Efeitos do treinamento aeróbico de baixa intensidade iniciado 24 h após infarto do miocárdio sobre a estrutura e função cardíaca de ratos
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2013-05-24
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Universidade Federal de Viçosa
Resumo
O presente estudo teve como objetivo verificar os efeitos do treinamento aeróbico de baixa intensidade iniciado 24 horas após a cirurgia isquêmica sobre a estrutura e função do miocárdio e cardiomiócitos de ratos submetidos ao infarto do miocárdio (IM) experimental. Ratos Wistar com 30 dias de idade foram divididos em 4 grupos: Sham Sedentário (SHSD, n=15), Sham Exercitado (SHEX, n=15), Infartado Sedentário (IMSD, n=15) e Infartado Exercitado (IMSD, n=15). Vinte e quatro horas após indução do IM e da cirurgia simulada (Sham), os animais dos grupos IMEX e SHEX foram colocados na esteira rolante com 5º de inclinação, por um período de 20 minutos por dia, onde correram à velocidade de 12m/min durante 5 dias consecutivos. No 6º e no 35º dias, estes animais foram submetidos à avaliação da tolerância ao esforço físico. A tolerância ao esforço físico foi estimada pela capacidade máxima de esforço físico em teste progressivo de corrida em esteira e quantificada pelo tempo total até a fadiga (TTF, min) neste teste. A velocidade máxima de corrida (VMC) obtida no teste do 6º dia foi utilizada para calcular a intensidade de corrida adotada no programa de treinamento (%VMC, m/min). Este programa consistiu de corrida em esteira (5 dias/semana, 60min/dia, inclinação de 5º) a 65-75% da VMC. Trinta e cinco dias após a indução do IM, os cardiomiócitos da região remanescente ao IM do ventrículo esquerdo (VE) de metade dos animais de cada grupo foram isolados por dispersão enzimática, após eutanásia. Os cardiomiócitos foram estimulados a 1Hz, em temperatura controlada (~37ºC), para mensuração da função contrátil. O restante dos animais foi usado para obtenção dos registros hemodinâmicos. Após este procedimento, estes animais sofreram eutanásia e os corações foram removidos, fixados e corados com Hematoxilina-eosina e Picrosirius red para análise histológica. Os resultados mostraram que o programa de exercício físico aplicado não comprometeu a sobrevivência dos animais infartados. Os animais exercitados apresentaram maior capacidade de corrida em relação aos sedentários (p<0,05). O peso do coração, peso relativo do coração, peso relativo do VE, volume cardíaco, área celular do cardiomiócito e o teor de água no pulmão foram maiores nos animais infartos em comparação com o Sham (P<0,05), mas sem diferença entre os grupos IMSD e IMEX. Além disso, o programa de corrida não atenuou o tamanho do infarto e a deposição de colágeno no miocárdio remanescente ao IM. O eletrocardiograma (ECG) demonstrou que os animais IM apresentaram elevação dos segmentos ST, prolongamento dos intervalos QT, QTc e da onda T, aumento na amplitude das ondas Q e T, e redução da amplitude da onda S, em relação aos animais Sham (p<0,05), imediatamente após a ligadura da ACADE. Entretanto, ao final do programa de corrida, não foram encontradas diferenças nestes parâmetros avaliados. Os ratos IM apresentaram aumento na frequência cardíaca (FC) de repouso, reduções na pressão sistólica do VE (PSVE) e da taxa máxima de elevação de pressão (dP/dtmáx), além da elevação da pressão diastólica final do VE (PDFVE) e da taxa máxima de declínio de pressão (dP/dtmin) (p<0,05). Contudo, o programa de treinamento físico aplicado reduziu a dP/dtmín e a FC de repouso além de aumentar a PSVE dos animais IM (p<0,05). A amplitude de contração e o tempo de relaxamento não foram alterados pelo IM. No entanto, os animais IM apresentaram aumento no tempo para o pico de contração celular, em comparação aos animais Sham (p<0,05), mas sem diferença entre os grupos IMSD e IMEX. Concluiu-se que o treinamento aeróbico de baixa intensidade iniciado 24 horas após o IM experimental e realizado durante 5 semanas não agravou o remodelamento cardíaco e atenuou os efeitos deletérios do IM sobre os parâmetros hemodinâmicos.
This study aimed at investigating the effects of low-intensity aerobic training initiated 24 hours after myocardial infarction (MI) on the structure and function of the myocardium and cardiomyocytes. Four-weeks old Wistar rats were divided into 4 groups: Sham Sedentary (SHSD, n=15), Sham exercised (SHEX, n=15), infarcted Sedentary (IMSD, n=15) and infarcted exercised (IMSD, n=15). Twenty-four hours after MI and sham operation animals from the training groups were placed on a treadmill with a 5º angle of inclination, during 20 minutes per day, at a speed of 12m/min for 5 consecutive days. On the 6th and 35th days animals were evaluated for tolerance to physical exertion. Exercise tolerance was estimated by the maximum physical exertion in a progressive treadmill running test and quantified by the total time until fatigue (TTF, min) achieved in the mentioned test. The maximum running speed (MRS) achieved in the 6th day test was used to calculate the intensity adopted in the training program (VMC%, m/min). This program consisted of treadmill running (5 days/week, 60min/day, and inclination of 5º) at a speed of 65-75% of MRS. Thirty-five days after the induction of MI, half of animals of each group were used for cardiomyocytes isolation. After euthanasia, cardiomyocytes were isolated from the non-infarcted area of the left ventricle (LV) by enzymatic dispersion. The cardiomyocytes were stimulated at 1Hz, under controlled temperature (~37°C) for measurements of contractile function. The remaining animals in each group were used to obtain in the hemodynamic recordings. After that, these animals were euthanized and the hearts were removed, fixed and stained with hematoxylin-eosin and picrosirius red for histological analysis. The exercise program did not affect the survival of infarcted animals. Animals in the training program had greater running capacity compared to sedentary (p<0.05). Heart weight, indexed heart weight, LV indexed weight, heart volume, cardiomyocyte area and water content in the lungs were greater in the MI groups (P <0.05) than in Sham groups. In addition, the running program did not attenuate the infarct size and collagen deposition in the remaining myocardium. Animals with MI had ST segment elevation, QT prolongation, increase of QTc and T wave amplitude, and reduced Q, S and T waves amplitude compared to Sham (p<0.05). However, at 35 days later no differences in these ECG parameters were observed. MI rats showed an increase in heart rate (HR) at rest, decreased LV systolic pressure (LVSP) and the maximum rate of pressure rise (dP/dtmax) and increased LV end-diastolic pressure (PDFLV) and minimum rate of pressure rise (dP/dtmin) (p <0.05). However, the training program was able to decreased resting HR, increase LVSP and decreased dP/dtmin in the MI group (p<0.05). The amplitude of contraction and relaxation time were not affected by MI. However, MI animals showed increased time to peak of cell contraction compared to sham animals (p<0.05), but no difference between groups IMSD and IMEX was observed. It is concluded that low-intensity aerobic training initiated 24 hours after MI for a period of 5 weeks did not impair cardiac remodeling and attenuated the deleterious effects of MI on hemodynamic parameters.
This study aimed at investigating the effects of low-intensity aerobic training initiated 24 hours after myocardial infarction (MI) on the structure and function of the myocardium and cardiomyocytes. Four-weeks old Wistar rats were divided into 4 groups: Sham Sedentary (SHSD, n=15), Sham exercised (SHEX, n=15), infarcted Sedentary (IMSD, n=15) and infarcted exercised (IMSD, n=15). Twenty-four hours after MI and sham operation animals from the training groups were placed on a treadmill with a 5º angle of inclination, during 20 minutes per day, at a speed of 12m/min for 5 consecutive days. On the 6th and 35th days animals were evaluated for tolerance to physical exertion. Exercise tolerance was estimated by the maximum physical exertion in a progressive treadmill running test and quantified by the total time until fatigue (TTF, min) achieved in the mentioned test. The maximum running speed (MRS) achieved in the 6th day test was used to calculate the intensity adopted in the training program (VMC%, m/min). This program consisted of treadmill running (5 days/week, 60min/day, and inclination of 5º) at a speed of 65-75% of MRS. Thirty-five days after the induction of MI, half of animals of each group were used for cardiomyocytes isolation. After euthanasia, cardiomyocytes were isolated from the non-infarcted area of the left ventricle (LV) by enzymatic dispersion. The cardiomyocytes were stimulated at 1Hz, under controlled temperature (~37°C) for measurements of contractile function. The remaining animals in each group were used to obtain in the hemodynamic recordings. After that, these animals were euthanized and the hearts were removed, fixed and stained with hematoxylin-eosin and picrosirius red for histological analysis. The exercise program did not affect the survival of infarcted animals. Animals in the training program had greater running capacity compared to sedentary (p<0.05). Heart weight, indexed heart weight, LV indexed weight, heart volume, cardiomyocyte area and water content in the lungs were greater in the MI groups (P <0.05) than in Sham groups. In addition, the running program did not attenuate the infarct size and collagen deposition in the remaining myocardium. Animals with MI had ST segment elevation, QT prolongation, increase of QTc and T wave amplitude, and reduced Q, S and T waves amplitude compared to Sham (p<0.05). However, at 35 days later no differences in these ECG parameters were observed. MI rats showed an increase in heart rate (HR) at rest, decreased LV systolic pressure (LVSP) and the maximum rate of pressure rise (dP/dtmax) and increased LV end-diastolic pressure (PDFLV) and minimum rate of pressure rise (dP/dtmin) (p <0.05). However, the training program was able to decreased resting HR, increase LVSP and decreased dP/dtmin in the MI group (p<0.05). The amplitude of contraction and relaxation time were not affected by MI. However, MI animals showed increased time to peak of cell contraction compared to sham animals (p<0.05), but no difference between groups IMSD and IMEX was observed. It is concluded that low-intensity aerobic training initiated 24 hours after MI for a period of 5 weeks did not impair cardiac remodeling and attenuated the deleterious effects of MI on hemodynamic parameters.
Descrição
Palavras-chave
Infarto de miocárdio, Função cardíaca, Treinamento físico, Myocardial infarction, Heart function, Physical training
Citação
RAMOS, Regiane Maria Soares. Effects of low-intensity aerobic exercise training initiated 24 h after myocardial infarction on heart structure and function of rats. 2013. 96 f. Dissertação (Mestrado em Aspectos sócio-culturais do movimento humano; Aspectos biodinâmicos do movimento humano) - Universidade Federal de Viçosa, Viçosa, 2013.