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The Journal of Clinical Endocrinology & Metabolism Vol. 82, No. 10 3342-3348
Copyright © 1997 by The Endocrine Society


Original Studies

Responses of Catecholestrogen Metabolism to Acute Graded Exercise in Normal Menstruating Women before and after Training1

Carl De Crée, Peter Ball, Bärbel Seidlitz, Gerrit Van Kranenburg, Peter Geurten and Hans A. Keizer

Interuniversity Project on Reproductive Endocrinology in Women and Exercise, the Department of Applied and Experimental Reproductive Endocrinology (C.D.C.), The Institute for Gyneco-Endocrinological Research, B-3000 Leuven 3, Belgium; the Department of Biochemical and Clinical Endocrinology (P.B., B.S.), Medical University of Lübeck, D-23538 Lübeck, Germany; and the Department of Movement Sciences (G.V.K., P.G., H.A.K.), Faculty of Health Sciences, University of Maastricht, NL-6200 MD Maastricht, The Netherlands

Address all correspondence and requests for reprints to: C. De Crée, M.D., Department of Applied and Experimental Reproductive Endocrinology, The Institute for Gyneco-Endocrinological Research, P.O. Box 134, B-3000 LEUVEN 3 (Belgium).

It has been hypothesized that exercise-related hypo-estrogenemia occurs as a consequence of increased competition of catecholestrogens (CE) for catechol-O-methyltransferase (COMT). This may result in higher norepinephrine (NE) concentrations, which could interfere with normal gonadotropin pulsatility. The present study investigates the effects of training on CE responses to acute exercise stress.

Nine untrained eumenorrheic women (mean percentage of body fat ±SD: 24.8 ± 3.1%) volunteered for an intensive 5-day training program. Resting, submaximal, and maximal (tmax) exercise plasma CE, estrogen, and catecholamine responses were determined pre- and post training in both the follicular (FPh) and luteal phase (LPh).

Acute exercise stress increased total primary 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 mean (±SE) plasma E, 2-OHE, and 2-MeOE concentrations were significantly lower (P < 0.05) at each exercise intensity (for 2-OHE: 332 ± 47 vs. 422 ± 57 pg/mL at tmax; for 2-MeOE: 317 ± 26 vs. 354 ± 34 pg/mL at tmax). Training produced opposite effects on 2-OHE:E ratios (an estimation of CE formation) during acute exercise in the FPh (reduction) and LPh (increase). The 2-MeOE:2-OHE ratio (an estimation of CE activity) showed significantly higher values at tmax in both menstrual phases after training (FPh: +11%; LPh: +23%; P < 0.05). After training, NE values were significantly higher (P < 0.05).

The major findings of this study were that: training lowers absolute concentrations of plasma estrogens and CE; the acute exercise challenge altered plasma estrogens but had little effect on CE; estimation of the formation and activity of CE suggests that formation and O-methylation of CE proportionately increases. These findings may be of importance for NE-mediated effects on gonadotropin release.




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Copyright © 1997 by The Endocrine Society