title: Enhanced glucose metabolism is preserved in cultured primary myotubes from obese donors in response to exercise training.
abstract: BACKGROUND
  It was suggested that human cultured primary myotubes retain the metabolic characteristics of their donor in vitro.
  
  
  OBJECTIVE
  The aim of the present study was to investigate whether the metabolic responses to endurance training are also conserved in culture.
  
  
  METHODS
  Middle-aged obese subjects completed an 8-week supervised aerobic exercise training program in which vastus lateralis muscle biopsies were collected before and after training.
  
  
  METHODS
  Anthropometric and blood parameters, as well as aerobic capacity, were assessed before and after training. Muscle biopsies were either used for Western blot analysis or digested to harvest myogenic progenitors that were differentiated into myotubes. Glucose oxidation, palmitate oxidation, and glycogen synthesis assays were performed on myotubes before and after training. Gene expression was assessed by real-time quantitative PCR.
  
  
  RESULTS
  Our data indicate that in parallel of in vivo improvement of whole-body aerobic capacity and glucose metabolism, biopsy-derived primary myotubes showed similar patterns in vitro. Indeed, glucose oxidation, glycogen synthesis, and inhibition of palmitate oxidation by glucose were enhanced in myotubes after training. This was associated with consistent changes in the expression of metabolism-linked genes such as GLUT1, PDK4, and PDHA1. Interestingly, no difference in myogenic differentiation capacity was observed before and after training.
  
  
  CONCLUSIONS
  Aerobic exercise training is associated with metabolic adaptations in vivo that are preserved in human cultured primary myotubes. It can be hypothesized that skeletal muscle microenvironmental changes induced by endurance training lead to metabolic imprinting on myogenic progenitor cells.
authors.affiliation: Institut National de la Santé et de la Recherche Médicale (INSERM), Unité Mixte de Recherche (UMR) 1048, Obesity Research Laboratory, 31432 Toulouse, France.
authors.forename: Virginie
authors.initials: V
authors.lastname: Bourlier
authors.forename: Céline
authors.initials: C
authors.lastname: Saint-Laurent
authors.forename: Katie
authors.initials: K
authors.lastname: Louche
authors.forename: Pierre-Marie
authors.initials: PM
authors.lastname: Badin
authors.forename: Claire
authors.initials: C
authors.lastname: Thalamas
authors.forename: Isabelle
authors.initials: I
authors.lastname: de Glisezinski
authors.forename: Dominique
authors.initials: D
authors.lastname: Langin
authors.forename: Coralie
authors.initials: C
authors.lastname: Sengenes
authors.forename: Cedric
authors.initials: C
authors.lastname: Moro
mesh_terms: D015444:Exercise; D005081:Exercise Therapy; D005947:Glucose / Q000378:metabolism*; D051272:Glucose Transporter Type 1 / Q000235:genetics / Q000378:metabolism; D006003:Glycogen / Q000096:biosynthesis; D006801:Humans; D008297:Male; D008875:Middle Aged; D018485:Muscle Fibers, Skeletal / Q000378:metabolism* / Q000473:pathology; D009765:Obesity / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D010084:Oxidation-Reduction; D019308:Palmitic Acid / Q000378:metabolism; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism; D030481:Pyruvate Dehydrogenase (Lipoamide) / Q000235:genetics / Q000378:metabolism; D000081382:Pyruvate Dehydrogenase Acetyl-Transferring Kinase; D052097:Quadriceps Muscle / Q000378:metabolism* / Q000473:pathology
chemical_list: D051272:Glucose Transporter Type 1; C000631432:PDK4 protein, human; D000081382:Pyruvate Dehydrogenase Acetyl-Transferring Kinase; D019308:Palmitic Acid; D006003:Glycogen; D030481:Pyruvate Dehydrogenase (Lipoamide); C065640:pyruvate dehydrogenase E1alpha subunit; D017346:Protein Serine-Threonine Kinases; D005947:Glucose