C. Decree et al., RESPONSES OF CATECHOLESTROGEN METABOLISM TO ACUTE GRADED-EXERCISE IN NORMAL MENSTRUATING WOMEN BEFORE AND AFTER TRAINING, The Journal of clinical endocrinology and metabolism, 82(10), 1997, pp. 3342-3348
It has been hypothesized that exercise-related hypo-estrogenemia occur
s as a consequence of increased competition of catecholestrogens (CE)
for catechol-O-methyltransferase (COMT). This may result in higher nor
epinephrine (NE) concentrations, which could interfere with normal gon
adotropin pulsatility. The present study investigates the effects of t
raining on CE responses to acute exercise stress. Nine untrained eumen
orrheic women (mean percentage of body fat +/-SD: 24.8 +/- 3.1%) volun
teered for an intensive 5-day training program. Resting, submaximal, a
nd maximal (t(max)) exercise plasma CE, estrogen, and catecholamine re
sponses were determined pre-and post training in both the follicular (
FPh) and luteal phase (LPh). Acute exercise stress increased total pri
macy estrogens (E) but had little effect on total 2-hydroxyestrogens (
2-OHE) and 2-hydroxyestrogen-monomethylethers (2-MeOE) (= O-methylated
CE after competition for catechol-O-methyltransferase). This pattern
was not significantly changed by training. However, posttraining LPh m
ean (+/- SE) plasma E, 2-OHE, and 2-MeOE concentrations were sig nific
antly lower (P < 0.05) at each exercise intensity (for 2-OHE: 332 +/-
47 vs. 422 +/- 57 pg/mL at t(max); for 2-MeOE: 317 +/- 26 vs. 354 +/-
34 pg/mL at t(max)). Training produced opposite effects on 2-OHE:E rat
ios (an estimation of CE formation) during acute exercise in the FPh (
reduction) and LPh (increase). The 2-MeOE:2-OHE ratio (an estimation o
f CE activity) showed significantly higher values at t(max) in both me
nstrual phases after training (FPh: + 11%; LPh: +23%; P < 0.05). After
training, NE values were significantly higher (P < 0.05). The major f
indings of this study were that: training lowers absolute concentratio
ns of plasma estrogens and CE; the acute exercise challenge altered pl
asma estrogens but had little effect on CE; estimation of the formatio
n and activity of CE suggests that formation and O-methylation of CE p
roportionately increases. These findings may be of importance for NE-m
ediated effects on gonadotropin release.