Transcriptional control, but not subcellular location, of PGC-1α is altered following exercise in a hot environment

Matthew W. Heesch, Robert J. Shute, Jodi L. Kreiling, Dustin R. Slivka

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25 Scopus citations

Abstract

The purpose of this study was to determine mitochondrial biogenesisrelated mRNA expression, binding of transcription factors to the peroxisome proliferator-activated receptor- coactivator 1- (PGC-1) promoter, and subcellular location of PGC-1 protein in human skeletal muscle following exercise in a hot environment compared with a room temperature environment. Recreationally trained males (n 11) completed two trials in a temperature-and humiditycontrolled environmental chamber. Each trial consisted of cycling in either a hot (H) or room temperature (C) environment (33 and 20C, respectively) for 1 h at 60% of maximum wattage (Wmax) followed by 3 h of supine recovery at room temperature. Muscle biopsies were taken from the vastus lateralis pre-, post-, and 3 h postexercise. PGC-1 mRNA increased post (P 0.039)-and 3 h postexercise in C (P 0.002). PGC-1, estrogen-related receptor- (ERR), and nuclear respiratory factor 1 (NRF-1) mRNA was all lower in H than C post (P 0.038, P<0.001, and P 0.030, respectively)-and 3 h postexercise (P 0.035, P 0.007, and P<0.001, respectively). Binding of cAMP response element-binding protein (CREB) (P 0.005), myocyte enhancer factor 2 (MEF2) (P 0.047), and FoxO forkhead box class-O1 (FoxO1) (P 0.010) to the promoter region of the PGC-1 gene was lower in H than C. Nuclear PGC-1 protein increased postexercise in both H and C (P 0.029) but was not different between trials (P 0.602). These data indicate that acute exercise in a hot environment blunts expression of mitochondrial biogenesis-related mRNA, due to decreased binding of CREB, MEF2, and FoxO1 to the PGC-1 promoter.

Original languageEnglish
Pages (from-to)741-749
Number of pages9
JournalJournal of Applied Physiology
Volume121
Issue number3
DOIs
StatePublished - Sep 2016

Funding

We thank Terrence Laursen, Matthew Bubak, Nicholas Dinan, and David Taylor La Salle for assistance with data collection. Additionally, we thank Dr. Kris Berg, Dr. Jeffery French, and Dr. Nicholas Stergiou for reviewing and providing feedback on the manuscript. This publication was made possible by National Institute for General Medical Science (NIGMS) Grant 5P20GM103427, a component of the National Institutes of Health (NIH) and its contents are the sole responsibility of the authors and do not necessarily represent the official views of NIGMS or NIH. Additional funding was provided by a Graduate Research and Creative Activity Grant from the University of Nebraska at Omaha Office for Research and Creative Activity.

Funder number
5P20GM103427

    Keywords

    • Heat stress
    • Mitochondrial biogenesis
    • Skeletal muscle

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