An acute bout of high-intensity interval training increases the nuclear abundance of PGC-1α and activates mitochondrial biogenesis in human skeletal muscle

Am J Physiol Regul Integr Comp Physiol. 2011 Jun;300(6):R1303-10. doi: 10.1152/ajpregu.00538.2010. Epub 2011 Mar 30.


Low-volume, high-intensity interval training (HIT) increases skeletal muscle mitochondrial capacity, yet little is known regarding potential mechanisms promoting this adaptive response. Our purpose was to examine molecular processes involved in mitochondrial biogenesis in human skeletal muscle in response to an acute bout of HIT. Eight healthy men performed 4 × 30-s bursts of all-out maximal intensity cycling interspersed with 4 min of rest. Muscle biopsy samples (vastus lateralis) were obtained immediately before and after exercise, and after 3 and 24 h of recovery. At rest, the majority of peroxisome proliferator-activated receptor γ coactivator (PGC)-1α, a master regulator of mitochondrial biogenesis, was detected in cytosolic fractions. Exercise activated p38 MAPK and AMPK in the cytosol. Nuclear PGC-1α protein increased 3 h into recovery from exercise, a time point that coincided with increased mRNA expression of mitochondrial genes. This was followed by an increase in mitochondrial protein content and enzyme activity after 24 h of recovery. These findings support the hypothesis that an acute bout of low-volume HIT activates mitochondrial biogenesis through a mechanism involving increased nuclear abundance of PGC-1α.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptation, Physiological / physiology
  • Adult
  • Biopsy
  • Cell Nucleus / metabolism*
  • Exercise / physiology*
  • Heart Rate / physiology
  • Heat-Shock Proteins / metabolism*
  • Humans
  • Male
  • Mitochondria, Muscle / physiology*
  • Muscle, Skeletal / metabolism*
  • Muscle, Skeletal / pathology
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
  • Physical Exertion / physiology*
  • Protein Kinases / metabolism
  • Transcription Factors / metabolism*
  • p38 Mitogen-Activated Protein Kinases / metabolism


  • Heat-Shock Proteins
  • PPARGC1A protein, human
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
  • Transcription Factors
  • Protein Kinases
  • AMP-activated protein kinase kinase
  • p38 Mitogen-Activated Protein Kinases