Functional hypothalamic amenorrhea (FHA), often termed stress-induced anovulation (SIA), is characterized by reduced GnRH drive and mild hypercortisolemia. The behavioral antecedents associated with the development of nonorganic forms of chronic anovulation and amenorrhea are variable. While voluntary undernutrition and increased activity, including excessive exercise, are commonly reported by women with FHA / SIA, the energy deficits created by these behaviors generally do not seem sufficient to independently disrupt GnRH drive. We therefore hypothesized that metabolic stress amplifies the impact of social stress. Available monkey and human data support this notion, but the mechanisms mediating this potentiation have not been fully explicated. Based on the foregoing considerations, we formulated three key questions regarding the pathogenesis of FHA / SIA. First, does metabolic challenge in the form of exercise elicit a comparable metabolic and endocrine response in eumenorrheic, ovulatory women and those with FHA / SIA? Second, to what extent is the increase in circulating cortisol observed in FHA communicated to the central nervous system? Third, will addressing problematic behaviors and attitudes reverse FHA? An understanding of the pathogenesis of FHA / SIA may help in treating couples with infertility, especially those who have subclinical forms of hypothalamic hypogonadism such as functional oligospermia and luteal insufficiency.