'Lymphocyte subsets, their responsiveness to mitogen and their capacity for glutamine oxidation and glycolysis were assessed in seven subjects before and after an acute bout of interval exercise, the purpose being to establish whether exercise is associated with alterations in lymphocyte metabolic capacities. The subjects exercised at 112 % of their maximal work capacity (as determined by pre-test) on a treadmill and performed 25 repeat tests, each of 1 min duration interrupted by 2 min rest periods. Venous blood samples were taken at rest and 3 min following completion of exercise. Acute exercise was associated with significant decreases in the percentage of T- (p <0.01) and B-cells (p <0.01) and an increase in the percentage of NK-cells (p <0.05). These changes were accompanied by a significant decrease in the responsiveness of peripheral blood lymphocytes to the mitogen concanavalin A (p <0.05). Acute exercise was also associated with profound changes in the metabolic capacities of peripheral blood lymphocytes: rates of (CO2)-C-14 production from [U-C-14]glutamine (19%: p <0.05) and lactate (27 %: p <0.05) production were increased significantly in response to interval exercise. Linear regression analysis revealed significant correlation between the exercise-mediated changes (%) in T- and NK-cells and changes (%) in both lymphocyte responsiveness to cancanavalin A and metabolic capacity, particularly glutamine oxidation to CO2. One interpretation of these data is that acute exercise promotes a redistribution in lymphocyte subsets, and that it is this redistribution that is the basis of both the impairment in lymphocyte responsiveness to mitogens and the increase in lymphocyte metabolic capacity, especially glutamine oxidation. This putative mechanism presumes that those cells that increase in proportion in response to acute exercise, particularly the non-proliferating NK-cells, have higher metabolic capacities, especially for glutamine oxidation, than those cells that decrease in proportion post-exercise, including both the T-and B-cells. Alternative mechanisms are discussed.