The Female Athlete Triad represents three interrelated conditions of (i) low energy availability (energy deficiency), presenting with or without disordered eating, (ii) menstrual dysfunction, and (iii) poor bone health, each of which can exist along a continuum of severity ranging from mild and moderate subclinical health concerns to severe clinical outcomes, including eating disorders, amenorrhea, and osteoporosis. This review provides a brief overview of the Female Athlete Triad, including updating the current thinking regarding energy availability and how it relates to reproductive function, and sets the stage for an initial working model of a similar syndrome in males that will be based on currently available evidence and will later be defined and referred to as a Male Athlete Triad by the newly re-named Female and Male Athlete Triad Coalition. A primary focus of this paper will be on the physiology of each Triad model with an emphasis on low energy availability and its role in reproductive function, with a brief introduction on its effects on bone health in men. From the data reviewed, (i) a specific threshold of energy availability below which menstrual disturbances are induced is not supported; (ii) it appears that the energetic, reproductive, and bone systems in men are more resilient to the effects of low energy availability compared to those of women, requiring more severe energetic perturbations before alterations are observed; and (iii) it appears that recovery of the hypothalamic pituitary gonadal axis can be observed more quickly in men than in women.

This is the second of two publications comprising the 2025 update to the 2014 Consensus Statement on treatment and return to play guidelines on the Female Athlete Triad (Triad). This paper pairs with the 2025 Update to the Female Athlete Triad Coalition Consensus Statement Part 1: State of the Science and Introduction of a New Adolescent Model (Sports Medicine, 2025), to focus on evidence-based revisions for screening, diagnosis, treatment, and clearance and return to play. Revised recommendations for managing eating disorders (ED)/disordered eating (DE) and non-pharmacological and pharmacological treatment of bone loss and abnormal menstrual cycles are included, as are the most recent clearance and return to play recommendations, inclusive of adolescent athletes. Recent research supports the adoption of revised criteria for defining and treating energy deficiency, moving away from the concept of an energy-availability threshold. Energy deficiency-induced menstrual disturbances can be reversed with a moderate increase in food intake and modest weight gain, but restoration of menses alone is not associated with high rates of ovulation or increased ovarian steroid levels until multiple consecutive normal length menstrual cycles are achieved. Revised guidelines for the diagnosis and treatment of functional hypothalamic oligo/amenorrhea are included with guidance on the confounding effects of hyperandrogenemia. Gynecological age and psychological stress are factors impacting the individual susceptibility to the Triad. The bone health spectrum of the Triad now includes bone stress injuries. Routes of administration via epidermal patch versus oral for pharmacological treatment of low bone density are discussed. The diagnosis, treatment, and return to play approaches for adolescents with the Triad are unique compared with those employed for adults and require age-appropriate clinical guidelines. The strength of the evidence-based statements is graded using an accepted taxonomy in which randomized controlled trials and observational data are considered the highest level of evidence.

Dietary consumption of prunes has favorable impacts on bone health, but more research is necessary to improve upon study designs and refine our understandings. We evaluated the effects of prunes (50 g or 100 g/d) on bone mineral density (BMD) in postmenopausal women during a 12-mo dietary intervention. Secondary outcomes include effects on bone biomarkers. The single-center, parallel-arm 12-mo randomized controlled trial tested the effects of 50 g and 100 g prunes compared with a control group on BMD (every 6 mo) and bone biomarkers in postmenopausal women. In total, 235 women (age 62.1 ± 5.0 y) were randomly allocated into control (n = 78), 50-g prune (n = 79), or 100-g prune (n = 78) groups. Compliance was 90.2 ± 1.8% and 87.1 ± 2.1% in the 50-g and 100-g prune groups. Dropout was 22%; however, the dropout rate was 41% for the 100-g prune group (compared with other groups: 10%, control; 15%, 50 g prune; P < 0.001). A group × time interaction for total hip BMD was observed in control compared with 50-g prune groups (P < 0.05) but not in control compared with 100-g prune groups (P > 0.05). Total hip BMD decreased –1.1 ± 0.2% in the control group at 12 mo, whereas the 50-g prune group preserved BMD (–0.3 ± 0.2%) at 12 mo (P < 0.05). Although hip fracture risk (FRAX) worsened in the control group at 6 mo compared with baseline (10.3 ± 0.5% compared with 9.8 ± 0.5%, P < 0.05), FRAX score was maintained in the pooled (50 g + 100 g) prune groups. A 50-g daily dose of prunes can prevent loss of total hip BMD in postmenopausal women after 6 mo, which persisted for 12 mo. Given that there was high compliance and retention at the 50-g dosage over 12 mo, we propose that the 50-g dose represents a valuable nonpharmacologic treatment strategy that can be used to preserve hip BMD in postmenopausal women and possibly reduce hip fracture risk. This trial was registered at clinicaltrials.gov as NCT02822378.

This study examined the effect of estradiol-β-17 across the menstrual cycle (MC) during aerobic exercise on energy substrate utilization and oxidation. Thirty-two eumenorrheic (age = 22.4 ± 3.8 y (mean ± SD)), physically active women participated in two steady-state running sessions at 65% of VO_2max, one during the early follicular and one during the luteal phase of the MC. Blood samples were collected at rest before each exercise session and analyzed for Estradiol-β-17 to confirm the MC phase. Carbohydrate (CHO) utilization and oxidation values were significantly lower (p < 0.05) in the luteal (utilization: 51.6 ± 16.7%; oxidation: 1.22 ± 0.56 g/min; effect size (ES) = 0.45, 0.27) than follicular phase (utilization: 58.2 ± 15.1%; oxidation: 1.38 ± 0.60 g/min) exercise sessions. Conversely, fat utilization and oxidation values were significantly (p < 0.05) higher in the luteal (utilization: 48.4 ± 16.7%; oxidation: 0.49 ± 0.19 g/min; ES = 0.45,0.28) than follicular phase (utilization: 41.8 ± 15.1%; oxidation: 0.41 ± 0.14 g/min). Estradiol-β-17 concentrations were significantly (p < 0.01) greater during the luteal (518.5 ± 285.4 pmol/L; ES = 0.75) than follicular phase (243.8 ± 143.2 pmol/L). Results suggest a greater use of fat and reduced amount of CHO usage during the luteal versus follicular phase, directly related to the change in resting estradiol-β-17. Future research should investigate the role these changes may play in female athletic performance.

Objective Determine the interrelations between reductions in energy availability (EA), luteinizing hormone (LH) pulse frequency, and the induction of menstrual disturbances in previously sedentary, ovulatory women. Methods Secondary analysis of a randomized controlled trial consisting of a 3-month controlled diet and supervised exercise program. EA was calculated daily by measured energy intake (kcal) and exercise energy expenditure (kcal) normalized to fat-free mass (kg) and averaged during baseline and each of 3 intervention menstrual cycles. Blood samples were obtained every 10 minutes for 24 hours in the early follicular phase before the intervention and after 3 months of diet and exercise (n = 14). LH pulse dynamics were assessed by Cluster. Linear mixed models determined whether EA predicts LH pulse frequency and LH pulse frequency predicts luteal phase defects (LPDs). Results Subjects were 20 ± 1 years old, 165.1 ± 1.4 cm tall, and weighed 58.9 ± 1.5 kg. LH pulse frequency decreased from 0.82 ± 0.06 pulses/h to 0.63 ± 0.09 pulses/h (P = 0.048) as a result of the intervention which produced modest (-3.2 ± 0.6 kg) weight loss. EA, averaged across a menstrual cycle, predicted LH pulse frequency (P = 0.003) such that a single-unit decrease in EA was associated with a 0.017 pulses/h decrease in LH pulse frequency. LH pulse frequency in cycles with LPDs was 49% of that observed in cycles with no menstrual disturbances and for every 0.1-unit decrease in LH pulse frequency, the odds of having an LPD were 22× greater than having an optimal ovulatory cycle (P = 0.01). Conclusions Modest reductions in EA over a prolonged period are associated with decreased LH pulse frequency and the induction of menstrual disturbances.