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This Article Full Text Full Text (PDF) All Versions of this Article: 294/2/E463    most recent 00666.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Leick, L. Articles by Pilegaard, H. Search for Related Content PubMed PubMed Citation Articles by Leick, L. Articles by Pilegaard, H.

PGC-1 is not mandatory for exercise- and training-induced adaptive gene responses in mouse skeletal muscle

¹Centre of Inflammation and Metabolism and Copenhagen Muscle Research Centre, Department of Molecular Biology, and ²Copenhagen Muscle Research Centre, Department of Human Physiology, Institute of Exercise and Sport Sciences, University of Copenhagen, Copenhagen, Denmark; and ³Institute of Neurosciences and Department of Cellular Biology, Physiology, and Immunology, Autonomous University of Barcelona, Barcelona, Spain

Submitted 18 October 2007 ; accepted in final form 6 December 2007

The aim of the present study was to test the hypothesis that peroxisome proliferator activated receptor- coactivator (PGC) 1 is required for exercise-induced adaptive gene responses in skeletal muscle. Whole body PGC-1 knockout (KO) and littermate wild-type (WT) mice performed a single treadmill-running exercise bout. Soleus and white gastrocnemius (WG) were obtained immediately, 2 h, or 6 h after exercise. Another group of PGC-1 KO and WT mice performed 5-wk exercise training. Soleus, WG, and quadriceps were obtained 37 h after the last training session. Resting muscles of the PGC-1 KO mice had lower (20%) cytochrome c (cyt c), cytochrome oxidase (COX) I, and aminolevulinate synthase (ALAS) 1 mRNA and protein levels than WT, but similar levels of AMP-activated protein kinase (AMPK) 1, AMPK2, and hexokinase (HK) II compared with WT mice. A single exercise bout increased phosphorylation of AMPK and acetyl-CoA carboxylase-β and the level of HKII mRNA similarly in WG of KO and WT. In contrast, cyt c mRNA in soleus was upregulated in WT muscles only. Exercise training increased cyt c, COXI, ALAS1, and HKII mRNA and protein levels equally in WT and KO animals, but cyt c, COXI, and ALAS1 expression remained 20% lower in KO animals. In conclusion, lack of PGC-1 reduced resting expression of cyt c, COXI, and ALAS1 and exercise-induced cyt c mRNA expression. However, PGC-1 is not mandatory for training-induced increases in ALAS1, COXI, and cyt c expression, showing that factors other than PGC-1 can exert these adaptations.

peroxisome proliferator-activated receptor- coactivator; mitochondrial biogenesis; gene expression

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