Exercise, skeletal muscle metabolism and health

 

Mark Hargreaves

Department of Physiology, The University of Melbourne, Australia

 

Skeletal muscle, by virtue of his mass and metabolic characteristics, has a major role in the regulation of whole body carbohydrate, lipid and protein metabolism.  A single exercise bout increases muscle insulin sensitivity and plasma triglyceride clearance, effects that are partly mediated by activation of key signalling pathways and downstream targets, hormonal changes and substrate depletion.  It has also been demonstrated that contracting skeletal muscle releases bioactive molecules (“myokines”) that contribute to physiological regulation during exercise and the systemic benefits of exercise.  Regular exercise training increases the capacity for substrate storage, mobilization and oxidation.  Key metabolic adaptations to training include increased muscle mitochondrial mass, enhanced sensitivity to various hormones, notably insulin, and increased expression of key enzymes and substrate transporters in skeletal muscle.  Collectively, these adaptations have positive benefits for metabolic and cardiovascular health.  In recent years, we have been particularly interested in the effects of acute and chronic exercise on skeletal muscle GLUT4 expression.  A single bout of exercise increases skeletal muscle GLUT4 mRNA and over time this results in increased GLUT4 protein expression.  A key transcriptional regulator is myocyte enhancer factor 2 (MEF2), which is subject to regulation by the class II histone deacetylase HDAC5 (a known transcriptional repressor) and phosphorylation.  Increased understanding of the molecular regulation of the expression of key proteins, such as GLUT4, is important to inform the development of optimal exercise interventions and associated therapeutic strategies to enhance health and well being.

 

The original work of the author has been supported by the Diabetes Australia Research Trust.    

 

Key words: exercise, skeletal muscle, mitochondria, GLUT4, MEF2, HDAC5