Changes of thyroid and cardiac function in exercise-induced sudden death model rats after excessive fatigue

Qian Yu; Yin Wei-Yao; yao; Li Hua

doi:10.3969/j.issn.2095-4344.2016.49.009

Abstract：BACKGROUND:Exercise fatigue can lead to lactic acid accumulation, metabolism decrease and energy intake disturbance fol owing by overtraining. Further, constant development of negative superposition after overtraining wil contribute to karoshi and exercise-induced sudden death. <br> OBJECTIVE:To investigate the changes of rat thyroid function under excessive fatigue state and to further explore the relationship between the exercise-induced sudden cardiac death and thyroid function. <br> METHODS:Seven rats were randomly selected from 30 male Sprague-Dawley rats as blank control group. The remaining rats were trained continuously with exhaustive loaded-swimming exercises to achieve the excessive fatigue state, and seven as fatigue group, seven as sudden death group. Rat samples were col ected immediately after exercise to observe the morphology, structure and intercel ular substance changes of thyroid fol icular epithelial cel s and cardiac muscle fibers by hematoxylin-eosin staining;levels of serum tri odothyronine (T3), tetraiodothyronine (T4), thyroid stimulating hormone (TSH) and lactic dehydrogenase 2 (LDH-2) were detected by ELISA. <br> RESULTS AND CONCLUSION:(1) In the sudden death group, intermyocardiac vessels expanded extremely, some thin myocardial fibers ruptured, and severe congestion and hemorrhage occurred;thyroid fol icles were in a hypochromatism with loose intercel ular substance, and extensive visible vacuolization in the fol icular col oid. (2) The levels of serum LDH-2 and T3 in the sudden death group were significantly higher than those in the blank control group (P<0.05). (3) The levels of serum T4 and TSH were the highest in the fatigue group, fol owed by sudden death group, and lowest in the blank control group (P<0.05). (4) These results suggest that excessive fatigue caused by long-term high-intensity training wil lead to thyroid morphological abnormality and myocardial impairment. Increasing serum LDH-2 fol owing excessive fatigue aggravates myocardial damages. Fatigue accumulation causing thyroid dysfunction, abnormal secretion of TSH, T3 and T4, may be one of the causes of exercise-induced sudden death. Exercise-induced sudden death belongs to a multiple organ dysfunction syndrome, and turbulence of thyroid causing cardiac structural and functional alteration may induce sudden cardiac death.