Differences in the cardiac proteome in rats selected for either low or high running capacity

Abstract

Selection on running capacity has created rat phenotypes of high capacity runners (HCR) that have enhanced cardiac function and low capacity runners (LCR) that exhibit features of metabolic syndrome. Proteins that regress with differences in running capacity may be mechanistically responsible for this divergence in disease risk. Hearts of 6 HCR and 6 LCR from generation 23 were analysed using difference in‐gel electrophoresis (DIGE) and protein spots were identified from database searches of tryptic peptide mass fingerprints and fragment ion mass spectra. The running capacity of HCR was 4‐fold greater than LCR. DIGE resolved 957 gel spots and proteins were identified unambiguously in 369 spots. Protein expression profiling detected 68 statistically significant (P<0.05; false discovery rate <10 %, calculated using q‐values) differences between HCR and LCR hearts. In HCR, there was robust up‐regulation of each enzyme of the beta‐oxidation pathway, whereas, LCR hearts were characterised by the modulation of enzymes associated with ketone body or amino acid metabolism. LCR also exhibited enhanced expression of antioxidant enzymes such as catalase and greater phosphorylation of alpha B‐crystallin at serine 59. Our data show that selection on running capacity is associated with changes in cardiac metabolism and oxidative stress pathways.