Luteal Phase Deficiency and Anovulation in Recreational Women
Luteal Phase Deficiency and Anovulation in Recreational Women
ABSTRACT & COMMENTARY
Synopsis: In sedentary women, 90% of all menstrual cycles were ovulatory, but in exercising women, only 45% were ovulatory. Of the remainder, 43% of cycles demonstrated luteal phase deficiency and 12% were anovulatory.
Source: De Souza MJ, et al. J Clin Endocrinol Metab 1998;83:4220-4232.
The purpose of this study was to determine menstrual cycle characteristics in women participating in moderate, recreational exercise who had regular menstrual cycle intervals. For three consecutive menstrual cycles, subjects collected daily urine samples for analysis of follicle stimulating hormone (FSH), estrone conjugates, pregnanediol-3-glucuronide, and creatinine. Urinary estrone is a metabolite of and marker for estradiol. Pregnanediol is a metabolite of and marker for progesterone. The 11 sedentary women and 24 recreational exercisers were similar in age, weight, gynecologic age, and menstrual cycle length. Despite regular menstrual cycle intervals of 28.8 days, 10% of sedentary women consistently had luteal phases that were less than 10 days and associated with decreased peak pregnanediol (< 3 mcg/mg creatinine). None of the sedentary women had anovulatory cycles. In comparison, recreational exercisers were more likely to display ovarian compromise (55%) than to meet criteria for ovulation (45%). In exercising women, energy availability was most decreased in those with anovulatory cycles. Menstrual interval was preserved in women with luteal phase deficiency because follicular phase lengths were longer when luteal phase durations were shorter. As a group, exercisers ran 17 miles a week and participated in five hours of other exercise weekly.
COMMENT BY SARAH L. BERGA, MD
Is energy availability the prime regulator of reproductive function? At least two types of reproductive compromise are due to altered metabolism. Polycystic ovary syndrome is associated with excessive energy efficiency and a proclivity toward weight gain. In the absence of insulin resistance, which is primarily a function of excess weight, women with polycystic ovary morphology remain ovulatory.1 Thus, too much energy availability can lead to reproductive compromise and increase the risk of diabetes in women with "thrifty metabolism."
Most women who experience restricted energy availability develop reproductive compromise. The only exception might be women with polycystic ovary syndrome. This study demonstrated that even when the menstrual cycle interval is preserved, restricted energy availability due to moderate running and recreational exercise can compromise ovulatory function. This result is not entirely unanticipated, but it is alarming. What should we tell young women? Certainly, those attempting conception might want to reduce or even cease recreational running because the occurrence of regular cycles does not mean that ovulatory function is sufficient to support implantation. What about those not immediately interested in pregnancy? It is even more difficult to know what to say. Does luteal phase deficiency due to recreational exercise have long-term deleterious consequences such as reduced bone accretion? In a separate study, De Souza and associates found no decrement in bone density as long as estrogen levels were not diminished.2 Perhaps restricted energy availability confers protection against cardiovascular disease and cancer by reducing the "stress" of oxidative metabolism. If an exercising woman with regular menstrual cycles is not seeking pregnancy, it seems doubtful that her reproductive status would be an issue for the patient or physician. Thus, most reproductive compromise in exercising women is likely to escape clinical detection. Until deleterious consequences are revealed, and in the absence of oligomenorrhea or amenorrhea, it is prudent not to scare women by advising against exercise.
References
1. Robinson S, et al. Clin Endocrinol (Oxf) 1993; 39:351-355.
2. De Souza MJ, et al. J Clin Endocrinol Metab 1997;82:2867-2876.
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