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

By J. Little, A. Safdar, G. Wilkin, M. Tarnopolsky, M. Gibala. Journal of Physiology, 2010

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Physiological adaptations to low‐volume, high‐intensity interval training in health and disease (2012, methodology): “Similar to endurance exercise (Wright et al. 2007; Little et al. 2010a), acute Wingate-based HIT may activate PGC-1 by increasing its nuclear translocation (Little et al. 2011b).”
Exercise metabolism and the molecular regulation of skeletal muscle adaptation. (2013, background): “Conversely, short-term interval training increases SIRT1 expression in skeletal muscle (Little et al., 2010), while higher SIRT3 protein is reported in Table 3.”
Metabolic Syndrome and Insulin Resistance: Underlying Causes and Modification by Exercise Training (2013, positive): “(401) used a more practical six sessions of 8 to 12 60-s cycle sprints at 100% of peak power output achieved during a VO2max test and noted 119% increases in GLUT-4.”
Low-volume high-intensity interval training reduces hyperglycemia and increases muscle mitochondrial capacity in patients with type 2 diabetes. (2011, methodology): “Given the potency of low-volume HIT to induce mitochondrial biogenesis in young, healthy subjects (8, 16), we hypothesized that HIT might also increase mitochondrial capacity in skeletal muscle of individuals with T2D.”