Luteinizing Hormone Pulsatility Is Disrupted at a Threshold of Energy Availability in Regularly Menstruating Women

TLDR

The study examined how luteinizing hormone (LH) pulsatility depends on energy availability by manipulating energy balance in 29 regularly menstruating, sedentary young women during the early follicular phase. Participants performed 15 kcal/kg lean body mass/day exercise at 70 % VO₂max while consuming a controlled diet to achieve energy availabilities of 45 and 10, 20, or 30 kcal/kg LBM/day in two randomized trials, with daily and 10‑minute interval blood sampling for LH and a panel of metabolic hormones. LH pulsatility was unchanged at 30 kcal/kg LBM/d but below this threshold frequency decreased and amplitude increased—especially in women with short luteal phases—mirroring changes in glucose, beta‑hydroxybutyrate, GH, and cortisol, demonstrating that LH pulsatility is disrupted only when energy availability falls below a critical level.

Abstract

To investigate the dependence of LH pulsatility on energy availability (dietary energy intake minus exercise energy expenditure), we measured LH pulsatility after manipulating the energy availability of 29 regularly menstruating, habitually sedentary, young women of normal body composition for 5 d in the early follicular phase. Subjects expended 15 kcal/kg of lean body mass (LBM) per day in supervised exercise at 70% of aerobic capacity while consuming a clinical dietary product to set energy availability at 45 and either 10, 20, or 30 kcal/kg LBM.d in two randomized trials separated by at least 2 months. Blood was sampled daily during treatments and at 10-min intervals for the next 24 h. Samples were assayed for LH, FSH, estradiol (E2), glucose, beta-hydroxybutyrate, insulin, cortisol, GH, IGF-I, IGF-I binding protein (IGFBP)-1, IGFBP-3, leptin, and T3. LH pulsatility was unaffected by an energy availability of 30 kcal/kg LBM.d (P > 0.3), but below this threshold LH pulse frequency decreased, whereas LH pulse amplitude increased (all P < 0.04). This disruption was more extreme in women with short luteal phases (P < 0.01). These incremental effects most closely resembled the effects of energy availability on plasma glucose, beta-hydroxybutyrate, GH, and cortisol and contrasted with the dependencies displayed by the other metabolic hormones (simultaneously P < 0.05). These results demonstrate that LH pulsatility is disrupted only below a threshold of energy availability deep into negative energy balance and suggest priorities for future investigations into the mechanism that mediates the nonlinear dependence of LH pulsatility on energy availability.