The female athlete triad represents one of the most critical clinical syndromes in sports medicine, exercise physiology, and clinical psychology, capturing the complex systemic interplay between nutritional intake, reproductive neuroendocrinology, and skeletal integrity. When athletes consistently operate under conditions of caloric deficit—whether secondary to clinical eating disorders, inadvertent underfueling, or rigorous volume demands—the downstream physiological repercussions can permanently impair metabolic equilibrium, fertility, and lifelong bone health.
Female Athlete Triad
1. Concise Definition
The female athlete triad is a medical syndrome recognized in active females characterized by three interrelated components: low energy availability (with or without an eating disorder), functional hypothalamic amenorrhea or menstrual irregularities, and diminished bone mineral density ranging from osteopenia to frank osteoporosis. Rather than existing as an all-or-nothing clinical presentation, the syndrome manifests along a continuous spectrum ranging from optimal health and physiological adaptation to severe, debilitating multisystem impairment.
In clinical practice, low energy availability acts as the primary driving etiology. When dietary caloric intake is insufficient to support the metabolic demands required for basic basal physiological processes after subtracting the energy expended in physical exercise, the body initiates profound neuroendocrine conservation pathways. These survival adaptations suppress reproductive axis function and impair bone remodeling dynamics, predisposing the athlete to stress fractures, cardiovascular dysfunction, metabolic suppression, and adverse psychological sequelae.
2. Etymology & Linguistic Origin
The term “athletic triad” or “female athlete triad” originates from modern medical English and sports science nomenclature. The word “triad” is derived from the Greek noun trias (genitive triados), signifying a grouping or assembly of three interconnected elements. The prefix “female” stems from the Latin femella (the diminutive form of femina, meaning woman), while “athlete” finds its roots in the ancient Greek athletes, representing a contestant or competitor in physical games, which in turn stems from athlon, denoting a contest or prize.
The specific clinical nomenclature emerged in 1992 during an ad-hoc consensus meeting of the American College of Sports Medicine (ACSM). Tasked with describing a recurring constellation of clinical symptoms observed in competitive collegiate and elite female competitors, the expert working group formally christened the syndrome the “Female Athlete Triad” to underscore the co-occurrence of disordered eating, amenorrhea, and osteoporosis. Over subsequent decades, the terminology evolved to accommodate non-disordered caloric deficiencies and subclinical bone losses.
3. Pronunciation & Grammatical Form
The term is pronounced phonetically in Standard American and British English as /ˈfiː.meɪl ˈæθ.liːt ˈtraɪ.æd/. Grammatically, it functions as an open compound noun phrase. In formal medical discourse, it is typically preceded by the definite article (“the female athlete triad”) and takes singular agreement in predicate constructions (e.g., “The female athlete triad represents an endocrine disruption”).
Common linguistic variants and abbreviations include “the Triad,” “athletic triad,” and the initialism “FAT.” However, professional literature primarily retains “the Triad” or integrates the construct into the broader contemporary framework known as Relative Energy Deficiency in Sport (REDs), which accounts for male athletes and a broader spectrum of physiological systems.
4. Detailed Conceptual Explanation
At its core, the female athlete triad is anchored by the concept of energy availability (EA). Energy availability is quantitatively defined as the dietary energy intake (measured in kilocalories) minus the exercise energy expenditure (kilocalories), normalized to fat-free mass (FFM) in kilograms: EA = (Dietary Energy Intake − Exercise Energy Expenditure) / Fat-Free Mass. In an optimal physiological state, an energy availability value of 45 kcal/kg FFM/day or higher guarantees sufficient caloric fuel for basal metabolic rate, cellular thermogenesis, immune maintenance, protein synthesis, and neuroendocrine signaling.
When an individual falls below an energy threshold—frequently established in laboratory research as falling below approximately 30 kcal/kg FFM/day—the central nervous system registers an existential threat to survival. The human organism possesses no redundant reserve for high-cost evolutionary processes such as mammalian reproduction during states of energy starvation. Consequently, the hypothalamic-pituitary-ovarian (HPO) axis undergoes profound down-regulation. The arcuate and paraventricular nuclei of the hypothalamus suppress the pulsatile secretion of gonadotropin-releasing hormone (GnRH).
Without rhythmic, high-frequency GnRH pulses, the anterior pituitary gland halts its pulsatile release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). This absence of gonadotropic stimulation arrests ovarian follicular development, causing systemic ovarian steroidogenesis to plummet. Circulating concentrations of 17β-estradiol drop to postmenopausal or early follicular baseline levels, producing functional hypothalamic amenorrhea (FHA). Simultaneously, the down-regulation of the thyroid axis (manifesting as low total and free triiodothyronine [T3] levels, often termed non-thyroidal illness syndrome) and elevated cortisol-to-insulin ratios further reduce resting energy expenditure.
The skeletal system serves as the third critical axis of the triad. Bone tissue is a metabolically dynamic organ undergoing perpetual cellular turnover through osteoclast-mediated bone resorption and osteoblast-mediated bone formation. Estradiol plays an essential anti-resorptive role in female skeletal physiology by inducing osteoclast apoptosis and suppressing pro-resorptive cytokines such as receptor activator of nuclear factor-κB ligand (RANKL). When hypoestrogenism develops, uninhibited osteoclastic activity rapidly degrades microarchitectural trabecular structure.
Crucially, low bone mineral density in the triad is not exclusively an endocrine disorder caused by estrogen deficiency; it is equally a metabolic disorder caused by energy deficiency. Osteoblasts are bioenergetically demanding cells. In states of low energy availability, circulating concentrations of anabolic hormones—most notably insulin-like growth factor 1 (IGF-1), insulin, and leptin—drop dramatically, while systemic levels of peptide YY, adiponectin, and ghrelin rise. Consequently, bone formation ceases or slows considerably at the exact moment that hypoestrogenic osteoclast activity accelerates resorption. The resulting uncoupling of bone turnover causes accelerated structural fragility, increasing the prospective risk of microfractures, macroscopic cortical stress fractures, and premature structural osteopenia.
5. Historical Development
Recognition of the health costs associated with rigorous athletic training emerged alongside the rapid increase in female sports participation following the passage of Title IX in the United States in 1972. Throughout the late 1970s and 1980s, running boom literature frequently romanticized exercise-induced amenorrhea, regarding the cessation of menses as a harmless badge of elite cardiovascular conditioning or an advantageous adaptation that spared athletes from cyclic blood loss and discomfort.
However, pioneer endocrinologists and orthopedic researchers in the mid-1980s—including Barbara Drinkwater and Christopher Cann—published groundbreaking studies demonstrating that young amenorrheic distance runners exhibited lumbar spine bone mineral densities equivalent to women in their seventies, accompanied by elevated incidences of vertebral compression fractures. In 1992, the American College of Sports Medicine convened an expert task force that formally defined the “Female Athlete Triad” as a clinical cluster comprising disordered eating, amenorrhea, and osteoporosis.
Recognizing that many athletes experienced subtle, subclinical presentations that failed to meet the rigid thresholds for clinical anorexia nervosa or catastrophic bone fractures, the ACSM issued a revised position stand in 2007. Led by Anne Loucks and colleagues, this landmark consensus redefined each component of the triad as a continuous spectrum. Energy availability moved from “disordered eating” to “low energy availability with or without an eating disorder”; menstrual status expanded from “amenorrhea” to “subclinical ovulatory dysfunction and oligomenorrhea”; and skeletal health transitioned from “osteoporosis” to “sub-optimal bone mineral density.”
In 2014, the Female Athlete Triad Coalition published updated clinical consensus guidelines for screening, diagnosis, and risk stratification. Concurrently, the International Olympic Committee (IOC) introduced the conceptual framework of Relative Energy Deficiency in Sport (REDs). The IOC model expanded the scope of the athletic triad to encompass male athletes, psychological antecedents, and systemic impairments across cardiovascular, gastrointestinal, immunological, and hematological health, positioning the triad as a recognized, foundational subcomponent of global energy deficiency syndromes.
6. Theoretical Foundations
The female athlete triad is conceptualized through several biological, evolutionary, and psychological frameworks. Biologically, the syndrome is governed by the Metabolic Energy Partitioning Theory. In evolutionary biology, this is recognized under Life History Theory, which dictates that an organism possesses finite caloric resources that must be strategically partitioned between maintenance, growth, physical activity, and reproduction. When incoming energetic resources decline precipitously, evolution favors somatic survival over reproductive proliferation. Energy is selectively diverted away from high-cost physiological enterprises—such as ovulation, gestational preparedness, and structural bone accretion—to preserve basic cellular neurochemistry, cardiovascular tone, and cellular respiration.
From an endocrinological perspective, the triad is grounded in the Hypothalamic Energy-Sensing Framework. The arcuate nucleus integrates peripheral metabolic cues: falling leptin levels from depleting adipocytes, decreased insulin from reduced carbohydrate ingestion, and rising ghrelin from gastric distension. These peripheral messengers signal low metabolic reserves to kisspeptin-expressing neurons within the rostral periventricular area and arcuate nucleus. Because kisspeptin is the primary upstream stimulator of GnRH release, the metabolic silencing of kisspeptin leads to downstream ovarian suppression.
Psychologically, the cognitive theories of eating pathology elucidate why athletes willingly endure or exacerbate extreme energy deficits. The Cognitive-Behavioral Model of Eating Disorders posits that perfectionistic traits, cognitive distortions regarding body composition, and high demands for control generate extreme dietary restraint. In athletic settings, this psychopathology intersects with athletic identity theory: when an individual’s self-worth is entirely entwined with athletic achievement, social reinforcement from coaches, teammates, and media creates intense pressure to achieve lean physical forms, reinforcing rigid dietary patterns.
7. Key Components, Types & Dimensions
The female athlete triad manifests across three interlocking clinical spectra, each spanning a continuum from optimal health to profound pathological impairment:
- The Energy Availability Spectrum: Ranges from Optimal Energy Availability (≥45 kcal/kg FFM/day), which preserves full physiological and metabolic function, through Low Energy Availability without an Eating Disorder (inadvertent underfueling due to high training load, poor nutritional literacy, or financial/time constraints), to Low Energy Availability with an Eating Disorder (intentional, highly restrictive intake driven by clinical pathology such as anorexia nervosa, bulimia nervosa, or avoidant/restrictive food intake disorder).
- The Menstrual Status Spectrum: Spans from Eumenorrhea (regular ovulatory cycles occurring every 21 to 35 days with normal luteal phase length), through Subclinical Menstrual Disturbances (including luteal phase defects with inadequate progesterone production and anovulatory cycles where bleeding may appear regular despite absent ovulation), to Oligomenorrhea (intermittent cycles exceeding 35 days) and Functional Hypothalamic Amenorrhea (the complete absence of menses for three or more consecutive months in post-menarchal females, or primary amenorrhea defined as the absence of menarche by age 15).
- The Bone Health Spectrum: Progresses from Optimal Bone Health (characterized by robust bone mineral density, well-mineralized cortical geometry, and balanced bone turnover rates), through Low Bone Mineral Density (defined in premenopausal athletic populations as a dual-energy X-ray absorptiometry [DXA] Z-score falling between −1.0 and −1.9 alongside secondary clinical risk factors), to Osteoporosis (characterized by a DXA Z-score ≤−2.0 accompanied by a history of clinically significant low-trauma bone fractures or repeated stress fractures).
8. Examples & Illustrative Cases
The practical manifestation of the female athlete triad frequently varies depending on the specific sport discipline, competitive level, and psychological profile of the individual. In aesthetic, endurance, and weight-class sports—such as cross-country running, artistic gymnastics, figure skating, rowing, and road cycling—the pressure to minimize mass while maximizing power-to-weight ratios dramatically inflates triad vulnerability.
Consider the illustrative case of a 19-year-old collegiate distance runner who increases her training volume from 45 to 70 miles per week while maintaining her habitual nutritional routine. She does not display clinical body image dissatisfaction; her underfueling is inadvertent, caused by suppressed appetite following high-intensity interval training and busy academic schedules. Within four months, her energy availability drops below 25 kcal/kg FFM/day. Her regular menstrual cycles become irregular (oligomenorrhea) and eventually halt altogether (secondary amenorrhea). Over six months, her circulating estrogen diminishes and systemic bone resorption accelerates. While running on flat terrain, she experiences acute, severe pain in her mid-tibia; an MRI confirms a high-grade cortical stress fracture. This case demonstrates non-psychopathological, inadvertent low energy availability resulting in severe skeletal consequences.
Contrast this with the case of a 16-year-old competitive ballet dancer who internalizes rigid aesthetic ideals reinforced by instructors. She deliberately restricts macronutrient intake, eliminating dietary fats and carbohydrates, and engages in unrecorded supplementary cardiovascular workouts. Here, low energy availability is intentional and coupled with disordered eating cognitions. Her menarche is delayed past her sixteenth birthday (primary amenorrhea), and her lumbar spine DXA scan reveals a Z-score of −2.3. The combination of intense mechanical impact without hormonal and energetic support leaves her with premature osteoporosis and multiple metatarsal stress fractures, threatening her athletic longevity.
9. Measurement & Assessment
Assessing the female athlete triad requires a comprehensive, multidisciplinary clinical approach integrating self-reported psychometric screening, precise physiological calculations, endocrine biomarker assays, and radiological imaging.
Initial screening is optimized through validated psychometric instruments, such as the Eating Disorder Examination Questionnaire (EDE-Q) and the Low Energy Availability in Females Questionnaire (LEAF-Q). The LEAF-Q evaluates physiological symptoms of insufficient energy intake, specifically interrogating gastrointestinal function, historical and current menstrual irregularities, and past musculoskeletal stress injuries.
Quantification of energy availability in clinical settings involves measuring dietary intake over consecutive representative days using detailed dietary logs analyzed by a registered sports dietitian, combined with objective measures of exercise energy expenditure using calibrated heart rate monitors, power meters, or indirect calorimetry. Fat-free mass is evaluated using dual-energy X-ray absorptiometry (DXA) or multi-frequency bioelectrical impedance analysis.
Endocrine and laboratory evaluation is essential to rule out confounding organic causes of amenorrhea and metabolic suppression. Diagnostic panels must examine:
- Serum beta-human chorionic gonadotropin (β-hCG) to exclude pregnancy.
- Thyroid-stimulating hormone (TSH) and free triiodothyronine (free T3), the latter functioning as a sensitive proxy marker for cellular energy deficit.
- Follicle-stimulating hormone (FSH), luteinizing hormone (LH), and total and free estradiol to assess the integrity of the hypothalamic-pituitary-ovarian axis.
- Serum prolactin to rule out pituitary prolactinomas.
- Total testosterone, androstenedione, and dehydroepiandrosterone sulfate (DHEA-S) to distinguish functional hypothalamic amenorrhea from polycystic ovary syndrome (PCOS).
- Metabolic and nutritional biomarkers, including ferritin, 25-hydroxyvitamin D, comprehensive metabolic panel, and fasting lipid profiles.
Bone mineral density must be evaluated using dual-energy X-ray absorptiometry. In premenopausal athletes, the International Society for Clinical Densitometry (ISCD) mandates the use of age- and sex-matched Z-scores rather than postmenopausal T-scores. Because athletes in weight-bearing sports generally demonstrate bone mineral density 10% to 20% higher than sedentary peers, an age-matched Z-score below −1.0 standard deviations in an athlete is considered abnormal and warrants immediate clinical intervention.
10. Applications & Practical Significance
The clinical, operational, and performance significance of the female athlete triad extends across sports organizations, educational institutions, and public health systems. In high-performance athletic environments, the triad represents a paradoxical performance saboteur: while short-term weight loss may yield transient improvements in power-to-weight ratio, persistent energy deficiency impairs glycogen synthesis, diminishes skeletal muscle protein synthesis, blunts training adaptation, accelerates cognitive fatigue, and dramatically increases injury rates.
To mitigate these risks, collegiate organizations such as the National Collegiate Athletic Association (NCAA) and international Olympic governing bodies have integrated triad risk assessment tools into mandatory pre-participation physical examinations (PPE). Athletes are stratified into low-, moderate-, or high-risk categories using point-based algorithms developed by the Female Athlete Triad Coalition. High-risk athletes—those exhibiting active anorexia nervosa, Z-scores ≤−2.0, or prolonged amenorrhea—are restricted from full sports clearance until measurable physiological recovery criteria are satisfied.
Within academic institutions and sports clubs, practical applications center on educational initiatives directed toward coaches, athletic trainers, and parents. Eradicating systemic sports cultures that celebrate excessive leanness, eliminating mandatory weigh-ins in aesthetic sports, and normalizing open discussions regarding normal menstrual function serve as crucial preventive interventions.
11. Research & Empirical Evidence
Decades of empirical research confirm the profound biological and psychological consequences of the triad. Seminal laboratory experiments conducted by Anne Loucks and colleagues demonstrated that reducing energy availability below 30 kcal/kg FFM/day disrupts LH pulsatility within as little as five days in healthy, previously eumenorrheic female volunteers. Furthermore, their research revealed that this disruption occurs independently of exercise-induced psychological stress, isolating energy availability as the causal biological trigger.
Extensive epidemiological work led by Mary Jane De Souza, Nancy Williams, and colleagues across diverse athletic cohorts demonstrated that subclinical ovulatory disturbances—such as luteal phase defects and anovulation—are common in exercising women who report seemingly regular monthly bleeding, indicating that overt amenorrhea represents only the final stage of long-standing reproductive suppression. Their randomized clinical trials, such as the REFUEL study, demonstrated that increasing daily energy intake by 300 to 600 kcal without altering exercise volume successfully restores normal menstrual cyclicity and improves peripheral markers of bone turnover.
Orthopedic and sports epidemiology investigations, including long-term prospective cohorts tracked by Adam Tenforde and Stuart Warden, have quantified the severe skeletal vulnerabilities associated with triad components. Athletes presenting with multiple triad risk factors experience an approximate fourfold to sixfold increase in the prospective incidence of bone stress injuries compared to their fully nourished, eumenorrheic peers. Crucially, longitudinal imaging demonstrates that bone microarchitectural deficits incurred during adolescent bone-building windows often persist into mid-adulthood, leaving permanent skeletal deficits even after menstrual function is restored.
12. Cultural & Cross-Cultural Considerations
The presentation and sociocultural drivers of the female athlete triad vary considerably across geographical regions, socioeconomic strata, and sport subcultures. In Western societies, the triad is often reinforced by pervasive thin-ideal internalization, hyper-individualistic competitive environments, and the commercialization of fitness culture, which equates extreme abdominal muscularity and low body fat with discipline and moral virtue.
Conversely, in non-Western cultures, the expression of energy deficiency may manifest without overt body dysmorphia or self-identified desires to attain thinness. For instance, in developing nations or resource-limited athletic pipelines, low energy availability frequently arises from food insecurity, arduous manual labor combined with sports training, and inadequate institutional dietary support, reflecting systemic nutritional deficits rather than psychological eating disorders.
Furthermore, cultural stigmas surrounding menstruation, reproductive health, and female athletic participation often suppress early identification. In many conservative or traditional cultural environments, discussions regarding menstrual cyclicity, menarche, and vaginal bleeding remain culturally taboo. Female athletes in these contexts may conceal irregular or absent menstruation from male coaching staff and sports medicine providers, delaying diagnostic workups until disabling bone fractures or severe systemic illnesses force medical intervention.
13. Criticisms, Debates & Limitations
The traditional female athlete triad construct has been subject to continuous academic debate and theoretical refinement. The primary critique emerged in 2014 when the International Olympic Committee introduced the concept of Relative Energy Deficiency in Sport (REDs). Proponents of the REDs framework argued that the historic triad was overly narrow, as it focused exclusively on three parameters in biological females, inadvertently neglecting male athletes who suffer corresponding hypogonadotropic hypogonadism, bone demineralization, and metabolic slowing under low energy availability. Furthermore, critics argued that the triad failed to explicitly incorporate non-reproductive consequences, such as immunological impairment, gastrointestinal dysfunction, hematological deficiencies, and cardiovascular abnormalities.
In response, researchers dedicated to the preservation of the Female Athlete Triad Coalition model argue that the triad maintains unmatched diagnostic precision and clinical utility. They assert that the triad captures the specific, well-validated neuroendocrine axis linking low energy availability, functional hypothalamic amenorrhea, and estrogen-mediated bone loss, and warn that overly expansive frameworks risk diluting focused clinical guidelines and validated screening protocols.
Another ongoing clinical controversy concerns pharmaceutical management. Historically, clinicians routinely prescribed combined oral contraceptive pills (COCPs) containing synthetic ethinylestradiol and progestins to amenorrheic athletes under the mistaken belief that chemically induced withdrawal bleeds protected bone health. Rigorous clinical trials have demonstrated that oral contraceptives fail to restore natural bone mineral density—partially because first-pass hepatic metabolism of oral ethinylestradiol suppresses circulating hepatic IGF-1, a crucial bone-trophic hormone. Current consensus statements caution against oral contraceptives as a primary treatment for triad-induced osteopenia, instead recommending non-pharmacological nutritional restoration or transdermal 17β-estradiol patches paired with cyclic micronized oral progesterone when pharmacological support is necessary.
14. Related Terms & Distinctions
A rigorous understanding of the female athlete triad requires differentiating it from related physiological and pathological conditions:
- Relative Energy Deficiency in Sport (REDs): A broader syndrome encompassing systemic physiological and psychological impairments caused by low energy availability across male and female athletes, of which the female athlete triad represents a specific, highly characterized subcomponent.
- Anorexia Nervosa: A psychiatric disorder characterized by body image distortion, an intense fear of gaining weight, and persistent behavior that interferes with weight gain. While anorexia nervosa frequently leads to the female athlete triad, the triad itself can occur entirely without eating disorder psychopathology through inadvertent underfueling.
- Polycystic Ovary Syndrome (PCOS): An endocrine disorder characterized by hyperandrogenism, ovulatory dysfunction, and polycystic ovarian morphology. Unlike triad-related functional hypothalamic amenorrhea (which presents with low LH and suppressed estrogen), PCOS typically presents with elevated LH-to-FSH ratios, hyperandrogenism, and preserved or elevated bone mineral density.
- Overtraining Syndrome (OTS): A state of chronic performance decrements resulting from systemic neurochemical and autonomic imbalance following prolonged training stress without adequate recovery. Although OTS and the triad frequently co-occur, OTS can occur in fully fueled athletes, whereas the triad requires an underlying energy availability deficit.
- Premature Ovarian Insufficiency (POI): The loss of normal ovarian function before age 40, characterized by hypergonadotropic hypogonadism (elevated FSH and LH due to the absence of ovarian follicular response). In contrast, triad-related amenorrhea is hypogonadotropic (FSH and LH are suppressed or inappropriately normal).
15. Summary / Key Takeaways
The female athlete triad remains a cornerstone clinical concept within sports medicine, linking nutritional behavior to systemic reproductive neuroendocrinology and long-term skeletal architecture. Driven fundamentally by low energy availability—whether arising from clinical eating disorders or unintended discrepancies between energy intake and training output—the syndrome triggers an evolutionary survival response that arrests the hypothalamic-pituitary-ovarian axis, leading to functional hypothalamic amenorrhea and accelerated bone demineralization.
Early screening, comprehensive interdisciplinary evaluation, and targeted intervention are critical to avoiding irreversible bone microarchitectural damage and chronic health complications. Clinical management must prioritize restoring energy availability through dietary realignments, volume management, and behavioral therapy, while avoiding the misleading use of oral contraceptives as a standalone therapeutic cure.
References
- De Souza, M. J., Nattiv, A., Joy, E., Misra, M., Williams, N. I., Mallinson, R. J., Gibbs, J. C., Olmsted, M., Goolsby, M., & Matheson, G. (2014). 2014 Female Athlete Triad Coalition Consensus Statement on treatment and return to play of the female athlete triad. British Journal of Sports Medicine, 48(4), 289–289. https://doi.org/10.1136/bjsports-2013-093218
- Loucks, A. B., Kiens, B., & Wright, H. H. (2011). Energy availability in athletes. Journal of Sports Sciences, 29(Suppl 1), S7–S15. https://doi.org/10.1080/02640414.2011.588839
- Mountjoy, M., Sundgot-Borgen, J., Burke, L., Carter, S., Stellingwerff, T., Lebrun, C., Ackland, T., Blauwet, C., Burrows, M., & Sherman, R. (2014). The IOC consensus statement: beyond the Female Athlete Triad—Relative Energy Deficiency in Sport (RED-S). British Journal of Sports Medicine, 48(7), 491–497. https://doi.org/10.1136/bjsports-2014-093502
- Nattiv, A., Loucks, A. B., Manore, M. M., Sanborn, C. F., Sundgot-Borgen, J., & Warren, M. P. (2007). American College of Sports Medicine position stand: The female athlete triad. Medicine & Science in Sports & Exercise, 39(10), 1867–1882. https://doi.org/10.1249/mss.0b013e318149f111
- Tenforde, A. S., Carlson, J. L., Chang, A., Sainani, K. L., Shultz, R., Kim, I. Y., Cutti, P., Golden, N. H., & Fredericson, M. (2017). Association of the female athlete triad risk assessment stratification to the development of bone stress injuries in collegiate athletes. The American Journal of Sports Medicine, 45(2), 302–310. https://doi.org/10.1177/0363546516665819