EFFECT OF RESISTANCE EXERCISE AND REDUCTION OF BLOOD FLOW ON MUSCLE GROWTH IN

抗阻运动和血流量减少对肌肉生长的影响

• 批准号: 7719201
• 负责人: Blake B Rasmussen
• 金额: $ 0.66万
• 依托单位: UNIVERSITY OF TEXAS MED BR GALVESTON
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-04-01 至 2009-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7719201
• 关键词: 70-kDa Ribosomal Protein S6 Kinases; Blood Vessels; Blood flow; Cardiac; Computer Retrieval of Information on Scientific Projects Database; Exercise; Funding; Grant; Growth; Hypoxia; Institution; Link; Muscle; Muscle Contraction; Muscle Proteins; Phosphorylation; Play; Protein Biosynthesis; Proteins; Protocols documentation; Rate; Research; Research Personnel; Resistance; Resources; Rest; Role; Sirolimus; Source; Translation Initiation; United States National Institutes of Health; Venous; angiogenesis; cell growth; design; human FRAP1 protein; hypoxia inducible factor 1; insight; mTOR Signaling Pathway; men; older men; protein degradation; transcription factor

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Rapamycin (mTOR) signaling pathway plays a significant role in stimulating translation initiation and muscle protein synthesis. Though both muscular contraction and hypoxia have been demonstrated to acutely up regulate AMPK activity, effect of hypoxia per se on muscle protein turnover is unknown. Additionally, recent studies have shown that hypoxia can up-regulate the mTOR signaling pathway through a transcription factor called hypoxia-inducible factor-1 (HIF1). Hypoxia induced angiogenesis and cardiac cell growths have been linked to HIF1; therefore, resistance exercise combined with restricted venous blood flow may further stimulate mTOR signaling pathway through HIF1. The specific aims are to: 1) to determine which component(s) of the mTOR signaling pathway are modified with muscular contraction combined with local hypoxia in older men. 2) To determine whether blood flow restriction during low-intensity exercise produces a larger increase in muscle protein synthesis than regular resistance exercise alone in older men. We will study groups of 24 older (60 yrs and above yrs) men after an overnight fast. The protocol is designed to study the modulations in mixed muscle protein fractional synthetic rate (FSR) and total protein content and phosphorylation status of components of the mTOR signaling pathway involved in translation initiation (mTOR, p70S6K, eIF2B, HIFs and AMPK) at rest and after low intensity resistance exercise with or without vascular occlusion. These studies will provide insight into the cellular mechanisms responsible for the enhanced hypertrophic effect of resistance exercise combined with reduced muscular blood flow.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目及 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 雷帕霉素 (mTOR) 信号通路在刺激翻译起始和肌肉蛋白合成中发挥重要作用。 尽管肌肉收缩和缺氧已被证明可以急剧上调 AMPK 活性，但缺氧本身对肌肉蛋白周转的影响尚不清楚。 此外，最近的研究表明，缺氧可以通过一种称为缺氧诱导因子-1 (HIF1) 的转录因子上调 mTOR 信号通路。 缺氧诱导的血管生成和心肌细胞生长与 HIF1 有关； 因此，抗阻运动结合限制静脉血流可能会通过HIF1进一步刺激mTOR信号通路。 具体目标是：1) 确定 mTOR 信号通路的哪些成分因老年男性的肌肉收缩和局部缺氧而被改变。 2) 确定低强度运动期间的血流限制是否比老年男性单独进行常规抗阻运动更能促进肌肉蛋白质合成。 我们将对 24 名老年男性（60 岁及以上）禁食过夜后进行研究。 该协议旨在研究混合肌肉蛋白分数合成率 (FSR) 和总蛋白含量的调节，以及参与翻译起始的 mTOR 信号通路成分（mTOR、p70S6K、eIF2B、HIF 和 AMPK）在休息和休息时的磷酸化状态。在有或没有血管闭塞的低强度阻力运动后。 这些研究将深入了解抵抗运动增强肥大效果并减少肌肉血流量的细胞机制。