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.

Moderate Physical Exercise Activates ATR2 Receptors, Improving Inflammation and Oxidative Stress in the Duodenum of 2K1C Hypertensive Rats.

Background: In addition to the cardiovascular and renal systems, the gastrointestinal tract also contains angiotensin ATR1a, ATR1b, and ATR2. We previously observed that the 2Kidney-1Clip hypertension model elicits physical exercise and gastrointestinal dysmotility, which is prevented by renin-angiotensin system blockers. Here, we investigate the effect of physical exercise on inflammation, stress biomarkers, and angiotensin II receptors in the duodenum of 2K1C rats. Methods: Arterial hypertension was induced by the 2K1C surgical model. The rats were allocated in Sham, 2K1C, or 2K1C+Exercise groups. One week after surgery, they were submitted to a physical exercise protocol (running 5x/week, 60min/day). Next, we assessed their intestinal contractility, cytokine levels (TNF-α, IL-1ß, and IL-6), oxidative stress levels (MPO, GSH, MDA, and SOD), and the gene expression of angiotensin receptors (ATR1A, ATR1B, and ATR2). Results: In comparison with the Sham group, the 2K1C arterial hypertension decreased (p<0.05) the intestinal contractility. In comparison with 2K1C, the 2K1C+Exercise group exhibited lower (p<0.05) MPO activity (22.04±5.90 vs. 78.95±18.09 UMPO/mg tissue) and higher (p<0.05) GSH concentrations in intestinal tissues (67.63±7.85 vs. 31.85±5.90mg NPSH/mg tissue). The 2K1C+Exercise group showed lower (p<0.05) cytokine levels in the intestine than 2K1C rats. In comparison with the Sham group, the 2K1C+Exercise rats showed higher (p<0.05) gene expression of ATR2 in the duodenum. Conclusion: 2K-1C hypertension elicits an oxidative stress and inflammation process in the duodenum. Physical exercise modulates the expression twice as much of ATR2 receptors, suggesting possible anti-inflammatory and antioxidant effects induced by exercise.

Role of cholecystokinin and oxytocin in slower gastric emptying induced by physical exercise in rats.

Vigorous exercise can induce gastrointestinal disorders such decreased gastric emptying pace, while low-intensity exercise can accelerate gastric motility. However, the mechanisms of these effects are still unknown. We investigated the possible neurohumoral mechanisms involved in these phenomena. In sedentary (Sed) and acute exercise (Ex) groups of rats, we assessed the activation of c-Fos in NTS and DVMN and the plasma levels of CCK and OXT. Separate groups received pretreatment with the oxytocin antagonist atosiban (AT), the cholecystokinin antagonist devazepide (DVZ), or the TRPV1 receptor inhibitor capsazepine (CAPZ). AT, DVZ and CAPZ treatments prevented (p<0.05) slower gastric emptying induced by acute exercise. The gene expression of OXT decreased (P<0.05) while that of CCK increased (P<0.05) in the gastric fundus and pylorus of the Ex group, while the plasma levels of OXT rose (p<0.05) and of CCK declined (p<5.05). We also observed activation (p<0.05) of c-Fos-sensitive neurons in the NTS and DVMN of exercised rats. In conclusion, acute exercise slowed gastric emptying by the vagal afferent pathway, which involved activation of CCK1/OXT/TRPV1 sensitivity.

L-Glutamine and Physical Exercise Prevent Intestinal Inflammation and Oxidative Stress Without Improving Gastric Dysmotility in Rats with Ulcerative Colitis.

The aim of this study was to evaluate the effects of glutamine supplementation or exercise on gastric emptying and intestinal inflammation in rats with ulcerative colitis (UC). Strength exercise consisted of jump training 4 × 10 repetitions/5 days a week/8 weeks with progressive overload. Endurance exercise consisted of swimming without overload for a period of 1 h a day/5 days a week/8 weeks. Another group (sedentary) of animals was supplemented with L-glutamine (1 g/kg of body weight) orally for 8 weeks before induction of UC. Colitis was induced by intra-colonic administration of 1 mL of 4% acetic acid. We assessed gastric emptying, macroscopic and microscopic scoring, oxidative stress markers, and IL-1ß, IL-6, and (TNF-α) levels. The UC significantly increased (p < 0.05) the gastric emptying compared with the saline control group. We observed a significantly decrease (p < 0.05) in body weight gain in UC rats compared with the control groups. Both exercise interventions and L-glutamine supplementation significantly prevented (p < 0.05) weight loss compared with the UC group. Strength and endurance exercises significantly prevented (p < 0.05) the increase of microscopic scores and oxidative stress (p < 0.05). L-glutamine supplementation in UC rats prevented hemorrhagic damage and improved oxidative stress markers (p < 0.05). Strength and endurance exercises and glutamine decreased the concentrations of inflammatory cytokines IL-1ß, IL-6, and TNF-α compared with the UC group (p < 0.05). Strength and endurance exercises and L-glutamine supplementation prevented intestinal inflammation and improved cytokines and oxidative stress levels without altering gastric dysmotility in rats with UC.

Acute Strength Exercise Decreases Satiety by Modifying Blood Cytokines Levels in Physically Active Men

Abstract Aim: Exercise elicits adaptations in several physiological systems, such as the gastrointestinal tract. We evaluated the effects of an acute strength exercise (acute-SE) on gastric satiety and its correlation with creatinine kinase (CK), lactate, and plasma cytokine levels in humans. Methods: Anthropometric parameters, body composition, muscular strength, and satiety (drink test protocol) at rest and exercise were assessed. Results: In the squat, bench press, and T-bar row exercises, we observed a significant decrease (p<0.05) in muscular strength in the second, third, and fourth sets compared with that in the first set. Compared with rest, we observed a significant increase (p<0.05) in CK and lactate levels after acute-SE. In the drink test, acute-SE significantly increased (p <0.05) the total intake, calories ingested, and a total time of ingestion. Concerning cytokines, there was a significant increase (p<0.05) after acute-SE of IL-1β and IL-6 levels at the beginning of the test and a decrease in IL-6, -10, -13, and TNF-α levels after acute-SE at the end of the test (p<0.05). There was a correlation between CK, lactate, and total intake after acute-SE (p<0.05) as well as between IL-6, 13, TNF-α, and volume ingested in the last score of the drink test after acute-SE (p<0.05). Conclusion: Acute-SE decreases satiety associated with changes in lactate, CK, and plasma cytokine levels in healthy humans.