Abstract

Exercise confers numerous health benefits, many of which are thought to stem from exercise-induced mitochondrial biogenesis (EIMB) in skeletal muscle. The transcriptional coactivator PGC-1α, a potent regulator of metabolism in numerous tissues, is widely believed to be required for EIMB. We show here that this is not the case. Mice engineered to lack PGC-1α specifically in skeletal muscle (Myo-PGC-1αKO mice) retained intact EIMB. The exercise capacity of these mice was comparable to littermate controls. Induction of metabolic genes after 2 weeks of in-cage voluntary wheel running was intact. Electron microscopy revealed no gross abnormalities in mitochondria, and the mitochondrial biogenic response to endurance exercise was as robust in Myo-PGC-1αKO mice as in wildtype mice. The induction of enzymatic activity of the electron transport chain by exercise was likewise unperturbed in Myo-PGC-1αKO mice. These data demonstrate that PGC-1α is dispensable for exercise-induced mitochondrial biogenesis in skeletal muscle, in sharp contrast to the prevalent assumption in the field.

Highlights

  • Endurance exercise is a powerful inducer of mitochondrial biogenesis in skeletal muscle [1,2,3]

  • The mice were generated by Cre/Lox recombination and transgenic expression of Cre with a myogenin/MEF2 promoter/enhancer construct, as previously described [35,52,53]. 12-week old female Myo-PGC-1aKO mice and littermate control mice were allowed to exercise in individually housed cages with hanging voluntary running wheels for 12 days

  • The Myo-PGC-1aKO mice provide a good system for assessing the effects of deleting proliferator-activated receptor gamma coactivator1a (PGC-1a) in skeletal muscle without any of the negative effects of germline deletion of PGC-1a

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Summary

Introduction

Endurance exercise is a powerful inducer of mitochondrial biogenesis in skeletal muscle [1,2,3]. Increases in mitochondrial function have been associated with a reduction in diabetes and obesity outcomes, delayed effects of aging, and improved exercise capacity [3,4,5,6]. Many of these benefits are likely due to increased expression of electron transport chain (ETC) enzymes and oxidative phosphorylation (OXPHOS). Members of the nuclear respiratory factor (NRF) and estrogenrelated receptor (ERR) families of transcription factors regulate the expression of the nuclear encoded genes [7,8,9], while Transcription factor A, mitochondrial (Tfam) regulates the expression of mitochondrial encoded genes [10]

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