Regular exercise is an essential component of prevention of obesity, but in adolescent young women, physical conditioning is associated to multiple endocrine aberrations and an increased risk of fractures. High-intensity exercise activates the hypothalamic-pituitary-adrenal axis (HPA), increases cortisol concentration, disrupts the menstrual cycle, and can lead to premature osteoporosis. In athletes, menstrual cyce disruption reflects decreased activity of the hypoyhalamic-pituitary -gonadal axis (HPG). Decreased bone mass is particularly alarming for adolescent young women as bone accretion reaches a plateau in the post-pubertal years, thereby rendering them vulnerable to life-long increased risk of osteporosis. There is a need to identify reliable predictors for exercise-induced amenorrhea in adolescents of normal weight. Cortisol is increased in athletes and studies in other populations have shown that an endogenous increase in cortisol is linked to bone loss. The proposed project will test the hypothesis that the activation of the HPA axis is a preditor of subsequent decrease of HPG activity and estrogen concentrations thereby increasing the risk of osteoporosis in active post-pubertal girls. We plan to conduct an intervention study on adolescent girls of 14 to 16 years of age and preparing for team sports or enrolling in a supervised training program. The study will be framed by the periods of on and off training as they are imposed in high schools. Cardiovascular fitness will be assessed by maximal oxygen consumption (VO2max) and outcomes of interest will be 24-hour cortisol concentrations, gonadotropins and bone density, as well as changes in body composition, leptin and insulin sensitivity. Our goal will be to identify early markers of declining gonadotropin function and bone health in postpubertal young women as they improve cardiovascular capacity
