Advertisement

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

Authors

  • Jonathan P. Little,

    1. Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, Hamilton, Ontario, Canada L8S 4K1
    Search for more papers by this author
  • Adeel Safdar,

    1. Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, Hamilton, Ontario, Canada L8S 4K1
    2. Departments of Pediatrics and Medicine, McMaster University, Hamilton, Ontario, Canada L8N 3Z5
    Search for more papers by this author
  • Geoffrey P. Wilkin,

    1. Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, Hamilton, Ontario, Canada L8S 4K1
    Search for more papers by this author
  • Mark A. Tarnopolsky,

    1. Departments of Pediatrics and Medicine, McMaster University, Hamilton, Ontario, Canada L8N 3Z5
    Search for more papers by this author
  • Martin J. Gibala

    1. Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, Hamilton, Ontario, Canada L8S 4K1
    Search for more papers by this author

Corresponding author M. J. Gibala: Department of Kinesiology, McMaster University, 1280 Main Street West, Hamilton, ON, Canada L8S 4K1.  Email: gibalam@mcmaster.ca

Abstract

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 ± 0.4 years, inline image ml kg−1 min−1) performed six training sessions over 2 weeks. Each session consisted of 8–12 × 60 s intervals at ∼100% of peak power output elicited during a ramp inline image peak test (355 ± 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 γ co-activator 1α (PGC-1α) was ∼25% higher after training (P < 0.05), but total PGC-1α protein content remained unchanged. Total SIRT1 content, a proposed activator of PGC-1α and mitochondrial biogenesis, was increased by ∼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-1α, and Tfam may be involved in coordinating mitochondrial adaptations in response to HIT in human skeletal muscle.

Ancillary