Pedro Paulo Menezes Scariot

Different exercise protocols improve metabolic syndrome markers, tissue triglycerides content and antioxidant status in rats

BackgroundAn increase in the prevalence of obesity entails great expenditure for governments. Physical exercise is a powerful tool in the combat against obesity and obesity-associated diseases. This study sought to determine the effect of three different exercise protocols on metabolic syndrome and lipid peroxidation markers and the activity of antioxidant enzymes in adult Wistar rats (120 days old).MethodsAnimals were randomly divided into four groups: the control (C) group was kept sedentary throughout the study; the aerobic group (A) swam1 h per day, 5 days per week, at 80% lactate threshold intensity; the strength group (S) performed strength training with four series of 10 jumps, 5 days per week; and the Concurrent group (AS) was trained using the aerobic protocol three days per week and the strength protocol two days per week.ResultsGroups A and S exhibited a reduction in body weight compared to group C. All exercised animals showed a reduction in triglyceride concentrations in fatty tissues and the liver. Exercised animals also exhibited a reduction in lipid peroxidation markers (TBARS) and an increase in serum superoxide dismutase activity. Animals in group A had increased levels of liver catalase and superoxide dismutase activities.ConclusionsWe concluded that all physical activity protocols improved the antioxidant systems of the animals and decreased the storage of triglycerides in the investigated tissues.

Strength Training Prevents Hyperinsulinemia, Insulin Resistance, and Inflammation Independent of Weight Loss in Fructose-Fed Animals.

The aim of this study was to compare the effects of aerobic, strength, and combined training on metabolic disorders induced by a fructose-rich diet. Wistar rats (120 days old) were randomized into five groups (n = 8–14): C (control diet and sedentary), F (fed the fructose-rich diet and sedentary), FA (fed the fructose-rich diet and subject to aerobic exercise), FS (fed the fructose-rich diet and subject to strength exercise), and FAS (fed the fructose-rich diet and subject to combined aerobic and strength exercises). After the 8-week experiment, glucose homeostasis, blood biochemistry, tissue triglycerides, and inflammation were evaluated and analyzed. The strength protocol exerted greater effects on glucose homeostasis, insulin sensitivity, and liver lipid contents than other protocols (all P < 0.05). All three exercise protocols induced a remarkable reduction in inflammation, tissue triglyceride content, and inflammatory pathways, which was achieved through c-Jun NH2-terminal kinase (JNK) phosphorylation and factor nuclear kappa B (NFkB) activation in both the liver and the muscle. Our data suggest that strength training reduced the severity of most of the metabolic disorders induced by a fructose-rich diet and could be the most effective strategy to prevent or treat fructose-induced metabolic diseases.

Wide housing space and chronic exercise enhance physical fitness and adipose tissue morphology in rats

The current cages commonly used in animal experiments can prevent rats from engaging in most forms of natural locomotion behaviors. These animals tend to exhibit sedentary habits. Here, we show that a combination of wide housing space and training exercise helps to reduce white adipose mass and to increase brown adipose mass. Thus, this combination is a useful strategy for truly enhancing the physical fitness of captive rats commonly used in exercise-related interventional studies and to maximize their welfare.

Mountain Ultramarathon Induces Early Increases of Muscle Damage, Inflammation, and Risk for Acute Renal Injury

Purpose: This study aimed to investigate changes in muscle damage during the course of a 217-km mountain ultramarathon (MUM). In an integrative perspective, inflammatory response and renal function were also studied. Methods: Six male ultra-runners were tested four times: pre-race, at 84 km, at 177 km, and immediately after the race. Blood samples were analyzed for serum muscle enzymes, acute-phase protein, cortisol, and renal function biomarkers. Results: Serum creatine kinase (CK), lactate dehydrogenase (LDH), and aspartate aminotransferase (AST) increased significantly throughout the race (P < 0.001, P < 0.001; P = 0.002, respectively), and effect size (ES) denoted a large magnitude of muscle damage. These enzymes increased from pre-race (132 ± 18, 371 ± 66, and 28 ± 3 U/L, respectively) to 84 km (30, 1.8, and 3.9-fold, respectively); further increased from 84 to 177 km (4.6, 2.9, and 6.1-fold, respectively), followed by a stable phase until the finish line. Regarding the inflammatory response, significant differences were found for C-reactive protein (CRP) (P < 0.001) and cortisol (P < 0.001). CRP increased from pre-race (0.9 ± 0.3 mg/L) to 177 km (243-fold), cortisol increased from pre-race (257 ± 30 mmol/L) to the 84 km (2.9-fold), and both remained augmented until the finish line. Significant changes were observed for creatinine (P = 0.03), urea (P = 0.001), and glomerular filtration rate (GFR) (P < 0.001), and ES confirmed a moderate magnitude of changes in renal function biomarkers. Creatinine and urea increased, and GFR decreased from pre-race (1.00 ± 0.03 mg/dL, 33 ± 6 mg/dL, and 89 ± 5 ml/min/1.73 m2, respectively) to 84 km (1.3, 3.5, and 0.7-fold, respectively), followed by a plateau phase until the finish line. Conclusion: This study shows evidence that muscle damage biomarkers presented early peak levels and they were followed by a plateau phase during the last segment of a 217-km MUM. The acute-phase response had a similar change of muscle damage. In addition, our data showed that our volunteers meet the risk criteria for acute kidney injury from 84 km until they finished the race, without demonstrating any clinical symptomatology.