title: Truncated splice variant PGC-1α4 is not associated with exercise-induced human muscle hypertrophy.
abstract: BACKGROUND
  A truncated PGC-1α splice variant (PGC-1α4) has been implicated in the regulation of resistance exercise (RE)-induced muscle hypertrophy, and basal expression levels said to be augmented in response to concurrent aerobic (AE) and RE training.
  
  
  OBJECTIVE
  The current study investigated human muscle truncated and non-truncated PGC-1α transcripts in response to both acute and chronic RE, and with or without preceding AE (AE+RE).
  
  
  METHODS
  Ten men performed 5 weeks of unilateral AE+RE and RE training. Before (untrained) and after (trained) this intervention, PGC-1α transcripts were assessed in vastus lateralis muscle biopsies obtained before and 3 h after acute RE, with or without preceding AE. Additionally, samples were collected 72 h after the last exercise bout of the training programme.
  
  
  RESULTS
  The truncated splice variant increased (P < 0.05) its expression after acute exercise regardless of mode. However, the expression was greater (P < 0.05) after AE+RE than RE. Other PGC-1α transcripts showed similar response. Truncated transcripts originated from both the alternative and proximal promoter, and AE+RE increased PGC-1α expression from both promoter sites. RE induced transcripts from the alternative promoter only. PGC-1α expressions after acute exercise were comparable across isoforms in both untrained and trained muscle. Steady-state levels of isoforms were unchanged after 5-week training (P > 0.05). Exercise-induced expression of PGC-1α variants did not correlate with changes in muscle size or strength (P > 0.05).
  
  
  CONCLUSIONS
  Our results do not support the view that truncated PGC-1α coordinates exercise-induced hypertrophy in human skeletal muscle. Rather, all PGC-1α isoforms appear to be regulated transiently in response to acute exercise and regardless of mode.
authors.affiliation: Department of Health Sciences, Mid Sweden University, Östersund, Sweden.
authors.forename: T R
authors.initials: TR
authors.lastname: Lundberg
authors.forename: R
authors.initials: R
authors.lastname: Fernandez-Gonzalo
authors.forename: J
authors.initials: J
authors.lastname: Norrbom
authors.forename: H
authors.initials: H
authors.lastname: Fischer
authors.forename: P A
authors.initials: PA
authors.lastname: Tesch
authors.forename: T
authors.initials: T
authors.lastname: Gustafsson
mesh_terms: D000328:Adult; D015444:Exercise / Q000502:physiology*; D006801:Humans; D006984:Hypertrophy / Q000235:genetics / Q000378:metabolism; D008297:Male; D018482:Muscle, Skeletal / Q000378:metabolism*; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; D020033:Protein Isoforms / Q000235:genetics / Q000378:metabolism; D060888:Real-Time Polymerase Chain Reaction; D055070:Resistance Training; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014157:Transcription Factors / Q000235:genetics* / Q000378:metabolism; D055815:Young Adult
chemical_list: C486497:PPARGC1A protein, human; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; D020033:Protein Isoforms; D014157:Transcription Factors
keywords: aerobic exercise; concurrent exercise; endurance; gene expression; muscle strength; resistance exercise