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The reported prevalence of low energy availability (LEA) in female and male track and field athletes is between 18% and 58% with the highest prevalence among athletes in endurance and jump events. In male athletes, LEA may result in reduced testosterone levels and libido along with impaired training capacity. In female track and field athletes, functional hypothalamic amenorrhea as consequence of LEA has been reported among 60% of elite middle- and long-distance athletes and 23% among elite sprinters. Health concerns with functional hypothalamic amenorrhea include impaired bone health, elevated risk for bone stress injury, and cardiovascular disease. Furthermore, LEA negatively affects recovery, muscle mass, neuromuscular function, and increases the risk of injuries and illness that may affect performance negatively. LEA in track and field athletes may occur due to intentional alterations in body mass or body composition, appetite changes, time constraints, or disordered eating behavior. Long-term LEA causes metabolic and physiological adaptations to prevent further weight loss, and athletes may therefore be weight stable yet have impaired physiological function secondary to LEA. Achieving or maintaining a lower body mass or fat levels through long-term LEA may therefore result in impaired health and performance as proposed in the Relative Energy Deficiency in Sport model. Preventive educational programs and screening to identify athletes with LEA are important for early intervention to prevent long-term secondary health consequences. Treatment for athletes is primarily to increase energy availability and often requires a team approach including a sport physician, sports dietitian, physiologist, and psychologist.

We aimed to (a) report energy availability (EA), metabolic/reproductive function, bone mineral density, and injury/illness rates in national/world-class female and male distance athletes and (b) investigate the robustness of various diagnostic criteria from the Female Athlete Triad (Triad), Low Energy Availability in Females Questionnaire, and relative energy deficiency in sport (RED-S) tools to identify risks associated with low EA. Athletes were distinguished according to benchmarks of reproductive function (amenorrheic [n = 13] vs. eumenorrheic [n = 22], low [lowest quartile of reference range; n = 10] versus normal testosterone [n = 14]), and EA calculated from 7-day food and training diaries (< or >30 kcal·kg⁻¹ fat-free mass·day⁻¹). Sex hormones (p < .001), triiodothyronine (p < .05), and bone mineral density (females, p < .05) were significantly lower in amenorrheic (37%) and low testosterone (40%; 15.1 ± 3.0 nmol/L) athletes, and bone injuries were ∼4.5-fold more prevalent in amenorrheic (effect size = 0.85, large) and low testosterone (effect size = 0.52, moderate) groups compared with others. Categorization of females and males using Triad or RED-S tools revealed that higher risk groups had significantly lower triiodothyronine (female and male Triad and RED-S: p < .05) and higher number of all-time fractures (male Triad: p < .001; male RED-S and female Triad: p < .01) as well as nonsignificant but markedly (up to 10-fold) higher number of training days lost to bone injuries during the preceding year. Based on the cross-sectional analysis, current reproductive function (questionnaires/blood hormone concentrations) appears to provide a more objective and accurate marker of optimal energy for health than the more error-prone and time-consuming dietary and training estimation of EA. This study also offers novel findings that athlete health is associated with EA indices.

The authors describe the implementation of a 3-week dietary intervention in elite race walkers at the Australian Institute of Sport, with a focus on the resources and strategies needed to accomplish a complex study of this scale. Interventions involved: traditional guidelines of high carbohydrate (CHO) availability for all training sessions; a periodized CHO diet which integrated sessions with low and high CHO availability within the same total CHO intake; and a ketogenic low-CHO high-fat diet. Seven-day menus and recipes were constructed for a communal eating setting to meet nutritional goals as well as individualized food preferences and special needs. Menus also included nutrition support before, during, and after exercise. Daily monitoring, via observation and food checklists, showed that energy and macronutrient targets were achieved. Diets were matched for energy (∼14.8 MJ/d) and protein (∼2.1 g·kg⁻¹·day⁻¹) and achieved desired differences for fat and CHO, with high CHO availability and periodized CHO availability: CHO = 8.5 g·kg⁻¹·day⁻¹, 60% energy, fat = 20% of energy and low-CHO high-fat diet: 0.5 g·kg⁻¹·day⁻¹ CHO, fat = 78% energy.  There were no differences in micronutrient intake or density between the high CHO availability and periodized CHO availability diets; however, the micronutrient density of the low-CHO high-fat diet was significantly lower. Daily food costs per athlete were similar for each diet (∼AU$ 27 ± 10). Successful implementation and monitoring of dietary interventions in sports nutrition research of the scale of the present study require meticulous planning and the expertise of chefs and sports dietitians. Different approaches to sports nutrition support raise practical challenges around cost, micronutrient density, accommodation of special needs, and sustainability.

This study implemented a 2-week high carbohydrate (CHO) diet intended to maximize CHO oxidation rates and examined the iron-regulatory response to a 26-km race walking effort. Twenty international-level, male race walkers were assigned to either a novel high CHO diet (MAX = 10 g/kg body mass CHO daily) inclusive of gut-training strategies, or a moderate CHO control diet (CON = 6 g/kg body mass CHO daily) for a 2-week training period. The athletes completed a 26-km race walking test protocol before and after the dietary intervention. Venous blood samples were collected pre-, post-, and 3 hr postexercise and measured for serum ferritin, interleukin-6, and hepcidin-25 concentrations. Similar decreases in serum ferritin (17–23%) occurred postintervention in MAX and CON. At the baseline, CON had a greater postexercise increase in interleukin-6 levels after 26 km of walking (20.1-fold, 95% CI [9.2, 35.7]) compared with MAX (10.2-fold, 95% CI [3.7, 18.7]). A similar finding was evident for hepcidin levels 3 hr postexercise (CON = 10.8-fold, 95% CI [4.8, 21.2]; MAX = 8.8-fold, 95% CI [3.9, 16.4]). Postintervention, there were no substantial differences in the interleukin-6 response (CON = 13.6-fold, 95% CI [9.2, 20.5]; MAX = 11.2-fold, 95% CI [6.5, 21.3]) or hepcidin levels (CON = 7.1-fold, 95% CI [2.1, 15.4]; MAX = 6.3-fold, 95% CI [1.8, 14.6]) between the dietary groups. Higher resting serum ferritin (p = .004) and hotter trial ambient temperatures (p = .014) were associated with greater hepcidin levels 3 hr postexercise. Very high CHO diets employed by endurance athletes to increase CHO oxidation have little impact on iron regulation in elite athletes. It appears that variations in serum ferritin concentration and ambient temperature, rather than dietary CHO, are associated with increased hepcidin concentrations 3 hr postexercise.