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Aging and the mitochondrial response to exercise training, measured by noninvasive 31P magnetic resonance spectroscopy

通过无创 31P 磁共振波谱测量衰老和线粒体对运动训练的反应

基本信息

批准号：
10417265
负责人：
OWEN T. CARMICHAEL
金额：
$ 61.05万
依托单位：
LSU PENNINGTON BIOMEDICAL RESEARCH CTR
依托单位国家：
美国
项目类别：
财政年份：
2020
资助国家：
美国
起止时间：
2020-09-01 至 2024-05-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10417265
关键词：
Acute Address Adult Aerobic Aerobic Exercise Age Aging Ancillary Study Attenuated Automobile Driving Bioenergetics Bioinformatics Biologic Characteristic Biological Biology Collaborations Collection DNA Methylation Data Disease Elderly Event Exercise Funding Health Health Benefit Individual Knowledge Light Link Magnetic Resonance Spectroscopy Measurement Measures Mitochondria Modality Molecular Molecular Profiling Multiomic Data Muscle Muscle Mitochondria Non-Insulin-Dependent Diabetes Mellitus Outcome Pathway interactions Persons Phenotype Phosphocreatine Physical Fitness Physical Function Physical activity Physiological Prevention Principal Investigator Proteomics Publishing Recovery Regulation Reporting Resistance Role Skeletal Muscle Technology Time Training Transducers United States National Institutes of Health VO2max Variant Work age group age related base cardiometabolism cardiorespiratory fitness clinically relevant epigenomics exercise prescription exercise training experience healthy aging improved in vivo inter-individual variation lipidomics member middle age mode of exercise muscular structure novel precision medicine programs resistance exercise response strength training transcriptomics vastus lateralis virtual young adult

项目摘要

Program Director/Principal Investigator (Last, First, Middle): Project Summary Reduced skeletal muscle mitochondrial oxidative capacity of skeletal muscle has been implicated in aging- related declines in cardiorespiratory fitness, physical functioning, and cardiometabolic health. Although exercise training in older adults increases mitochondrial capacity, virtually all of the data is reported in terms of average responses within groups. Yet within groups, there is enormous inter-individual variation in these responses. Two specific questions remain regarding the significance and implications of exercise-induced changes in mitochondrial capacity. 1) Does exercise improve mitochondrial capacity similarly in older and younger adults? 2) What are the molecular signatures within skeletal muscle that associate with improvements in mitochondrial capacity in older and younger adults? We will address these major gaps in knowledge by objectively assessing the spectrum of mitochondrial capacity responses to exercise in vivo, investigating the underlying molecular regulation of exercise responses, and relating the mitochondrial responses and molecular factors to clinically-relevant outcomes such as exercise-induced improvements in cardiorespiratory fitness (VO2max). The NIH-funded Molecular Transducers of Physical Activity Consortium (MoTrPAC) funds collection of comprehensive molecular signatures from biospecimens before and after 12 weeks of aerobic and resistance exercise training in healthy adults spanning the adult age span. This ancillary study will synergize with MoTrPAC and will add measurements of mitochondrial capacity of the skeletal muscle via non-invasive 31P magnetic resonance spectroscopy (31P-MRS) before and after training in 420 individuals across a wide age range (18 to 60+). Aim 1 is to assess differences in the mitochondrial capacity response to exercise training across the agespan and between aerobic and resistance training. Aim 2 is to identify molecular transducers of mitochondrial capacity induced by exercise. Primary hypotheses are that a proportion of individuals will not improve mitochondrial capacity following exercise training regardless of modality; age per se will not correlate with mitochondrial capacity responses; that greater improvements in mitochondrial capacity will associate similarly with greater improvements in cardiorespiratory fitness in younger and older adults; and that mitochondrial capacity responses will be greater with aerobic training compared to resistance training but aerobic-resistance differences will be similar across age groups. The impact of the project is that it will leverage the high-throughput `omics' technologies and exercise studies provided by MoTrPAC to shed light on mechanisms underlying the variation in mitochondrial capacity responses linked to health benefits of physical activity in older adults. OMB No. 0925-0001/0002 (Rev. 01/18 Approved Through 03/31/2020) Page Continuation Format Page

项目总监/首席调查员(最后、第一、中间)：项目摘要骨骼肌线粒体氧化能力降低与衰老有关-- 心肺功能、身体功能和心脏代谢健康方面的相关下降。虽然老年人的运动训练增加了线粒体的能力，几乎所有的数据都是以小组内的平均反应。然而，在群体内部，在这些方面存在着巨大的个体差异回应。关于运动诱导的意义和影响，还有两个具体的问题线粒体能力的变化。1)锻炼是否同样能提高老年人和老年人的线粒体能力年轻人？2)骨骼肌中与进步相关的分子特征是什么？老年人和年轻人的线粒体能力？我们将通过以下方式解决这些知识上的主要差距客观评估在体运动对线粒体能力的反应谱，调查运动反应的潜在分子调控及其与线粒体反应和分子的关系影响临床相关结果的因素，如运动导致的心肺功能改善 (VO2max)。美国国立卫生研究院资助的体力活动分子传感器联合会(MoTrPAC)基金需氧12周和12周后生物旋毛虫综合分子特征的收集跨越成人年龄跨度的健康成年人的阻力运动训练。这项辅助研究将使使用MoTrPAC，并将通过非侵入性增加骨骼肌线粒体容量的测量 420名不同年龄段受试者训练前后的31P磁共振波谱分析范围(18到60+)。目的1是评估线粒体对运动训练的反应能力的差异。在各个年龄段，在有氧训练和耐力训练之间。目标2是鉴定分子换能器运动诱导的线粒体能力。基本假设是，一定比例的人不会在运动训练后提高线粒体能力，无论是哪种形式；年龄本身不会相关线粒体能力的反应；线粒体能力的更大改善将与同样，年轻人和老年人的心肺健康状况也有更大的改善；与阻力训练相比，有氧训练的线粒体能力反应更大，但不同年龄段的有氧耐力差异将是相似的。该项目的影响是，它将利用MoTrPAC提供的高通量“组学”技术和运动研究来阐明线粒体容量反应变化的机制与体力活动的健康益处有关老年人的活动。 OMB编号0925-0001/0002(01/18修订版批准至2020年3月31日)页面续格式页面