The researchers found that so-called AMP-activated protein kinase (AMPK) slows down in the skeletal muscle of 2-year-old rats relative to 3-month-old rats. A chief regulator of whole-body energy balance, AMPK in skeletal muscle stimulates the oxidation of fatty acids and the production, or biogenesis, of power-producing mitochondria that burn fat and fuel cells, according to the researchers.
The new findings might help to explain "what happens as we age," said Gerald I. Shulman, a Howard Hughes Medical Institute investigator at Yale University School of Medicine.
Earlier studies have shown that, in comparison to 20-year-old adults, even lean and healthy people in their seventies show a higher incidence of fat buildup in their muscle and livers and a deficiency in mitochondrial function, Shulman explained. These metabolic shifts have been implicated in the increased prevalence of insulin resistance and type 2 diabetes that occurs with aging.
"The message of this paper is that, with aging, the AMPK pathway has reduced activity," Shulman said. "So, one probably has to work harder to maintain the same level of fat oxidation and mitochondrial biogenesis in muscle."
The number of mitochondria within muscle largely determines its metabolic capacity. The mitochondrial composition of fibers in different muscles corresponds to the jobs that they do, and muscle can be "reprogrammed" through exercise.
For example, Shulman said, the skeletal muscles of marathon runners typically have much greater mitochondrial content and a greater capacity to burn fat. Those properties can most likely be attribu