The Association between Weight Loss Induced Suppression of LH Pulsatility and Metabolic Hormones

Open Access
Figurelle, Morgan Elizabeth
Area of Honors:
Bachelor of Science
Document Type:
Thesis Supervisors:
  • Nancy I. Williams, Thesis Supervisor
  • Stephen Jacob Piazza, Honors Advisor
  • cortisol
  • ghrelin
  • LH pulsatility
  • EAMD
It has been demonstrated that ghrelin and cortisol are elevated in women with exercise-associated menstrual disturbances (EAMD). Additionally, it is suggested that ghrelin is a key factor contributing to the suppression of luteinizing hormone (LH) pulse frequency, a proxy indicator of menstrual function. However, the mechanism by which ghrelin modulates LH pulsatility is unknown. The purpose of this study was to test the hypothesis that cortisol is a potential intermediary in the association between ghrelin and LH in normal weight, sedentary women subsequent to a controlled feeding and exercise intervention designed to induce an energy deficit. This study was part of a larger study designed to assess the endocrine and reproductive changes in women in response to an intervention controlling food intake and supervised exercise (5 days/week). Subjects (5 sedentary controls [C], 16 exercising energy deficit [Edef]) were studied at baseline (BL) and subsequent to (Post) the 3-month intervention. Blood samples were obtained every 10 minutes for 24 hours and assayed using radioimmunoassay for total ghrelin. Immulite was used to measure serum concentrations of LH and ELISA was utilized to measure concentrations of 24-hour urinary cortisol. Statistical analyses included paired T-tests, ANOVA and stepwise linear regression. Subjects in the Edef group lost a significant amount of body weight (58.4 ± 1.1 kg to 55.3 ± 1.2 kg, p < 0.001), body fat percentage (28.3 ± 1.2 to 24.6 ± 1.2, p < 0.001), body fat mass (16.6 ± 0.8 kg to 13.7 ± 0.9 kg, p < 0.001), and increased VO2 max (37.1 ± 1.1 ml/kg/min to 43.0 ± 1.5 ml/kg/min, p = 0.001) whereas C subjects remained weight stable (p = 0.146). Ghrelin AUC (28903 ± 2739 to 34799 ± 3382, p = 0.002), 24-hour mean (1216.9 ± 126.3 to 1457.8 ± 150.3, p = 0.002) and peak (1602.4 ± 153.2 to 2007.2 ± 214.7, p = 0.003) as well as 24-hour cortisol (40.7 ± 3.4 to 57.3 ± 5.9, p = 0.018) significantly increased whereas LH pulse frequency (0.81 ± 0.06 to 0.63 ± 0.08, p = 0.047) significantly decreased from BL to post in the Edef group while there was no change exhibited in the C group in any ghrelin parameter, 24-hour cortisol or LH pulse frequency (p > 0.05). In the Edef group, the change in ghrelin AUC (p < 0.001) and the change in body weight (p = 0.03) significantly predicted the change in 24-hour cortisol. Also observed in the Edef group, the change in ghrelin 24-hour mean (p = 0.01) was the only significant predictor of the change in LH pulse frequency. Thus, the association between cortisol and LH was not demonstrated in this study. In conclusion, cortisol may be also be involved in the suppression of the HPO axis, but is likely not an intermediary in the association between ghrelin and LH.