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Acute high‐intensity exercise increases the nuclear abundance of PGC‐1α in equine skeletal muscle
Author(s) -
Mukai Kazutaka,
Kitaoka Yu,
Ohmura Hajime,
Takahashi Toshiyuki,
Matsui Akira,
Aida Hiroko
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.lb821
Subject(s) - mitochondrial biogenesis , skeletal muscle , cytosol , coactivator , mitochondrion , medicine , endocrinology , nucleus , biology , chemistry , microbiology and biotechnology , transcription factor , gene , biochemistry , enzyme
Peroxisome proliferator‐activated receptor gamma coactivator (PGC) ‐1α is a transcriptional coactivator that plays a key role in coordinating mitochondrial biogenesis. It was recently shown in rodent and human skeletal muscles that acute exercise causes a shift in the subcellular localization of PGC‐1α from the cytosol to the nucleus, allowing PGC‐1α to coactivate transcription factors and increase mitochondrial gene expression, but there are no equine data. Our purpose was to examine PGC‐1α protein content in cytosolic and nuclear fractions of equine skeletal muscle following an acute bout of high‐intensity exercise. Ten Thoroughbred horses ran at 115% of maximal oxygen consumption until exhaustion and needle biopsy samples were obtained from the gluteus medius muscle before and immediately after exercise, and after 4 and 24 h of recovery. In response to acute exercise, nuclear PGC‐1α protein significantly increased after 24 h of recovery (p<0.05), but cytosolic PGC‐1α protein was unchanged compared with rest. These results suggest that acute exercise causes translocation of cytosolic PGC‐1α protein to the nucleus to activate mitochondrial biogenesis in horses.