MECHANISMS OF SKELETAL MUSCLE FATIGUE

骨骼肌疲劳的机制

• 批准号: 2899870
• 负责人: Jay H. Williams
• 金额: $ 22.74万
• 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/2899870
• 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 活动常常会导致疲劳。疲劳的影响是 最常见于运动场、工作场所等场所 康复诊所。在大多数情况下，骨骼肌疲劳会导致 运动表现和工作效率下降。然而，在一些 在某些情况下，疲劳会增加人们对骨科和骨科疾病的敏感性 肌肉腱损伤，并可能导致肌肉酸痛。 尽管这些后果以及疲劳造成的个人和经济成本 众所周知，引起这种现象的机制并不完全 明白了。如果要开发方法来预防和减轻疲劳和 其最终结果，那么疲劳过程必须充分 明白了。拟议研究的总体目标是获得见解 介导骨骼肌疲劳的机制。疲劳似乎 兴奋-收缩耦合过程改变的结果 继发于肌浆网功能特性的变化 和收缩装置或横向之间的通信 小管和 SR。多年来，人们都知道疲劳的发生是 与肌糖原水平降低和积累有关 乳酸。此外，其他糖酵解代谢物也在体内升高。 肌纤维。这表明碳水化合物代谢的某些方面 影响骨骼肌的力量输出，可能是糖原的消耗或 代谢物的积累。据此，本次会议的具体目标 建议如下。首先，确定糖原代谢物是否改变 CA SR功能以及TT-SR通信。其次，判断是否 体外糖原提取会改变 CA 和 SR 功能以及 TT-SR 沟通。第三，为了确定骨骼肌中的糖原是否耗尽， vivo，改变 CA 和 SR 功能以及 TT-SR 通讯。结果 拟议的实验将提供有关 介导骨骼肌疲劳的机制。此外，还将尝试 确定肌糖原水平、CHO 代谢和 疲劳过程。