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Controversy exists as to whether the metabolic activity of the brain as a whole increases during physical exercise. For example, there appears to be no change in brain O2 uptake during cycling (Zobl et al. 1965; Madsen et al. 1993), whereas during vigorous exercise on the treadmill an increase in brain O2 uptake and a tendency for glucose uptake to increase has been reported (Scheinberg et al. 1954). In the case of mental stress, there is no appreciable change in brain O2 uptake but there is an increase in cerebral glucose uptake (Madsen et al. 1995a). Thus, the rate of glucose uptake is enhanced compared to that of O2. Interestingly, the ‘uncoupling’ between the O2 and glucose uptake rates is sustained even after the cessation of brain activation (Madsen et al. 1995a,b) and may be associated with a decrease in the glycogen level in the brain (Madsen et al. 1995a). During maximal exercise, blood lactate increases to as much as 30 mmol l−1 (Nielsen, 1999) and the brain is known to take up lactate (Ahlborg & Wahren, 1972). Lactate transport across mammalian plasma membranes is mainly carrier mediated (Poole et al. 1993) and a monocarboxylate transporter is found in rat brain endothelium cells (Gerhart et al. 1997). Brain tissue, including neurons (Dringen et al. 1993) and astrocytes (Tildon et al. 1993), possesses the capacity to take up and utilise lactate as an energy source. In fact, lactate rather than glucose may be the primary energy source during neuronal activation (Larrabee, 1996) when lactate is supplied by the glial cells to the neurons (Poitry-Yamate et al. 1995). A positive arterial-jugular venous concentration difference (a–v difference) for lactate has been demonstrated in the dog (Nemoto et al. 1974; Avogaro et al. 1990) and in humans during cardiopulmonary resuscitation (Rivers et al. 1991). Taken together, these reports led us to hypothesise that the metabolic rate for the brain is increased during exercise and also in the recovery phase when lactate, in addition to glucose and O2, is taken into consideration as a metabolic substrate. Therefore, we investigated the a–v differences for glucose, lactate and O2 at rest, during exercise and in the immediate recovery period. Since arterial CO2 tension increases during moderate exercise and decreases during maximal exercise (Jorgensen et al. 1992), we applied an index of the metabolic rate of the brain that would be independent of flow, i.e. we calculated the O2/carbohydrate uptake ratio. In a separate experiment in the rat, we investigated whether an increase in blood lactate per se would influence brain uptake of lactate.