跳至主要内容
临床试验/NCT02792621
NCT02792621已完成不适用

Assessing the Effects of Increased Mitochondrial Function on Skeletal Muscle Performance in Older Men; a Pilot Study

Royal Devon and Exeter NHS Foundation Trust2 个研究点 分布在 1 个国家目标入组 16 人开始时间: 2016年11月8日最近更新:
适应症

试验速览

阶段
不适用
状态
已完成
发起方
入组人数
16
试验地点
2
主要终点
Change in mitochondrial function

研究概览

简要总结

As people grow older skeletal muscle gradually becomes smaller and weaker, causing reduced mobility and quality of life. To understand and reverse this negative process investigators need to find new ways of improving the ability of muscle to perform physical activity. There is some evidence that supplements may improve how the mitochondria work, and investigators want to explore this idea in more detail, by measuring how the muscles work and respond to exercise before and after taking the supplement. This will give us the basic information investigators would need to see if this is a useful idea.

详细描述

A defining feature of ageing is loss of muscle mass ('sarcopenia') and associated functional weakness ('dynapenia'). A common characteristic of dynapenia is lowered mitochondrial content and metabolic function, causing reduced aerobic capacity, increased sensations of effort and impaired lipid oxidation (with resultant glucose intolerance). Exercise training improves mitochondrial and muscle function in ageing populations, however such adaptations remain below that of young counterparts, suggesting alternative approaches are required. Pre-clinical studies show that dietary supplementation with precursors of nicotinamide adenine dinucleotide (NAD+) restore mitochondrial biogenesis and oxidative capacity in ageing rodents and diabetic humans. However, whether NAD+ precursors rejuvenate mitochondrial capacity and, ultimately, muscle function in older humans is unknown. This pilot project will therefore investigate the efficacy of NAD+ precursor supplementation for increasing muscle performance in normally active older men, combined with examination of the molecular and metabolic mechanisms regulating physiological responses.

研究设计

研究类型
Interventional
分配方式
Randomized
干预模型
Parallel
主要目的
Prevention
盲法
Quadruple (Participant, Care Provider, Investigator, Outcomes Assessor)

入排标准

年龄范围
65 Years 至 75 Years(Older Adult)
性别
Male
接受健康志愿者

入选标准

  • Age between 65-75 years
  • Body mass index between 19-29
  • No active cardiovascular or metabolic disease
  • No active respiratory disease
  • No current musculoskeletal injuries
  • A sedentary lifestyle (i.e. does not engage in strenuous, planned physical activity)
  • The ability to give informed consent

排除标准

  • Currently taking a statin drug or NSAIDs
  • Have a current peptic ulcer
  • Have any renal impairment
  • Have a known hypersensitivity to Acipimox

结局指标

主要结局

Change in mitochondrial function

时间窗: Baseline, day 7, day 14

Mitochondria will be extracted from muscle samples immediately post-biopsy (biopsies taken baseline, day 7 and day 14) and analysed for content and subsequently for oxidative respiratory function using the Seahorse technique, and maximal rates of Adenosine Triphosphate (ATP) production.

次要结局

  • Chronic changes in habitual muscle protein synthetic rates(Baseline and then daily for 14 days)

研究者

发起方
Royal Devon and Exeter NHS Foundation Trust
申办方类型
Other
责任方
Sponsor

研究点 (2)

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