A practical model of low-volume high-intensity interval training induces mitochondrial biogenesis in human skeletal muscle: potential mechanisms

J Physiol. 2010 Mar 15;588(Pt 6):1011-22. doi: 10.1113/jphysiol.2009.181743. Epub 2010 Jan 25.


High-intensity interval training (HIT) induces skeletal muscle metabolic and performance adaptations that resemble traditional endurance training despite a low total exercise volume. Most HIT studies have employed 'all out', variable-load exercise interventions (e.g. repeated Wingate tests) that may not be safe, practical and/or well tolerated by certain individuals. Our purpose was to determine the performance, metabolic and molecular adaptations to a more practical model of low-volume HIT. Seven men (21 + or - 0.4 years, V(O2peak) = 46 + or - 2 ml kg(-1) min(-1)) performed six training sessions over 2 weeks. Each session consisted of 8-12 x 60 s intervals at approximately 100% of peak power output elicited during a ramp V(O2) peak test (355 + or - 10 W) separated by 75 s of recovery. Training increased exercise capacity, as assessed by significant improvements on both 50 kJ and 750 kJ cycling time trials (P < 0.05 for both). Skeletal muscle (vastus lateralis) biopsy samples obtained before and after training revealed increased maximal activity of citrate synthase (CS) and cytochrome c oxidase (COX) as well as total protein content of CS, COX subunits II and IV, and the mitochondrial transcription factor A (Tfam) (P < 0.05 for all). Nuclear abundance of peroxisome proliferator-activated receptor gamma co-activator 1alpha (PGC-1alpha) was approximately 25% higher after training (P < 0.05), but total PGC-1alpha protein content remained unchanged. Total SIRT1 content, a proposed activator of PGC-1alpha and mitochondrial biogenesis, was increased by approximately 56% following training (P < 0.05). Training also increased resting muscle glycogen and total GLUT4 protein content (both P < 0.05). This study demonstrates that a practical model of low volume HIT is a potent stimulus for increasing skeletal muscle mitochondrial capacity and improving exercise performance. The results also suggest that increases in SIRT1, nuclear PGC-1alpha, and Tfam may be involved in coordinating mitochondrial adaptations in response to HIT in human skeletal muscle.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptation, Physiological / physiology*
  • Biopsy
  • Citrate (si)-Synthase / metabolism
  • DNA-Binding Proteins / metabolism
  • Electron Transport Complex IV / metabolism
  • Energy Metabolism / physiology
  • Exercise / physiology*
  • Glucose Transporter Type 4 / metabolism
  • Glycogen / metabolism
  • Heat-Shock Proteins / metabolism
  • Humans
  • Male
  • Mitochondria, Muscle / enzymology
  • Mitochondria, Muscle / physiology*
  • Mitochondrial Proteins / metabolism
  • Models, Biological*
  • Muscle, Skeletal / pathology
  • Muscle, Skeletal / physiology*
  • Oxygen Consumption / physiology
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
  • Sirtuin 1 / metabolism
  • Transcription Factors / metabolism
  • Young Adult


  • DNA-Binding Proteins
  • Glucose Transporter Type 4
  • Heat-Shock Proteins
  • Mitochondrial Proteins
  • PPARGC1A protein, human
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
  • SLC2A4 protein, human
  • TFAM protein, human
  • Transcription Factors
  • Glycogen
  • Electron Transport Complex IV
  • Citrate (si)-Synthase
  • SIRT1 protein, human
  • Sirtuin 1