Training intensity modulates changes in PGC-1α and p53 protein content and mitochondrial respiration, but not markers of mitochondrial content in human skeletal muscle

FASEB J. 2016 Feb;30(2):959-70. doi: 10.1096/fj.15-276907. Epub 2015 Nov 16.


Exercise training has been associated with increased mitochondrial content and respiration. However, no study to date has compared in parallel how training at different intensities affects mitochondrial respiration and markers of mitochondrial biogenesis. Twenty-nine healthy men performed 4 wk (12 cycling sessions) of either sprint interval training [SIT; 4-10 × 30-s all-out bouts at ∼200% of peak power output (WPeak)], high-intensity interval training (HIIT; 4-7 × 4-min intervals at ∼90% WPeak), or sublactate threshold continuous training (STCT; 20-36 min at ∼65% WPeak). The STCT and HIIT groups were matched for total work. Resting biopsy samples (vastus lateralis) were obtained before and after training. The maximal mitochondrial respiration in permeabilized muscle fibers increased significantly only after SIT (25%). Similarly, the protein content of peroxisome proliferator-activated receptor γ coactivator (PGC)-1α, p53, and plant homeodomain finger-containing protein 20 (PHF20) increased only after SIT (60-90%). Conversely, citrate synthase activity, and the protein content of TFAM and subunits of the electron transport system complexes remained unchanged throughout. Our findings suggest that training intensity is an important factor that regulates training-induced changes in mitochondrial respiration and that there is an apparent dissociation between training-induced changes in mitochondrial respiration and mitochondrial content. Moreover, changes in the protein content of PGC-1α, p53, and PHF20 are more strongly associated with training-induced changes in mitochondrial respiration than mitochondrial content.

Keywords: PHF20; TFAM; exercise; mitochondrial biogenesis; mitochondrial remodeling.

Publication types

  • Randomized Controlled Trial
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Antigens, Neoplasm / metabolism
  • Biomarkers, Tumor / metabolism
  • DNA-Binding Proteins
  • Exercise / physiology*
  • Humans
  • Male
  • Mitochondria, Muscle / metabolism*
  • Muscle Proteins / metabolism*
  • Muscle, Skeletal / metabolism*
  • Oxygen Consumption / physiology*
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
  • Transcription Factors / metabolism*
  • Tumor Suppressor Protein p53 / metabolism*


  • Antigens, Neoplasm
  • Biomarkers, Tumor
  • DNA-Binding Proteins
  • Muscle Proteins
  • PHF20 protein, human
  • PPARGC1A protein, human
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
  • TP53 protein, human
  • Transcription Factors
  • Tumor Suppressor Protein p53