The Effect Of Astaxanthin On Myocardial Metabolism In Acute High Intense Exercise Rats

Objective:To learn the metabolic mechanism of rat myocardium about acute high intense exercise or astaxanthin.Methods:The male SD rats weight were about 190±10g,and therer were 32 week-7 healthy rats,which were randomly divided into 4 groups.They were the control group（group C）,exercise group（group E）,medicine supplementary group（group M）and medicine supplementary and exercise group（group EM）.Astaxanthin was given to M and EM groups at 25mg/kg/d,and soybean oil was given to C and E groups at the same amount.Every group of rats were given adaptive exercise training on the first day,and the athletic ability of the rats was tested by increasing load exercise on the 20th day.The speed was confirmed at 21m/min by 75%VO_2max obtained and Bedford’s paper.On the 29th day,the rats in E and EM groups took the last one-time high-intensity treadmill exercise at a speed of 24m/min,5min,8 times with a gradient of-16°and an interval of1min.The rat myocardium was collected immediately after running（within10min）,and the samples were tested by LC-MS after they were processed.XCMS,SIMCA-P,Excel and Origin software were used to image and data processing and analysis to find significantly different metabolites.Metabolic pathways and the potential markers were analyzed by Met-PA and KEGG databases.Results:As the standard of VIP>1,p<0.05,FC>1.5 or FC<0.67,（1）Compared with group C,group E had 32 different metabolic markers in myocardium.32 different metabolites were involved in 26 metabolic pathways,and 6 of them were potential target pathways for acute intense exercise,including linoleic acid metabolism,fructose and mannose metabolism,amino sugar and nucleotide sugar metabolic pathway,nicotinate and nicotinamide metabolism,arginine biosynthesis,and pyrimidine metabolism.And 12potential markers:the level of SOPC,Cytidine monophosphate N-acetylneuraminic acid,thymidine,thymine,uracil（p<0.01）,L-Aspartate,PC,L-Arginine,D-Mannose 1-phosphate、D-mannose、linoleic acid（p<0.05）were increased significantly,but the level of nicotinamide（p<0.05）decreased significantly;（2）Comparing with group C,group M had 39 different metabolic markers,which involved in 14 metabolic pathways.And six of them were potential target pathway for astaxanthin supplement.It included amino sugar and nucleotide sugar metabolic pathway,galactose metabolic pathway,fructose and mannose metabolic pathway,glycolysis/gluconeogenesis,starch and sucrose metabolic pathway,pentose phosphate pathway.And 16 potential markers:the level of D-Ribose 5-phosphate,D-Mannose-6-phosphate,D-Glucose6-phosphate,6-Phospho-D-gluconate,D-Lactose,phosphoenolpyruvate,sucrose,galactinol,α-D-Galactose 1-phosphate,D-Erythrose 4-phosphate,D-Mannose,α-D-glucose,D-Ribulose 5-phosphate,β-D-Fructose 6-phosphate（p<0.01）,stachyose,D-Mannose 1-phosphate（p<0.05）significantly increased.（3）Compared with group E,group EM had 15 different metabolic markers,which involved in 9 metabolic pathways,and among which3 were potential targeting pathways of astaxanthin on acute intense exercise,including linoleic acid metabolism,Glutathione metabolism,cysteine and methionine metabolism.And 6 potential markers:the level of S-Adenosylmethionine increased significantly（p<0.05）,the level of SOPC,3-phosphoserine,glutathione（p<0.01）,linoleic acid,5-L-Glutamyl-L-alanine（p<0.05）were significantly decreased.Conclusion:（1）Acute high-intensity exercise can cause disorders of lipid and glucose metabolism in the myocardium of rats,and the body compensates to enhance amino acid metabolism to protect myocardium.（2）Astaxanthin supplementation can make the myocardial sugar metabolism more active,lipid metabolism does not change significantly,and the myocardial energy supply is more sufficient.（3）Astaxanthin supplementation can improve myocardial lipid metabolism of rats with acute high-intensity exercise,provide needed energy for the body,and promote amino acid metabolism to protect the myocardium.