Abstract

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REFERENCES

Discussion
Board

The female athlete triad is associated with disordered eating, amenorrhea and osteoporosis. Various authors suggest that it begins with disordered eating. An important type of eating disorder is anorexia nervosa, which has one of the highest mortality rates of any psychiatric disorder. Competitive female athletes are at increased risk for anorexia nervosa. This is a complex disorder associated with multiple predisposing, percepitating and perpetuating factors. Animal modeling is one way to focus on specific aspects of the problem.

The most popular animal model is the weight-loss syndrome produced by freely induced wheel-running exercise in animals maintained on a moderate food restriction schedule. Compared to animals that are exposed to either variable alone, the simultaneous imposition of both variables causes profound weight loss. We have argued that the syndrome models two features of anorexia nervosa: hyperactivity and freely induced weight loss. Others argue that it is also associated with an 'activity-based anorexia.' However, since the reduction in food intake is at least partly experimenter induced, and because animals exposed to the syndrome eat similar amounts compared to animals weight-reduced to the same extent by simple food restriction, we argued that the term 'anorexia' should not be applied to the syndrome.

Other data we have collected suggest that beta-endorphin is not involved in the syndrome. Finally, we have data implicating serotonin in the phenomenon, which we describe as an exercise-stress syndrome. The purpose of this presentation will be to review the literature on the syndrome and propose that it is highly relevant to the female athelete triad. For example, it has been known for nearly 40 years that the it produces profound negative energy balance. It is also well established that it produces anesterous and activation of the hypothalamo-pituitary-adrenal axis, which can negatively impact bone. To our knowledge, there are no reports in the literature demonstrating that the syndrome changes bone homoeostasis. The reason for this, however, is that this possibility has not been heretofore considered. There are a variety of other treatments that can be used to model anorexia nervosa. These include chronic infusion of appetite suppressant drugs, chemical neurotoxins, and electrolytic brain lesions. However, there are relatively few model systems as pertinent to the female athlete triad as the exercise-stress syndrome.

We conclude that the exercise-stress syndrome is relevant to both the endocrinology and osteology of the female athlete triad. Consequently, the model is positioned to promote research in both psychoneuroendocrinology as well as psychoneuro-osteology.

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Poster Number PAaravich0470
Keywords: anorexia nervosa, exercise, bone, body weight, female athlete triad