Mitochondrial bioenergetics from ipsilateral cortex following mild brain contusion and subsequent pioglitazone administration. Mice received either sham surgery or CCI followed by pioglitazone (20 mg/kg/day) initiated at either 0.25, 3, 12, or 24 h post-injury. An osmotic pump was inserted to ensure delivery of 20 mg/kg/day; mitochondria were then isolated from the ipsilateral cortex at 48 h post-injury, and bioenergetics were assayed using the Seahorse technology. There were no significant changes in State III_CI or State IV mitochondrial bioenergetics between groups in any subpopulation. However, there was a significant increase in State V_CI respiration in vehicle sham and 0.25 h pioglitazone (Pio) CCI groups compared to vehicle CCI in total mitochondria. One-way ANOVA, compared to vehicle CCI, Dunnett’s post hoc. *P < 0.037. F_5,26 = 3.525. State V Complex I-mediated maximal mitochondrial respiration was unaltered in glia-enriched mitochondria. In synaptic mitochondria, there was a significant increase in State V_CI respiration in vehicle sham and 0.25 h Pio CCI groups compared to vehicle CCI. One-way ANOVA, compared to vehicle CCI, Dunnett’s post hoc. *P < 0.049. F_5,26 = 4.14. There was a significant increase in State V_CII respiration in vehicle sham and 0.25 h Pio CCI groups compared to vehicle CCI in total mitochondria. One-way ANOVA, compared to vehicle CCI, Dunnett’s post hoc. *P < 0.022. F_5,26 = 3.15. State V Complex II-mediated maximal mitochondrial respiration was unaltered in glia-enriched mitochondria. In synaptic mitochondria, there was a significant increase in State V_CII respiration in vehicle sham and 0.25 h Pio CCI groups compared to vehicle CCI. One-way ANOVA, compared to vehicle CCI, Dunnett’s post hoc. *P < 0.029. F_5,26 = 3.48. Per cent OCR values represented as mean ± SEM with individual data points, N = 4–8/group. Data presented as percentage of sham.