Treinamento resistido previne o desenvolvimento de hipertensão arterial pulmonar em ratos expostos à fumaça secundária de cigarro
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Data
2019-01-25
Autores
Moreno, Ana Caroline Rippi [UNESP]
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Universidade Estadual Paulista (Unesp)
Resumo
O tabagismo é uma das maiores ameaças à saúde pública. A exposição à fumaça secundária de cigarro está associada com mais de 50 doenças, destacando o enfisema pulmonar. O treinamento resistido (TR) é uma ferramenta eficaz para a prevenção e promoção da saúde. Pouco se sabe sobre efeitos de treinamento resistido em tecidos muscular cardíaco e esquelético de modelos experimentais expostos à fumaça secundária de cigarro. O objetivo deste estudo é avaliar o efeito do treinamento resistido em ratos expostos a fumaça secundária do cigarro. Trinta e dois ratos Wistar foram divididos em quatro grupos: Controle Sedentário (CS), Fumante Sedentário (FS), Controle Exercitado (CE) e Fumante Exercitado (FE). Os animais dos grupos FS e FE foram expostos à fumaça secundária de quatro cigarros por 30 minutos duas vezes ao dia, cinco dias na semana. Os animais exercitados (CE e FE) foram submetidos ao teste de carga máxima suportada (CMS) e o treinamento utilizado foi subida em escada vertical com incremento, uma vez ao dia, cinco dias por semana. Ambas intervenções foram realizadas por 16 semanas. Após a eutanásia foi coletado sangue para dosagem de glicemia, colesterol total, HDL e triglicerídeos. Coração, traqueia, pulmão, fígado e músculo gastrocnêmio foram coletados para análise anatomopatológicas. A análise gênica de marcadores da dinâmica e biogênese mitocondrial foi realizada pela técnica de RT-PCR em fragmentos do coração e músculo gastrocnêmio. Observou que os animais CS apresentaram maior ganho comparado a todos demais grupos (p<0,05), o grupo CE maior do que os grupos fumantes (FS e FE; p<0,05) e o grupo FE menor ganho comparado com todos (p<0,05), associado ao menor consumo de ração (p=0,0005). O grupo FE apresentou redução de HDL (FE vs CE p=0,02). Nos grupos fumantes (FS e FE) houve presença de enfisema pulmonar (FS e FE vs CS e CE p<0,0001) e aumento da espessura da artéria pulmonar (FS vs CS e CE e FE vs CS, p=0,003). No coração houve aumento na espessura do ventrículo direito nos animais FS vs CS, CE e FE (p<0,0001). No fígado observou-se aumento de macrófagos nos animais fumantes (FS e FE vs CS p=0,002). No músculo esquelético os animais FE apresentaram redução do diâmetro das fibras musculares (FE vs CS e CE p=0,0002). Na análise gênica foi observado aumento de Fis1 em gastrocnêmio de FS vs CS (p=0,05) e Ppargc1a em coração de FE vs FS (p=0,01). Portanto, conclui-se que embora não tenha prevenido Enfisema e HP, o TR em ratos fumantes preveniu hipertensão arterial pulmonar possivelmente por melhorar a capacidade oxidadiva do músculo cardíaco (aumento de Ppargc1a), o que poderia resultar na prevenção do aumento do VD. Entretanto, resultados negativos foram encontrados na ingestão e peso corporal, músculo esquelético (redução do diâmetro das fibras) e no perfil de lipoproteínas (redução do HDL).
Smoking is one of the greatest threats to public health. Exposure to secondhand smoke is associated with more than 50 diseases, most notably pulmonary emphysema. Resistance training is an effective tool for prevention and health promotion. Little is known about the effects of high intensity resistance training on cardiac and skeletal muscle tissues of experimental models exposed to cigarette smoke. The aim of this study is to evaluate the effect of resistance training in rats exposed to secondary cigarette smoke. Thirty-two Wistar rats were divided into four groups: Sedentary Control (SC), Sedentary Smoker (SS), Exercised Control (EC) and Exercised Smoker (ES). Animals from the SS and ES groups were exposed to the smoke from four cigarrettes for 30 minutes twice daily, five days a week. The animals exercised (EC and ES) underwent the maximum supported load test (CMS) and the utilized training was the climb on a vertical ladder with increment, once a day, five days a week. Both interventions were performed for 16 weeks. After euthanasia, blood was collected to measure fasting blood glucose dosage, total cholesterol, HDL, and triglycerides. Heart, trachea, lung, liver and gastrocnemius muscle were collected for anatomopathological analysis. Gene analysis of dynamics markers and mitochondrial biogenesis was performed by the RT-PCR technique in fragments of the heart and gastrocnemius muscle. It was observed that SC animals showed a higher gain compared to all other groups (p <0.05), the EC group showed a higher gain than the smoking groups (SS and ES, p <0.05) and the ES group had a lower gain compared to all (p <0.05), associated with lower feed intake (p = 0.0005). The ES group had HDL reduction (ES vs EC p = 0.02). Pulmonary emphysema (SS and SE vs SC and EC p <0.0001) and pulmonary artery thickness enlargement (SS vs SC and EC and ES vs SC, p = 0.003) were found in the smoking groups (SS and ES). In the heart, there was increase in the right ventricle in the animals from SS vs SC, EC and ES (p <0.0001). In the liver, it was observed increase of macrophages in the smokers animals (SS and ES vs. SC p = 0.002). In the skeletal muscle, ES animals presented reduction of muscle fibers (ES vs SC and EC p = 0.0002). In the gene analysis, it was observed an increase of Fis1 in gastrocnemius of SS vs SC (p = 0.05) and Ppargc1a in the heart of ES vs SS (p = 0.01). Therefore, it was concluded that although it did not prevent Emphysema and HP, the RT in smokers rats has prevented pulmonary arterial hypertension possibly by improving the oxidative capacity of the cardiac muscle (increase of Ppargc1a), which could result in the prevention of increased VD. However, negative results were found in the intake and body weight, skeletal muscle (reduction of fiber diameter) and lipoprotein profile (HDL reduction).
Smoking is one of the greatest threats to public health. Exposure to secondhand smoke is associated with more than 50 diseases, most notably pulmonary emphysema. Resistance training is an effective tool for prevention and health promotion. Little is known about the effects of high intensity resistance training on cardiac and skeletal muscle tissues of experimental models exposed to cigarette smoke. The aim of this study is to evaluate the effect of resistance training in rats exposed to secondary cigarette smoke. Thirty-two Wistar rats were divided into four groups: Sedentary Control (SC), Sedentary Smoker (SS), Exercised Control (EC) and Exercised Smoker (ES). Animals from the SS and ES groups were exposed to the smoke from four cigarrettes for 30 minutes twice daily, five days a week. The animals exercised (EC and ES) underwent the maximum supported load test (CMS) and the utilized training was the climb on a vertical ladder with increment, once a day, five days a week. Both interventions were performed for 16 weeks. After euthanasia, blood was collected to measure fasting blood glucose dosage, total cholesterol, HDL, and triglycerides. Heart, trachea, lung, liver and gastrocnemius muscle were collected for anatomopathological analysis. Gene analysis of dynamics markers and mitochondrial biogenesis was performed by the RT-PCR technique in fragments of the heart and gastrocnemius muscle. It was observed that SC animals showed a higher gain compared to all other groups (p <0.05), the EC group showed a higher gain than the smoking groups (SS and ES, p <0.05) and the ES group had a lower gain compared to all (p <0.05), associated with lower feed intake (p = 0.0005). The ES group had HDL reduction (ES vs EC p = 0.02). Pulmonary emphysema (SS and SE vs SC and EC p <0.0001) and pulmonary artery thickness enlargement (SS vs SC and EC and ES vs SC, p = 0.003) were found in the smoking groups (SS and ES). In the heart, there was increase in the right ventricle in the animals from SS vs SC, EC and ES (p <0.0001). In the liver, it was observed increase of macrophages in the smokers animals (SS and ES vs. SC p = 0.002). In the skeletal muscle, ES animals presented reduction of muscle fibers (ES vs SC and EC p = 0.0002). In the gene analysis, it was observed an increase of Fis1 in gastrocnemius of SS vs SC (p = 0.05) and Ppargc1a in the heart of ES vs SS (p = 0.01). Therefore, it was concluded that although it did not prevent Emphysema and HP, the RT in smokers rats has prevented pulmonary arterial hypertension possibly by improving the oxidative capacity of the cardiac muscle (increase of Ppargc1a), which could result in the prevention of increased VD. However, negative results were found in the intake and body weight, skeletal muscle (reduction of fiber diameter) and lipoprotein profile (HDL reduction).
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Palavras-chave
Pgc1a, Fumaça secundária, Força muscular, Enfisema pulmonar, Mitocôndria, Ratos Wistar, Secondhand smoke, Muscle strenght, Pulmonary emphysema, Mitochondria, Wistar rats