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PGC‐1[alpha] and upstream regulators in human skeletal muscle
Author(s) -
Norrbom Jessica,
Rundqvist Helene,
Sundberg Carl Johan,
Jansson Eva,
Gustafsson Thomas
Publication year - 2008
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.22.1_supplement.753.10
Subject(s) - skeletal muscle , ampk , mitochondrial biogenesis , endocrinology , medicine , activator (genetics) , calcineurin , phosphorylation , nfat , chemistry , biology , microbiology and biotechnology , mitochondrion , protein kinase a , receptor , transplantation
A central component in skeletal muscle remodelling to regular exercise is a higher mitochondrial density. The co‐activator PGC‐1α has been described as a central player in mitochondrial biogenesis and several signaling pathways have been shown to influence PGC‐1α transcription such as calcineurin, MAPK p38 and AMPK in various experimental settings. The aim of the present study was to evaluate the importance of the above‐mentioned pathways and their effect on exercise‐induced PGC‐1α transcription. Skeletal muscle biopsies were obtained from the vastus lateralis muscle from 12 healthy males before, directly after and 2 h after 45 min one‐legged knee extension exercise. One leg exercised with restricted blood flow (R‐leg), the other with non‐restricted blood flow (NR‐leg). Results & Conclusion: PGC‐1α mRNA expression increased significantly 2 h after exercise in the R‐leg, but not in the NR‐leg. The p38 phosphorylation and MCIP‐1 mRNA (a marker of calcineurin activation) increased following exercise regardless of blood flow condition. For pAMPK there was an increased activation in the R‐leg, which could be a possible explanation for the differential regulation of PGC‐1α.