From the BBC: researcher "compared the skeletal muscle of three-month-old rats and two-year-olds. They found that a process called AMP-activated protein kinase (AMPK) slowed down in the older animals. AMPK's role in skeletal muscle is to stimulate the body to burn off fat and to fuel cells, via the production of mitochondria - cells' power sources. ... a person would have to work harder when trying to maintain the same benefits from exercise as they did when they were young. AMPK activity in our skeletal muscle is probably a good thing because it activation stimulates glucose uptake, increases fat oxidation [fat burning], and promotes mitochondrial biogenesis [production]." As Randall Parker points out, this looks a lot like an evolutionary adaptation to minimize damage caused by increasing numbers of cells taken over by age-damaged mitochondria - which has the effect instead of making insulin resistance, type 2 diabetes and age-related muscle loss (sarcopenia) the order of the day. Expect to hear more on this in the next few years as scientists determine where AMPK fits within the hierarchy of cause and effect in aging.