Markers of human skeletal muscle mitochondrial biogenesis and quality control: Effects of age and aerobic exercise training

Adam R. Konopka, Miranda K. Suer, Christopher A. Wolff, Matthew P. Harber

Research output: Contribution to journalArticlepeer-review

Abstract

Perturbations in mitochondrial health may foster age-related losses of aerobic capacity (VO2peak) and skeletal muscle size. However, limited data exist regarding mitochondrial dynamics in aging human skeletal muscle and the influence of exercise. The purpose of this study was to examine proteins regulating mitochondrial biogenesis and dynamics, VO2peak, and skeletal muscle size before and after aerobic exercise training in young men (20 ± 1 y) and older men (74 ± 3 y). Exercise-induced skeletal muscle hypertrophy occurred independent of age, whereas the improvement in VO 2peak was more pronounced in young men. Aerobic exercise training increased proteins involved with mitochondrial biogenesis, fusion, and fission, independent of age. This is the first study to examine pathways of mitochondrial quality control in aging human skeletal muscle with aerobic exercise training. These data indicate normal aging does not influence proteins associated with mitochondrial health or the ability to respond to aerobic exercise training at the mitochondrial and skeletal muscle levels.

Original languageEnglish (US)
Pages (from-to)371-378
Number of pages8
JournalJournals of Gerontology - Series A Biological Sciences and Medical Sciences
Volume69
Issue number4
DOIs
StatePublished - Apr 2014
Externally publishedYes

Keywords

  • FIS1
  • Hypertrophy.
  • Mitochondrial dynamics
  • Mitofusin
  • PGC-1α
  • Sarcopenia

ASJC Scopus subject areas

  • Aging
  • Geriatrics and Gerontology

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