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: 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, Symbol ml kg-1 min-1) performed six training sessions over 2 weeks. Each session consisted of 8-12 x 60 s intervals at ~100% of peak power output elicited during a ramp Symbol 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 [gamma] co-activator 1[alpha] (PGC-1[alpha]) was ~25% higher after training (P < 0.05), but total PGC-1[alpha] protein content remained unchanged. Total SIRT1 content, a proposed activator of PGC-1[alpha] 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-1[alpha], and Tfam may be involved in coordinating mitochondrial adaptations in response to HIT in human skeletal muscle.

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