Affiliations 

  • 1 Institute of Integrative Biology, University of Liverpool, Liverpool L69 7ZB, UK
  • 2 Molecular Histology and Cell Growth Unit, INGM - Fondazione Istituto Nazionale Genetica Molecolare, 20122 Milan, Italy
  • 3 Department of Medicine, University of East Anglia, Norwich Research Park, Norwich NR4 7TJ, UK
  • 4 Institute of Integrative Biology, University of Liverpool, Liverpool L69 7ZB, UK; School of Biosciences and Biotechnology, Universiti Kebangsaan Malaysia, 43600 Bangi, Selangor, Malaysia
  • 5 Centre for Proteome Research, Institute of Integrative Biology, University of Liverpool, Liverpool L69 7ZB, UK
  • 6 School of Biosciences, University of Birmingham, Birmingham B15 2TT, UK
  • 7 Pennington Biomedical Research Center, Baton Rouge, LA 70808, USA
  • 8 German Mouse Clinic, Institute of Experimental Genetics, Helmholtz Zentrum München, German Research Center for Environmental Health, Ingolstädter Landstr. 1, 85764 Neuherberg, Germany
  • 9 Sport and Exercise Sciences, Liverpool John Moores University, Liverpool L3 3AF, UK
  • 10 School of Biomedical Sciences, University of Leeds, Leeds LS2 9JT, UK
  • 11 Institute of Ageing and Chronic Disease, University of Liverpool, Liverpool L7 8TX, UK
  • 12 Molecular Histology and Cell Growth Unit, INGM - Fondazione Istituto Nazionale Genetica Molecolare, 20122 Milan, Italy; Dipartimento di Bioscienze, Università degli Studi di Milano, 20133 Milan, Italy
  • 13 Institute of Integrative Biology, University of Liverpool, Liverpool L69 7ZB, UK. Electronic address: f.falciani@liverpool.ac.uk
Cell Rep, 2017 Nov 07;21(6):1507-1520.
PMID: 29117557 DOI: 10.1016/j.celrep.2017.10.040

Abstract

Regular endurance training improves muscle oxidative capacity and reduces the risk of age-related disorders. Understanding the molecular networks underlying this phenomenon is crucial. Here, by exploiting the power of computational modeling, we show that endurance training induces profound changes in gene regulatory networks linking signaling and selective control of translation to energy metabolism and tissue remodeling. We discovered that knockdown of the mTOR-independent factor Eif6, which we predicted to be a key regulator of this process, affects mitochondrial respiration efficiency, ROS production, and exercise performance. Our work demonstrates the validity of a data-driven approach to understanding muscle homeostasis.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.