SAT-208 Effects of Metabolic and Psychological Stressors on Serum 24-Hour Cortisol and Luteinizing Hormone

Exercising women with functional hypothalamic amenorrhea (FHA) experience disrupted luteinizing hormone pulsatility which has been linked to low energy availability. While the susceptibility to life stressors in also linked to reproductive axis suppression, the contribution of psychosocial stress to FHA in exercising women is unclear. Our aim was to prospectively determine the relations between indicators of psychosocial and metabolic stressors on the change in LH pulse dynamics during a three-month diet and exercise intervention causing moderate weight loss in previously untrained, ovulatory, collage age women studied across an academic year. We also explored the potential role of cortisol as an indicator of both metabolic and psychosocial stress in the change in LH. This is a secondary analysis from a previously published randomized, controlled trial demonstrating the causal role of low energy availability in the disruption of the menstrual cycle. Here, we report on 21 women aged (18 to 24 yrs), BMI (21.7± 1.9 kg/m(2)), aerobic capacity (37.5 ± 5.3 ml/kg/min) who completed a baseline menstrual cycle and three intervention menstrual cycles of a controlled diet (55% carbohydrates, 30% protein, 15% fat) and supervised aerobic exercise (5 days/wk, 30-90 min/day, 60-80% maximum heart rate). We assessed anthropometrics, aerobic capacity, psychosocial stress (Perceived Stress Scale), and metabolic hormones throughout the intervention. 24 hour LH pulse dynamics (q10 min) and diurnal patterns of cortisol (q60 min) were determined in the early follicular phase prior to the intervention and in the follicular phase of the 3(rd) intervention cycle or in the post intervention cycle. Pre to post comparisons were determined with paired t-tests, and Pearson bivariate correlations assessed associations. Subjects lost weight pre=57.8±4.9 kg to post=55.0±4.6 kg (p<0.001) and gained aerobic capacity pre=37.5 ± 5.3 ml/kg/min to post= 42.3 ± 5.9 ml/kg/min (p=.003). LH pulse frequency declined pre=0.79±0.23 pulses/hr to post=0.60±.29 pulses/hr (p=0.014), but mean LH and pulse amplitude were unchanged. 24 hour cortisol area under the curve increased significantly from pre=6716 ±3839 µg*day/dL to post=8515 ±2259 µg*day/dL (p=0.003). Increases in cortisol AUC were associated with a decline in LH pulse frequency R=-0.472; (p=0.048). The change in PSS was not associated with the change in LH or the change in cortisol. Body weight declines were associated with increases in cortisol AUC R= -0.473, (p=0.03) and the decline in LH pulse frequency R= 0.523; (p=0.026). These results suggest that the initial perturbation of LH pulsatility with moderate diet and exercise is largely metabolically driven and not influenced by individual responses to life stressors experienced across the academic year.