Effect Of Exercise Fatigue On Energy Metabolism Of Skeletal Muscle In Rats And Its Mechanism

Objective:to establish a rat model of exercise fatigue by increasing treadmill training,and to explore the effect of exhaustion exercise on energy metabolism of skeletal muscle fibers in rats and its molecular mechanism.Methods:30 healthy male Wistar rats?8 weeks old?and 10 control group?randomly selected?were selected as the D group,and the rest 20 served as exercise fatigue models by multistage incremental treadmill exercise.Exercise program?slope0⁰,load is divided into two groups:fatigue group;fatigue two groups?.The blood glucose,serum insulin,muscle glycogen,blood urea nitrogen,blood lactic acid,muscle lactic acid content,glycogen synthetase,phospho fructose kinase and mitochondrial isocatate dehydrogenase activity of three groups of rats immediately after exhaustive exercise were tested.RT-PCR technique was used to determine the gene expression of AMPK-mTOR-HIF-1?in the four muscle cells of bone.Results:1)immediately after exhaustive exercise,the body weight of group P₁ and P₂ decreased after exercise compared with group P₁ and P_2,and the difference between group P₁ and group P₁ was significant?P<0.01?,and there was a difference in P₂ group?P<0.05?.After exercise,the body weight of group P₂ was lower than that in group P₁?P<0.05?.There was no difference in the weight of the other groups before exercise.2)the content of blood sugar,serum insulin and muscle glycogen decreased?P<0.05?in group P₁ and group P₂ compared with group D,and there was a significant decrease in blood sugar,and the difference was significant?P<0.01?.The activity of glycogen synthetase in group P₁ was higher than that in group D?P<0.05?.The activity of glycogen synthetase in group P₂ was significantly higher than that in group D,and the difference was significant?P<0.01?.There is no difference between the P₁ and the P₂group.3)the blood urea nitrogen,blood lactate and muscle lactic acid concentration in group P₁ were significantly higher than those in group D?P<0.01?;the blood urea nitrogen concentration in group P₂ was significantly higher than that in group D?P<0.01?;the concentration of lactate and muscle lactate in P₂ group was higher than that in D group?P<0.05?.There is no difference between the P₁ and the P₂ group.4)there was no significant difference in the content of ATP in the three groups.The content of AMP and AMP/ATP in the P₁ and P₂ groups were significantly higher than those in the D group,and the difference was significant?P<0.01?.There is no difference between the P₁ and the P₂ group.5)the activity of fructose phosphoric acid kinase in group P₁ and P₂ was higher than that in group D,which was different?P<0.05?.The activity of ISO-citrate dehydrogenase in group P₁ and P₂ was significantly higher than that in group D,and the difference was significant?P<0.01?.There is no difference between the P₁ and the P₂ group.6)the activity of AMPK in group P₁ and P₂ was significantly higher than that in group D,and the difference was significant?P<0.01?.The activity of mTORC1 in group P₁ was lower than that in group D,and there was a difference?P<0.05?.The activity of mTORC1 in the P₂group was significantly lower than that in the D group,and the difference was significant?P<0.01?.There is no difference between the P₁ and the P₂ group.There was no difference in the Ct?dR?values of mTORC2 and HIF-1?in the three groups of rats.Conclusions:1.Experimental results show that exercise intensity has no significant effect on the indicators involved in the experiment.2.The change of AMP/ATP ratio during exercise can activate AMPK,ascribed to the increase of AMP.3.After exercise induced fatigue,the blood glucose concentration,serum insulin concentration and muscle glycogen content decreased significantly in rats.The activities of blood urea nitrogen,blood lactate and muscle lactate,glycogen synthetase,phospho fructose kinase and isoccitrate dehydrogenase activity increased significantly.After exhaustive exercise,blood sugar decreased,negative feedback of hypoglycemia regulated islet beta cells,reduced insulin secretion,decreased insulin concentration significantly,and played a protective role in islet cells.In order to delay the production of fatigue,the muscle stimulated GLUT4 to transposition from the intima to the outer membrane of the cell.The increase of glucose transport rate corresponded to the increase of GS activity.The body promotes glucose transport through a non insulin pathway.Its physiological mechanism is:slow muscle contraction after exhaustive exercise leads to a sharp increase in intracellular AMP content.The target protein AMPK is activated by allosteric,and then stimulates the related signal transduction pathway to enhance the utilization of fatty acids and glucose in the peripheral tissue,especially the skeletal muscle,and promote the energy balance.In order to delay the occurrence of sports fatigue.