Low body fat masses of elite female gymnasts are favoured for the current aesthetic appeal required for complex movements performed by the gymnasts. Optimal nutritional intake relative to physical training regimes is essential for pubertal development. Here we evaluate how high intensity training in combination with nutritional intake affects pubertal development. Twenty-two female (13.6 +/- 1.0 years) and 18 male (12.4 +/- 1.6 years) elite gymnasts from national cadres were enlisted in this study. Skeletal maturation and hormonal levels of the hypophyseal, gonadal, and adrenal axes were estimated. Prepubertal and pubertal stages were determined, and body composition was measured using two indirect methods. Whereas female gymnasts showed bone retardation (1.7 years), reduced height potential, minimal fat mass (4.3 +/- 1.3 kg), no significant increase in pubertal oestradiol levels (17.6 +/- 4.2 pg/ml vs. 23.9 +/- 13.4 pg/ml), and delayed menarche (2.3 years), male gymnasts displayed virtually unaltered pubertal development due to different training regimes. Nutritional intake was insufficient in all gymnasts although to a lesser extent for male gymnasts. Intensive physical training of elite female gymnasts combined with inadequate nutritional intake can alter the normal pattern of pubertal development. In female gymnasts the onset of menarche can be influenced by keeping the amount of fat mass low. There is a peripubertal change favouring fat mass over muscle mass in females while there is a net gain of muscle mass during pubertal development in males.

Adjustment of serum leptin levels in elite gymnasts for gender, pubertal stage and BMI or % body fat reveals inappropriately low values. The reason for this hypoleptinemia is most probably insufficient caloric intake. The data suggest that hypoleptinemia in turn causes delayed puberty and growth in this particular group of athletes.

Muscles and bones of patients with congenital heart disease (CHD) are subject to various potentially deleterious influences during growth. The aim of the present study was to analyse the outcome of bone and muscle parameters in adolescents and young adults with a spectrum of CHD. Bone and muscle parameters of the forearm were examined at two standard sites, 4% and 65%, in 29 adolescents and young adults with CHD, aged 14-24 years, by quantitative computed tomography. For the entire study population, bone and muscle parameters did not deviate significantly from the reference values except for age- and gender-corrected body height (ASDS-height: -0.6+/-1.2, p=0.01). Both age- and gender- and height- and gender-corrected (HSDS) abnormal bone mass (BMC) was found at the distal radius in patients with Fontan repair (ASDS-BMC4%: -1.5+/-0.9, p=0.008; HSDS-BMC4%: -1.2+/-1.0, p=0.05) and in those in NYHA class III (ASDS-BMC4%: -1.3+/-0.4, p=0.001; HSDS-BMC4%: -1.4+/-0.5, p=0.004). There was minimal overlap between Fontan patients (n=6) and NYHA class III (5 Fontan patients were in NYHA class I or II). In conclusion, most patients with CHD show a normal muscle and bone development in proportion to their reduced body height. Further follow-up is required to determine whether patients in a worse clinical status (NYHA III) and those with single ventricle physiology are at increased risk of osteoporosis and fractures.

Leptin, the product of the ob-gene, is specifically released by adipocytes. In addition to its metabolic function it seems to affect the feedback-mechanisms of the hypothalamic-pituitary-gonadal-axis. We studied 13 female juvenile elite gymnasts with anorexia athletica (AA) and 9 female patients with anorexia nervosa (AN) regarding the relation between leptin, fat stores, and the reproductive hormone levels. Leptin levels in females with anorexia nervosa (Tanner stage B4 [median]; mean age: 17.8 +/- 1.7 years) were low (2.9 +/- 2.7 microg/L), and were related to body mass index (BMI) (r = 0.71; p = 0.03) and percentage body fat mass (r = 0.78; p = 0.01). Leptin levels of the elite gymnasts were even more decreased (1.2 +/- 0.8 microg/L) caused by the low amount of fat stores. Leptin correlated with BMI (r= 0.77; p = 0.004) and the percentage body fat mass (r = 0.6; p = 0.04). In elite gymnasts leptin levels correlated with CA showing an age-dependent increase (r= 0.59; p = 0.04). Oestradiol was secreted at a low level in both groups (AN: 25.6 +/- 17.4 microg/L; AA: 24.4 +/- 13.5 microg/L). A delay in menarche and a retarded bone maturation occurred in AA. Our results clearly show that leptin levels are low in restrained eaters. Leptin levels represent the fat stores in the body and play a permissive role for female pubertal development. There is evidence that the mechanisms leading to a dysregulation of the reproductive-axis in patients with AN are comparable with those leading to delayed puberty in juvenile elite gymnasts with AA. This implies that AN and AA are overlapping groups and AA can lead to the development of AN.