title: Human muscle gene expression following resistance exercise and blood flow restriction.
abstract: BACKGROUND
  Blood flow restriction in combination with low-intensity resistance exercise (REFR) increases skeletal muscle size to a similar extent as compared with traditional high-intensity resistance exercise training. However, there are limited data describing the molecular adaptations that occur after REFR.
  
  
  OBJECTIVE
  To determine whether hypoxia inducible factor-1 alpha (HIF-1alpha) and REDD1 mRNA are expressed differently in REFR compared with low-intensity resistance exercise with no blood flow restriction (CONTROL). Secondly, to determine whether low-intensity resistance exercise is able to induce changes in mRNA expression of several anabolic and catabolic genes as typically seen with high-intensity resistance exercise.
  
  
  METHODS
  Six subjects were studied at baseline and 3 h after a bout of leg resistance exercise (20% 1RM) in REFR and CONTROL subjects. Each subject participated in both groups, with 3 wk separating each visit. Muscle biopsy samples were analyzed for mRNA expression, using qRT-PCR.
  
  
  RESULTS
  Our primary finding was that there were no differences between CONTROL and REFR for any of the selected genes at 3 h after exercise (P > 0.05). However, low-intensity resistance exercise increased HIF-1alpha, p21, MyoD, and muscle RING finger 1 (MuRF1) mRNA expression and decreased REDD1 and myostatin mRNA expression in both groups (P < 0.05).
  
  
  CONCLUSIONS
  Low-intensity resistance exercise can alter skeletal muscle mRNA expression of several genes associated with muscle growth and remodeling, such as REDD1, HIF-1alpha, MyoD, MuRF1, and myostatin. Further, the results from REFR and CONTROL were similar, indicating that the changes in early postexercise gene expression were attributable to the low-intensity resistance exercise bout, and not blood flow restriction.
authors.affiliation: Department of Physical Therapy, University of Texas Medical Branch, Galveston, TX, USA.
authors.forename: Micah J
authors.initials: MJ
authors.lastname: Drummond
authors.forename: Satoshi
authors.initials: S
authors.lastname: Fujita
authors.forename: Takashi
authors.initials: T
authors.lastname: Abe
authors.forename: Abe
authors.initials: A
authors.lastname: Takashi
authors.forename: Hans C
authors.initials: HC
authors.lastname: Dreyer
authors.forename: Elena
authors.initials: E
authors.lastname: Volpi
authors.forename: Blake B
authors.initials: BB
authors.lastname: Rasmussen
mesh_terms: D000222:Adaptation, Physiological; D000328:Adult; D016022:Case-Control Studies; D018592:Cross-Over Studies; D015870:Gene Expression; D006801:Humans; D007537:Isometric Contraction / Q000502:physiology*; D008297:Male; D018482:Muscle, Skeletal / Q000098:blood supply / Q000502:physiology*; D055435:Myostatin; D011446:Prospective Studies; D011494:Protein Kinases; D012333:RNA, Messenger / Q000235:genetics; D015424:Reperfusion; D058570:TOR Serine-Threonine Kinases; D016212:Transforming Growth Factor beta; D014891:Weight Lifting / Q000502:physiology*
chemical_list: C525911:MSTN protein, human; D055435:Myostatin; D012333:RNA, Messenger; D016212:Transforming Growth Factor beta; D011494:Protein Kinases; C546842:MTOR protein, human; D058570:TOR Serine-Threonine Kinases