Novel Factors for Muscle Mass and Strength in Adults

影响成人肌肉质量和力量的新因素

• 批准号: 9175681
• 负责人: Shivani Sahni
• 金额: $ 35.75万
• 依托单位: HEBREW REHABILITATION CENTER FOR AGED
• 依托单位国家: 美国
• 财政年份: 2016
• 资助国家: 美国
• 起止时间: 2016-08-15 至 2019-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9175681
• 关键词: Accounting; Address; Adult; Affect; Age; Aging; American; Amino Acids; Antioxidants; Ascorbic Acid; Blood Vessels; Blood flow; Carnitine; Carotenoids; Characteristics; Coenzymes; Collagen; Communities; DNA copy number; Data; Diet; Elderly; Fracture; Future; Gait speed; Goals; Hand Strength; Health; Individual; Inflammation; Insulin; Intake; Intervention; Intervention Studies; Knowledge; Link; Measures; Mediating; Mitochondria; Mitochondrial DNA; Modality; Modeling; Muscle; Muscle Proteins; Muscle function; Muscular Atrophy; Outcome; Oxidative Stress; Participant; Pathway interactions; Perfusion; Physical Function; Physical activity; Physiological; Public Health; Rest; Risk Factors; Role; Skeletal Muscle; Time; Upper Extremity; Validation; Vitamin E; Woman; Work; age related; age-related muscle loss; arm; base; brachial artery; cardiovascular health; cohort; combat; disability; fall risk; insight; men; multimodality; muscle form; muscle strength; novel; offspring; prevent; protein intake; reduced muscle mass; response; time use

ABSTRACT / PROJECT SUMMARY Age-related decline in muscle mass and strength is an important public health issue. Future interventions will depend on identifying the physiologic pathways involved in these muscle changes and consequent physical function. We propose to investigate novel risk factors and identify associated pathways that affect age-related declines in muscle mass, quality, strength and gait speed. Our long term goal is to identify novel risk factors and associated pathways that affect age-related declines in muscle and physical function. The objective is to determine the roles of antioxidant intake, vascular function and mitochondrial function in loss of muscle mass, quality, strength and gait speed in adult men and women, providing new public health insights. We hypothesize that low antioxidant intake, impaired vascular function and lower mitochondrial DNA copy number (mtDNA-CN) will each contribute towards decreased muscle mass, quality, strength and gait speed, even accounting for established risk factors. We will address this work via 4 aims using up to 1,912 participants from a well- characterized cohort, the Framingham Offspring Study. Aim 1 will examine the association of antioxidant intakes (Vitamin C, Vitamin E and total carotenoids) with measures of muscle mass, quality, strength [defined as appendicular lean muscle mass/height2, grip strength-to-arm lean mass ratio (arm muscle quality), change in appendicular lean muscle mass/height2, change in grip strength over time] and change in gait speed. Aim 2 will examine the association of vascular function (assessed by brachial artery resting characteristics, hyperemic flow response and aortic stiffness with measures of muscle mass, quality, strength and change in gait speed. Aim 3 will examine the association of mtDNA-CN with measures of muscle mass, quality, strength and change in gait speed. Finally, Aim 4 will examine the combined effect of the novel risk factors evaluated from Aims 1-3 along with established risk factors (protein intake, physical activity and inflammation), on measures of muscle mass, quality, strength and change in gait speed. We plan to validate the findings from these aims by using a validation cohort, the Cardiovascular Health Study. The expected outcome is evidence for low antioxidant intake, impaired vascular and low mtDNA-CN as novel risk factors for age-related decrease in muscle mass, quality, strength and gait speed. The significance of the proposed work is that it will increase our understanding of individual contributions and combined effect of the proposed novel risk factors on age-related declines in muscle and physical function. This study will provide a strong basis for future multi-modality intervention studies aimed at reducing or preventing age-related declines in muscle and their debilitating consequences among older adults. 1

摘要/项目摘要 与年龄相关的肌肉质量和力量的下降是一个重要的公共健康问题。未来的干预措施将 依赖于确定这些肌肉变化和随后的生理变化所涉及的生理路径 功能。我们建议调查新的风险因素，并确定影响年龄相关的相关途径。 肌肉质量、质量、力量和步态速度下降。我们的长期目标是识别新的风险因素 以及影响与年龄相关的肌肉和身体功能下降的相关途径。我们的目标是 确定抗氧化剂摄入量、血管功能和线粒体功能在肌肉质量损失中的作用， 成年男性和女性的质量、力量和步速，提供新的公共卫生见解。我们假设 抗氧化剂摄入量低，血管功能受损，线粒体DNA拷贝数(mtDNA-CN)减少 是否每个人都会导致肌肉质量、质量、力量和步速下降，即使考虑到 已确定的风险因素。我们将通过4个目标解决这项工作，使用来自一口井的多达1,912名参与者- 弗雷明翰后代研究的特征队列。目标1将研究抗氧化剂之间的联系 摄入量(维生素C、维生素E和类胡萝卜素总量)，测量肌肉质量、质量、力量[定义 如附件瘦肌肉质量/身高2，握力与手臂瘦质量比(手臂肌肉质量)，变化 在阑尾瘦肌肉质量/身高2中，握力随时间的变化]和步态速度的变化。目标2 将检查血管功能的关联性(通过臂动脉静息特征来评估， 充血血流反应和主动脉僵硬与肌肉质量、力量和变化的测量 步态速度。目标3将检查线粒体DNA-CN与肌肉质量、质量、力量的测量之间的关系 以及步态速度的变化。最后，目标4将检验评估的新风险因素的综合影响。 从目标1-3以及已确定的危险因素(蛋白质摄入量、体力活动和炎症)， 衡量肌肉质量、质量、力量和步态速度变化的指标。我们计划从以下方面验证这些发现 这些目标是通过使用验证队列-心血管健康研究-来实现的。 预期的结果是抗氧化剂摄入量低、血管受损和线粒体DNA-CN低作为新的证据。 与年龄相关的肌肉质量、质量、力量和步速下降的危险因素。这一事件的意义 拟议的工作是，它将增加我们对个人贡献和 提出了与年龄相关的肌肉和身体功能下降的新风险因素。这项研究将提供一个 为未来旨在减少或防止年龄相关性下降的多模式干预研究奠定了坚实的基础 在老年人中的肌肉及其衰弱的后果。 1