911 resultados para Exercício intervalado


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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Dexamethasone (DEXA) is a synthetic glucocorticoid widely used in the handling of several drugs, for its proven benefits in fighting inflammation and allergies. Despite their benefits, their chronic use leads to several side effects that include changes in the body in the metabolism of carbohydrates, lipids and proteins. Moreover, being an anti-inflammatory, acts on the arachidonic acid pathway, reducing the expression of the enzyme cyclooxygenase (COX-2) and growth factor derived from the endothelium of blood vessels (VEGF) in various tissues. However, its effects on the myocardium are still uncertain. The physical training (PT), in turn, promotes effects contrary to those caused by chronic use of DEXA, however, little is known about the preventive effects of TF in the side effects of Dexa in the myocardium. Therefore, the aim of this study was to determine if the TF has the ability to prevent and/or mitigate the effects of Dexa in protein expression of COX-2 and VEGF in the myocardium. Forty animals were divided into 4 groups: sedentary control (SC), sedentary treated with Dexa (SD), trained control (TC) and Trained treated with Dexa (TD) and submitted to a protocol of physical training on the treadmill for 70 days (1 h/day-5 days per week, 60% of physical capacity) or kept sedentary. Over the past 10 days, rats were treated with Dexa (Decadron, 0.5 mg/kg per day, ip) or saline. During training the animals were weighed weekly and during treatment daily. At the end of treatment was made to measure fasting glucose levels of animals. The rats were killed with excess anesthesia and cardiac muscle was removed, weighed, homogenized, centrifuged and stored at -20° C for analysis of protein expression of VEGF and COX-2 by Western blotting technique. Treatment with dexamethasone caused a weight loss of 18% in sedentary animals and 13% in trained as well as elevated levels of fasting glucose in sedentary (88%). The TF was unable to mitigate the loss in...

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Muscle atrophy is always associated with Dexamethasone (Dexa) treatment, however the mechanisms are not completely understood. This study investigated the effects of Dexa on myostatin and p70S6K protein expression and if previous exercise training (T) can attenuate these effects. Eighty rats were distributed into 4 groups: sedentary control (SC), sedentary treated with Dexa (SD; 0,5 mg/kg per day, i.p., 10 days), trained control (TC) and trained treated with Dexa (TD) and underwent a training period where they were either submitted to a running protocol (60% of physical capacity, 5 days/week for 8 weeks) or kept sedentary. After T period, animals underwent Dexa treatment concomitant with training. Western Blot was performed to identify myostatin and p70S6k protein expression in the tibialis anterior (TA) and soleus (SOL) muscle. Ten days of Dexa treatment increased fasting glucose (SD=+62%), however previous T attenuated this increase (TD=+20%, p<0.05). Dexa determined significant decrease in body weight in TD (-22%) and SD (-25%), followed by TA weight reduction in SD (-23%) and TD (-20%). Previous training could not avoid these decreases. Myostatin protein expression was not altered by dexa treatment or training in TA muscle but in SOL muscle it was significantly modified after T, regardless of treatment (TC=+%23 and TD=+25) compared with their respective controls. The protein p70S6K was not modified neither by dexa nor training in any of the analyzed muscle or condition. The results of this study allowed us to conclude that previous training attenuates the hyperglycemia induced by Dexa, however it did not prevent the body or muscle weight reductions. Even in the presence of muscle atrophy, the expression of myostatin and p70S6K do not justify the mechanisms of muscle loss induced by Dexa, which suggests that other catabolic or anabolic proteins could be involved in the process of muscle atrophy after 10 days of treatment with Dexa

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Introduction: physical exercise has been recommended as a non-pharmacological, therapeutic strategy in the treatment of important cardiovascular risk factors. Objective: to analyze the impact of an exercise program, tailored to the reality of the Family Health Units (FHU), on body composition, cardiovascular risk factors and Framingham score in obese postmenopausal. Methods: 70 women between 50 and 79 years, sedentary, obese and without menstruating for at least twelve months, were randomly assigned to a trained group (TG) (n = 35) and an untrained (GnT) (n = 35). The GT took 20 weeks of a physical exercise program with three weekly sessions, consisting of monitoring activities and heating (10 minutes), 25 minutes of exercise flexibility and strength, 50 minute walk with intensity between 50-65% of VO2max and 5-minute cool-down. The GnT was instructed to maintain their normal activities. Results: TG showed significant reductions in body mass index (30,1+3,7 vs. 29,3+3,7; p=0,0001), waist circumference (93,3+10,3 vs. 89,1+10,4; p=0,0001), percentage of fat (54,2+2,9 vs. 53,2+3,3; p=0,0001), systolic blood pressure (128,0+14,6 vs. 119,2+10,3; p=0,0001), triglycerides (148,4+66,1 vs. 122,8+40,7; p=0,006), VLDL cholesterol (29,7+13,2 vs. 24,5+8,0; p=0,005) and Framingham score (13,08+4,0 vs. 11,77+4,1; p=0,010). In the untrained group were observed significant increases in the percentage of fat (55,0+4,0 vs. 57,0+3,8; p=0,0001), systolic blood pressure (128,6+10,5 vs. 133,7+12,0; p=0,001), fasting glucose (95,2+18,4 vs. 113,7+28,8; p=0,001) and Framingham score (12,82+3,2 vs. 13,91+4,0; p=0,043), but also decreases levels of HDL cholesterol (55,1+10,5 vs. 51,7+11,0; p=0,017). Conclusion: the exercise program, adapted to the conditions of FHU, was effective in reducing cardiovascular risk factors in obese postmenopausal women served by the SUS program.

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The exercise-induced collapse (EIC) is a hereditary disease characterized by muscle weakness, impaired locomotion and collapse after intense exercise. This autossomic recessive disorder affects mainly Labrador Retriever presenting the mutation c.767G>T in the dynamin 1 (DNM1) gene. The objective of this study is to report the first case of exercise-induced collapse in Labrador Retriever in Brazil. The molecular test detected the specific genetic mutation and confirmed the clinical diagnosis in a Labrador Retriever with clinical history of weakness and collapse after exercise. It is important to include this disease as part of the differential diagnosis of neuromuscular diseases in Labrador Retriever and use the molecular test to guide matings.

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Introduction: The rest interval between bouts is a crucial variable of resistance training to ensure recovery of neuromuscular capacity. Objective: To compare the effect of rest interval between repeated bouts of resistance training on neuromuscular capacity of trained men. Methods: Eight resistance-trained men (21.6 +/- 3.3 years, 75.1 +/- 11.3 kg, 178.2 +/- 6.8 cm) performed two randomized and crossover resistance exercise bouts, repeated with rest interval of 24h or 48h. The bouts consisted of horizontal, inclined and declined bench press performed with five sets of 10 repetitions with an intensity of 70% of one repetition maximum (1RM) for each exercise. Neuromuscular performance post-exercise bout (strength, power and speed), was assessed with an accelerometer (Myotest (R)), with a load of 50% 1RM, in the bench press exercise. Results: Both sessions (24 and 48h) showed significant reduction (P < 0.05) in the neuromuscular capacity (strength, power and speed) post-exercise bout, returning to baseline values within 24h (P> 0.05). Conclusion: The results suggest that the rest interval of 24h is sufficient for recovery of neuromuscular performance in upper limbs of resistance-trained men.

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