Rats artificially selected as low capacity runners (LCR) exhibit features of the metabolic syndrome, and blunted exercise training-induced cardiac hypertrophy compared with high capacity runners (HCR). We tested the hypothesis that the divergent cardiac phenotypes may be due to diminished activation of signaling proteins in LCR vs HCR rats. LCR (n=18) and HCR (n=18) rats were randomly assigned to acute exercise or control groups. Ten minutes after a 10-min bout of high intensity treadmill exercise, rats were euthanized, and left ventricles (LV) were harvested. LV homogenates were immunoblotted for phosphorylated and total levels of extracellular regulated kinase (ERK1/2), c-Jun N-terminal kinase (JNK), p38, Akt, S6, and the ribosomal S6 protein kinases S6K and p90RSK. Alterations in protein ubiquitination were examined as an index of protein turnover. In LCR and HCR rats, S6 was activated to a similar extent after exercise (5-fold vs control), as were JNK1/2, p38, and ERK1/2 (each 1.5-fold). Exercise significantly reduced ubiquitination of some proteins, suggesting diminished post-exercise protein degradation. That no significant LCR/HCR differences were observed 10-min post-exercise in the signaling pathways studied herein suggests that the source of the differing cardiac phenotypes in LCR/HCR rats may involve differing activation times and/or other signaling pathways.