title: Aerobic interval training attenuates remodelling and mitochondrial dysfunction in the post-infarction failing rat heart.
abstract: OBJECTIVE
  Following a large myocardial infarction (MI), remaining viable muscle often undergoes pathological remodelling and progresses towards chronic heart failure. Mitochondria may also be affected by this process and, due to their functional importance, likely contribute to the progression of the disease. Aerobic interval training (AIT) has been shown effective in diminishing pathological myocardial transformation, but the effects of AIT on mitochondrial function in hearts undergoing remodelling are not known.
  
  
  RESULTS
  Adult female Sprague-Dawley rats were randomized to either 8 weeks of aerobic interval treadmill running (5 days/week), which started 4 weeks after left coronary artery ligation (MI-Trained), or a sedentary group (MI-Sedentary). Echocardiography was performed before and after the 8-week period, at which point the left ventricles (LVs) were also harvested. Twelve weeks after surgery, MI-Sedentary rats had significantly lower LV fractional shortening compared with MI-Trained rats. Complex I-dependent respiration assessed in isolated LV mitochondria was decreased by ∼37% in MI-Sedentary and 17% in MI-Trained animals (group differences P < 0.05), compared with sham-operated animals. This was paralleled with diminished ATP production and increased degree of protein oxidation in MI-Sedentary rats. The enzymatic activity of complex I was also decreased to a greater extent in MI-Sedentary than in MI-Trained animals, with no evidence of its reduced expression. When complex II substrate was used, no differences among the three groups were observed.
  
  
  CONCLUSIONS
  Exercise reduces LV contractile deterioration in post-infarction heart failure and alleviates the extent of mitochondrial dysfunction, which is paralleled with preserved complex I activity.
authors.affiliation: Department of Physiology, University of Split School of Medicine, Soltanska 2, Split 21000, Croatia.
authors.forename: Jasenka
authors.initials: J
authors.lastname: Kraljevic
authors.forename: Jasna
authors.initials: J
authors.lastname: Marinovic
authors.forename: Danijel
authors.initials: D
authors.lastname: Pravdic
authors.forename: Petra
authors.initials: P
authors.lastname: Zubin
authors.forename: Zeljko
authors.initials: Z
authors.lastname: Dujic
authors.forename: Ulrik
authors.initials: U
authors.lastname: Wisloff
authors.forename: Marko
authors.initials: M
authors.lastname: Ljubkovic
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D042967:Electron Transport Complex I / Q000378:metabolism; D042963:Electron Transport Complex II / Q000378:metabolism; D004734:Energy Metabolism; D005081:Exercise Therapy; D005260:Female; D006333:Heart Failure / Q000000981:diagnostic imaging / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology / Q000628:therapy*; D008929:Mitochondria, Heart / Q000378:metabolism*; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000150:complications*; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D014463:Ultrasonography; D016277:Ventricular Function, Left; D020257:Ventricular Remodeling
chemical_list: D042963:Electron Transport Complex II; D042967:Electron Transport Complex I
keywords: Aerobic interval training; Animal model; Heart failure; Mitochondria; Myocardial infarction