Previous exercise training increases levels of PPAR-α in long-term post-myocardial infarction in rats, which is correlated with better inflammatory response

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. METHODS AND 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). CONCLUSION: 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.

Prior exercise training does not prevent acute cardiac alterations after myocardial infarction in female rats

OBJECTIVE: This study aimed to investigate whether previous exercise training could prevent or attenuate acute cardiac alterations after myocardial infarction. METHODS: Female rats were submitted to swim training (1 h/day; 5 days/week) or allowed to remain sedentary for 8 weeks. Afterwards, they were randomly assigned to left coronary artery occlusion or sham surgery. After this procedure, the rats remained sedentary for one week until euthanasia. Cardiac structural and functional analyses were performed using Doppler echocardiography. The rats that had a moderate or large infarct size were included in the evaluations. The data (mean + SEM) were analyzed using a two-way ANOVA model followed byTukey's post-hoc test. RESULTS: After the surgery, no significant difference between the exercise and sedentary groups was observed in the left ventricular infarct sizes (34.58 + 3.04 vs. 37.59 + 3.07). In another group of rats evaluated with Evans blue 1 h after myocardial infarction, no siginificant difference in the area at risk was observed between the exercised and sedentary rats (49.73 + 1.52 vs. 45.48 + 3.49). The changes in the left ventricular fractional areas for the exercised and sedentary myocardial infarction groups (36 + 2 percent and 39 + 3 percent, respectively) were smaller than those for the exercise sham surgery (ES, 67+1 percent) and sedentary sham surgery (SS, 69 + 2 percent) groups. The E/A was higher in the sedentary myocardial infarction (4.4 + 0.3) and exercised myocardial infarction (5.5 + 0.3) rats than in the SS (2.4 + 0.1) and ES (2.2 + 0.1) rats. CONCLUSION: Previous swim training of female rats does not attenuate systolic and diastolic function alterations after myocardial infarction induced by left coronary artery occlusion, suggesting that cardioprotection cannot be provided by exercise training in this experimental model.

A função mecânica do miocárdio remanescente a um infarto do miocárdio é normal durante o período de cicatrização, embora exista insuficiência cardíaca / Mechanical function is normal in remanent myocardium during the healing period of myocardial infarction - despite congestive heart failure

OBJETIVO: A relação temporal entre disfunção ventricular (DV) após infarto do miocárdio (IM) e função mecânica do miocárdio remanescente não está estabelecida. O trabalho analisou, por ecodopplercardiograma (ECO), a função ventricular de ratos com IM de grandes dimensões e a função mecânica de músculos papilares (MP) no término do período de cicatrização. MÉTODOS: Estudados ECO e MP de 9 ratos Wistar (IM), três semanas após IM e 9 controles (C). Determinaram-se: tensão desenvolvida (TD) e sua primeira derivada positiva e negativa, tempo de pico de tensão, tensão de repouso e tempo de relaxamento a 50 por cento de TD em concentrações de cálcio (em mM) de 0,5, 1,0, 1,5, 2,0 e 2,5. Após rianodina, foram promovidas contrações tetânicas em concentrações de cálcio de 1,5, 2,5 e 5,0. RESULTADOS: O ECO caracterizou DV com marcada anormalidade do volume diastólico e da fração de ejeção do VE, além de nítido padrão restritivo do fluxo sangüíneo pela valva mitral. Não foi identificada diferença significante entre os dados de mecânica miocárdica dos ratos IM e C. CONCLUSÃO: A insuficiência cardíaca (IC) que ocorre em ratos com IM > 40 por cento do VE, no final do período de cicatrização, não depende de disfunção miocárdica. As modificações estruturais da câmara e a menor população de miócitos devem fundamentar a DV e a IC.