Endurance and resistance training are known to improve insulin sensitivity in healthy, sedentary and insulin resistant individuals. A single bout of endurance exercise has been suggested to improve insulin sensitivity for up to 48 hours (Perseghin et al. 1996). There is evidence to show that increased glucose uptake and glycogen synthase activity may be directly related to decreases in muscle glycogen post-exercise (Nielsen et al. 2001). On the other hand, very little is known about the acute effects of resistance exercise in humans. The aim of this study therefore was to investigate the blood glucose response to a 75 g oral glucose tolerance test (OGTT) 6 h after a high intensity bout of either resistance (RE) or endurance exercise (EE). In an attempt to replete muscle glycogen stores and thus pinpoint potential effects to the insulin signalling cascade, a carbohydrate/protein beverage was consumed within the first h post-exercise 18 subjects were investigated both after exercise and in a control trial without exercise. 9 subjects (Age = 21 ± 1 years, BMI = 22.8 ± 0.6 kg/m², ♂/♀ = 6/3) completed 1 h of EE (cycle ergometry at 75% Wmax) and 9 (Age = 23 ± 0 years, BMI = 23.9 ± 0.3 kg/m², ♂/♀ = 6/3) completed a RE bout (3 sets of 10 repetitions to failure) covering all major muscle groups. All subjects ingested 1.5 L of a carbohydrate (200g) protein beverage (50g) both within 1 h after exercise and in the control trial. An OGTT was performed 6 h post-exercise. Only water was consumed in the period between ingestion of the beverage and the start of the OGTT. Blood glucose concentrations following the OGTT shown by area under the curve decreased 16% in the RE group (822 ± 68 v. 694 ± 23 mmol l^-1 120 min) but were unchanged in the EE group (784 ± 40 v. 834 ± 59 mmol l^-1 120 min) (P < 0.05). Blood insulin concentrations remained unchanged in both the RE and EE groups (4978.74 ± 706.46 v. 4458.07 ± 597.79 μU ml^-1 120 min and 4117.61 ± 590.28 v. 3918.04 ± 351.65 μU ml^-1 120 min respectively) (P > 0.05). The results suggest that improved insulin sensitivity following a single bout of RE or EE occurs through different mechanisms. It is probable that the improvement of EE reported in previous studies is dependent on the depletion of glycogen stores and, therefore, is not seen in this study. On the other hand the results show that the lowered blood glucose response following RE is still present after re-feeding with carbohydrate and protein immediately post-exercise. Therefore, in line with recent animal studies (Hernandez et al. 2000), these results suggest that the reduction in blood glucose following RE may involve other mechanisms such as increased activation of the insulin signalling cascade.