Traumatic brain injury initiates a cascade of events including increased oxidative stress that contributes to the period of generalized metabolic depression. Previously, sodium and ethyl pyruvate and glucose supplementation were shown to reduce cell death and improve recovery following experimental TBI. In this study we used 13C NMR spectroscopy to determine if sodium pyruvate, ethyl pyruvate or glucose supplementation influences the activity of metabolic pathways associated with the intracellular redox state and oxidative metabolism. Our findings show improvements in astrocyte anaplerotic metabolism following all fuel treatments. Only animals treated with sodium pyruvate showed improved oxidative metabolism in neurons. None of the fuel treatments reduced the amount of glucose metabolized via the pentose phosphate pathway. The restoration of astrocyte metabolism by these fuels may partially underlie their abilities to improve cerebral glucose utilization and to reduce neuronal loss following experimental TBI.