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BACKGROUND:Resveratrol is a natural antioxidant extracted from plants.Its mechanism of improving exercise-induced fatigue mainly focuses on the protective effect against oxidative stress and inflammation.In this study,the protective mechanism of resveratrol on exercise-induced fatigue was mainly discussed from the perspective of gluconeogenesis. OBJECTIVE:To investigate the effect of resveratrol on gluconeogenesis in exercise-induced fatigue rats. METHODS:After 1 week of adaptive training,male Sprague-Dawley rats were randomly divided into 4 groups with 12 rats in each group:blank control group,resveratrol group,exercise group,resveratrol + exercise group.Weight-bearing swimming training was used to simulate long-term medium-high intensity exercise.After swimming with a weight of 5%for 1 hour every day,50 mg/kg resveratrol solution or the same volume of dimethyl sulfoxide solvent were given orally,6 days a week,for a total of 6 weeks.Samples were collected 24 hours after the last exercise,and the levels of urea nitrogen,creatine kinase,blood glucose,liver glycogen and lactic acid and pyruvate in liver tissue were detected by the kit.The activity of phosphoenolpyruvate carboxykinase was detected by microassay,and the activity of glucose-6-phosphatase was detected by enzyme-linked immunosorbent assay.Real-time fluorescence quantitative PCR was used to detect the gene expression of silent information regulator 1,cAMP-response element binding protein and peroxisome proliferator-activated receptor-γ coactivator-1α. RESULTS AND CONCLUSION:In the exercise group,plasma urea nitrogen and creatine kinase levels of rats were significantly increased(both P<0.05),liver lactate and pyruvate levels and lactate/pyruvate ratio were significantly increased(all P<0.01),and blood glucose and liver glycogen contents were significantly decreased(both P<0.01).Resveratrol supplementation could effectively improve the above conditions.Exercise significantly decreased the activities of phosphoenolpyruvate carboxykinase and glucose-6-phosphatase(P<0.01,P<0.05),and resveratrol supplementation significantly increased the activity of phosphoenolpyruvate carboxykinase in liver tissue(P<0.01).The mRNA expression levels of silent information regulator 1,cAMP-response element binding protein and peroxisome proliferator-activated receptor-γ coactivator-1α in liver tissue of the exercise group were significantly decreased(all P<0.01),while resveratrol supplementation could significantly increase the gene expression levels of this pathway.To conclude,resveratrol can relieve exercise-induced fatigue caused by long-term medium-high intensity exercise,and its mechanism may be related to up-regulating the gluconeogenesis regulatory pathway,improving rate-limiting enzyme activity,promoting liver gluconeogenesis,and increasing blood glucose and liver glycogen levels.
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BACKGROUND:Type 2 diabetes is often accompanied by renal dysfunction.Increasing studies have shown that exercise can alleviate metabolic disorders and renal dysfunction in diabetic patients.However,the specific mechanism underlying the renal protective effect of exercise in patients with type 2 diabetes is rarely reported. OBJECTIVE:To investigate whether aerobic exercise can improve renal function in type 2 diabetic rats by inhibiting transforming growth factor β1/Notch1 pathway. METHODS:Male Sprague-Dawley rats were randomly divided into normal control group and diabetes model group.After successful modeling,they were randomly divided into diabetes control group and diabetes exercise group.Rats in the diabetes exercise group were subjected to an 8-week aerobic exercise.Samples were collected after exercise,and the relevant indexes of glucose and lipid metabolism and renal function were detected by automatic biochemical analyzer and ELISA.The microscopic structure of renal cortex was observed by electron microscope.ELISA and RT-PCR were used to detect the expression of related proteins and genes in rat kidney tissue. RESULTS AND CONCLUSION:Compared with the normal control group,fasting blood glucose,total cholesterol,and triglyceride levels and insulin resistance index were significantly increased in the diabetic control group(P＜0.05).Aerobic exercise could significantly reduce fasting blood glucose and triglyceride levels(P＜0.05).Compared with the normal control group,the diabetic control group had significantly increased contents of urinary microalbumin,serum urea nitrogen and serum creatinine(P＜0.01),thickened renal basement membrane,mesangial matrix hyperplasia,accompanied by a certain degree of foot process fusion,and obvious lesion of the kidney.Aerobic exercise could significantly down-regulate the overexpressions of urinary microalbumin,serum urea nitrogen and serum creatinine in type 2 diabetic rats(P＜0.01),and significantly improve the pathological changes of the kidney in diabetic rats.Compared with the normal control group,the protein and gene expression levels of transforming growth factor β1,Notch1,Jagged1 and Hes1 in rat kidney tissue were significantly increased in the diabetic control group(P＜0.01).Aerobic exercise had a highly significant inhibitory effect on the overexpression of transforming growth factor β1,Notch1 and Jagged1 proteins and genes(P＜0.01)and also significantly inhibited the overexpression of Hes1 protein(P＜0.05).In conclusion,aerobic exercise can protect renal function and delay the pathological progression of the kidney in diabetic rats,which may be achieved by inhibiting the overexpression of transforming growth factor β1/Notch1 signaling pathway.
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BACKGROUND:Studies have shown that resveratrol can relieve exercise-induced fatigue and protect the heart,but its action mechanism needs further study. OBJECTIVE:To explore the protective effect and regulatory mechanism of resveratrol on ventricular remodeling in exercise-induced fatigue rats. METHODS:Totally 48 male Sprague-Dawley rats were randomly divided into four groups,with 12 rats in each group.Rats in the blank control group were fed conventionally.After one week of adaptive training,rats in the exercise-related fatigue group and exercise-related fatigue with resveratrol supplement group were trained by 6-week weight-bearing swimming(5%body mass lead block fixed in the tail,70%-80%maximal oxygen uptake intensity),6 days a week,60 minutes a day.Rats in the resveratrol supplement group and exercise-related fatigue with resveratrol supplement group were given resveratrol(50 mg/kg per day)by gavage one hour after exercise intervention.Blank control group and exercise-related fatigue group were given the same volume of 2%dimethyl sulfoxide,6 days a week,once a day for 6 weeks.The body mass and heart mass of the rats were measured 24 hours after the last intervention.Plasma creatine kinase isoenzyme,cardiac troponin 1,pyruvate dehydrogenase and uncoupling protein 1 levels in myocardial tissue were determined by ELISA.The mRNA expression levels of ventricular remodeling-related factor Foxp1,transforming growth factor β1 and endothelin 1 were detected by RT-PCR. RESULTS AND CONCLUSION:Compared with the blank control group,the body mass of rats decreased and the heart mass increased in the exercise-related fatigue group(P＜0.05).Compared with the exercise-related fatigue group,the body mass and heart mass of the rats reduced in the exercise-related fatigue with resveratrol supplement group(P＜0.05).Compared with the blank control group,the levels of creatine kinase isoenzyme,cardiac troponin 1 and uncoupling protein 1 increased(P＜0.01),and the level of pyruvate dehydrogenase decreased(P＜0.01)in the exercise-related fatigue group.Compared with the exercise-related fatigue group,the levels of creatine kinase isoenzyme,myocardial troponin 1 and uncoupling protein 1 decreased(P＜0.05),and the level of pyruvate dehydrogenase increased(P＜0.05)in the exercise-related fatigue with resveratrol supplement group.Compared with the blank control group,the expression of the Foxp1 gene decreased(P＜0.01),and the expression of transforming growth factor β1 and endothelin 1 gene increased(P＜0.01)in the myocardium of the exercise-related fatigue group.Compared with the exercise-related fatigue group,the expression of the Foxp1 gene in the myocardium of the exercise-related fatigue with resveratrol supplement group increased(P＜0.01),while the expression of the transforming growth factor β1 and endothelin 1 gene decreased(P＜0.05).It is suggested that exercise-induced fatigue can promote myocardial adaptability and cause compensatory hypertrophy.Resveratrol can improve myocardial injury and energy metabolism and delay ventricular energy remodeling in rats.This effect may be related to the regulation of Foxp1/transforming growth factor β1/endothelin 1 signaling pathway.
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BACKGROUND/OBJECTIVES@#To investigate the effect and regulatory mechanism of resveratrol supplementation on the mitochondrial energy metabolism of rats with exerciseinduced fatigue.MATERIALS/METHODS: Forty-eight Sprague-Dawley male rats were divided randomly into a blank control group (C), resveratrol group (R), exercise group (E), and exercise and resveratrol group (ER), with 12 rats in each group. Group ER and group E performed 6-wk swimming training with 5% wt-bearing, 60 min each time, 6 days a wk. Group ER was given resveratrol 50 mg/kg by gavage one hour after exercise; group R was only given resveratrol 50 mg/kg by gavage; group C and group E were fed normally. The same volume of solvent was given by gavage every day. @*RESULTS@#Resveratrol supplementation could reduce the plasma blood urea nitrogen content, creatine kinase activity, and malondialdehyde content in the skeletal muscle, increase the total superoxide dismutase activity in the skeletal muscle, and improve the fatigue state.Resveratrol supplementation could improve the activities of Ca2+ -Mg2+ -ATPase, Na+ -K+ -ATPase, succinate dehydrogenase, and citrate synthase in the skeletal muscle. Furthermore, resveratrol supplementation could up-regulate the sirtuin 1 (SIRT1)-proliferator-activated receptor gamma coactivator-1α (PGC-1α)-nuclear respiratory factor 1 pathway. @*CONCLUSIONS@#Resveratrol supplementation could promote mitochondrial biosynthesis via the SIRT1/PGC-1α pathway, increase the activity of the mitochondrial energy metabolismrelated enzymes, improve the antioxidant capacity of the body, and promote recovery from exercise-induced fatigue.
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Objective To examine the separate or combined effects of aerobic exercise and AlaGln administration on patients with type 2 diabetes mellitus(T2DM).Methods T2DM was induced in rats by feeding a high-fat diet and injecting a low dose of streptozocin.Then they were trained for 8 weeks with or without administration of alanyl glutamine(Ala-Gln).At the end of training,the content of fasting serum glucose (FBG),insulin (INS),C-peptide and glucagon like peptide-1 (GLP-1) were measured and homeostasis model assessment of insulin resistance (HOMA-IR) was calculated.Results Compared with the normal rats,significant increase was observed in the FBG concentration(P＜0.05)and HOMA-IR(P＜0.05),but significant decrease in C-peptide(P＜0.05) and GLP-1(P＜0.01) of the type 2 diabetic rats.Aerobic exercise resulted in significant decrease in the FBG and HOMA-IR levels,but significant increase in the concentration of C-peptide(P＜0.01).Ala-Gln administration reduced FBG (P＜0.05),and promoted the concentrations of serum insulin (P＜0.05),C-peptide (P＜0.01) and GLP-1(P＜0.05) significantly.The combination of aerobic exercise with Ala-Gln administration had a significant interaction on promoting serum insulin(P＜0.05),but not on decreasing FBG and HOMA-IR,or increasing C-peptide and GLP-1.Conclusion The aerobic exercise or Ala-Gln administration can significantly lower blood glucose levels by improving the impaired insulin secretion in type 2 diabetic rats,and their combination has a synergistic effect on promoting insulin secretion.
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Objective To explore the effect of hypoxic training on the barrier function of intestinal mucous membrane and underlying mechanism in rats.Methods Eighty 5-week-old male Sprague-Dawley rats were randomly divided into a control group,an exercise training group,a hypoxia control group and a hypoxia exercise group,each of 20.The altitude training was conducted through swimming training in artificial hypoxia environment.Two and 6 weeks after the intervention,the tissue structure and ultrastructure of small intestine mucosa were observed.The content of diamine oxidase (DAO)and D-lactate (D-LA),tumor necrosis factor-α (TNF-α)and nuclear factor κB (NF-κB)in plasma and the mRNA level of occludin in ileal tissue were measured.Results (1)Electron microscopy data showed that,after six weeks,compared with the control group,the microvilli of rats in the exercise training group were sparser and arranged irregularly.Furthermore,the gap between epithelial cells became wider.In addition,the number of mitochondria decreased significantly and cristae were vague.For the hypoxia control group,the microvilli shortened significantly and arranged irregularly.Moreover,the gap between cells became wider with partial denatured mitochondria.For the Hypoxia exercise group,the number of mucosal epithelium microvilli in the bowels reduced significantly and the microvilli shortened significantly.Similar to that of the hypoxia control group,the gap between epithelium cells growed wider.However,the cellular structure were fuzzier,and the denature of mitochondria worsened,with the cristae being vague even disappearing partially.(2)Two weeks of exercise training reduced the number of intestinal microvilli significantly (P＜0.01),but increased the plasma level of the DAO and D-LA,as well as the expression level of NF-κB in intestinal tissue significantly (P＜0.05).Hypoxic exposure significantly reduced the mRNA level of oceludin in small intestine (P＜0.01),but significantly increased the plasma level of DAO and D-LA (P＜0.05 vs.control)and the expression of TNF-α and NF-κB in small intestine (P＜0.01).There was no significant interaction between two weeks of exercise training and hypoxia exposure either on the reduction of the number and height of intestinal microvilli,or the transcription level of occluding in small intestine,or the plasma level of DAO and D-LA,or the expression of TNF-α and NF-κB in small intestine (P＞0.05).(3)Both exercise training for six weeks and hypoxia exposure significantly reduced the number and height of microvilli in small intestine (P＜0.01)and the occludin level in small intestine,but significantly increased the plasma level of DAO and DLA (P＜0.01),the expression of TNF-α (P＜0.01,P＜0.05)and NF-κB (P＜0.01).Meanwhile there was significant interaction between six-week exercise training and hypoxia exposure on decreasing the number (P＜0.01)and the height (P＜0.05)of microvilli in small intestine.Conclusion (1)Both intensive training and hypoxia exposure can impair intestinal mucosal barrier function and the extent of damage is correlated with the duration of training and hypoxia exposure.(2)Hypoxic exposure and intensive training may reduce the expression of occludin mRNA through increasing the expression of TNF-α and NF-κB in the small intestine,which in turn increases intestinal permeability and intestinal mucosa inju