Treinamento resistido de intensidade moderada preserva a função vascular mediada por insulina na artéria mesentérica de ratos tratados com dexametasona

Introduction: Glucocorticoids (GC) are used as antiallergic and anti-inflammatory drugs, but their excessive use causes metabolic disorders, resulting in the appearance of metabolic syndrome (MS) and, therefore, endothelial dysfunction. Thus, resistance exercise has been an important alternative in the prevention and treatment of these metabolic disorders that lead to damage to the endothelium, preventing the development of cardiovascular diseases. Objective: To evaluate the capacity of resistance training (RT) to prevent metabolic and vascular changes induced by GC. Methods: Wistar rats were divided into groups: Control (CO), Dexamethasone (DEX) and Dexamethasone + RT (DEX+RT) and weighed weekly. Animals CO, DEX and DEX+RT were adapted (5 days/5 min/day) in the squat device. After adaptation, the groups were submitted to the test of a maximum repetition (1RM), repeated every 2 weeks to maintain the desired intensity. The DEX+RT group was submitted to an RT protocol in 3 series of 10 repetitions, 3 times/week for 8 weeks and with an intensity of 60% of the maximum load established in the 1RM test. The CO and DEX groups were submitted to a fictitious exercise. In the eighth week of resistance training, dexamethasone (DEXA, 2.0 mg/kg, via i.p) was administered for 7 days in the DEX and DEX+RT and 0.9% NaCl groups in the CO group. 48 hours after 1RM, animals were fasted for 8 hours and glucose, insulin, total cholesterol (TC), triglyceride (TG), low density lipoprotein (LDL-c) and high density lipoprotein (HDL- c) have been verified. After that, the animals were anesthetized and sacrificed, the superior mesenteric artery was removed and sectioned into rings, and mounted in vats for an isolated organ. Endothelium-dependent vasodilation was achieved through concentration-response curves for insulin, in rings pre-contracted with phenylephrine (Phe). Then, concentration-response curves were obtained for the CO, DEX and DEX+RT groups, in the absence and in the presence of PI3K, NOS, ETA receptor inhibitors, and the vasoconstriction induced by FEN in the absence and presence was also evaluated. of L-NAME. Results: glucose, insulin, CT, TG, LDL-c were increased and HDL-c reduced in the DEX group, but these changes were prevented in the DEX+RT group. Insulin-induced vasodilation was reduced in the DEX group compared to the CO group, however, DEX+TR increased vasodilation in relation to the DEX group. When we evaluated the participation of PI3K after incubation with LY294002, there was a reduction in relaxation in the CO group, while in the DEX group, vasodilation was abolished, showing a similarly contractile effect in the presence of NOS inhibitor, being inhibited with BQ123. However, the contractile effect was abolished in the DEX+RT group. The vasoconstrictor response induced by Phe, increased in the DEX group compared to CO, being reduced in the DEX+RT group. Additionally, after incubation with L-NAME, the vasoconstrictor response was high in all groups, being lower in the CO and DEX+RT group than in the DEX group. Conclusion: RT in the presence of high doses of glucocorticoids, prevented damage to the PI3K/eNOS vasodilator pathway, in addition to attenuating the MAPK/ET-1 vasoconstrictor pathway.Introdução: Os glicocorticoides (GC) são utilizados como antialérgicos e anti-inflamatórios, mas o seu uso prolongado pode causar distúrbios metabólicos, podendo levar ao desenvolvimento da disfunção endotelial. Por outro lado, o treinamento resistido (TR) de intensidade moderada tem sido uma alternativa importante na prevenção e tratamento desses distúrbios metabólicos e que causam danos no endotélio. Objetivo: Avaliar a capacidade do TR em preservar as alterações metabólicas e vasculares induzidas por GC. Métodos: Ratos Wistar foram divididos em grupos: Controle (CO), Dexametasona (DEX) e Dexametasona+TR (DEX+TR) e pesados semanalmente. Os animais CO, DEX e DEX+TR foram adaptados (5 dias/5 min/dia) no aparelho de agachamento. Após a adaptação, os grupos foram submetidos ao teste de uma repetição máxima (1RM), repetido a cada 2 semanas para manter a intensidade desejada. O grupo DEX+TR foi submetido ao protocolo de TR com 3 séries de 10 repetições, 3 vezes/semana durante 8 semanas e intensidade de 60% da carga máxima estabelecida no teste de 1RM. Os grupos CO e DEX foram submetidos a um exercício fictício. Na oitava semana de treinamento resistido, administrou-se dexametasona (DEXA, 2,0 mg/kg, via i.p) por 7 dias, nos grupos DEX e DEX+TR e NaCl a 0,9% no grupo CO. 48 horas após o 1RM, os animais foram mantidos em um jejum de 8 horas e a glicose, insulina, colesterol total (CT), triglicerídeo (TG), lipoproteína de baixa densidade (LDL-c) e lipoproteína de alta densidade (HDL-c) foram verificadas. Após isso, os animais foram anestesiados e eutanasiados, a artéria mesentérica superior foi removida e seccionada em anéis, e montados em cubas para órgãos isolados. A vasodilatação dependente de endotélio foi obtida através de curvas concentração-resposta para a insulina, em anéis pré-contraídos com fenilefrina (FEN). Em seguida, foram obtidas curvas concentração-respostas para os grupos CO, DEX e DEX+TR, na ausência e na presença dos inibidores da fosfatidilinositol 3-quinase (PI3K) utilizando LY294002, da óxido nítrico sintase (NOS) utilizando L-NAME, do receptor de endotelina A (ETA) utilizando BQ123, também foi avaliada a vasoconstrição induzida por FEN na ausência e presença de L-NAME. Resultados: a glicose, insulina, CT, TG, LDL-c foram aumentadas e HDL-c reduzido no grupo DEX, porém essas alterações foram prevenidas no grupo DEX+TR. Já a vasodilatação induzida por insulina foi reduzida no grupo DEX comparado ao grupo CO, entretanto, o DEX+TR aumentou a vasodilatação em relação ao grupo DEX. Quando avaliamos a participação da PI3K após a incubação com LY294002, houve redução do relaxamento no grupo CO, enquanto no grupo DEX a vasodilatação foi abolida, mostrando um efeito contrátil semelhantemente na presença do inibidor da NOS, sendo inibida com o BQ123. Porém, o efeito contrátil foi abolido no grupo DEX+TR. Já resposta vasoconstrictora induzida por FEN, aumentou no grupo DEX comparado ao CO, sendo reduzida no grupo DEX+TR. Adicionalmente, após a incubação com L-NAME, a resposta vasoconstrictora foi elevada em todos os grupos, sendo menor no grupo CO e DEX+RT comparado ao grupo DEX. Conclusão: o TR na presença de glicocorticoides, preservou danos na via vasodilatadora PI3K/eNOS, além de atenuar a via vasoconstritora MAPK/ET-1.Aracaj

Effects of One Resistance Exercise Session on Vascular Smooth Muscle of Hypertensive Rats

AbstractBackground:Hypertension is a public health problem and increases the incidence of cardiovascular diseases.Objective:To evaluate the effects of a resistance exercise session on the contractile and relaxing mechanisms of vascular smooth muscle in mesenteric arteries of NG-nitro L-arginine methyl ester (L-NAME)-induced hypertensive rats.Methods:Wistar rats were divided into three groups: control (C), hypertensive (H), and exercised hypertensive (EH). Hypertension was induced by administration of 20 mg/kg of L-NAME for 7 days prior to experimental protocols. The resistance exercise protocol consisted of 10 sets of 10 repetitions and intensity of 40% of one repetition maximum. The reactivity of vascular smooth muscle was evaluated by concentration&#8209;response curves to phenylephrine (PHEN), potassium chloride (KCl) and sodium nitroprusside (SNP).Results:Rats treated with L-NAME showed an increase (p < 0.001) in systolic blood pressure (SBP), diastolic blood pressure (DBP) and mean arterial pressure (MAP) compared to the initial period of induction. No difference in PHEN sensitivity was observed between groups H and EH. Acute resistance exercise reduced (p < 0.001) the contractile response induced by KCl at concentrations of 40 and 60 mM in group EH. Greater (p < 0.01) smooth muscle sensitivity to NPS was observed in group EH as compared to group H.Conclusion:One resistance exercise session reduces the contractile response induced by KCl in addition to increasing the sensitivity of smooth muscle to NO in mesenteric arteries of hypertensive rats

Avaliação do teste de 1600m sobre marcadores de estresse oxidativo e danos musculares em corredores juvenis

 Evaluation of the 1600m test on markers of oxidative stress and muscle damage in young runners The intense and prolonged physical exercise can cause oxidative stress and muscular damages, generating damage in the performance of the athlete. The aim of this study was to investigate the acute effect of the 1600m test on oxidative stress and muscle damage in young runners. Nine adolescents between 15 and 18 years of age participated in this study. The 1600m test was performed to evaluate the aerobic capacity, where the volunteers performed four laps on the 400m lane, making a total of 1600m. There was no increase in the tissue oxidative stress marker evaluated by the TBARS in the post-test. In relation to the antioxidant enzyme, the protocol did not promote an increase of glutathione activity. Plasma concentrations of lactate dehydrogenase and creatine kinase had a significant increase after the 1600m test compared to the pre-test. It was concluded that the 1600m test promotes muscle damage, however no oxidative stress was generated.O exercício físico intenso e prolongado pode ocasionar estresse oxidativo e danos musculares, gerando prejuízo no desempenho do atleta.  O estudo tem como objetivo investigar o efeito agudo do teste de 1600m sobre o estresse oxidativo e danos musculares em corredores juvenis. Participaram desse estudo nove adolescentes entre 15 e 18 anos de idade. Foi realizado o teste de 1600m para avaliar a capacidade aeróbia, onde os voluntários realizaram quatro voltas em pista de 400m, perfazendo um total de 1600m. Não houve aumento no marcador de estresse oxidativo tecidual avaliado pelo TBARS no pós-teste. Em relação à enzima antioxidante, o protocolo não promoveu um aumento da atividade da glutationa. Nas concentrações plasmáticas de lactato desidrogenase e da creatina quinase tiveram um aumento significativo depois do teste de 1600m comparado ao pré-teste. Conclui-se que o teste de 1600m promove danos musculares, no entanto não foi gerado estresse oxidativo

Resistance Exercise Restores Endothelial Function and Reduces Blood Pressure in Type 1 Diabetic Rats

Background: Resistance exercise effects on cardiovascular parameters are not consistent. Objectives: The effects of resistance exercise on changes in blood glucose, blood pressure and vascular reactivity were evaluated in diabetic rats. Methods: Wistar rats were divided into three groups: control group (n = 8); sedentary diabetic (n = 8); and trained diabetic (n = 8). Resistance exercise was carried out in a squat device for rats and consisted of three sets of ten repetitions with an intensity of 50%, three times per week, for eight weeks. Changes in vascular reactivity were evaluated in superior mesenteric artery rings. Results: A significant reduction in the maximum response of acetylcholine-induced relaxation was observed in the sedentary diabetic group (78.1 ± 2%) and an increase in the trained diabetic group (95 ± 3%) without changing potency. In the presence of NG-nitro-L-arginine methyl ester, the acetylcholine-induced relaxation was significantly reduced in the control and trained diabetic groups, but not in the sedentary diabetic group. Furthermore, a significant increase (p < 0.05) in mean arterial blood pressure was observed in the sedentary diabetic group (104.9 ± 5 to 126.7 ± 5 mmHg) as compared to that in the control group. However, the trained diabetic group showed a significant decrease (p < 0.05) in the mean arterial blood pressure levels (126.7 ± 5 to 105.1 ± 4 mmHg) as compared to the sedentary diabetic group. Conclusions: Resistance exercise could restore endothelial function and prevent an increase in arterial blood pressure in type 1 diabetic rats