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Sports Fatigue In Rat Striatum Neurons Glucose Transport Effects And Its Mechanism Research

Posted on:2015-12-31Degree:MasterType:Thesis
Country:ChinaCandidate:S WangFull Text:PDF
GTID:2347330422483618Subject:Human Movement Science
Abstract/Summary:PDF Full Text Request
In the exercise fatigue, Brain tissue energy depletion,must rely on constantly glucoseobtained from the blood in order to maintain normal metabolic activities and functions.Motorneurons but also due to the impact of local metabolites and afferent nerve system, decreasedability to work, also needs to rely on the glucose in the blood to maintain metabolicbalance.The glucose transporter3(GLUT3) as the neurons facilitated glucose transportercarrier, and glucose molecule with high affinity, glucose transporter responsible for glucosetransport from the extracellular space to the neurons, which maturity and neuronal functionrelated to the regulation of brain tissue, reflects local tissue utilization of glucose and maturityof neurons, play a protective role in the brain.Experimental objective: Glucose is the main energy metabolism in the brain to providethe material, which is able to supply a steady stream of energy supply to meet the continuousexercise of the brain.To maintain blood glucose levels normal function of the brain plays avital role, insulin promotes the peripheral tissue glucose uptake and utilization, acceleratedglycogen synthesis, decreased blood glucose.In addition, lactic acid as a substrate for brainenergy metabolism, mainly through gluconeogenesis to glucose to maintain blood glucosebalance and for organizations to use.When the functional activity of neurons increases,inadequate energy supply, should need to rely on glucose transporter GLUT3to meet theirfunctional activity and maintain normal energy metabolism of the brain. The paper establishesthe fatigue model in rats, observe and analyze changes in relevant indicators of changes inlevels of iatrical neurons in rat brain cells GLUT3mRNA and protein expression, as well asglucose, lactic acid, serum insulin, glycogen, etc., aimed at Analysis of the exercise for thefatigue to exhaustion in the immediate situation neuronal GLUT3glucose transporter andsports fatigue and recovery factors GLUT3transport, investigate the effect of glucosetransporters in the sports fatigue mechanisms to delay the exercise of fatigue, speed laboratoryevidence provided during the energy supply.Experiment methods: Experimental animal models to adult male Wistar rats for the study,the use of multi-level Treadmill exercise sports fatigue pattern established in rats.Will beadaptive training treadmill rats were randomly divided into control group and fatigue groupafter screening. In addition to the control group, and the remaining rats were in accordance with the multi-level incremental exercise fatigue scheme, cycle7days.6days ago carried theload level as follows: Class I load rating of15m/min, treadmill exercise time was30min; IILevel load rating of20m/min, treadmill exercise time was30min; Level III load rating of25m/min, treadmill exercise time was60min,Slope are0°; rats7days after treadmill exerciseto class III load level, has been running at a speed of25m/min to exhaustion. Level I loadrating of15m/min, treadmill exercise time was30min; II Level load rating of20m/min,treadmill exercise time was30min three load rating of25m/min, treadmill exercise time was60min,6days.Measured immediately after exhaustive exercise levels in each group of ratsglucose, glycogen and lactate levels, using insulin radioimmunoassay kit serum insulin levels,Reverse transcription-polymerase chain reaction (RT-PCR) were determined before and afterfatigue striatal neurons GLUT3genes are expressed, Immune histochemical methoddetermination of fatigue before and after the striatum GLUT3protein expression.Experiment results:(1)Judge index of sports fatigue in rats: see rats from the behavioral in treadmill exerciseform by the ground type into voldemort type, stranded in the end of the runway at electricalstimulation, paddle; all cannot make rats to continue running;Compared with control group,the sports fatigue rats weight slightly lower after;And from the rat tail vein blood detectsmovement fatigue immediate blood urea nitrogen concentration decreased, blood lactic acidconcentration increased.(2)Rats compared with control group, the exercise fatigue instantly, concentration ofblood glucose, serum insulin, blood lactic acid levels increased significantly, cerebralglycogen content is reduced, the differences were statistically significant(p<0.01,p<0.05)?(3)Compared with control group, the exercise fatigue instantly, a significant reduction inthe rat striatum glucose concentration, a marked increase in the concentration of lactic acid,were statistically significant(p<0.01)(4)Compared with control group, the exercise fatigue instantly glucose transporters in therat striatum neurons GLUT3mRNAexpression intensity significantly enhanced.(5)Immunohistochemical results showed that, in comparison with control group rats ran'smotion to fatigue immediate striatal neurons positive staining with larger area, circumferenceis small, the difference has statistical significance(p<0.05);HE staining results showed that, incomparison with control group rats ran's motion to fatigue instantly striatal neurons nuclear area is larger, the perimeter is longer, but it has a much smaller nuclear/cytoplasmic ratios,and the differences were statistically significant(p<0.05).Experiment conclusion:(1)Treadmill exercise on Wistar rats (SPF) behavioral judgment, biochemical indicatorsof detection, proved with the method of one-time exhaustion exercise successful exercisefatigue model is established.(2)Rat treadmill exercise for a long time to fatigue instantly, energy consumption islarger, the glucose oxidation decomposition of the speed and the amount is larger, so the bloodsugar levels relatively quiet condition serious decline;Persistent hypoglycemia causes cerebralglycogen reserves drop;The depletion of glycogen, the concentration of lactic acidconcentration significantly higher than the quiet condition.Serious lack of supply, so the bodyenergy to produce fatigue, movement is terminated.(3)Persistent hypoglycemia and a lot of blood lactic acid accumulation caused a graveshortage of brain tissue of glucose uptake, then appeared the striatum reduced glucose andlactic acid content increased.(4)Compared with control group, the rats ran's motion to fatigue, immediately striatalneurons GLUT3protein expression and higher GLUT3mRNA expression, may be a protectivereaction of the body's resistance fatigue GLUT3mRNA expression increases, thus promote thesynthesis of protein.
Keywords/Search Tags:Sports fatigue, corpus striatum, neurons, glucose transporter, mechanism, Rats
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