These studies determined the role of carbohydrate deficit from acute exercise on postprandial triglyceride elevation (PPTG). In Study 1, when energy expenditure was held constant in the exercise trials, both acute moderate (~50% VO₂ peak; MIE) and high intensity endurance exercise (90% VO₂ peak intervals; HIE) were effective to lower PPTG compared to a non-exercise control [CON; 54.9 (13.5) % and 75.2 (15.5) %, respectively, relative to CON, p<0.05], with HIE significantly lower than MIE (p=0.03). Total postprandial fat oxidation was increased in both MIE [83.3 (10.6) %] and HIE [89.1 (9.8) %] compared to CON [69.0 (16.1) %, p<0.05), with HIE significantly greater then MIE (p=0.012). These effects occurred in the absence of any change in glucose tolerance. In Study 2, when an isoenergetic meal was provided immediately after an acute exercise session (80 min; 60 min at ~65% VO₂peak and 10, 2 min intervals) consisting of either low carbohydrate (EX+LCHO) or high carbohydrate content (EX+HCHO), PPTG was siginificantly higher in EX+HCHO compared to EX+LCHO [449 (118) mg/dL/4h and 325 (63) mg/dL/4h, respectively, p=0.03], despite similar energy balance. Furthermore, postprandial fat oxidation was higher in EX+LCHO compared to EX+HCHO [256.7 (57.6) kcal/4h and 209.4 (56) kcal/4h, respectively, p=0.002]. PPTG was significantly related to fat oxidation (r=-0.61), fasting plasma [beta]-hydroxybutyrate (r=-0.62) and carbohydrate deficit (r=0.51), but not energy deficit (r=0.25). In summary, these data suggest that post-exercise carbohydrate balance from both increasing carbohydrate oxidation during exercise (i.e., exercise intensity) or by reducing post-exercise carbohydrate intake, is an important determinant of PPTG-lowering effects of exercise and that this may result from changes in fat oxidation. / text