摘要
目的:为进一步探讨运动性月经失调(AMI)的机制提供理论依据。方法:在建立递增负荷训练的运动性闭经动物模型的基础上,对大鼠下丘脑弓状核神经元和垂体促性腺细胞超微结构进行观察。结果:电镜下,7周训练组大鼠下丘脑弓状核神经元轴突髓鞘分离、树突肿胀,核周质线粒体空泡变。垂体促性腺激素(Gn)细胞、生长激素(GH)细胞、促肾上腺皮质激素(ACTH)细胞的粗面内质网扩张,线粒体嵴断裂和肿胀。尤其是促性腺细胞粗面内质网极度扩张,出现类似性腺阉割细胞(Ⅳ型)和脱颗粒细胞(Ⅴ型)。休息1周后未见恢复。结论:运动性动情周期抑制发生在下丘脑水平,短期休息调整不能恢复。下丘脑-垂体轴细胞超微结构的改变与运动强度和运动时间密切相关。
Objective: To show the mechanism of the ultrastructural change of Hypothalamus-Pituitary axis in women with athletic menstrual cycle irregularities (AMI). Methods: At first establish a rat model similar to athletic menstrual irregularities by incremental training, then observe the ultrastructural change of arcuate nucleus neuron in hypothalamus and gonadotroph in pituitary. Results: In training group A, the axon of arcuate nucleus neuron is separated from its myelin sheath, swelling in dendrite and vacuolation in mitochondrion. Rough endoplasmic reticulum(RER) expands in gonadotroph, somatotroph and corticotroph as well as swelling of mitochondrion with crista broken. Especially the swelling of RER in gonadotroph is so striking that it looks just like castration cell (type Ⅳ) and degranulation cell (type Ⅴ). Recovery is not found after rest for 1 week. Conclusion: Hypothalamus is the most important level correlated with AMI. Its change cannot recover through short period of rest. There is a close relationship between the ultrastructural change in hypothalamus-pituitary axis and training intensity and duration.
出处
《中国运动医学杂志》
CAS
CSCD
北大核心
2001年第3期260-262,共3页
Chinese Journal of Sports Medicine
关键词
运动性动情周期抑制
递增负荷训练
大鼠
下丘脑-垂体轴
细胞超微结构
athletic menstrual cycle irregularities, incremental training, rat, Hypothalamus-Pituitary axis, cell ultrastructure