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Articles in PresS, published online ahead of print July 18, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.01051.2001
Submitted on December 5, 2001
Accepted on July 1, 2002
level in the heart is improved by exercise training
1 Department of Internal Medicine, Institute of Clinical Medicine, Tsukuba, Ibaraki, Japan
2 Institute of Health and Sport Sciences, Tsukuba, Ibaraki, Japan
* To whom correspondence should be addressed. E-mail: t-miyauc{at}md.tsukuba.ac.jp.
Exercise training improves aging-induced decrease of fatty acid (FA) metabolic capacity in the heart. However, the mechanisms for improving FA metabolic capacity in the heart by exercise training are unclear. Peroxisome proliferator-activated receptor (PPAR)-, a transcriptional activator, regulates many genes of FA metabolic enzymes. We hypothesized that PPAR- contributes to exercise training-induced improvement of FA metabolic capacity in the aged heart. To investigate whether PPAR- and its target genes in the aged heart are affected by exercise training, we used hearts of sedentary young rat (Sedentary-young group; 4 months old), sedentary aged rat (Sedentary-aged group; 23 months old), and swim-trained aged rat (Trained-aged group; 23 months old, swimming training for 8 weeks). The mRNA and protein expression of PPAR- in the heart was significantly lower in the Sedentary-aged group compared with the Sedentary-young group, and was significantly higher in the Trained-aged group compared with the Sedentary-aged group. The activity of PPAR- DNA binding to the transcriptional regulating region on the FA metabolic enzyme genes in heart and the mRNA expression of 3-hydroxyacyl CoA dehydrogenase (HAD) and carnitine palmitoyl transferase-I, which are PPAR- target genes, in heart was significantly lower in the Sedentary-aged group compared with the Sedentary-young group, and was significantly higher in the Trained-aged group compared with the Sedentary-aged group. Furthermore, the enzyme activity of HAD in heart was significantly lower in the Sedentary-aged group compared with the Sedentary-young group, and was significantly higher in the Trained-aged group compared with the Sedentary-aged group. These findings suggest that exercise training improves aging-induced decreases in myocardial PPAR- mRNA and protein expressions, PPAR- DNA binding activity, and its target gene expression in the heart. Consequently myocardial FA metabolic enzyme activity was improved in the Trained-aged hearts. Therefore, it is considered that the regulatory system of myocardial PPAR- participates in a mechanism of adaptations of FA metabolic capacity in the heart for aging and subsequent exercise training.
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