الملخص
OBJECTIVES: The present study was performed to investigate 1) whether aerobic exercise training prior to myocardial infarction would prevent cardiac dysfunction and structural deterioration and 2) whether the potential cardiac benefits of aerobic exercise training would be associated with preserved morphological and contractile properties of cardiomyocytes in post-infarct remodeled myocardium. METHODS: Male Wistar rats underwent an aerobic exercise training protocol for eight weeks. The rats were then assigned to sham surgery (SHAM), sedentary lifestyle and myocardial infarction or exercise training and myocardial infarction groups and were evaluated 15 days after the surgery. Left ventricular tissue was analyzed histologically, and the contractile function of isolated myocytes was measured. Student's t-test was used to analyze infarct size and ventricular wall thickness, and the other parameters were analyzed by the Kruskal-Wallis test followed by Dunn's test or a one-way analysis of variance followed by Tukey's test (p<0.05). RESULTS: Myocardial infarctions in exercise-trained animals resulted in a smaller myocardial infarction extension, a thicker infarcted wall and less collagen accumulation as compared to myocardial infarctions in sedentary animals. Myocardial infarction-induced left ventricular dilation and cardiac dysfunction, as evaluated by +dP/dt and -dP/dt, were both prevented by previous aerobic exercise training. Moreover, aerobic exercise training preserved cardiac myocyte shortening, improved the maximum shortening and relengthening velocities in infarcted hearts and enhanced responsiveness to calcium. CONCLUSION: Previous aerobic exercise training attenuated the cardiac dysfunction and structural deterioration promoted by myocardial infarction, and such benefits were associated with preserved cardiomyocyte morphological and contractile properties. .
الموضوعات
Animals , Male , Rats , Heart/physiopathology , Myocardial Infarction/physiopathology , Myocardial Infarction/prevention & control , Myocytes, Cardiac/physiology , Physical Conditioning, Animal/physiology , Blood Pressure/physiology , Hemodynamics/physiology , Myocardial Contraction/physiology , Random Allocation , Rats, Wistar , Time Factors , Ventricular Function, Left/physiologyالملخص
FUNDAMENTO: O diabete experimental promove disfunção contrátil em cardiomiócitos, mas os efeitos do treinamento em natação nesta disfunção não são conhecidos. OBJETIVO: Testar os efeitos de um programa de treino em natação (PTN) sobre a disfunção contrátil de cardiomiócitos de ratos com diabete experimental. MÉTODOS: Ratos Wistar (idade: 30 dias; peso corporal médio: 84,19 g) com diabete induzida por estreptozotocina (60 mg/kg de peso corporal; glicemia > 300 mg/dl) foram alocados em diabéticos sedentários (DS, n = 10) e diabéticos exercitados (DE, n = 13). Animais da mesma idade e peso serviram de controles sedentários (CS, n = 10) e controles exercitados (CE, n = 06). Os animais DE e CE foram submetidos a um PTN (05 dias/semana, 90 min/dia), por 08 semanas. Os miócitos do ventrículo esquerdo (VE) foram isolados e estimulados eletricamente a 3,0 Hz em temperatura ambiente (∼ 25º C). RESULTADOS: O diabete reduziu a função contrátil nos cardiomiócitos dos animais em relação aos controles (i.e., menor amplitude de contração, maior tempo de contração e relaxamento). O PTN atenuou a redução na amplitude de contração (CS, 11 ± 0,2 por cento vs DE, 11,6 ± 0,2 por cento), o tempo para o pico de contração (CS, 319 ± 5,8 ms vs DE, 333 ± 4,8 ms) e o tempo para 50 por cento de relaxamento (CS, 619 ± 22,2 ms vs DE, 698 ± 18,6 ms) dos cardiomiócitos dos animais diabéticos. O diabete reduziu as dimensões dos cardiomiócitos, porém, o PTN minimizou a redução da largura e volume celular, sem alterar o comprimento. CONCLUSÃO: O programa de treino em natação atenuou a disfunção contrátil dos miócitos do VE de ratos com diabete experimental.
BACKGROUND: Experimental diabetes promotes contractile dysfunction in cardiomyocytes, but the effects of swimming in this disorder are not known. OBJECTIVE: To test the effects of a swimming training program (STP) on cardiomyocyte contractile dysfunction in rats with experimental diabetes. METHODS: Wistar rats (age: 30 days; mean body weight: 84.19 g) with diabetes induced by streptozotocin (60 mg/kg body weight; glucose > 300 mg/dl) were divided into sedentary diabetic rats (SD, n = 10) and exercised diabetic rats (ED, n = 13). Animals of same age and weight served as sedentary controls (SC, n = 10) and exercised controls (EC, n = 06). Animals and ED and EC underwent a STP (05 days/week, 90 min/day) for 08 weeks. Left ventricular (LV) myocytes were isolated and electrically stimulated at 3.0 Hz at room temperature (∼ 25º C). RESULTS: Diabetes reduced contractile function in cardiomyocytes of animals compared to controls (i.e., lower amplitude of contraction, longer duration of contraction and relaxation). The STP attenuated the reduced amplitude of contraction (SC, 11 ± 0.2 percent vs ED, 11.6 ± 0.2 percent), time to peak contraction (SC, 319 ± 5.8 ms vs ED, 333 ± 4.8 ms) and time to 50.0 percent of relaxation (SC, 619 ± 22.2 ms vs ED 698 ± 18.6 ms) of cardiomyocytes of diabetic rats. Diabetes reduced the size of cardiomyocytes, however, the STP minimized the reduction of cell volume and width, without changing length. CONCLUSION: The swimming training program attenuated the contractile dysfunction of the LV myocytes of rats with experimental diabetes.
FUNDAMENTO: La diabetes experimental promueve el trastorno contráctil de los cardiomiocitos, pero los efectos del entrenamiento en natación en este trastorno no se conocen. OBJETIVO: Probar los efectos de un programa de capacitación en natación (PTN) sobre el trastorno contráctil de cardiomiocitos de ratas con diabetes experimental. MÉTODOS: Ratas Wistar (edad: 30 días, peso corporal medio: 84,19 g) con diabetes inducida por estreptozotocina (60 mg/kg de peso corporal, glucosa > 300 mg/dl) fueron divididos en diabéticos sedentarios (DS, n = 10) y diabéticos ejercitados (DE, n = 13). Animales de la misma edad y peso sirvieron de controles sedentarios (CS, n = 10) y controles ejercitados (CE, n = 06). Los animales DE y CE se sometieron a un PTN (05 días/semana, 90 min/día), por 08 semanas. Los miocitos del ventrículo izquierdo (VI) fueron aislados y estimulados eléctricamente a 3,0 Hz en temperatura ambiente (~ 25º C). RESULTADOS: La diabetes disminuyó la función contráctil de los cardiomiocitos de los animales en comparación con los controles (es decir, menor amplitud de la contracción, la duración de la contracción y relajación). El PTN atenuó la reducción de la amplitud de la contracción (CS, 11 ± 0,2 por ciento frente a la DE, 11,6 ± 0,2 por ciento), el tiempo para la contracción máxima (CS, 319 ± 5,8 ms vs DE, 333 ± 4,8 ms) y el tiempo para el 50 por ciento de relajación (CS, 619 ± 22,2 ms vs DE, 698 ± 18,6 ms) de los cardiomiocitos de los animales diabéticos. La diabetes redujo las dimensiones de los cardiomiocitos, sin embargo, el PTN minimizó la reducción de la anchura y volumen celular, sin cambiar la longitud. CONCLUSIÓN: El programa de entrenamiento de natación atenuó la disfunción contráctil de los miocitos del VI de las ratas con diabetes experimental.
الموضوعات
Animals , Rats , Diabetes Mellitus, Experimental/physiopathology , Myocardial Contraction/physiology , Myocytes, Cardiac/physiology , Physical Conditioning, Animal/physiology , Swimming/physiology , Rats, Wistar , Time Factors , Ventricular Function, Left/physiologyالملخص
Enquanto o exercício aeróbico regular promove adaptações benéficas ao músculo esquelético, o exercício físico exaustivo induz lesões musculares. O objetivo deste estudo foi verificar se um programa de natação com baixa intensidade é capaz de proteger músculos esqueléticos contra lesões induzidas por exercício exaustivo. Ratos Wistar (peso: 376,50 ± 4,36g; idade: 90 dias) foram divididos aleatoriamente em quatro grupos: controle sedentário (CS); sedentário submetido a teste de exaustão (SE); treinado em natação (TN); treinado em natação submetido a teste de exaustão (TNE). Animais dos grupos TN e TNE foram submetidos a um programa de natação sem sobrecarga por 90 minutos/dia, cinco dias/semana, durante 17 semanas. Após este período, os grupos SE e TNE foram submetidos a um teste de exaustão em natação. Após eutanásia, fragmentos dos músculos sóleo e reto femoral foram coletados e submetidos à análise histológica e de proteínas de choque térmico (HSP70). Os resultados mostraram que o tempo até a exaustão foi maior no grupo TNE que no SE (125,0 ± 6,0 vs. 90,0 ± 8,5min, respectivamente, P < 0,05). Os níveis de lactato sanguíneo durante o teste e exaustão foram menores no grupo TNE que no SE (5,31 ± 0,22 vs. 8,76 ± 0,59mmol/L, respectivamente, P < 0,05). A frequência de fibras lesadas nos músculos foi maior nos grupos SE (sóleo: 34,86 ± 0,04; reto femoral: 37,57 ± 0,07) e TNE (sóleo: 41,57 ± 0,08; reto femoral: 39,57 ± 0,05), comparada aos grupos CS (sóleo: 13,88 ± 0,81; reto femoral: 16,75 ± 0,79) e TN (sóleo: 24,14 ± 0,06; reto femoral: 24,0 ± 0,05), respectivamente (P < 0,05). Não houve diferença significativa nos níveis de HSP70 dos músculos analisados entre os quatro grupos. Concluimos que apesar do treinamento em natação melhorar o desempenho dos animais no teste de exaustão, não promoveu proteção aos seus músculos esqueléticos contra as lesões induzidas pelo exercício exaustivo.
While regular aerobic exercise promotes beneficial adaptations to the skeletal muscle, acute exhaustive exercise causes structural damage to the skeletal muscle cells. The aim of this study was to verify whether a low-intensity swimming program protects the skeletal muscles against damage induced by exhaustive exercise. Male Wistar rats (weight: 376.50 4.36g; age: 90 days) were randomly divided into four groups: sedentary control (SC, N=8); sedentary submitted to exhaustive test (SE, N=7); swimming trained (TN, N=7); swimming trained submitted to exhaustive test (TNE, N=7). Animals of TN and TNE groups were submitted to a swimming regimen without overload for 90 min/day, 5 days/wk, during 17 weeks. Forty-eight hours after the last training session, animals from SE and TNE groups were submitted to an exhaustive exercise protocol. At sacrifice, fragments of soleus and rectus femoris muscles were collected and submitted to histological analysis and heat shock protein (HSP70) expression measurement. The results showed that the time until exhaustion was greater in the STE than in SE group (125.0 6.00 vs. 90.0 8.48 min, respectively, P<0.05). The levels of blood lactate during exhaustive exercise were lower in animals from TNE than SE (5.31 ± 0.22 vs. 876 ± 0.59 mmol/L, respectively, P<0.05)The frequency of damaged fibers in the muscles was greater in SE (soleus: 34.86±0.04; rectus femoris: 37.57 ± 0.07) and STE (soleus: 41.57±0.08; rectus femoris: 39.57 ± 0.05), compared to groups SC (soleus: 13.88±0.81; rectus femoris: 16.75 ± 0.79) and ST (soleus: 24.14±0.06; rectus femoris: 24.0 ± 0.05), respectively (P<0.05). There was no significant difference at the HSP70 levels of the analyzed muscles among the four groups (P>0.05). In conclusion, although a low-intensity swimming training increased the animals' performance in the exhaustive exercise test, it did not protect their skeletal muscles against damage induced by exhaustive exercise.