过度疲劳状态下运动性猝死模型大鼠甲状腺及心脏功能变化

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

背景:疲劳过度累积会引起机体一系列的变化,乳酸堆积、机体代谢速率减慢、能量摄取障碍等,导致过度训练。当发生过度训练时机能将出现负叠加现象,而负叠加过程的发展终会导致过劳死、运动性猝死的发生。目的:为研究过度疲劳状态下大鼠甲状腺功能的变化情况,进一步探索"心源性"运动性猝死与甲状腺功能的关系。方法:将30只雄性SD大鼠,随机抽取7只作为空白对照组,其余大鼠进行力竭性负重游泳训练至过度疲劳,其中疲劳组7只,运动性猝死大鼠7只,运动后即刻取材进行以下测定:(1)苏木精-伊红染色观察甲状腺滤泡上皮细胞、心肌纤维形态结构及细胞间质的变化;(2)ELISA检测血清三碘甲状腺原氨酸(甲状腺素,T3)、四碘甲状腺原氨酸(甲状腺素,T4)、促甲状腺激素、血清乳酸脱氢酶2水平。结果与结论:(1)运动性运动性猝死组大鼠甲状腺滤泡淡染,细胞间质疏松,部分滤泡胶质出现大量空泡;心肌间血管极度扩张,心肌纤维纤细,部分肌纤维断裂,心肌充血出血严重;(2)运动性猝死组大鼠血清中乳酸脱氢酶2浓度明显高于空白对照组(P<0.05);(3)运动性猝死组血清中T3、T4浓度明显高于对照组(P<0.05),且T4显著低于疲劳组(P<0.01),促甲状腺激素浓度明显高于对照组(P<0.05),且显著低于疲劳组(P<0.01)。(4)结果提示,长期大强度运动导致过度疲劳,甲状腺形态结构发生病理性改变;过度疲劳状态下发生的运动性猝死大鼠心肌细胞形态结构受到损害;过度疲劳时血清乳酸脱氢酶2水平升高加重心肌损伤;过度疲劳不断累积导致甲状腺功能紊乱,促甲状腺激素、T3、T4分泌异常,从而引起机体运动过程中代谢紊乱、能量供应不足并器官衰竭,可能诱发运动性猝死;运动性猝死是多器官多系统交互作用的结果,甲状腺功能紊乱引起心脏结构功能改变可能诱发"心源性"运动猝死。

BACKGROUND： Exercise fatigue can lead to lactic acid accumulation, metabolism decrease and energy intake disturbance following by overtraining. Further, constant development of negative superposition after overtraining will contribute to karoshi and exercise-induced sudden death. 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. 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 collected immediately after exercise to observe the morphology, structure and intercellular substance changes of thyroid follicular epithelial cells and cardiac muscle fibers by hematoxylin-eosin staining; levels of serum triiodothyronine（T3）, tetraiodothyronine（T4）, thyroid stimulating hormone（TSH） and lactic dehydrogenase 2（LDH-2） were detected by ELISA. 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 follicles were in a hypochromatism with loose intercellular substance, and extensive visible vacuolization in the follicular colloid.（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, followed 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 will lead to thyroid morphological abnormality and myocardial impairment. Increasing serum LDH-2 following 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.