Cerebral oxygen/glucose ratio is low during sensory stimulation and rises above normal during recovery: Excess glucose consumption during stimulationis not accounted for by lactate efflux from or accumulation in brain tissue

Functional activation stimulates CMRglc more than CMRO2 and raises lactate levels in brain. This has been interpreted as evidence that brain work is s upported mainly by energy derived from anaerobic glycolysis, To determine i f lactate production accounts for the "excess" glucose consumption, cerebra l arteriovenous differences were measured in conscious rats before, during, and 15 minutes after sensory stimulation; the brains were rapidly frozen i n situ immediately after completion of blood sampling and assayed for metab olite levels. The molar O-2/glucose uptake ratio fell from 6.1 +/- 1.1 (mea n +/- SD) before stimulation to 5.0 +/- 1.1 during activation (P < 0.01); l actate efflux from brain to blood was detectable at rest but not during sti mulation. By 15 minutes after activation, O-2 and lactate arteriovenous dif ferences normalized, whereas that for glucose fell, causing the O-2/glucose ratio to rise above preactivation levels to 7.7 +/- 2.6 (P < 0.01). Brain glucose levels remained stable through all stages of activity. Brain lactat e levels nearly doubled during stimulation but normalized within 15 minutes of recovery. Brain glycogen content fell during activation and declined fu rther during recovery. These results indicate that brain glucose metabolism is not in a steady state during and shortly after activation. Furthermore, efflux from and increased content of lactate in the brain tissue accounted for less than 54% of the "excess" glucose used during stimulation, indicat ing that a shift to anaerobic glycolysis does not fully explain the disprop ortionately greater increases in CMRglc above that of CMRO2 in functionally activated brain. These results also suggest that the apparent dissociation between glucose utilization and O-2 consumption during functional activati on reflects only a temporal displacement; during activation, glycolysis inc reases more than oxidative metabolism, leading to accumulation of products in intermediary metabolic pools that are subsequently consumed and oxidized during recovery.