Molecular switches between the troponin T and I isoforms are known to occur in various conditions, but the results from studies of failing human hearts with various etiologies are contradictory and it is not certain whether troponin isoform changes occur. Therefore, the molecular switching of troponin isoforms during normal development and heart failure (HF) after myocardial infarction were investigated in Sprague-Dawley rats at the fetal, neonate, and normal adult stages, and in a postinfarction adult HF group. During normal development, switching from the fetal to the adult pattern of the troponin T and I isoforms was observed. Immunoblotting of postinfarction failing hearts revealed a marked increase in the fetal isoform of cardiac TnT (cTnT) (fetal/adult cTnT isoforms: normal adult = 0.61 +/- 0.09 vs postinfarction HF = 1.59 +/- 0.13, p < 0.001). Also, the amount of the adult troponin I (TnI) isoform decreased significantly in the postinfarction failing heart. In the semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) with glyceraldehyde-3-phosphate-dehydrogenase (GAPDH) as an internal standard, the mRNA of fetal cTnT increased in the postinfarction failing heart (fetal cTnT/GAPDH: control = 0.22 vs HF rat = 0.84, p < 0.05). Therefore, molecular switching of the troponin T and I isoforms occurred during the normal development of the rat, and there was re-expression of the fetal pattern of the isoforms in the postinfarction failing heart of the adult rat.