CATECHOLAMINE RESPONSES TO ACUTE AND CHRONIC EXERCISE ACCORDING TO MENSTRUAL STATUSDear Editor-in-Chief:Sympathoadrenal activity increases proportionately with the intensity of the exercise and is closely associated with oxygen availability (2,5). In their recent study, Schaal et al. (8) observed reduced plasma norepinephrine (NE) responses to an acute exercise in amenorrheic women when compared to foUicular-phase eumenorrheie women. The authors opine that their findings lend support to the hypothesis that amenorrheic women may experience hypoglycemia-associated autonomie failure-induced suppression of catecholamine (CA) responses to acute exercise. This view deserves further scrutiny especially in the light of the results reported by previous studies.For example, from two extensive studies (2,3) on CA metabolism and exercise-related menstrual irregularities (ERMI), we learn that:1. Acute exercise responses of both NE and epinephrine (EPI) are cycle-and menstrual status-dependent. 2. Menstrual cycle-dependent differences in resting plasma CA disappear with increased training and loss of cycle regularity, while baseline levels of NE significantly increase. 3. Exhaustive training and loss of cycle regularity increase (rather than decrease) plasma NE (and, to some, extent dopamine) at V02max but do not affect EPI responses.Those findings are consistent with the hypothesis that periodic marked elevations in NE levels during maximal exercise may interfere with pulsatile luteinizing hormone release (1) and thus lead to ERMI, although they raise questions about hypoglycemia-associated autonomie failure as a suitable explanation for ERMI. We also note that, in the study by Schaal et al. (8), neither the amenorrheic subjects' HR nor arterial blood pressure at maximal exercise was lower despite their apparent reduced plasma CA responses.In an estrogen-poor environment such as the follicular phase, catechol-0-methyltransferase activity is approximately 20% reduced, whereas it tends to acutely increase with acidosis and in response to chronic exercise (4). ERMI (irrespective of energy balance issues) or loss of fat mass will cause a shift in estrogen metabolism from loa-to C-2 hydroxylase oxidation (3). C-2-substituted estrogens, with their hybrid estrogen/CA structure, exhibit a higher affinity for catechol-0-methyltransferase than CA (3,4) does, the net result potentially being an important decrease in the metabolic clearance rate of CA, which, too, is hard to reconcile with the conclusions by Schaal et al.Brain cortisol may play a role in eating disorders because it interacts with tryptophan and serotonin metabolism. However, the ERMI cortisol data by Schaal et al. show no significant differences. Cortisol levels in ERMI often may represent mere artifacts that would be neutralized by simple correction for caffeine intake or plasma volume (6). Reduced CA responses, hypothetically speaking, could be the result of a simultaneous decrease in CA blood production rate and a much higher increase in metabolic clearance rate. Su...