Abstract:

BACKGROUND: Exhaustive exercise is a movement that exceeds the physiological limits of humans or animals. High-intensity motor exercise can disturb the homeostasis, causing a series of stress reactions, and excessive stress can lead to damage and dysfunction.
OBJECTIVE: To analyze the related factors to sudden cardiac death by exercise-induced fatigue model of rat cardiomyocytes.
METHODS: One hundred and thirty Sprague-Dawley rats were provided by Chengdu Dashuo Biotechnology Co., Ltd. Seven rats were randomly selected to as blank control group, and the remaining rats were used to establish the fatigue model (continuous swimming training, 36 hours per times). Then the negative superposition state of over-recovery was the state of over-fatigue. Seven rats were sacrificed and recorded as fatigue groups A, B and C after 3x36 hours, 6x36 hours and 9x36 hours of training, respectively. The rats died during training or within 24 hours after training (excluding inhaled water) regarded as exercise-induced sudden death group. Apoptosis of cardiomyocytes was detected by TUNEL. Bax and Bcl-2 expression in myocardium was detected by immunohistochemistry. Cell morphology was observed by hematoxylin-eosin staining.
RESULTS AND CONCLUSION: (1) In the sudden death group, the myocardial fibers were thinner than those in the other groups, some myocardial fibers were broken, the vessels were extremely dilated, and the myocardium was severely necrotic with hyperemia and hemorrhage. (2) Apoptotic index of cardiomyocytes and number of apoptotic cardiomyocytes in the fatigue and sudden death groups were significantly increased (P < 0.05). (3) The number of pro-apoptotic proteins in rat heart tissues were increased significantly in the state of excessive fatigue (P < 0.05), and the content of the apoptotic inhibiting protein Bcl-2 was decreased significantly (P < 0.01). (4) These results imply that continuous training can lead to excessive fatigue in rats, which will lead to changes in the morphological structure of rat cardiac cells and even lead to damage. Meanwhile, abnormal expression of Bcl-2 and Bax proteins in the cardiac tissue will occur. The damage of cardiomyocytes leads to apoptosis of cardiomyocytes, and the number of cardiomyocytes is significantly reduced, which affects the structure and function of the whole heart and eventually leads to sudden cardiac death.

中国组织工程研究杂志出版内容重点：组织构建；骨细胞；软骨细胞；细胞培养；成纤维细胞；血管内皮细胞；骨质疏松；组织工程

Key words: exercise induced fatigue, excessive fatigue, cardiomyocyte apoptosis, Bax, Bal-2, pro-apoptotic proteins, sudden cardiac death