Author(s): KAMEMOTO, K., SAKAMAKI-SUNAGA, M. , Institution: OSAKA SANGYO UNIVERSITY, Country: JAPAN, Abstract-ID: 1253

INTRODUCTION:
Long-term or severe low energy availability in athletes leads to health impairments and declines in athletic performance (1). While a laboratory-based study reported that energy availability (EA) ≤ 30 kcal/kg FFM/day impaired endocrine and metabolic function (2), its effects on appetite-regulating hormones involved remain inadequately investigated. Elevated appetite-regulating hormones ghrelin and peptide tyrosine tyrosine (PYY) have been reported in women with hypothalamic amenorrhea (3,4) or anorexia nervosa (5). This study examined the relationship between energy availability (EA), appetite-regulating hormones and eating behavior in female athletes.
METHODS:
Ten female university track and field athletes (means ± SD, age: 20.1 ± 1.0 years, body mass index: 21.1 ± 2.5 kg/m2, %body fat: 21.9 ± 4.6%) competing in jumping disciplines. Body composition was assessed using dual-energy X-ray absorptiometry (DXA). EA was calculated over three consecutive days during the training season from dietary records and training logs. Exercise energy expenditure (EEE) was estimated by using metabolic equivalents. Blood samples were collected in the early morning following an overnight fast for analysis of follicle stimulating hormone, luteinizing hormone, estradiol, insulin, acylated ghrelin, PYY3-36, and glucose. The Eating Attitudes Test-26 (EAT-26) assessed eating behavior. Mann-Whitney U tests and Spearman's rank correlation coefficients were used for statistical analysis. Statistical significance was set at P < 0.05.
RESULTS:
Mean EA was 26.1 ± 11.0 kcal/kg FFM/day, with five participants below and five at or above 30 kcal/kg FFM/day. The EA≥30 group had significantly lower exercise energy expenditure (EEE) and significantly higher energy, fat, and carbohydrate intakes compared to the EA<30 group (all P < 0.016). Acylated ghrelin and PYY3-36 showed no significant differences in the EA≥30 versus EA<30 groups (P = 0.465, P = 0.754, respectively), and no correlation with EA (P = 0.960, P = 0.627, respectively). EA positively correlated with insulin, energy intake, and carbohydrate intake (all P < 0.042). Two participants scored ≥ 20 on the EAT-26, indicating possible eating disorders. EAT-26 scores negatively correlated with insulin, glucose, and fat intake (all P < 0.014).
CONCLUSION:
In this small sample of female track and field athletes, appetite-regulating hormones (acylated ghrelin and PYY3-36) showed no association with EA, despite variation in EA levels. However, insulin correlated with both EA and eating disorder risk scores, suggesting its potential utility as a physiological marker of energy balance in athletes.