Glycolysis and the significance of lactate in traumatic brain injury.
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanisms, cerebral microdialysis studies, and preliminary clinical reports
PubMed 25904838 · doi:10.3389/fnins.2015.00112
What was done
Narrative review evaluating the role of glycolysis, brain extracellular lactate elevation, and the lactate/pyruvate ratio in traumatic brain injury (TBI). The authors synthesize evidence regarding the astrocyte-neuron lactate shuttle hypothesis, 13C-labeled microdialysis tracer studies assessing tricarboxylic acid cycle utilization, and preliminary trials of intravenous exogenous lactate supplementation.
What was found
The abstract reports no numerical findings, effect sizes, or sample statistics. It summarizes that high extracellular lactate is statistically associated with poor clinical outcomes, but 13C microdialysis demonstrates that neurons can metabolize lactate into glutamine via the tricarboxylic acid cycle. High extracellular lactate may therefore signify neuronal inability to consume astrocyte-derived lactate (metabolic uncoupling). Intravenous exogenous lactate supplementation showed beneficial effects on surrogate endpoints.
Why it matters
Reframes post-TBI lactate from a toxic waste byproduct of hypoxia into an active oxidative substrate, providing a mechanistic rationale for exploring exogenous lactate therapy in neurocritical care.
Limits
As a narrative review, it provides no original clinical data or systematic quantitative synthesis. Therapeutic evidence is limited to surrogate endpoints without proven effects on long-term neurological recovery or survival.
Cited by
- contradicts Following traumatic brain injury, cerebral glycolysis is impaired, leaving neurons starving for preferred lactate fuel.