Influência do exercício físico resistido sobre a remodelação cardíaca de ratos com infarto do miocárdio
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Data
2019-02-25
Autores
Rodrigues, Éder Anderson
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Universidade Estadual Paulista (Unesp)
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Introdução: O exercício físico é considerado importante estratégia terapêutica para pacientes com insuficiência cardíaca (IC) estável. A compreensão dos benefícios do exercício na IC resultou, principalmente, de investigações com exercício aeróbio, uma vez que treinamento muscular resistido não era considerado seguro. Mais recentemente, exercícios resistidos têm sido recomendados na IC. Os mecanismos envolvidos nos efeitos do exercício resistido sobre o miocárdio ainda não estão esclarecidos. Neste estudo, foi avaliado os efeitos do exercício físico resistido, durante o processo de remodelação cardíaca, sobre alterações cardíacas estruturais, funcionais e moleculares induzidas por infarto do miocárdio (IM) em ratos. Métodos: Três meses após a indução do IM, ratos Wistar foram divididos em três grupos: Sham (n=20); IM sedentário (IM-Sed, n=20); IM submetido a exercício físico resistido (IM-R, n=20). Os ratos treinaram 3 vezes por semana durante três meses subindo escada com diferentes cargas. A avaliação das estruturas cardíacas e função ventricular foi realizada por ecocardiograma. O menor diâmetro dos miócitos foi analisado em cortes histológicos corados por hematoxilina e eosina. A avaliação do metabolismo energético, hidroperóxido de lipídeo, enzimas antioxidantes, malonaldeído (MDA) e carbonilação de proteínas foi realizada por espectrofotometria. A análise de mRNAs das subunidades da enzima NADPH oxidase Nox2, Nox4, p22phox e p47phox e dos genes de referência ciclofilina e gliceraldeído-3-fosfato desidrogenase (GAPDH) foi realizada por reação em cadeia da polimerase em tempo real após transcrição reversa (RT-PCR). A análise estatística foi feita por ANOVA complementada pelo teste de Tukey ou teste de Dunn’s. Resultados: O exercício resistido melhorou a capacidade de carga máxima e não alterou as estruturas cardíacas e o função do ventrículo esquerdo. Os valores do menor diâmetro das fibras cardíacas foram menores no grupo IM-Sed que no Sham e IM-R. A atividade da lactato desidrogenase foi menor no grupo IM-Sed que no Sham e foi restaurada pelo exercício resistido. A atividade da catalase foi menor nos grupos infartados. O hidroperóxido de lipídeo foi menor no grupo IM-R que no IM-Sed. A expressão da p47phox foi menor no grupo IM-Sed. Conclusões: Ratos com infarto do miocárdio apresentam remodelação cardíaca caracterizada por dilatação do átrio e ventrículo esquerdos, disfunção sistólica, e redução da atividade da lactato desidrogenase e catalase, e da subunidade p47phox do complexo da NADPH oxidase no miocárdio. O exercício resistido iniciado tardiamente é seguro, bem tolerado, aumenta a capacidade muscular de carga máxima, reduz o estresse oxidativo, e preserva a atividade da lactato desidrogenase e a expressão gênica da subunidade p47phox do complexo da NADPH oxidase miocárdica em ratos infartados.
Introduction: Physical exercise is considered an important therapeutic strategy for patients with stable heart failure (HF). The understanding of the benefits of exercise in HF resulted mainly from aerobic exercise investigations, since resistance muscle training was not considered safe. More recently, resistance exercises have been recommended in HF. The mechanisms involved in the effects of resistance exercise on the myocardium have not yet been clarified. In this study, the effects of resistive physical exercise during cardiac remodeling on structural, functional and molecular cardiac changes induced by myocardial infarction (MI) in rats were evaluated. METHODS: Three months after MI induction, Wistar rats were divided into three groups: Sham (n = 20); Sedentary IM (IM-Sed, n = 20); IM subjected to resisted physical exercise (IM-R, n = 20). The rats trained three times a week for three months climbing ladders with different loads. The evaluation of cardiac structures and ventricular function was performed by echocardiogram. The smaller diameter of myocytes was analyzed in histological sections stained with hematoxylin and eosin. The evaluation of energy metabolism, lipid hydroperoxide, antioxidant enzymes, malonaldehyde (MDA) and protein carbonylation was performed by spectrophotometry. Analysis of mRNAs of the subunits of the NADPH oxidase enzyme Nox2, Nox4, p22phox and p47phox and the reference genes cyclophilin and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) were performed by real-time polymerase chain reaction after reverse transcription (RT- PCR). Statistical analysis was performed by ANOVA complemented by the Tukey test or Dunn's test. Results: Resistance exercise improved maximal load capacity and did not alter cardiac structures and left ventricular function. The values of the smaller diameter of the cardiac fibers were smaller in the IM-Sed group than in the Sham and IM-R groups. Lactate dehydrogenase activity was lower in the IM-Sed group than in Sham and was restored by resistance exercise. Catalase activity was lower in the infarcted groups. Lipid hydroperoxide was lower in the IM-R group than in IM-Sed. The expression of p47phox was lower in the IM-Sed group. Conclusions: Rats with myocardial infarction present with cardiac remodeling characterized by dilation of the left atrium and ventricle, systolic dysfunction, and reduction of lactate dehydrogenase and catalase activity, and the p47phox subunit of the NADPH oxidase complex in the myocardium. Late-onset resistance exercise is safe, well-tolerated, maximizes muscle load, reduces oxidative stress, and preserves lactate dehydrogenase activity and the gene expression of the p47phox subunit of the myocardial NADPH oxidase complex in infarcted rats.
Introduction: Physical exercise is considered an important therapeutic strategy for patients with stable heart failure (HF). The understanding of the benefits of exercise in HF resulted mainly from aerobic exercise investigations, since resistance muscle training was not considered safe. More recently, resistance exercises have been recommended in HF. The mechanisms involved in the effects of resistance exercise on the myocardium have not yet been clarified. In this study, the effects of resistive physical exercise during cardiac remodeling on structural, functional and molecular cardiac changes induced by myocardial infarction (MI) in rats were evaluated. METHODS: Three months after MI induction, Wistar rats were divided into three groups: Sham (n = 20); Sedentary IM (IM-Sed, n = 20); IM subjected to resisted physical exercise (IM-R, n = 20). The rats trained three times a week for three months climbing ladders with different loads. The evaluation of cardiac structures and ventricular function was performed by echocardiogram. The smaller diameter of myocytes was analyzed in histological sections stained with hematoxylin and eosin. The evaluation of energy metabolism, lipid hydroperoxide, antioxidant enzymes, malonaldehyde (MDA) and protein carbonylation was performed by spectrophotometry. Analysis of mRNAs of the subunits of the NADPH oxidase enzyme Nox2, Nox4, p22phox and p47phox and the reference genes cyclophilin and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) were performed by real-time polymerase chain reaction after reverse transcription (RT- PCR). Statistical analysis was performed by ANOVA complemented by the Tukey test or Dunn's test. Results: Resistance exercise improved maximal load capacity and did not alter cardiac structures and left ventricular function. The values of the smaller diameter of the cardiac fibers were smaller in the IM-Sed group than in the Sham and IM-R groups. Lactate dehydrogenase activity was lower in the IM-Sed group than in Sham and was restored by resistance exercise. Catalase activity was lower in the infarcted groups. Lipid hydroperoxide was lower in the IM-R group than in IM-Sed. The expression of p47phox was lower in the IM-Sed group. Conclusions: Rats with myocardial infarction present with cardiac remodeling characterized by dilation of the left atrium and ventricle, systolic dysfunction, and reduction of lactate dehydrogenase and catalase activity, and the p47phox subunit of the NADPH oxidase complex in the myocardium. Late-onset resistance exercise is safe, well-tolerated, maximizes muscle load, reduces oxidative stress, and preserves lactate dehydrogenase activity and the gene expression of the p47phox subunit of the myocardial NADPH oxidase complex in infarcted rats.
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Palavras-chave
infarto do miocárdio, insuficiência cardíaca, remodelação cardíaca, exercício resistido, estresse oxidativo