title: Previous exercise training increases levels of PPAR-α in long-term post-myocardial infarction in rats, which is correlated with better inflammatory response.
abstract: OBJECTIVE
  Exercise is a protective factor for cardiovascular morbidity and mortality, with unclear mechanisms. Changing the myocardial metabolism causes harmful consequences for heart function and exercise contributes to metabolic adjustment modulation. Peroxisome proliferator-activated receptors (PPARs) are also myocardium metabolism regulators capable of decreasing the inflammatory response. We hypothesized that PPAR-α is involved in the beneficial effects of previous exercise on myocardial infarction (MI) and cardiac function, changing the expression of metabolic and inflammatory response regulators and reducing myocardial apoptosis, which partially explains the better outcome.
  
  
  RESULTS
  Exercised rats engaged in swimming sessions for 60 min/day, 5 days/week, for 8 weeks. Both the exercised rats and sedentary rats were randomized to MI surgery and followed for 1 week (EI1 or SI1) or 4 weeks (EI4 or SI4) of healing or to sham groups. Echocardiography was employed to detect left ventricular function and the infarct size. Additionally, the TUNEL technique was used to assess apoptosis and immunohistochemistry was used to quantitatively analyze the PPAR-α, TNF-α and NF-κB antigens in the infarcted and non-infarcted myocardium. MI-related mortality was higher in SI4 than in EI4 (25% vs 12%), without a difference in MI size. SI4 exhibited a lower shortening fraction than EI4 did (24% vs 35%) and a higher apoptosis/area rate (3.97±0.61 vs 1.90±1.82) in infarcted areas (both p=0.001). Immunohistochemistry also revealed higher TNF-α levels in SI1 than in EI1 (9.59 vs 4.09, p<0.001) in infarcted areas. In non-infarcted areas, EI4 showed higher levels of TNF-α and positive correlations between PPAR-α and NF-κB (r=0.75, p=0.02), in contrast to SI4 (r=0.05, p=0.87).
  
  
  CONCLUSIONS
  Previously exercised animals had better long-term ventricular function post-MI, in addition to lower levels of local inflammatory markers and less myocardial apoptosis, which seemed to be related to the presence of PPAR-α.
authors.affiliation: Laboratório de Patologia Cardíaca, Instituto do Coração (InCor), Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo/, SP, Brazil.
authors.forename: Marília Harumi Higuchi
authors.initials: MH
authors.lastname: Santos
authors.affiliation: Laboratório de Patologia Cardíaca, Instituto do Coração (InCor), Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo/, SP, Brazil.
authors.forename: Maria de Lourdes
authors.initials: Mde L
authors.lastname: Higuchi
authors.affiliation: Universidade Federal de São Paulo (UNIFESP), Cardiologia, São Paulo/, Brazil.
authors.forename: Paulo J F
authors.initials: PJ
authors.lastname: Tucci
authors.affiliation: Laboratório de Patologia Cardíaca, Instituto do Coração (InCor), Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo/, SP, Brazil.
authors.forename: Shérrira M
authors.initials: SM
authors.lastname: Garavelo
authors.affiliation: Laboratório de Patologia Cardíaca, Instituto do Coração (InCor), Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo/, SP, Brazil.
authors.forename: Márcia M
authors.initials: MM
authors.lastname: Reis
authors.affiliation: Fisiologia Cardíaca, São Paulo/, SP, Brazil.
authors.forename: Ednei L
authors.initials: EL
authors.lastname: Antonio
authors.affiliation: Laboratório de Patologia Cardíaca, Instituto do Coração (InCor), Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo/, SP, Brazil.
authors.forename: Andrey J
authors.initials: AJ
authors.lastname: Serra
authors.affiliation: Laboratório de Patologia Cardíaca, Instituto do Coração (InCor), Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo/, SP, Brazil.
authors.forename: Raul Cavalcante
authors.initials: RC
authors.lastname: Maranhão
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D005260:Female; D007249:Inflammation / Q000378:metabolism; D023421:Models, Animal; D009203:Myocardial Infarction / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000473:pathology; D016328:NF-kappa B / Q000378:metabolism; D047493:PPAR alpha / Q000032:analysis / Q000378:metabolism*; D010805:Physical Conditioning, Animal / Q000502:physiology*; D011897:Random Allocation; D017208:Rats, Wistar; D013995:Time; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014463:Ultrasonography; D016276:Ventricular Function / Q000502:physiology
chemical_list: D016328:NF-kappa B; D047493:PPAR alpha; D014409:Tumor Necrosis Factor-alpha