Mitochondrial oxidative capacity and NAD+ biosynthesis are reduced in human sarcopenia across ethnicities

Nat Commun. 2019 Dec 20;10(1):5808. doi: 10.1038/s41467-019-13694-1.

Abstract

The causes of impaired skeletal muscle mass and strength during aging are well-studied in healthy populations. Less is known on pathological age-related muscle wasting and weakness termed sarcopenia, which directly impacts physical autonomy and survival. Here, we compare genome-wide transcriptional changes of sarcopenia versus age-matched controls in muscle biopsies from 119 older men from Singapore, Hertfordshire UK and Jamaica. Individuals with sarcopenia reproducibly demonstrate a prominent transcriptional signature of mitochondrial bioenergetic dysfunction in skeletal muscle, with low PGC-1α/ERRα signalling, and downregulation of oxidative phosphorylation and mitochondrial proteostasis genes. These changes translate functionally into fewer mitochondria, reduced mitochondrial respiratory complex expression and activity, and low NAD+ levels through perturbed NAD+ biosynthesis and salvage in sarcopenic muscle. We provide an integrated molecular profile of human sarcopenia across ethnicities, demonstrating a fundamental role of altered mitochondrial metabolism in the pathological loss of skeletal muscle mass and function in older people.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Aged, 80 and over
  • Aging / physiology*
  • Biopsy
  • Case-Control Studies
  • Energy Metabolism / physiology
  • Humans
  • Jamaica
  • Male
  • Middle Aged
  • Mitochondria / metabolism
  • Mitochondria / pathology*
  • Muscle, Skeletal / cytology
  • Muscle, Skeletal / metabolism
  • Muscle, Skeletal / pathology*
  • NAD / biosynthesis*
  • Oxidation-Reduction
  • Oxidative Phosphorylation
  • Oxidative Stress / physiology
  • Proteostasis
  • Sarcopenia / ethnology
  • Sarcopenia / pathology*
  • Singapore
  • United Kingdom

Substances

  • NAD