The Mechanisms And Preventions Of Cardiovascular System Injury Induced By High-intensity Exercise

Background High-intensity exercise, as a strong source of stress, can cause obvious oxidative stress injury of myocardial cell and cardiac structure and function change, which leads to myocardial ischemia, arrhythmia, cardiac insufficiency, and even sudden cardiac death. However, the exact mechanism of myocardial injury induced by high-intensity exercise remains unclear, lacking of no effective protective measures. Objective In this study, the characteristics and effects of high-intensity exercise on changes of cardiac function was studied. Then, we evaluated the effects of FOX03 A and its potential mechanism in myocardial damage caused by high-intensity exercise. Furthermore, the protective role of Allicin, used as a kind of preventive drug, on myocardial injury induced by high-intensity exercise were analyzed.Section One The effects of on-site simulation high-intensity training on cardiovascular system functionMethods 100 military soldiers or officers were allocated to high-intensity group, while 70 logistics staff were assigned to control group. Serologicals index including cardiac-specific Troponin I-Ultra (TnI-Ultra), cardiac-specific Troponin T-High sensitivity (TnT-hs), human heart fatty acid binding protein (HUMAN H-FABP), cortisol (COR) and high sensitivity C-reactive protein (hs-CRP) were detected.40 subjects were randomly selected from high-intensity group, and 36 person from control group accordingly.12-lead dynamic cardiograph analysis system as well as heart rate variability analysis system were adopt for statistics analysis in this study.Results1. Both groups indicated a lower incidence of severe ventricular arrhythmia. High-intensity group showed more voluntary of sinus arrhythmia and intermittent Type1 Second-degree AV block. However, the number of atrial premature beats and ventricular premature beats increased remarkably in control group.2. All time-domain indicators of heart rate variability of high-intensity group significantly lower than control.3. TnI-Ultra、TnT-hs、H-FABP、COR and hs-CRP level of high-intensity group were obviously higher than that of control group with a statistically significant differences (P< 0.05).Conclusions1. High-intensity military training may induce the officers and soldiers into the obvious stress state.2. High strength training can lead to reduction of heart rate variability, increase in the incidence of all kinds of arrhythmia, and increase the risk of malignant arrhythmia and myocardial minor damage.Section Two The mechanisms and preventions of FOXO3a on rat myocardial oxidative stress caused by exhaustive exerciseMethod 80 adult Sprague-Dawley rats were divided into 8 groups, control group,swimming exhaustion group (SW group), treadmill exhaustion group (TM group),swimming exhaustion and low dose allicin group(SW+AL-L group), swimming exhaustion and high dose allicin group (SW+AL-H group), treadmill exhaustion and low dose allicin group (TM+AL-L group), treadmill exhaustion and high dose allicin group (TM+AL-H group),10 for each group. With swimming exhaustion and treadmill exhaustion training setting as a source of stress and allicin as a means of intervention, we established an stress rat model. Serologicals index including cardiac-specific Troponin I-Ultra(TnI-Ultra), cardiac-specific Troponin T-High sensitivity (TnT-hs), heart fatty acid binding protein (H-FABP), cortisol (COR) and high sensitivity C-reactive protein (hs-CRP) were all measured. The tissue structural changes of rats myocardium were observed with HE stain; cardiomyocytes apoptosis evaluated with TUNEL;the mRNA levels of AKT、FOXO3A、Bax、Bcl-xl and Sirtl mRNAwere measured with qRT-PCR; the changes of protein level of AKT、P-AKT (S473)、 FOXO3A、P-FOXO3A(Thr32)、Bax、Bcl-xl and Sirtl were measured with Western Blot;the protein expression of cytochrome C and cleaved caspase 3 were analyzed by immunohistochemical stain.Results1. Compared with Control group, serological indexes of swimming exhaustion and treadmill exhaustion group all raise, and SW group and TM group among the most obvious ones, and serological indexes has reduced to a certain extent after application of allicin intervention.2. HE staining suggests that SW and TM group myocardial fibers horizontal stripes disappear, granular degeneration, fatty degeneration and even myocardial cell necrosis occur, myocardial fibers clearance, interstitial capillary hyperplasia increase in some of myocardial cells.Muscle fibers swelling, myocardial fibers clearance, myocardial cell and degeneration, necrosis relieve among allicin intervention group, especially when allicin used in high dose.3. TUNEL indicates that myocardial apoptosis index of SW and TM group were significantly higher than that of Control group, but declined after the application of allicin intervention. Furthermore, the apoptosis index of high dose group was obviously lower than the low dose group.4. SW group remains a constant total AKT protein expression level, however, P-AKT、P-FOXO3A、FOXO3A、 Sirtl and Bcl-xl levels decrease, and Bax, cytochrome C、cleaved caspase 3 levels and Bax/Bcl-xl ratio rise on the contrary. After application intervention of allicin,P-AKT、P-FOXO3A、FOXO3A、Sirtl and Bcl-xl protein expression level increased significantly compared with SW group; Bax、cytochrome C and cleaved caspase 3 protein expression levels significantly decreased, especially in high dose group. Protein expression change of exhausted treadmill exercise groups share the same trend with exhaustion swimming exercise groups.Conclusions1. Swimming exhaustion exercise and treadmill exhaustion exercise both lead to myocardial oxidative stress injury in rats.2. Myocardial oxidative stress damage caused by exhaustion exercise may be mediated via FOX03A/AKT pathway.3. Allicin could protect rat myocardial micro damage from stress through FOX03A/AKT pathway...