Exercise-Induced Stress Responses of Amenorrheic and Eumenorrheic Runners

Publisher Website
Google Scholar
Abstract
The role of stress in exercise-associated amenorrhea was investigated. Sex hormones [FSH, LH, androstenedione (A), testosterone, estrone, and 17β-estradiol (E2)], stress hormones [dehydroepiandrosterone, cortisol (F), PRL, norepinephrine, and epinephrine] and psychological status (Profile of Mood States and State-Trait Anxiety Inventory) were measured at rest and in response to a 40-min 80% of maximal aerobic power (V̇O2max) run in highly trained eumenorrheic (n = 8) and amenorrheic (n = 7) women runners matched for fatness [eumenorrheic, 16.5 ± 2.3% (±SD); amenorrheic, 14.9 ± 4.8] and maximal aerobic power (eumenorrheic, 58.9 ± 5.7 ml/kg min; amenorrheic, 59.8 ± 4.6). Eumenorrheic runners were tested between days 3 and 8 of the follicular phase. At rest, decreased plasma FSH, LH, and E2 concentrations were found in amenorrheic women [eumenorrheic FSH, 10.5 ±4.1 mlU/ml; amenorrheic FSH, 4.9 ± 1.6 (P < 0.01); eumenorrheic LH, 14.1 ± 6.1 mlU/ml; amenorrheic LH, 5.1 ± 1.7 (P < 0.01); eumenorrheic E2) 20 ± 9 pg/ml; amenorrheic E2, 7 ± 6 (P < 0.05)]. Other sex and stress hormones and psychological measurements were similar in the two groups and were within the normal range. Ventilatory, cardiovascular, thermoregulatory, and psychological responses to the submaximal run were identical. Among eumenorrheic women, all stress hormones and A increased after exercise, but PRL, F, and A were unchanged among amenorrheic women. Estrone, E2, and testosterone did not change in either group. These observations are inconsistent with a general stress hypothesis of exercise-associated amenorrhea as well as with more specific hyperprolactinemic and hyperandrogenic hypotheses. In amenorrheic women, failure of PRL to increase in response to exercise may be due to their lack of E2, while failure of F and A to increase may indicate reduced adrenal 3β-hydroxysteroid dehydrogehase/isomerase activity.