Reproductive Endocrinology and Sports Medicine Department of Applied and Experimental Reproductive Endocrinology Institute for Gyneco-Endocrinological Research B-3000 Leuven 3, Belgium
Since the 1970s, the problem of exercise-induced menstrual irregularities and its possible consequences (osteoporosis, subfertility) has been recognized and studied in detail. Warren et al. (1) present a chrestomathy of theirs and a number of other North American authors who have delivered important contributions to our understanding of the etiology and reproductive health of female athletes. It is suggested that secondary amenorrhea, inadequate luteal phase, and the female athlete triad are a caused by a disturbance of normal GnRH pulsatility, which is provoked by weight loss or dietary restriction. Indeed, studies of Loucks et al. (2) have clearly pointed out how a disturbance of a critical energy balance, possibly accompanied by low T3 levels, may lead to menstrual problems.
However, we feel that the clear focus of North American authors on this specific mechanism seems to have led to a generalized belief that this is the sole mechanism involved or, in other words, that all or most exercise-induced menstrual problems result from a poor energy balance.
Nevertheless, Keizer et al. (3) have clearly shown that
exercise-intensity on its own can produce the same menstrual
problems in eucaloric athletes. Subsequent investigations by ourselves
(4), Russel et al. (5), and Snow et al. (6) have
demonstrated that regular high-intensity exercise leads to a shift in
estrogen metabolism from 16- to C-2 oxidation and formation of the
so-called catecholestrogens. The intrahypothalamic interactions between
increased catecholestrogen formation and norepinephrine exerts
important effects on the GnRH oscillator, which can produce menstrual
problems. This mechanism may be activated without any interference from
an individuals energy balance, and it is even speculated that changes
in eating behavior might even be secondary to such steroid-mediated
intrahypothalamic and metabolic effects.
Finally, it is opportune to mention that there are several subtle, but numerous differences between menstrual problems that seem to find their origin in eating behavior and those purely resulting from exercise. Such differences are reflected in a specific hormonal profile (differences in T3, IGFBP-1, 17,20-desmolase, among others), but it has also been speculated that disturbed eating behavior form of menstrual problems in athletes might be genetically predisposed and associated with the so-called 5-HT2A receptor (-1438 AA) promoter polymorphism.
The laboratory techniques required for the analysis of some of these mechanism are complicated and laborious, but it does not justify that our attention is reduced to the impact of diet. Only a comprehensive approach linking diet, hormone metabolism, and genetics will lead to a full understanding of the etiology of exercise-induced menstrual problems.
References
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