Effect of anaerobic resistance training on gastric emptying of solids, nutritional parameters and food behavior in the rats treated with dexamethasone.

Dexamethasone (Dexa) is a potent glucocorticoid that can trigger side effects, such as neuromuscular, cardiovascular, and gastric motility disorders. Exercise can ameliorate gastrointestinal disorders. However, it is not clear whether exercise can modulate the side effects of using Dexa on gastric motility. To investigate the role of anaerobic resistance training (ART) on gastric motility and feeding behavior of rats treated with dexamethasone, rats were divided into three groups: control (Ctrl), dexamethasone (Dexa), and anaerobic resistance training + dexamethasone (ARTDexa). Anaerobic resistance training (ART) consisted of climbing a vertical ladder 5 days/week (with intensity of 50% to 100% of the maximum overload/8 weeks). At the end of the ART or control period, the rats received Dexa (1 mg/kg i.p) for 10 consecutive days. In the end, we evaluated anthropometric parameters and feeding behavior, heart rate, gastric emptying, and lipid profile in all groups. We observed significant decrease (p < 0.05) in body weight and food intake in the Dexa and ARTDexa groups compared to the control. Dexa promoted significant tachycardia (p < 0.05) and a decrease (p < 0.05) in the r-r' interval. The ART significantly prevented (p < 0.05) cardiovascular effects. Dexa induced a decrease (p < 0.05) in gastric emptying compared to the control group. On the other hand, ART significantly prevented (p < 0.05) the decrease in gastric emptying compared to Dexa. The chronic use of Dexa caused tachycardia, decreased food intake, and decreased gastric emptying. The ART modulated cardiovascular parameters, improving tachycardia. In addition, this exercise prevented gastric dysmotility induced by dexamethasone.

Influence of the physical exercise on decrease in the gastric emptying and alter appetite and food behavior in rats dexamethasone-treatment.

The chronic use of Dexamethasone (Dex) induced hyperglycemia and insulin resistance. On the other hand, physical exercise attenuates the symptoms induced by Dex in many physiological systems. However, the effect of the exercise on the changes in gastric motility induced by dexamethasone remains unknown. We hypothesized that low-intensity aerobic exercise modulates the metabolic effects induced by Dex-treatment by modifying the gastrointestinal function and feeding behavior in rats. Male rats were distributed into the following groups: Control (Ctrl), Dex (1.0 mg/kg, i.p.), Exercise (Ctrl + Exercise 5%) and (Dex1.0 + Exercise 5%). The exercise protocol was swimming for 5 consecutive days. We assessed the murinometric and nutritional indices, food intake, blood glucose by (ipGTT) and the gastric emptying rate of a liquid test meal were assessed in all rats. We observed a significant decrease (p < .05) in the gastric emptying in Dex1.0 group in relation to Ctrl group. The exercise prevented decrease in the gastric emptying (p < .05) in Dex1.0 + EX5% group when compared with Dex1.0 groups. The Dex1.0 group induced a significantly increase (p < .05) in glycaemia vs Ctrl group. The hyperglycemia was improving (p < .05) in the Dex1.0 + Ex5% compared with Dex1.0 groups. We observed a positive correlation (p < .05, and r = 0.7065) between gastric retention vs glycaemia in the Dex1.0 groups. The Dex1.0 reduced (p < .05) the body weight and altered body composition, promoting hypophagia. IL-6 increased (p < .05) at gastric fundus in Ex5% compared with Ctrl groups. In conclusion, the use of Dex1.0 decreases gastric emptying, promotes hyperglycemia and modifies feeding behavior. The low-intensity exercise prevents hyperglycemia, thus improving gastric dysmotility without improving the anthropometric parameters.

Moderate-intensity exercise and renin angiotensin system blockade improve the renovascular hypertension (2K1C)-induced gastric dysmotility in rats.

Actually, arterial hypertension is a major public health concern, which involves the renin angiotensin aldosterone system (RAS), via activation of the angiotensin receptors AT1 and AT2 of the cardiovascular system. Although angiotensin is an important stimulant of the gut permeability to sodium and water, little is known about the effects of arterial hypertension on gut motor behavior. Thus, we evaluated in rats the effect of hypertension induced by two-kidney one-clip (2K1C) model on the gastric motility, as well as the influence of exercise and RAS blockers treatment in such phenomenon. One week after surgery the rats were treated with Aliskiren (50 mg·kg-1, p.o.), Captopril (50 mg·kg-1, p.o.) or Losartan (10 mg·kg-1, p.o). Other group of rats was submitted to swimming with 5% body weight overload. After 4 weeks of physical training or pharmacological treatment, we assessed the gastric retention in all groups (GR) of a liquid test meal, the mean arterial pressure (MAP), the heart rate (HR) and the HR variation (HRV) as well as the in vitro contractility of gastric fundus. Renovascular hypertension increased (p < 0.05) the GR, MAP and HR, a phenomenon prevented by pretreatment with RAS blockers or exercise. The two kidney one-clip Hypertension (2K1C) decreased (p < 0.05) the gastric fundus responsiveness, a phenomenon also prevented by exercise. It conclusion, renovascular hypertension delays the gastric emptying of liquids, a phenomenon involving the activation of RAS, where exercise or blockade with aliskiren, captopril and losartan prevent gastric dysmotility.