Beitins I Z, McArthur J W, Turnbull B A, Skrinar G S, Bullen B A
Department of Pediatrics, University of Michigan, Ann Arbor 48109.
J Clin Endocrinol Metab. 1991 Jun;72(6):1350-8. doi: 10.1210/jcem-72-6-1350.
We have previously reported that during 2 months of strenuous exercise, untrained young women with documented ovulatory menstrual cycles developed secondary oligoamenorrhea and luteal phase defects. In this study we tested the hypothesis that such abnormalities arise by altered neuroendocrine regulation of menstrual hormone secretion and that weight loss potentiates such effects. We supply a detailed analysis of the 20 cycles, of the total of 53, in which luteal phase abnormalities occurred. During the control month and 2 exercise months, all subjects collected daily overnight urine samples for the determination of LH, FSH, estriol (E3), and free progesterone (P) excretion by RIAs and creatinine by chemical assay. The characteristics of the abnormal luteal phase cycles were determined by comparing the excreted hormone levels and patterns during the control cycles with those of exercise cycles. The area under the curve (AUC) for each hormone was calculated for the follicular and luteal phases of each cycle. Six of the exercise cycles exhibited an inadequate luteal phase. This was characterized by a mean integrated P area of 202.4 (SEM, -61.8) nmol/day.nmol creatinine, compared with 331.7 (SEM, 64.7) during the corresponding control cycles, over a period of 9 or more days after the urinary LH peak to the onset of menses. Fourteen of the exercise cycles exhibited a short luteal phase. This was characterized by a mean integrated P area of 75.9 (30.9) nmol/day.nmol creatinine, compared to 267 (61.7) during the corresponding control cycles, over a span of 8 days or less from the urinary LH peak to the onset of menses. Additional abnormalities occurred only in the short luteal phase cycles. These included an increase in the length and AUC for E3 of the follicular phase and a decrease in the AUC of LH during the luteal phase. We conclude that the initiation of strenuous endurance training in previously ovulating untrained women frequently leads to corpus luteum dysfunction associated with insufficient P secretion and, in the case of short luteal phase cycles, decreased luteal phase length. That exercise may alter the neuroendocrine system is suggested by a delay in the ovulatory LH peak in spite of increased E3 excretion; moreover, less LH is excreted during the luteal phase. The lack of positive feedback to estrogens and decreased LH secretion during the luteal phase could compromise corpus luteum function. In contrast, decreased free P excretion was the sole abnormality noted in menstrual cycles with an inadequate luteal phase.
我们之前曾报道，在2个月的剧烈运动期间，有排卵性月经周期记录的未受过训练的年轻女性出现了继发性月经过少和黄体期缺陷。在本研究中，我们检验了这样一种假设，即这些异常是由月经激素分泌的神经内分泌调节改变引起的，且体重减轻会增强这种影响。我们对53个周期中的20个出现黄体期异常的周期进行了详细分析。在对照月和2个运动月期间，所有受试者每天收集过夜尿液样本，通过放射免疫分析法测定促黄体生成素（LH）、促卵泡生成素（FSH）、雌三醇（E3）和游离孕酮（P）的排泄量，并通过化学分析法测定肌酐。通过比较对照周期和运动周期中排泄的激素水平及模式，确定异常黄体期周期的特征。计算每个周期卵泡期和黄体期每种激素的曲线下面积（AUC）。6个运动周期表现出黄体期不足。其特征是在尿LH峰至月经开始后的9天或更长时间内，平均整合P面积为202.4（标准误，-61.8）nmol/天·nmol肌酐，而相应对照周期为331.7（标准误，64.7）。14个运动周期表现出黄体期缩短。其特征是在尿LH峰至月经开始后的8天或更短时间内，平均整合P面积为75.9（30.9）nmol/天·nmol肌酐, 而相应对照周期为267（61.7）。其他异常仅出现在黄体期缩短的周期中。这些异常包括卵泡期E3的长度和AUC增加，以及黄体期LH的AUC降低。我们得出结论，在之前有排卵的未受过训练的女性中开始剧烈耐力训练，常常会导致黄体功能障碍，伴有P分泌不足，在黄体期缩短的周期中，黄体期长度会缩短。尽管E3排泄增加，但排卵LH峰延迟，这表明运动可能会改变神经内分泌系统；此外，黄体期LH排泄减少。黄体期对雌激素缺乏正反馈以及LH分泌减少可能会损害黄体功能。相比之下，在黄体期不足的月经周期中，游离P排泄减少是唯一观察到的异常。
