A reduced cerebral metabolic ratio in exercise reflects metabolism and not accumulation of lactate within the human brain.

During maximal exercise lactate taken up by the human brain contributes to reduce the cerebral metabolic ratio, O(2)/(glucose + 1/2 lactate), but it is not known whether the lactate is metabolized or if it accumulates in a distribution volume. In one experiment the cerebral arterio-venous differences (AV) for O(2), glucose (glc) and lactate (lac) were evaluated in nine healthy subjects at rest and during and after exercise to exhaustion. The cerebrospinal fluid (CSF) was drained through a lumbar puncture immediately after exercise, while control values were obtained from six other healthy young subjects. In a second experiment magnetic resonance spectroscopy ((1)H-MRS) was performed after exhaustive exercise to assess lactate levels in the brain (n = 5). Exercise increased the AV(O2) from 3.2 +/- 0.1 at rest to 3.5 +/- 0.2 mM (mean +/-s.e.m.; P < 0.05) and the AV(glc) from 0.6 +/- 0.0 to 0.9 +/- 0.1 mM (P < 0.01). Notably, the AV(lac) increased from 0.0 +/- 0.0 to 1.3 +/- 0.2 mm at the point of exhaustion (P < 0.01). Thus, maximal exercise reduced the cerebral metabolic ratio from 6.0 +/- 0.3 to 2.8 +/- 0.2 (P < 0.05) and it remained low during the early recovery. Despite this, the CSF concentration of lactate postexercise (1.2 +/- 0.1 mM; n= 7) was not different from baseline (1.4 +/- 0.1 mM; n= 6). Also, the (1)H-MRS signal from lactate obtained after exercise was smaller than the estimated detection limit of approximately 1.5 mM. The finding that an increase in lactate could not be detected in the CSF or within the brain rules out accumulation in a distribution volume and indicates that the lactate taken up by the brain is metabolized.