Exercise training improves the aging-induced downregulation of myosin heavy 
chain (MHC) and sarcoplasmic reticulum (SR) Ca(2+)-ATPase, which participate in 
the regulation of cardiac contraction and relaxation. Thyroid hormone receptor 
(TR), a transcriptional activator, affected the regulation of gene expression of 
MHC and SR Ca(2+)-ATPase. We hypothesized that myocardial TR signaling 
contributes to a molecular mechanism of exercise training-induced improvement of 
MHC and SR Ca(2+)-ATPase genes with cardiac function in old age. We investigated 
whether TR signaling and gene expression of MHC and SR Ca(2+)-ATPase in the aged 
heart are affected by exercise training, using the hearts of sedentary young 
rats (4 mo old), sedentary aged rats (23 mo old), and trained aged rats (23 mo 
old, swimming training for 8 wk). Trained aged rats showed improvement in 
cardiac function. Expression of TR-alpha1 and TR-beta1 proteins in the heart 
were significantly lower in sedentary aged rats than in sedentary young rats and 
were significantly higher in trained aged rats than in sedentary aged rats. The 
activity of TR DNA binding to the transcriptional regulatory region in the 
alpha-MHC and SR Ca(2+)-ATPase genes and the mRNA and protein expression of 
alpha-MHC and SR Ca(2+)-ATPase in the heart and plasma 3,3'-triiodothyronine and 
thyroxine levels were altered in association with changes in the myocardial TR 
protein levels. These findings suggest that exercise training improves the 
aging-induced downregulation of myocardial TR signaling-mediated transcription 
of MHC and SR Ca(2+)-ATPase genes, thereby contributing to the improvement of 
cardiac function in trained aged hearts.