Ventilated, chloralose anesthetized cats were subjected to 3.2 atmosphere fluid percussion injury and compared with sham operated controls. In both groups, global cerebral blood flow (CBF), cerebral metabolic rate of oxygen utilization (CMRO₂), cerebral metabolic rate of glucose utilization (CMRGI), and ³¹P magnetic resonance spectroscopy (MRS) determinations of tissue pH (pH_i) phosphocreatine (PCr), and inorganic phosphate (Pi) were measured before and 5, 15, 30, and 60 min post-trauma. Following trauma, pH decreased slightly 30 min following trauma and gradually returned to normal. CMRO₂, CBF, and arterial pO₂ remained at control values throughout the experiment while CMRGI increased 243% at 5 min post-injury then rapidly returned to control values. This combination of acidosis and increased glucose utilization indicates that trauma causes a transient isolated increase in cerebral glycolysis and may be important to consider when investigating the etiology of post traumatic acidosis.