Reproductive dysfunction is common in female athletes and is indicated symptomatically by delayed menarche (primary amenorrhoea) in girls, and by a cessation of menses (secondary amenorrhoea) or sporadic menses (oligomenorrhoea) in adolescents and young women. These menstrual disturbances reflect different degrees of ovarian suppression and are accompanied by inadequate follicular development and impaired fertility. Exercise associated ovarian suppression coincides with a multitude of metabolic and physiological disturbances that can impact deleteriously on health. Of particular prominence is a disruption of bone metabolism, which reduces bone acquisition during adolescence and elicits premature bone loss in adulthood.¹

The mechanism of exercise associated ovarian suppression is neuroendocrine dysfunction.² The accompanying menstrual disturbance is termed functional hypothalamic amenorrhoea (FHA), which denotes its origin and attributes its aetiology to a reversible adaptation to physiological or emotional stress. In FHA, there is disruption of the pulsatile release of gonadotropin releasing hormone (GnRH) from the arcuate nucleus of the hypothalamus, which alters the pulsatile release of the pituitary gonadotropin, luteinising hormone (LH). The consequence is diminished ovarian stimulation.² At present, the precise cause of this neuroendocrine dysfunction is equivocal. A number of aetiological factors have been implicated, which tend to coincide in affected athletes, and include physical training itself, weight loss or the maintenance of a reduced body fat content, and low cellular energy (or specifically glucose) availability.³ Energy availability is assessed practically as dietary energy intake minus exercise energy expenditure.³

Fundamental insight into the aetiology of exercise associated ovarian suppression has emerged from observations of the prevalence of the disorder among different cohorts of athletes, in conjunction with their physical, nutritional, …