Literature examining the effects of aerobic exercise training on excess postexercise oxygen consumption (EPOC) is sparse. In this study, 9 male participants (19-32 yr) trained (EX) for 12 wk, and 10 in a control group (CON) maintained normal activity. VO(2max), rectal temperature (T(re)), epinephrine, norepinephrine, free fatty acids (FFA), insulin, glucose, blood lactate (BLA), and EPOC were measured before (PRE) and after (POST) the intervention. EPOC at PRE was measured for 120 min after 30 min of treadmill running at 70% VO(2max). EX completed 2 EPOC trials at POST, i.e., at the same absolute (ABS) and relative (REL) intensity; 1 EPOC test for CON served as both the ABS and REL trial because no significant change in VO(2max) was noted. During the ABS trial, total EPOC decreased significantly (p < .01) from PRE (39.4 ± 3.6 kcal) to POST (31.7 ± 2.2 kcal). T(re), epinephrine, insulin, glucose, and BLA at end-exercise or during recovery were significantly lower and FFA significantly higher after training. Training did not significantly affect EPOC during the REL trial; however, epinephrine was significantly lower, and norepinephrine and FFA, significantly higher, at endexercise after training. Results indicate that EPOC varies as a function of relative rather than absolute metabolic stress and that training improves the efficiency of metabolic regulation during recovery from exercise. Mechanisms for the decreased magnitude of EPOC in the ABS trial include decreases in BLA, T(re), and perhaps epinephrine-mediated hepatic glucose production and insulin-mediated glucose uptake.