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To investigate the effect of high-intensity exhaustive exercise on body and the molecular mechanism of oxidative stress regulating apoptosis of cardiovascular endothelial cells (CVECs), 70 college students who took an aerobics course were recruited as the research subjects, all of which were divided into the high-intensity group (35 students) and the moderate-intensity group (35 students). The Internet of Things- (IoT-) based human exercise information monitoring system was employed to collect the electrocardiogram, serum indexes, and oxidative stress indexes of the two groups of subjects after exercise. Moreover, 30 clean male SD rats were divided into exhaustive exercise group ( n = 10 ), routine exercise group ( n = 10 ), and blank control group ( n = 10 ) using treadmill exercise as stress source, and various physiological indexes of the three groups were compared. In human experiments, the time-domain indexes of heart rate variability (HRV), 50 ms in the total number of sinus heartbeats (PNN50), the standard deviation of all NN intervals (SDNN), standard deviation of mean NN interval (SDANN), standard deviation of difference between adjacent NN intervals (SDSD), root mean square (RMSSD) in the high intensity group were lower than those in the moderate intensity group ( P &lt; 0.05 ). The levels of T-sensitive troponin I (Tnl-ultra), cortisol (COR), high-sensitive troponin T (TnT-hs), high-sensitive C-reactive protein (hs-CRP), and human heart-type fatty acid binding protein (HUMAN H-FABP) in high intensity group were higher than those in moderate intensity group ( P &lt; 0.05 ). Experiments on animals found that SOD content and mRNA expression of fork-head box 03A (FOX03A) and silencing-information regulator 1 (Sirtl) in serum of rats in exhaustion exercise group were lower than those in the routine exercise group and blank control group, while lactate dehydrogenase (LDH) and malondialdehyde (MDA) contents were opposite ( P &lt; 0.05 ). In short, strenuous exercise made the body in the state of acute stress, leading to the disturbance of cardiac autonomic nervous function and sympathetic nervous function, and increasing the risk of malignant arrhythmia. Oxidative stress induced by exhaustive exercise may promote the apoptosis of CVECs by reducing the expression of Sirtl and FOX03A and locating FOX03A to the nucleus.

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Assessment of Exhaustive Exercise under Internet of Things Exercise Monitoring System and Mechanism Analysis of Cardiovascular Endothelial Cell Apoptosis Induced by Oxidative Stress