The purpose of this study was to determine if improved supramaximal exercise performance in trained cyclists following caffeine ingestion was associated with enhanced O(2) uptake (VO2 kinetics), increased anaerobic energy provision (accumulated O(2)-AO(2)-deficit), or a reduction in the accumulation of metabolites (for example, K(+)) associated with muscular fatigue. Six highly trained male cyclists (VO2peak 68 +/- 8 mL kg(-1) min(-1)) performed supramaximal (120% VO2peak) exercise bouts to exhaustion on an electronically braked cycle ergometer, following double-blind and randomized ingestion of caffeine/placebo (5 mg kg(-1)). Time to exhaustion (TE), VO2 kinetics, AO(2) deficit, blood lactate (La(-)), plasma potassium (K(+)), caffeine and paraxanthine concentrations were measured. Caffeine ingestion elicited significant increases in TE (14.8%, p < 0.01) and AO(2) deficit (6.5%, p < 0.05). In contrast, no changes were observed in AO(2) deficit at isotime, VO2 kinetics, blood [La(-)] at exhaustion or peak [K(+)] following caffeine ingestion. However, [K(+)] was significantly reduced (13.4%, p < 0.01) during warm-up cycling immediately prior to the onset of the supramaximal bout for the caffeine trials, compared with placebo. It appears that caffeine ingestion is beneficial to supramaximal cycling performance in highly trained men. The reduced plasma [K(+)] during submaximal warm-up cycling may prolong the time taken to reach critical [K(+)] at exhaustion, thus delaying fatigue. Considering caffeine ingestion did not change VO2 kinetics or isotime AO(2) deficit, increases in absolute AO(2) deficit may be a consequence of prolonged TE, rather than causal.