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

doi:10.3969/j.issn.2095-4344.2016.49.009

Abstract

Abstract:

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.

中国组织工程研究杂志出版内容重点：肾移植；肝移植；移植；心脏移植；组织移植；皮肤移植；皮瓣移植；血管移植；器官移植；组织工程

Key words: Death, Sudden, Thyroxine, Fatigue, Glycolysis, Tissue Engineering

CLC Number:

R318

Qian Yu, Yin Wei-yao, Li Hua. Changes of thyroid and cardiac function in exercise-induced sudden death model rats after excessive fatigue[J]. Chinese Journal of Tissue Engineering Research, 2016, 20(49): 7356-7363.

Figures/Tables 2

2.2 材料、方法的改进本实验共分为2个阶段：造模阶段和实验阶段。造模阶段参照殷劲教授等[14]的糖酵解供能运动疲劳模型对大鼠进行运动疲劳造模，造模成功后在实验方法上进行了一定的改进，将造模阶段的大、中、小三周期交替训练改为连续大运动量训练，使大鼠过度疲劳，并进入疲劳的付叠加状态，而在过度疲劳状态下出现的非呛水性死亡记为实验运动性猝死组。 2.3 模型稳定性研究实验动物模型参照殷劲教授等的糖酵解供能运动疲劳模型进行1周造模，该模型已被证实并使用，实验模型具有可靠性、稳定性。 2.4 苏木精-伊红染色结果 2.4.1 甲状腺苏木精-伊红染色结果空白组滤泡上皮细胞排列紧密，未见异常；疲劳组可见部分滤泡淡染，而运动性猝死组除部分滤泡淡染，还可见细胞间质疏松，部分滤泡胶质出现大量空泡(图2)。 2.4.2 心肌组织苏木精-伊红染色结果空白组大鼠心肌细胞纤维排列整齐，细胞间质致密均匀，未见异常；疲劳组可见心肌纤维纤细，出现部分断裂；而运动性猝死组心肌间血管极度扩张，大部分心肌纤维断裂，心肌充血出血严重出现严重坏死,心肌纤维溶解坏死(图3)。 2.5 血清指标检测结果 2.5.1 血清乳酸脱氢酶2检测结果空白组血清中乳酸脱氢酶2浓度较低，疲劳组与运动性猝死组血清乳酸脱氢酶2浓度较高(图4)。同时，疲劳组较空白组显著升高(60.6±18.8)，(25.0±7.4) mol/L，P < 0.01)，运动性猝死组[(44.0±14.2)mol/L]血清中乳酸脱氢酶2的浓度低于疲劳组(P < 0.05)。 2.5.2 血清T3、T4检测结果疲劳组与运动性猝死组血清中T3、T4浓度均高于空白组[T3：(323.0±90.0)，(246.3±75.7)，(23.0±10.0) mol/L，P < 0.01和P < 0.05；T4：(637.0±52.0)，(320.3±85.0)，(177.0±70.0) mol/L，P < 0.01和P < 0.05)，其中，运动性猝死组较疲劳组含量有所降低。与空白组相比，运动性猝死组T3、T4浓度显著升高(P < 0.05)，差异有显著性意义(图5，图6)。 2.5.3 血清促甲状腺激素检测结果空白组血清中促甲状腺激素浓度较低，疲劳组与运动性猝死组血清促甲状腺激素浓度较高(图7)。同时，疲劳组较空白组显著升高[(37.27±6.47)，(14.93±3.79) mol/L，P < 0.01]，运动性猝死组血清中促甲状腺激素的浓度[(22.94±2.10) mol/L]低于疲劳组，与空白组相比显著升高(P < 0.05)。"

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