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...

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Veröffentlicht in:The Journal of physiology 2010-03, Vol.588 (6), p.1011-1022
Hauptverfasser: Little, Jonathan P., Safdar, Adeel, Wilkin, Geoffrey P., Tarnopolsky, Mark A., Gibala, Martin J.
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Sprache:eng
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Zusammenfassung: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, 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 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. Muscles respond to exercise training by developing physiological changes that improve their performance. It has been found that the changes brought about by traditional endurance training can also be produced by high‐intensity interval training. Here a practical form of such training is outlined and shown to be effective (as indicated by changes in mitochondrial capacity and exercise performance). It involves spending 20–30 min, three days a week in cycling that consists of ten 60‐second periods of high‐intensity exercise wi
ISSN:0022-3751
1469-7793
DOI:10.1113/jphysiol.2009.181743