It is well known that women athletes engaged in strenuous physical exercise and endurance training may develop "athletic menstrual irregularities" (AMI). Although many studies have appeared dealing with the immediate endocrinological and physiological changes in these women, the underlying mechanisms have remained unknown to date. A number of hypotheses have been put forward, the most well-known among them, for example, defending the existence of a critical percent of body fat necessary to trigger or maintain normal menstruation. All these theories have, however, their own, sometimes numerous, methodological inaccuracies and a teleological way of investigation. Spectacular, and perhaps promising new developments concern the possible involvement of endogenous opioid peptides and catecholestrogens in these processes. In basal circumstances beta-endorphin, the most well-known endogenous substance with opiate-like activity, may decrease LH levels by suppressing hypothalamic GnRH. This phenomenon is, however, only observed during the estrogen-dominant late-follicular and mid-luteal phases. As for catecholestrogens, it appears essential to differentiate between, for example, the 2- and 4-hydroxy derivatives of both estrone and estradiol. While some of these catecholestrogens obviously seem to suppress LH levels, others seem to potentiate and induce the LH surge. In any case, similar to beta-endorphin, these activities of catecholestrogens appear to depend upon the essential presence of a sufficiently estrogenic environment. In addition, both endogenous opioid peptides and some of the catecholestrogens appear to be able to suppress prolactin release, probably by interfering with its inhibiting factor dopamine. Other effects of catecholestrogens may include the control of the luteolysis-potent prostaglandin F2 alpha. Although a number of studies have investigated the behaviour of beta-endorphin during and post-exercise, similar studies investigating catecholestrogens as to their relation to physical exercise are almost nonexistent. This, in association with the numerous methodological inaccuracies of various studies, makes it difficult to draw any firm conclusion. As to formulate new hypotheses, the only reasonable suggestion considers the possible existence of a complex feedback system including catecholestrogens and endogenous opioid peptides. Furthermore, recommendations made in this survey may be helpful in designing new, perhaps more firmly supported and appropriate future studies.