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To assess the roles of endogenous estrogen (E[SUB2]) and progesterone (P[SUB4]) in regulating exercise carbohydrate use, we used pharmacological suppression and replacement to create three distinct hormonal environments: baseline (B), with E[SUB2] and P[SUB4] low; estrogen only (E), with E[SUB2] high and P[SUB4] low; and estrogen/progesterone (E + P), with E[SUB2] and P[SUB4] high. Blood glucose uptake (R[SUBd]), total carbohydrate oxidation (CHO[SUBox]), and estimated muscle glycogen utilization (EMGU) were assessed during 60 min of submaximal exercise by use of stable isotope dilution and indirect calorimetry in eight eumenorrheic women. Compared with B (1.26 ± 0.04 g/rain) and E + P (1.27 ± 0.04 g/min), CHO[SUBox] was lower with E (1.05 ± 0.02 g/min). Glucose R[SUBd] tended to be lower with E and E + P relative to B. EMGU was 25% lower with E than with B or E + P. Plasma free fatty acids (FFA) were inversely related to EMGU (r[SUP2] = 0.49). The data suggest that estrogen lowers CHO[SUBox] by reducing EMGU and glucose R[SUBd]. Progesterone increases EMGU but not glucose R[SUBd]. The opposing actions of E[SUB2] and P[SUB4] on EMGU may be mediated by their impact on FFA availability or vice versa. [ABSTRACT FROM AUTHOR]