5/10 Creation of New Mitochondria
Mitochondria are little cell powerhouses that produce energy (ATP). In simple terms, they take the fat and carbohydrates you either eat or store and convert them to usable energy. The more mitochondria you have, the more efficiently your body utilizes the calories you consume.
The number of mitochondria you have can be increased by creating a demand for more energy production. In fact, HIIT is a potent stimulus for the creation of new mitochondria
Developing more mitochondria will help you produce more energy in your muscle, allow you to train harder for longer and so burn more calories. A win win situation when you train smart!
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A practical model of low-volume high-intensity interval training induces mitochondrial biogenesis in human skeletal muscle: potential mechanisms
Jonathan P. Little1, Adeel Safdar1,2, Geoffrey P. Wilkin1, Mark A. Tarnopolsky2, Martin J. Gibala1
Article first published online: 12 MAR 2010
© 2010 The Authors. Journal compilation © 2010 The Physiological Society
The Journal of Physiology
Volume 588, Issue 6, pages 1011–1022, March 2010
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.
Reference Study 
Brief intense interval exercise activates AMPK and p38 MAPK signaling and increases the expression of PGC-1α in human skeletal muscle
Martin J. Gibala1, Sean L. McGee2, Andrew P. Garnham3, Kirsten F. Howlett3, Rodney J. Snow3, and Mark Hargreaves2
+ Author Affiliations
1Department of Kinesiology, McMaster University, Hamilton, Ontario, Canada; 2Department of Physiology, The University of Melbourne, Melbourne, Victoria; and 3School of Exercise and Nutrition Sciences, Deakin University, Burwood, Victoria, Australia
Address for reprint requests and other correspondence: M. Gibala, Dept. of Kinesiology, McMaster Univ., 1280 Main St. West, Hamilton, Ontario, Canada L8S 4K1 (e-mail: email@example.com)
Submitted 8 July 2008. Accepted in final form 20 December 2008.
From a cell signaling perspective, short-duration intense muscular work is typically associated with resistance training and linked to pathways that stimulate growth. However, brief repeated sessions of sprint or high-intensity interval exercise induce rapid phenotypic changes that resemble traditional endurance training. We tested the hypothesis that an acute session of intense intermittent cycle exercise would activate signaling cascades linked to mitochondrial biogenesis in human skeletal muscle. Biopsies (vastus lateralis) were obtained from six young men who performed four 30-s “all out” exercise bouts interspersed with 4 min of rest (<80 kJ total work). Phosphorylation of AMP-activated protein kinase (AMPK; subunits α1 and α2) and the p38 mitogen-activated protein kinase (MAPK) was higher (P ≤ 0.05) immediately after bout 4 vs. preexercise. Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) mRNA was increased approximately twofold above rest after 3 h of recovery (P ≤ 0.05); however, PGC-1α protein content was unchanged. In contrast, phosphorylation of protein kinase B/Akt (Thr308 and Ser473) tended to decrease, and downstream targets linked to hypertrophy (p70 ribosomal S6 kinase and 4E binding protein 1) were unchanged after exercise and recovery. We conclude that signaling through AMPK and p38 MAPK to PGC-1α may explain in part the metabolic remodeling induced by low-volume intense interval exercise, including mitochondrial biogenesis and an increased capacity for glucose and fatty acid oxidation.
Reference Study 
An acute bout of high-intensity interval training increases the nuclear abundance of PGC-1α and activates mitochondrial biogenesis in human skeletal muscle
Jonathan P. Little , Adeel Safdar , David Bishop , Mark A. Tarnopolsky , Martin J. Gibala
American Journal of Physiology – Regulatory, Integrative and Comparative PhysiologyPublished 1 June 2011Vol. 300no. R1303-R1310DOI: 10.1152/ajpregu.00538.2010)