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.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 雷帕霉素（MTOR）信号通路在刺激翻译起始和肌肉蛋白合成中起着重要作用。 尽管已经证明肌肉收缩和缺氧急性地调节AMPK活性，但缺氧本身对肌肉蛋白更新的影响尚不清楚。 此外，最近的研究表明，缺氧可以通过称为低氧诱导因子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脏细胞生长已与HIF1相关。 因此，耐药性运动与受限的静脉血流可能进一步刺激通过HIF1刺激MTOR信号通路。 具体目的是：1）确定MTOR信号传导途径的哪些成分与肌肉收缩结合结合局部缺氧的老年男性。 2）确定在低强度运动中的血流限制是否会比仅在老年男性中单独的常规耐药性运动产生更大的肌肉蛋白质合成。 快速过夜后，我们将研究24个年龄较大（60岁及以上）男性的小组。 该协议旨在研究混合肌肉蛋白分数合成速率（FSR）和总蛋白质含量和总蛋白质含量和磷酸化状态的MTOR信号传导途径的组件（MTOR，P70S6K，EIF2B，EIF2B，HIFS和AMPK），在静止和无效的耐受性运动后，p70S6K，p70S6K，EIF2B，HIFS和AMPK）。 这些研究将洞悉导致抗性运动增强的肥大性作用以及肌肉血流减少的肥大作用。