Swimming Training Induced Myocardial Peroxynitrite Generation Mechanism

The research on oxidative stress has been about30years old. With the in-depthresearch of ROS and RNS，especially for NO，the emphasis on research oxidativestress, and the nitro-oxidative stress (nitrosative stress) is proposed. NADPH oxidasewas previously considered to be proprietary enzyme phagocytes, but recentlydiscovered that it is also present in many other cells. Gradually increasing evidencesuggests that NADPH oxidase is also involved in the exercise-induced myocardialROS production. NOS is the only synthase in living creature, which includes threesubtypes nNOS、eNOS、iNOS. Different exercise load isoforms are not the same, theincrease in the expression of an enzyme can lead to increased NO production. Basedon recent research,This study assumes that, after long-term swimming training,NADPH oxidase in myocardial induced generation of O?2and NOS generated NO intoof ONOO" by catalytic reaction.Research Methods:60mice were randomly divided into6groups:(1) control group (C group);(2)control+drug group (CA group);(3) swimming training group (T group);(4)swimming+drug group (TA group);(5) Weight swimming group;(6) Weightswimming group+drug group (OTA group). Swimming with loads of1to5%of bodyweight. Training every day,60minutes,6times a week for8weeks. Tail vein injectionof NADPH oxidase inhibitor Apocynin (lOmg/kg body weight) in the last twopre-training, at the end of the last training24hours after sampling.Research results：(1)After8weeks of training, the training body weight of mice is lower than thequiet group, high-intensity swimming training group than the moderate-intensitytraining group.(2)after8weeks of training, the last movement after24hours in the traininggroup Hb concentration decreased (P <0.05).(3)Mice by8weeks of free swimming or1%to5%weight loading swimmingtraining, compared to the end of the campaign after24h，with sedentary control group(C group): T group ONOO-content increased (P <0.01); TA group, OT group,ONOOievels significantly increased (P <0.05). CA group compared with group C，nosignificant change (P>0.05). TA group compared with the T group, the OTA group and OT group, the ONOO-content decreased (P <0.05).(4) After8weeks of free swimming or1%to5%of body weight loadingswimming training, compared with the C group，T group, TA group, OT group, OTAgroup, iNOS in a very significant increased (P <0.01). TA group and T group, the OTAgroup and OT group compared to the expression of iNOS has decreased, but there wasno significant difference.Research conclusions：1.8weeks of training, the mice in each group Hb decline，suggesting thatlong-term moderate-intensity and high-intensity aerobic training, reduced movementof the body’s blood oxygen transport capacity.2.8weeks of training, the exercise group than in the quiet group weightdecreased, indicating that the increase in exercise load. High-intensity exercise loaddecreased more than the moderate-intensity exercise load, indicating a greater load ofhigh-intensity exercise in mice body into a state of fatigue.3.8weeks of different load swimming training, the end of the campaign24hoursafter myocardial ONOO-signiifcantly increased, the two exercise load ONOO-nosignificant difference; applied NADPH oxidase inhibitor, reduced myocardialONOO-generation, the inference is that the ROS due to the decrease. The increase inreactive oxygen species generated by the the prompt exercise-induced myocardialNADPH oxidase pathway lead to myocardial ONOO-increase mechanism.4.Thelong-term swimming training-induced myocardial iNOS expressionincreased, thus resulting in the increase of NO，which led to the increased formation ofONOO-. The prompt exercise-induced myocardial expression of iNOS rise is one ofthe mechanisms leading to myocardial ONOO-increased.