OBJECTIVE:The aim of the present study was to evaluate the effect of both swimming and resistance training on tumor necrosis factor-alpha and interleukin-10 expression, adipocyte area and lipid profiles in rats fed a high-fat diet.METHODS:The study was conducted over an eight-week period on Wistar adult rats, who were divided into six groups as follows (n = 10 per group): sedentary chow diet, sedentary high-fat diet, swimming plus chow diet, swimming plus high-fat diet, resistance training plus chow diet, and resistance training plus high-fat diet. Rats in the resistance training groups climbed a vertical ladder with weights on their tails once every three days. The swimming groups swam for 60 minutes/day, five days/week.RESULTS:The high-fat diet groups had higher body weights, a greater amount of adipose tissue, and higher tumor necrosis factor-alpha expression in the visceral adipose tissue. Furthermore, the high-fat diet promoted a negative change in the lipid profile. In the resistance training high-fat group, the tumor necrosis factor-alpha expression was lower than that in the swimming high-fat and sedentary high-fat groups. Moreover, smaller visceral and retroperitoneal adipocyte areas were found in the resistance training high-fat group than in the sedentary high-fat group. In the swimming high-fat group, the tumor necrosis factor-alpha expression was lower and the epididymal and retroperitoneal adipocyte areas were smaller compared with the sedentary high-fat group.CONCLUSION:The results showed that both exercise modalities improved the lipid profile, adiposity and obesity-associated inflammation in rats, suggesting their use as an alternative to control the deleterious effects of a high-fat diet in humans.

The purpose of the present study was to evaluate the effects of the resistance training (RT) on the lipid profile and metabolism, oxidative stress, and activity of metalloproteinase-2 (MMP-2) in the left ventricle (LV) of dietinduced obesity rats. Methods: Forty males Wistar rats 90 days-old were grouped into four groups (n=10): i) Sedentary group (SED); ii) Obese sedentary group, feed with high-fat diet (Ob-SED); iii) Resistance Trained group (RT), and iv) Obese Resistance trained group (Ob-RT). The LV was assayed to Obesity index, LV lipid content, citrate synthase activity, lipid peroxidation (TBARS), enzymatic and non-enzymatic antioxidant systems, lipid profile, cardio-metabolic parameters, and activity of MMP-2. Results: High-fat diet was associated with manifestations of the obesity, body mass gain, and increased obesity index, accompanied by an alteration in the lipid profile. On the other hand, RT was able to prevent body weight gain, to reduce the obesity index and to improve the lipid profile, to elevate the activation of the citrate synthase, and to decrease MMP-2 activity in the LV of obese rats. Conclusion: RT positively modulated blood lipid profile and antioxidant enzymes preventing the increased activity of MMP-2 in the left ventricle from rats fed with high-fat diet.

The data demonstrated that moderate intensity RT prevented obesity-induced cardiovascular disorders simultaneously with reduced inflammatory responses and modifications of RAS in the NTS.

Angiotensin II increases and decreases arterial pressure by acting at angiotensin type 1 and type 2 receptors respectively. Renovascular hypertensive rats exhibit a high level of activity of the peripheral and central renin-angiotensin system. Therefore, in the present study we evaluated the effect of increasing the expression of angiotensin type 2 receptors in the solitary-vagal complex [nucleus of the solitary tract/dorsal motor nucleus of the vagus], a key brainstem region for cardiovascular regulation, on the development of renovascular hypertension. Holtzman normotensive rats were implanted with a silver clip around the left renal artery to induce 2 kidney-1 clip renovascular hypertension. Three weeks later, rats were microinjected in the solitary-vagal complex with either an adeno-associated virus to increase the expression of angiotensin type 2 receptors, or with a control vector. We observed that increasing angiotensin type 2 receptor expression in the solitary-vagal complex attenuated the development of renovascular hypertension and also reversed the impairment of the baroreflex and the increase in the low frequency component of systolic blood pressure observed in renovascular hypertensive rats. Further, an observed decrease in mRNA levels of angiotensin converting enzyme 2 in the solitary-vagal complex of renovascular hypertensive rats was restored to control levels following viral-mediated increases in angiotensin type 2 receptors at this site. Collectively, these data demonstrate specific and beneficial effects of angiotensin type 2 receptors via the brain of hypertensive rats, and suggest that central angiotensin type 2 receptors may be a potential target for therapeutics in renovascular hypertension.

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