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Ramping up the signal: promoting endurance training adaptation in skeletal muscle by nutritional manipulation
Author(s) -
Hawley John A,
Morton James P
Publication year - 2014
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12246
Subject(s) - mitochondrial biogenesis , skeletal muscle , endurance training , glycogen , biology , protein kinase a , cellular adaptation , microbiology and biotechnology , mitochondrion , peroxisome , medicine , endocrinology , receptor , kinase , gene , biochemistry
Summary Mitochondrial biogenesis in skeletal muscle results from the cumulative effect of transient increases in m RNA transcripts encoding mitochondrial proteins in response to repeated exercise sessions. This process requires the coordinated expression of both nuclear and mitochondrial (mt) DNA genomes and is regulated, for the most part, by the peroxisome proliferator‐activated receptor γ coactivator 1 α . Several other exercise‐inducible proteins also play important roles in promoting an endurance phenotype, including AMP‐activated protein kinase, p38 mitogen‐activated protein kinase and tumour suppressor protein p53. Commencing endurance‐based exercise with low muscle glycogen availability results in greater activation of many of these signalling proteins compared with when the same exercise is undertaken with normal glycogen concentration, suggesting that nutrient availability is a potent signal that can modulate the acute cellular responses to a single bout of exercise. When exercise sessions are repeated in the face of low glycogen availability (i.e. chronic training), the phenotypic adaptations resulting from such interventions are also augmented.