NDLI: Molecular responses to high-intensity interval exercise.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Gibala, Martin
Description	Country affiliation: Canada Author Affiliation: Gibala M ( Department of Kinesiology, McMaster University, 1280 Main Street West, Hamilton, ON L8S 4K1, Canada. gibalam@mcmaster.ca)
Abstract	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 high-intensity interval exercise training (HIT) induce rapid phenotypic changes that resemble traditional endurance training. Given the oxidative phenotype that is rapidly upregulated by HIT, it is plausible that metabolic adaptations to this type of exercise could be mediated in part through signaling pathways normally associated with endurance training. A key controller of oxidative enzyme expression in skeletal muscle is peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC-1alpha), a transcriptional coactivator that serves to coordinate mitochondrial biogenesis. Most studies of acute PGC-1alpha regulation in humans have used very prolonged exercise interventions; however, it was recently shown that a surprisingly small dose of very intense interval exercise, equivalent to only 2 min of all-out cycling, was sufficient to increase PGC-1alpha mRNA during recovery. Intense interval exercise has also been shown to acutely increase the activity of signaling pathways linked to PGC-1alpha and mitochondrial biogenesis, including AMP-activated protein kinase (alpha1 and alpha2 subunits) and the p38 mitogen-activated protein kinase. In contrast, signaling pathways linked to muscle growth, including protein kinase B/Akt and downstream targets p70 ribosomal S6 kinase and 4E binding protein 1, are generally unchanged after acute interval exercise. Signaling through AMP-activated protein kinase and p38 mitogen-activated protein kinase to PGC-1alpha may therefore explain, in part, the metabolic remodeling induced by HIT, including mitochondrial biogenesis and an increased capacity for glucose and fatty acid oxidation.
File Format	HTM / HTML
ISSN	17155312
Issue Number	3
Volume Number	34
e-ISSN	17155320
Journal	Applied Physiology, Nutrition, and Metabolism
Language	English
Publisher	Canadian Science Publishing
Publisher Date	2009-06-01
Publisher Place	Canada
Access Restriction	Subscribed
Subject Keyword	Discipline Physiology Discipline Metabolism Discipline Nutritional Sciences Discipline Sports Medicine Exercise Physiology Muscle, Skeletal Amp-activated Protein Kinases Metabolism Adaptation, Physiological Humans Mitochondria Proto-oncogene Proteins C-akt Journal Article Research Support, Non-u.s. Gov't Review
Content Type	Text
Resource Type	Article
Subject	Nutrition and Dietetics Physiology Endocrinology, Diabetes and Metabolism Physiology (medical) Sports Science

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