title: Exercise training prior to myocardial infarction attenuates cardiac deterioration and cardiomyocyte dysfunction in rats.
abstract: OBJECTIVE
  The present study was performed to investigate 1) whether aerobic exercise training prior to myocardial infarction would prevent cardiac dysfunction and structural deterioration and 2) whether the potential cardiac benefits of aerobic exercise training would be associated with preserved morphological and contractile properties of cardiomyocytes in post-infarct remodeled myocardium.
  
  
  METHODS
  Male Wistar rats underwent an aerobic exercise training protocol for eight weeks. The rats were then assigned to sham surgery (SHAM), sedentary lifestyle and myocardial infarction or exercise training and myocardial infarction groups and were evaluated 15 days after the surgery. Left ventricular tissue was analyzed histologically, and the contractile function of isolated myocytes was measured. Student's t-test was used to analyze infarct size and ventricular wall thickness, and the other parameters were analyzed by the Kruskal-Wallis test followed by Dunn's test or a one-way analysis of variance followed by Tukey's test (p<0.05).
  
  
  RESULTS
  Myocardial infarctions in exercise-trained animals resulted in a smaller myocardial infarction extension, a thicker infarcted wall and less collagen accumulation as compared to myocardial infarctions in sedentary animals. Myocardial infarction-induced left ventricular dilation and cardiac dysfunction, as evaluated by +dP/dt and -dP/dt, were both prevented by previous aerobic exercise training. Moreover, aerobic exercise training preserved cardiac myocyte shortening, improved the maximum shortening and relengthening velocities in infarcted hearts and enhanced responsiveness to calcium.
  
  
  CONCLUSIONS
  Previous aerobic exercise training attenuated the cardiac dysfunction and structural deterioration promoted by myocardial infarction, and such benefits were associated with preserved cardiomyocyte morphological and contractile properties.
authors.affiliation: Department of General Biology, Federal University of Viçosa, Viçosa/G, Brazil. luizbozi@usp.br
authors.forename: Luiz Henrique Marchesi
authors.initials: LH
authors.lastname: Bozi
authors.forename: Izabel Regina dos Santos Costa
authors.initials: IR
authors.lastname: Maldonado
authors.forename: Marcelo Perim
authors.initials: MP
authors.lastname: Baldo
authors.forename: Márcia Ferreira da
authors.initials: MF
authors.lastname: Silva
authors.forename: José Bianco Nascimento
authors.initials: JB
authors.lastname: Moreira
authors.forename: Rômulo Dias
authors.initials: RD
authors.lastname: Novaes
authors.forename: Regiane Maria Soares
authors.initials: RM
authors.lastname: Ramos
authors.forename: José Geraldo
authors.initials: JG
authors.lastname: Mill
authors.forename: Patricia Chakur
authors.initials: PC
authors.lastname: Brum
authors.forename: Leonardo Bonato
authors.initials: LB
authors.lastname: Felix
authors.forename: Thales Nicolau Prímola
authors.initials: TN
authors.lastname: Gomes
authors.forename: Antônio José
authors.initials: AJ
authors.lastname: Natali
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D006321:Heart / Q000503:physiopathology*; D006439:Hemodynamics / Q000502:physiology; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology; D009203:Myocardial Infarction / Q000503:physiopathology* / Q000517:prevention & control*; D032383:Myocytes, Cardiac / Q000502:physiology*; D010805:Physical Conditioning, Animal / Q000502:physiology*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D016277:Ventricular Function, Left / Q000502:physiology