Veldhuis J D, Evans W S, Demers L M, Thorner M O, Wakat D, Rogol A D
J Clin Endocrinol Metab. 1985 Sep;61(3):557-63. doi: 10.1210/jcem-61-3-557.
We tested the hypothesis that the neuroendocrine control of gonadotropin secretion is altered in certain women distance runners with secondary amenorrhea. To this end, we quantitated the frequency and amplitude of spontaneous pulsatile LH secretion during a 24-h interval in nine such women. The ability of the pituitary gland to release LH normally was assessed by administration of graded bolus doses of GnRH during the subsequent 8 h. Compared to normally menstruating women, six of nine amenorrheic distance runners had a distinct reduction in spontaneous LH pulse frequency, with one, three, six, five, four, or two pulses per 24 h (normal, 8-15 pulses/24 h). This reduction in LH pulse frequency occurred without any significant alterations in plasma concentrations of estradiol and free testosterone or 24-h integrated serum concentrations of LH, FSH, or PRL. Moreover, in long-distance runners, the capacity of the pituitary gland to release LH was normal or accentuated in response to exogenous pulses of GnRH. In the six women athletes with diminished spontaneous LH pulsatility, acute ovarian responsiveness also was normal, since serum estradiol concentrations increased normally in response to the GnRH-induced LH pulses. Although long-distance runners had significantly lower estimated percent body fat compared to control women, specific changes in pulsatile gonadotropin release did not correlate with degree of body leanness. In summary, certain long-distance runners with secondary amenorrhea or severe oligomenorrhea have unambiguously decreased spontaneous LH pulse frequency with intact pituitary responsiveness to GnRH. This neuroendocrine disturbance may be relevant to exercise-associated amenorrhea, since pulsatile LH release is a prerequisite for cyclic ovarian function. We speculate that such alterations in pulsatile LH release in exercising women reflect an adaptive response of the hypothalamic pulse generator controlling the intermittent GnRH signal to the pituitary gland. The basis for amenorrhea in the remaining runners who have normal pulsatile properties of LH release is not known.
某些患有继发性闭经的女子长跑运动员，其促性腺激素分泌的神经内分泌控制发生了改变。为此，我们对9名此类女性在24小时内自发性促黄体生成素（LH）脉冲式分泌的频率和幅度进行了定量分析。在随后的8小时内，通过给予递增剂量的促性腺激素释放激素（GnRH）推注，评估垂体正常释放LH的能力。与正常月经周期的女性相比，9名闭经的长跑运动员中有6人自发性LH脉冲频率明显降低，每24小时分别有1、3、6、5、4或2次脉冲（正常为8 - 15次脉冲/24小时）。LH脉冲频率的降低在雌二醇、游离睾酮的血浆浓度或LH、促卵泡生成素（FSH）或催乳素（PRL）的24小时综合血清浓度方面没有任何显著变化的情况下发生。此外，在长跑运动员中，垂体对GnRH外源性脉冲释放LH的能力正常或增强。在6名自发性LH脉冲性减弱的女性运动员中，急性卵巢反应性也正常，因为血清雌二醇浓度对GnRH诱导的LH脉冲反应正常增加。尽管长跑运动员与对照女性相比，估计体脂百分比显著更低，但脉冲式促性腺激素释放的特定变化与身体消瘦程度无关。总之，某些患有继发性闭经或严重月经过少的长跑运动员，其自发性LH脉冲频率明确降低，但垂体对GnRH的反应性正常。这种神经内分泌紊乱可能与运动相关的闭经有关，因为脉冲式LH释放是周期性卵巢功能的先决条件。我们推测，运动女性中LH脉冲式释放的这种改变反映了控制向垂体间歇性GnRH信号的下丘脑脉冲发生器的适应性反应。其余LH释放具有正常脉冲特性的长跑运动员闭经的原因尚不清楚。
