽管这些后果以及疲劳的个人和经济成本是 众所周知，冥想这种现象的机制并非完全 理解。是否要开发用于预防和减轻疲劳和 它的最终结果，然后必须完全疲劳过程 理解。拟议研究的总体目标是获得见识 进入介导骨骼肌疲劳的机制。疲劳似乎 激发 - 收集耦合过程的变化导致 继发于肌质网的功能特性变化的继发于此 以及收缩设备或横向之间的通信 小管和SR。多年以来，众所周知，疲劳的发作是 与肌肉糖原水平的降低和积累有关 乳酸。另外，其他糖酵解代谢物在 肌肉纤维。这表明碳水化合物代谢的某些方面 影响骨骼肌力量的输出，可能是糖原的耗竭或 代谢物的积累。因此，这是特定目标 建议如下。首先，确定糖原代谢物是否改变Ca 和SR功能以及TT-SR通信。第二，确定是否 糖原提取，体外，改变Ca和SR功能以及TT-SR 沟通。第三，确定骨骼肌中是否糖原耗竭 Vivo，Vivo，CA和SR功能以及TT-SR通信。结果 拟议的实验将提供有关该实验的急需信息 介导骨骼肌疲劳的机制。此外，它将尝试 确定肌肉糖原水平，CHO代谢与 疲劳过程。