title: Exercise training leads to a reduction of elevated myostatin levels in patients with chronic heart failure.
abstract: BACKGROUND
  In chronic heart failure (CHF), cardiac cachexia is often associated with the terminal stage of this disease. In animal studies it has been demonstrated that myostatin, a key regulator of skeletal muscle mass, is elevated in advanced stages of this syndrome.
  
  
  METHODS
  The aim of the present study was to investigate the expression of myostatin in patients with late stage CHF (NYHA IIIb) in comparison to healthy subjects. Furthermore the effects of physical exercise on myostatin were analyzed.
  
  
  METHODS
  Twenty-four patients were either randomized to a sedentary control group (CHF-S) or exercise training (CHF-E). At baseline and after 12 weeks mRNA and myostatin protein in the peripheral skeletal muscle as well as myostatin serum concentration were measured. Furthermore 12 age-matched healthy men were compared to all patients at baseline (HC).
  
  
  RESULTS
  CHF patients showed a two-fold increase of myostatin mRNA (p = 0.05) and a 1.7-fold (p = 0.01) augmentation of protein content in skeletal muscle compared to healthy subjects. In late-stage CHF, exercise training led to a 36% reduction of the mRNA and a 23% decrease of the myostatin protein compared to baseline. The serum concentration of myostatin revealed no significant alteration between the groups.
  
  
  CONCLUSIONS
  In the skeletal muscle, myostatin increases significantly in the course of CHF. The observed effects of a significant reduction of myostatin in skeletal muscle after 12 weeks of exercise training demonstrate the reversibility of molecular changes that might be able to halt the devastating process of muscle wasting in chronic heart failure.
authors: Department of Internal Medicine/Cardiology, University of Leipzig, Heart Center, Struempellstrasse 39, Leipzig, Germany. linkea@medizin.uni-leipzig.de
authors: Karsten
authors: K
authors: Lenk
authors: Sandra
authors: S
authors: Erbs
authors: Robert
authors: R
authors: Höllriegel
authors: Ephraim
authors: E
authors: Beck
authors: Axel
authors: A
authors: Linke
authors: Stephan
authors: S
authors: Gielen
authors: Sven Möbius
authors: SM
authors: Winkler
authors: Marcus
authors: M
authors: Sandri
authors: Rainer
authors: R
authors: Hambrecht
authors: Gerhard
authors: G
authors: Schuler
authors: Volker
authors: V
authors: Adams
mesh_terms: D000368:Aged; D001642:Bicycling; D015415:Biomarkers / Q000097:blood; D016009:Chi-Square Distribution; D002908:Chronic Disease; D015536:Down-Regulation; D005081:Exercise Therapy; D005858:Germany; D006333:Heart Failure / Q000097:blood / Q000235:genetics / Q000503:physiopathology / Q000628:therapy*; D006801:Humans; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000378:metabolism*; D055435:Myostatin / Q000097:blood* / Q000235:genetics; D012333:RNA, Messenger / Q000378:metabolism; D057185:Sedentary Behavior; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D015415:Biomarkers; C525911:MSTN protein, human; D055435:Myostatin; D012333:RNA, Messenger