A practical model of low-volume high-intensity interval training induces mitochondrial biogenesis in human skeletal muscle: potential mechanisms.
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.
Little
Jonathan P
JP
Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, Hamilton, Ontario, Canada L8S 4K1.
Safdar
Adeel
A
Wilkin
Geoffrey P
GP
Tarnopolsky
Mark A
MA
Gibala
Martin J
MJ
D000222:Adaptation, Physiological / Q000502:physiology*; D001706:Biopsy; D002950:Citrate (si)-Synthase / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000378:metabolism; D003576:Electron Transport Complex IV / Q000378:metabolism; D004734:Energy Metabolism / Q000502:physiology; D015444:Exercise / Q000502:physiology*; D051275:Glucose Transporter Type 4 / Q000378:metabolism; D006003:Glycogen / Q000378:metabolism; D006360:Heat-Shock Proteins / Q000378:metabolism; D006801:Humans; D008297:Male; D008931:Mitochondria, Muscle / Q000201:enzymology / Q000502:physiology*; D024101:Mitochondrial Proteins / Q000378:metabolism; D008954:Models, Biological; D018482:Muscle, Skeletal / Q000473:pathology / Q000502:physiology*; D010101:Oxygen Consumption / Q000502:physiology; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; D056564:Sirtuin 1 / Q000378:metabolism; D014157:Transcription Factors / Q000378:metabolism; D055815:Young Adult
D004268:DNA-Binding Proteins; D051275:Glucose Transporter Type 4; D006360:Heat-Shock Proteins; D024101:Mitochondrial Proteins; C486497:PPARGC1A protein, human; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; C495692:SLC2A4 protein, human; C499631:TFAM protein, human; D014157:Transcription Factors; D006003:Glycogen; D003576:Electron Transport Complex IV; D002950:Citrate (si)-Synthase; C447939:SIRT1 protein, human; D056564:Sirtuin 1