Rats selectively bred for high capacity running (HCR) or low capacity running (LCR) display divergence for intrinsic aerobic capacity and hepatic mitochondrial oxidative capacity, both factors associated with susceptibility for nonalcoholic fatty liver disease (NAFLD). Here we tested if HCR and LCR rats display differences in susceptibility for hepatic steatosis following 16 weeks of high fat diets (HFD) with either 45% or 60% of kcals from fat. The HCR were protected against HFD-induced hepatic steatosis while only the 60%HFD induced steatosis in LCR as marked by a doubling of liver triglycerides. Hepatic complete fatty acid oxidation (FAO) and mitochondrial respiratory capacity were all lower in the LCR compared to HCR. The LCR also displayed lower hepatic complete and incomplete FAO in the presence of etomoxir, suggesting a reduced role for non-carnitine palmitoyltransferase-1 mediated lipid catabolism in LCR vs. HCR. Hepatic complete FAO and mitochondrial respiration were largely unaffected by either chronic HFD; however, 60% HFD feeding markedly reduced 2-pyruvate oxidation, a marker of TCA cycle flux, and mitochondrial complete FAO only in the LCR rats. The LCR displayed lower levels of hepatic long chain acylcarnitines than the HCR but maintained similar levels of hepatic acetyl-carnitine levels, further supporting lower rates of β-oxidation, and TCA cycle flux in the LCR than HCR. Finally, only the LCR displayed early reductions in TCA cycle genes after the acute initiation of a HFD. In conclusion, intrinsically high aerobic capacity confers protection against high fat diet-induced hepatic steatosis through elevated hepatic mitochondrial oxidative capacity.