| BackgroundAs a global public health problem,the health hazards of air pollut ion have a great impact on human survival and production.As air particulate pollution levels increase,so does the morbidity and mortality of all causes and other related diseases.A large number of epidemiology has been confirmed that there is a significant positive correlation between outdoor air pollutants and the incidence of cardiovascular disease(CVD).Globally,air pollution causes twice as many deaths from cardiovascular disease each year as respiratory diseases.Inhalable particulate matter PM2.5 is the leading cause of cardiovascular injury and disease in air pollution.Mitochondria are abundant in myocardial tissue,providing energy for heart activity,and mitochondria are often one of the targets of particulate matter attacks in the exposed environment of PM2.5 inhalable particulate matter.Studies have shown that many heart diseases are associated with the destruction of mitochondrial dynamic balance.Therefore,according to existing studies,inhalable particulate matter PM2.5 induces cardiovascular injury mainly caused by oxidative stress and mitochondrial dynamic balance destructi on.Long-term regular movement can improve the body's adaptive performance at the cellular,tissue,organ and system levels.The study found that long-term regular exercise can effectively improve the contraction function and diastolic function of the heart muscle and enhance the function of the heart.However,the benefits of exercise-induced cardiovascular system are strength-dependent,the greater the intensity of exercise,the greater the health benefits.Interval Training(IT)is derived from intermittent exercise training programs and is a sport mode that alternates between high-intensity exercise loads and low-intensity recovery activities.Intermittent exercise,because of its adjustable characteristics,is conducive to improving heart function,with certain heart protection benefits.Studies have found that exercise activities under the exposure of particulate pollution,that is,exercise compound particles will increase the damage of particulate matter to the body,so that the body in sports face greater health risks.Pre-exercise can improve cardiovascular damage caused by particulate matter exposure;the study found.This study explores whether aerobic intermittent exercise can improve heart damage caused by acute and subacute exposure of inhalable particulate matter PM2.5 through aerobic intermittent exercise intervention on heart function,and further explores its internal mechanism.Objection(1)To investigate the effects of PM2.5 acute exposure on heart function of intermittent exercise intervention.(2)To investigate the effect of PM2.5 sub-acute exposure on heart function and its potential mechanism of action.MethodsStudy I:(1)Experimental animal groups:Randomly divided Wistar rats into blank control group(C),low concentration exposure group(L),medium concentration exposure group(M),high concentration exposure group(H),aerobic intermittent training group(E),exercise intervention low concentration exposure group(EL),exercise intervention concentration exposure group(EM)and exercise intervention high concentration exposure group(EH);(2)Aerobic intermittent training:after the maximum oxygen test,all exercise groups were subjected to aerobic intermittent exercise intervention(8 weeks,5 times/week,1 hour/time),high intensity of 40m/min,low intensity of 15 m/min;(3)Acute exposure to respirable particulates:after you complete the exercise intervention,exposure to different concentrations of particulate matter concentration in acute exposure group,exposed for 6 hours straight,low concentration exposure group is 55.5 to 150.4?g/m3,medium concentration exposure group is 150.5to 250.4?g/m3,high concentration exposure group is 250.5 to 500.4?g/m3;experimental indicator detection:after completing PM2.5 exposure,the function and morphology of the left ventricle of Wistar rats were determined using Vevo?2100 high-resolution small animal ultrasound imaging system.The heart muscle tissue of rats was dyed using HE staining technol ogy.Prepare mitochondrial transmission electron slices of the heart muscle in rats and observe the microstructure changes of myocardial cells and myocar dial mitochondria using a transmission electron microscope.To detect changes in oxidative stress markers in myocardial tissue homogenization;(5)Using the t-test to analyze the different indicators between groups.Study II:(1)Experimental animal grouping:Randomly divided The Wistar Rats Into Blank Control Group(C),Subacute Exposure Group(P),Aerobic Intermittent Exercise Group(E)And Exercise Intervention Subacute Exposure Group(EP);(2)Exercise Intervention:After The Maximum Oxygen Test,All Exercise Groups Were Subjected To Aerobic Intermit tent Exercise Intervention(Same As The Study I);(3)Inhalable particulate matter subacute exposure:After completing the exercise intervention,the inhalable particulate matter PM2.5 subacute exposure,continuous exposure for three weeks(21 days),6 hours per day;(4)experimental indicator detection:each group of Wistar rats completed PM2.5 exposure,using Vevo?2100 high-resolution small animal ultrasound imaging system to determine the left ventricle function and morphology of Wistar rats.HE staining technique was used to dye the heart muscle tissue of rats to determine the damage to the tissue.Prepare mitochondrial transmission electron slices of the heart muscle in rats and observe the microstructure changes of myocardial cells and myocardial mitochondria using a transmission electron microscope.Detection of changes in expression of myocardial mitochondr ial fusion/splitting proteins(Mfn1/2,OPA1 and Drp1),as well as ERK1/2-JNK-P53 signal pathway proteins in myocardial tissue homogenization;(5)Using the t-test to analyze the different indicators between groups.ResultsStudy I:(1)Acute exposure concentration:In acute exposure studies with different concentrations of PM2.5 inhalable particulate matter,the average concentrations of low,medium and high concentration exposure were 149.16±30.88?g/m3,269.31±30.79?g/m3 and 509.84±36.74?g/m3;(2)Left ventricle function and structure:the group H compared to the group C,the E/A,SR and S increased significantly(p<0.01),the Decel increased significantly(p<0.05),and E/SR is significantly reduced(p<0.01).The group EM compared to the group M,the S,LVIDd and LVVold was significantly increased(p<0.05),the E/A and E are significantly reduced(p<0.05);The group EH compared to the group H,the S,LVIDd and LVVold was significantly increased(p<0.01),the SV is significantly reduced(p<0.05),the E/A and E are significantly reduced(p<0.01).(3)HE staining and ultra-microstructure:with the increase of exposure dose,myocar dial inflammation and myocardial cells and myocardial mitochondria and muscle damage have increased changes,exercise intervention can alleviate myocardial inflammation and myocardial cells and myocardial mitochondria and muscle damage degree increased;(4)Oxidative stress markers:the group H compared to the control group,the SOD is significantly reduced(p<0.01)and the GSH-Px is significantly reduced(p<0.05).The group EH compared to the group H,the LPO concentration was significantly reduced(p<0.05).Study II:(1)Subacute exposure concentration:the average concentration during exposure was 233.63±201.47?g/m3;(2)Left ventricle function and structure:the group P compared to the control group,the S increased significantly(p<0.01),and the A and the EF were reduced significantly(p<0.05).The group E compared to the control group,the S reduced significantly(p<0.01).The group EP compared to the group P,the EF and the LVPWd increased significantly(p<0.05),and the S reduced significantly(p<0.01);(3)HE staining and ultra-microstructure:after inhalable PM2.5subacute exposure,it can lead to myocardial cell and myocar dial mitochondria and muscle damage,and exercise intervention can be alleviated due to Impairment of myocardial cells induced by PM2.5 subacute exposure and myocardial mitochondria and muscle filaments;(4)mitochondrial fusion fission protein:the group P compared to the control group,the mitochondr ial fusion proteins Mfn1,Mfn2 and OPA1 are significantly reduced(p<0.05).The group EP compared with the group P,the mitochondrial fusion protein Mfn2 and OPA1 increased significantly(p<0.05),and the Mfn1 increased(p>0.05,ES=1.3);(5)Signal pathway:the group P compared with the control group,p ERK1/2,RERK1/2,p JNK1/2 increased significantly(p<0.01),and p53 increased(p>0.05,ES=0.21).The group EP compared to the control group.Compared with the subacute exposure group,the p ERK1/2 and p JNK1/2 increased significantly(p<0.05)and the RERK1/2 increased significantly(p<0.01),and the P53(p>0.05,ES=0.29).Conclusions(1)8 weeks of aerobic intermittent exercise can improve PM2.5 acute exposure to damage to cardiomyopathy and mitochondria,promote the relief of diastolic functional damage to the heart,especially in the medium and high concentration groups,the improvement effect is obvious,which may be related to exercise to reduce inflammation and enhance the body's antioxidant capacity.(2)3 weeks PM2.5 subacute exposure leads to a decrease in left ventricular diastolic contraction function,damage to myocardial tissue and mitochondria,8 weeks of aerobic intermittent exercise can effectively relieve PM2.5 subacute exposure caused by the damage to the heart structure and function.(3)3 weeks PM2.5 subacute exposure may be involved in PGC-1 alpha-regulated mitochondria fusion/splitting through the signaling pathway of ERK1/2-JNK-P53,and 8 weeks of aerobic intermittent exercise can be effective Reduce the activation status of ERK1/2-JNK-P53 signal pathway caused by PM2.5subacute exposure,increase the content of PGC-1 alpha,promote the increase of mitochondrial fusion protein expression,and reduce the degree of damage to mitochondria. |
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