Following traumatic brain injury, cerebral glycolysis is impaired, leaving neurons starving for preferred lactate fuel.
"Now to answer your question about why is the injured brain suffering, for some reason the breakdown of sugar, or glycolysis, in the brain is impaired after injury. Now the product of that is lactate, and neurons run on lactate as the preferred fuel. So in part, the brain is starving." (said at 0:29:41)
The claim misstates the primary metabolic impairment that occurs following traumatic brain injury (TBI). Following TBI, cerebral glycolysis is typically accelerated (a phenomenon known as acute hyperglycolysis) rather than impaired. Lactate is the end product of glycolysis; its elevation in TBI results from increased glycolytic flux combined with downstream mitochondrial dysfunction (impaired oxidative phosphorylation in the TCA cycle) or hypoxia, which prevents efficient mitochondrial oxidation of pyruvate and lactate. If glycolysis were impaired, lactate production would be reduced rather than increased. Under the astrocyte-neuron lactate shuttle model, astrocytic glycolysis produces lactate that neurons can utilize as an energy substrate, but the brain's energetic deficit after TBI stems from mitochondrial dysfunction and metabolic uncoupling rather than an inability to break down glucose via glycolysis.
- contradicts: Glycolysis and the significance of lactate in traumatic brain injury. (Frontiers in neuroscience 2015)
"In TBI, glycolytic lactate is ascribed to hypoxia or mitochondrial dysfunction, although the precise nature of the latter is incompletely understood." (abstract, passage verified)
pubmedfull study (doi) - context: Cerebral Lactate Metabolism After Traumatic Brain Injury. (Current neurology and neuroscience reports 2016)
"Glutamate-induced activation of glycolysis stimulates lactate production from glucose in astrocytes, with subsequent lactate transfer to neurons (astrocyte-neuron lactate shuttle)." (abstract, passage verified)
pubmedfull study (doi)