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Am J Physiol Regul Integr Comp Physiol (May 14, 2008). doi:10.1152/ajpregu.00880.2007
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Submitted on December 10, 2007
Accepted on May 9, 2008

Tea catechin ingestion combined with habitual exercise suppresses the aging-associated decline in physical performance in senescence-accelerated mice

Takatoshi Murase1*, Satoshi Haramizu1, Noriyasu Ota1, and Tadashi Hase1

1 Biological Science Laboratories, Kao Corporation, Haga-gun, Tochigi, Japan

* To whom correspondence should be addressed. E-mail: murase.takatoshi{at}kao.co.jp.

Catechins, which are abundant in green tea, possess a variety of biologic actions, and their clinical application has been extensively investigated. In this study, we examined the effects of tea catechins and regular exercise on the aging-associated decline in physical performance in senescence-accelerated prone mice (SAMP1) and age-matched senescence-accelerated resistant mice (SAMR1). The endurance capacity of SAMR1 mice, measured as the running time to exhaustion, tended to increase over the 8-week experimental period, whereas that of SAMP1 mice decreased by 17%. On the other hand, the endurance capacity of SAMP1 mice fed 0.35% (w/w) catechins remained at the initial level and was significantly higher than that of SAMP1 mice not fed catechins. In SAMP1 mice fed catechins and given exercise, oxygen consumption was significantly increased, and there was an increase in skeletal muscle fatty acid {beta}-oxidation. The mRNA levels of mitochondria-related molecules, such as peroxisome proliferator-activated receptor-{gamma} coactivator-1, cytochrome c oxidase-II, III, and IV in skeletal muscle were also higher in SAMP1 mice given both catechins and exercise. Moreover, oxidative stress measured as thiobarbituric reactive substances was lower in SAMP1 groups fed catechins than in the SAMP1 control group. These results suggest that long-term intake of catechins, together with habitual exercise, is beneficial for suppressing the aging-related decline in physical performance and energy metabolism, and that these effects are due, at least in part, to improved mitochondrial function in skeletal muscle.







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