Background： Exercise-associated menstrual dysfunction （EAMD） is a common health problem in female athletes as a part of female athlete triad （FAT）, a condition related to low energy availability. In this study, w...Background： Exercise-associated menstrual dysfunction （EAMD） is a common health problem in female athletes as a part of female athlete triad （FAT）, a condition related to low energy availability. In this study, we explored the possibility that carbohydrate supplements can improve the status of EAMD and prevent exercise-induced ovarian injury in a FAT rat model. This research aimed to provide experimental evidence with regard to the relationship of energy intervention and EAMD. Methods： Forty-five female Sprague-Dawley rats （2 months old） were randomly divided into five experimental groups： control group （C）, 9-week exercise as model for EAMD （E）, post-EAMD recovery group （R）, oligosaccharide intervention group （O）, and glucose intervention group （G）. All rats were sacrificed at the end of 9 weeks. Serum samples were collected for measuring gonadotropin releasing hormone, follicle stimulating hormone, luteinizing hormone, 1713-estradiol and progesterone levels. The ovaries were taken for investigation of exercise- and carbohydrate-induced follicular subcellular structure changes. Results： Exercise induced irregular menstrual cycles and ovary subcellular structural damages, such as swollenness of mitochondria in rats from groups E and R. Both glucose and oligosaccharide supplements restored well-differentiated mitochondria in the ovarian follicular cells, and a significant improvement of endoplasmic reticulum and Golgi in swollenness in theca cells in groups O and G compared to groups C, E, and R. There was no difference in mitochondria subcellular structural changes between groups O and G. Group E showed attenuation of serum levels of 17β-estradiol and progesterone compared to C. There were no differences of 17β-estradiol serum levels among groups O, G, and R, while group G showed a lower level of progesterone than C. Conclusion： Female adult rats with 9-week continuous exercise can cause menstrual dysregulation as a model for EAMD. Post-EAMD intervention with glucose and oligosaccharide intake can normalize the menstrual cycle, restore the follicular subcellular structure, and reverse the exercise-induced reduction of ovary sex hormones. It suggests a positive feedback of hypothalamus-pituitary-ovary axis might be involved in the molecular mechanisms of energy intake in treating EAMD.展开更多
基金supported by Shanghai Key Laboratory of Human Sport Competence Development and Maintenance,Shanghai University of Sport(NO.11DZ2261100)
文摘Background： Exercise-associated menstrual dysfunction （EAMD） is a common health problem in female athletes as a part of female athlete triad （FAT）, a condition related to low energy availability. In this study, we explored the possibility that carbohydrate supplements can improve the status of EAMD and prevent exercise-induced ovarian injury in a FAT rat model. This research aimed to provide experimental evidence with regard to the relationship of energy intervention and EAMD. Methods： Forty-five female Sprague-Dawley rats （2 months old） were randomly divided into five experimental groups： control group （C）, 9-week exercise as model for EAMD （E）, post-EAMD recovery group （R）, oligosaccharide intervention group （O）, and glucose intervention group （G）. All rats were sacrificed at the end of 9 weeks. Serum samples were collected for measuring gonadotropin releasing hormone, follicle stimulating hormone, luteinizing hormone, 1713-estradiol and progesterone levels. The ovaries were taken for investigation of exercise- and carbohydrate-induced follicular subcellular structure changes. Results： Exercise induced irregular menstrual cycles and ovary subcellular structural damages, such as swollenness of mitochondria in rats from groups E and R. Both glucose and oligosaccharide supplements restored well-differentiated mitochondria in the ovarian follicular cells, and a significant improvement of endoplasmic reticulum and Golgi in swollenness in theca cells in groups O and G compared to groups C, E, and R. There was no difference in mitochondria subcellular structural changes between groups O and G. Group E showed attenuation of serum levels of 17β-estradiol and progesterone compared to C. There were no differences of 17β-estradiol serum levels among groups O, G, and R, while group G showed a lower level of progesterone than C. Conclusion： Female adult rats with 9-week continuous exercise can cause menstrual dysregulation as a model for EAMD. Post-EAMD intervention with glucose and oligosaccharide intake can normalize the menstrual cycle, restore the follicular subcellular structure, and reverse the exercise-induced reduction of ovary sex hormones. It suggests a positive feedback of hypothalamus-pituitary-ovary axis might be involved in the molecular mechanisms of energy intake in treating EAMD.
