The Effect Of MCU On Myocardial Mitochondria Calcium Metabolism In High Intensity Exercise Preconditioning

Objective:To observe the effect of exercise preconditioning on myocardial mitochondrial calcium metabolism after intensive exercise in rats,and to explore the role of mitochondrial calcium monodirectional transporter（MCU）in improving myocardial mitochondrial calcium metabolism disorder caused by exercise preconditioning.Methods:Thirty-two 8-week-old male SD rats were randomly divided into control group（C group,n=8）and one-time high intensity exercise group（EE group）after feeding for one week.（EP group）received 4 weeks treadmill exercise pretreatment（0°,30m/min,1h/d,5d/w）,but C,EE and Y groups were not treated in this period.After 4 weeks,EE group and EP group had one-time high intensity exercise（30m/mim）.In group Y,after intraperitoneal injection of MCU inhibitor,a one-time high intensity exercise（30m/mim to exhaustion）was carried out,and materials were obtained immediately.Measurement of Muscle Fiber Cross Sectional Area（CSA）by HE Staining Technique and Image J Measurement Software,The expression of MCU and MICu1 protein,the activity of Ca²⁺-ATPase and the contents of mitochondria and cytoplasmic Ca²⁺were measured by Westernblot method in each group of rats.Results:（1）Compared with the C group,the MCU protein expression in the EE group and the Y group was significantly increased（P<0.05）;the EP group was increased,but there was no statistical difference（P>0.05）;compared with the EE group Compared with it,the EP group and the Y group decreased,but there was no statistical difference（P>0.05）.（2）Compared with group C,MICU1 protein expression in EE group and EP group decreased slightly,and expression in group Y increased.However,there was no statistical difference（P>0.05）;compared with the EE group,the EP group decreased and the Y group increased,but there was no statistical difference（P>0.05）.（3）Compared with group C,the concentration of Ca²⁺in the myocardial mitochondria of the EE group increased,but the EP group and the Y group were significantly lower than the C group（P<0.05）;the EP group and the Y group were lower than the EE group,but there Statistical difference（P>0.05）.（4）Compared with group C,the concentration of Ca²⁺in the myocardial cytoplasm of the EE group decreased slightly,but there was no statistical difference（P>0.05）.The EP group and the Y group were significantly higher than the C group;compared with the EE group,EP group and Y group increased significantly（P<0.05,P<0.01）.（5）Compared with group C,the myocardial Ca²⁺-ATPase activity of the three groups decreased slightly,but the difference was not significant（P>0.05）.Conclusions:One-time high-intensity exercise can cause myocardial injury,in which myocardial mitochondrial function is damaged,causing mitochondrial calcium overload.Exercise preconditioning,as a means of ischemic preconditioning,can produce certain protective effects on myocardium.Exercise preconditioning can reduce myocardial mitochondrial calcium overload caused by one-time high-intensity exercise.The mechanism may be related to exercise preconditioning reducing the transport of calcium ions from cytoplasm to mitochondria by MCU and inhibiting exercise after MCU protein activity.Similar results as exercise preconditioning also support this possible mechanism.