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(改编自申请者的摘要)：急性骨骼肌 运动往往会导致疲劳的发展。疲劳的影响是 最常出现在体育场馆、工作场所和 康复诊所。在大多数情况下，骨骼肌疲劳会导致 运动成绩和工作效率下降。然而，在许多情况下 在某些情况下，疲劳会增加人们对骨科和 肌肉-肌腱损伤，可能导致肌肉酸痛。 尽管这些后果以及疲劳的个人和经济成本是 众所周知，冥想这一现象的机制并不完全 明白了。如果要开发出预防和缓解疲劳和 它的最终结果，那么当务之急是疲劳过程 明白了。拟议研究的总体目标是获得洞察力 研究调节骨骼肌疲劳的机制。疲劳感似乎 由兴奋-收缩耦合过程中的变化引起的 继发于肌浆网功能特性的改变 与收缩装置或在横行之间的沟通 小管和SR。多年来，人们都知道疲劳的开始是 与肌肉糖原水平的降低和积聚有关 乳酸盐。此外，其他糖酵解代谢物在体内升高 肌肉纤维。这表明碳水化合物新陈代谢的某些方面 影响骨骼肌力输出，可能是糖原耗竭或 代谢产物的积累。因此，这一行动的具体目标是 建议如下。首先，确定糖原代谢物是否会改变CA 和SR功能以及TT-SR通信。第二，确定是否 体外提取糖原可改变CA和SR功能以及TT-SR 沟通。第三，为了确定骨骼肌糖原耗竭是否 Vivo，改变CA和SR的功能以及TT-SR的通讯。结果是 拟议中的实验将提供关于 调节骨骼肌疲劳的机制。此外，它还将尝试 确定肌肉糖原水平、CHO代谢和 疲劳过程。