Power-Boosting Protein in Muscle Declines With Age

That's why even fit older people may need to work harder to stay slim, study says

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TUESDAY, Feb. 6, 2007 (HealthDay News) -- An age-related decline in a power-boosting signal in muscle may be the reason why older people have to exercise harder than younger people in order to get the same benefits, suggests a U.S. study.

Reporting in the February issue of the journal Cell Metabolism, researchers found that AMP-activated protein kinase (AMPK) worked more slowly in the skeletal muscle of 2-year-old rats than in 3-month-old rats.

In skeletal muscle, AMPK stimulates the oxidation of fatty acids and the production of power-producing mitochondria that burn fat and fuel cells, the researchers said.

"The message of this paper is that, with aging, the AMPK pathway has reduced activity. So, one probably has to work harder to maintain the same level of fat oxidation and mitochondrial biogenesis (production) in muscle," Gerald I. Shulman, a Howard Hughes Medical Institute investigator at Yale University School of Medicine, said in a prepared statement.

He noted that earlier studies showed that even lean and healthy people in their 70s have a higher incidence of fat buildup in their muscles and a deficiency in mitochondria function than 20-year-olds.

Age-related reduction in AMPK activity may also be linked to increased rates of insulin resistance and type 2 diabetes in older people, Shulman said.

"In regards to insulin resistance and type 2 diabetes, having more AMPK activity in our skeletal muscle is probably a good thing, because AMPK activation stimulates glucose uptake, increases fat oxidation, and promotes mitochondrial biogenesis," he said.

More information

The U.S. National Library of Medicine explains age-related changes in bones, muscles and joints.

SOURCE: Cell Press, news release, Feb. 6, 2007


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