The etiology of amenorrhea in exercising women is linked to a mismatch between caloric intake and high levels of exercise energy expenditure that results in a chronic energy deficit. This in turn stimulates compensatory mechanisms such as weight loss, metabolic hormone alterations, or energy conservation that subsequently causes a central suppression of reproductive function and concomitant hypoestrogenism. This suppression of reproductive function is associated with stress fractures, loss of bone mineral density, the failure to achieve peak bone mass, osteopenia, and osteoporosis. It has generally been accepted that the chronic hypoestrogenism is the major cause of bone loss in exercising women. However, the effects of food restriction and energy deficiency on bone mineral density likely represents an estrogen-independent mechanism for bone loss that involves some of the metabolic-related hormones altered with exercise-associated amenorrhea. These hormones (IGF-1 and leptin) play an important role in modulating bone turnover and bone mineral density in these women.