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Letters to the Editor |
Department of Obstetrics and Gynecology Columbia University College of Physicians and Surgeons Center for Menopause, Hormonal Disorders, and Women’s Health New York, New York 10032
Dr. De Crée raises interesting issues fundamental to the pathophysiology of exercise-induced amenorrhea: can exercise alone induce the spectrum of reproductive dysfunction—from inadequate luteal phases to a prolonged hypoestrogenic hypothalamic amenorrhea? Severe exhaustive exercise may affect GnRH pulses both in women (1 2 ) and the primate (3 ), although Loucks et al. (1 ), in their carefully controlled studies, suggest that an energy deficit is necessary to achieve suppression of LH pulses. However, other than alterations in follicular and luteal length of menstrual cycle, it has been difficult to reproduce prospectively the hypoestrogenic amenorrhea or even the anovulatory state. Research is plagued by the lack of longitudinal studies, use of different exercise models, the difficulty of controlling for caloric intake, and the importance of genetic issues; and, as most researchers have noted, there may be interindividual differences, particularly in adaptations to previous training (2 ). The well-described changes in estrogen metabolism seen with exercise have also been noted with nutritional deprivation, and it is difficult to attribute these metabolic changes to exercise stress alone (4 5 ). Bullen et al. (6 ), in their careful prospective study, found that the most severe dysfunction in young women following a standard exercise regimen occurred with weight loss, despite the careful effort to maintain the encaloric state. Also, recent data suggest that an adaptation to "disordered eating" is subtle and must be searched for by specific measures (7 8 9 ), and it isnot part of most clinical studies on exercise. Further complicating these issues is a menstrual dysfunction similar to polycystic ovarian syndrome, which is described in swimmers and may be confused with athletic hypothalamic amenorrhea (10 ).
Three observations, in particular, suggest that energy deficit or an adaptation to large caloric needs may be fundamental to at least the prolonged hypothalamic amenorrheic state: low levels or an altered diurnal rhythm of leptin seem to be part of the physiologic process (11 ) and the intimate association of the exercise-induced problem with osteopenia. In fact, recent research challenges the accepted notion that estrogen deficiency is the primary cause of bone loss in this syndrome as the pattern of bone remodeling is atypical of the estrogen deficient state (12 ). Thirdly, experiments in women runners suggest that a physiological paradox exists: a large energy output is not compensated for by increased caloric intake, yet weight loss does not occur (13 ).
Lastly, it is more than likely that genetic issues are of fundamental importance to the development of the syndrome—the hypothesis that the susceptible reproductive system may show a genetic promoter pathway is intriguing. Teleologically, shutdown of the reproductive system may be an appropriate adaptive mechanism, and the adaptations may be more efficiently expressed in some individuals than others. Certainly exploration of all of these issues is important to the understanding of an interesting neuroendocrine syndrome.
Footnotes
Received July 30, 1999. Accepted August 30, 1999. Address correspondence to: Carl De Crée, M.D., Associate Professor of Reproductive Endocrinology and Sports Medicine, Department of Applied and Reproductive Endocrinology, Institute for Gyneco-Endocrinological Research, P.O. Box 134, B-3000 Leuven 3, Belgium.
Received September 17, 1999. Accepted September 17, 1999. Address correspondence to: Michelle P. Warren, Department of Obstetrics and Gynecology, Columbia University College of Physicians and Surgeons, Center for Women’s Health, 622 West 168th Street, Room PH16-20, New York, New York 10032.
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