University of Calgary researchers say good old-fashioned calorie counting is the way to go when it comes to maintaining youthful muscles as we grow old.

In a study using rats the team found that elderly rats on a calorie-restricted diet had the muscle mass and function of much younger rats.

Russ Hepple, a physiologist at the University of Calgary's Kinesiology department, says the old rats had the muscles of a 20-year-old rat.

The rats were specially bred at the U.S. -based National Institute of Aging and from a very young age were fed a diet rich in nutrition but which was 40 per cent lighter in calories than normal.

Rats fed a normal diet lost 50 per cent of their muscle mass and 50 per cent of their muscle function at old age.

This study is the second by Hepple and his team which is examining the effects of calorie restricted diets.

The study found that elderly rodents on the strict diet experienced only a 20 per cent drop in muscle mass and no loss of muscle function.

The researchers say it has been known for some time that a calorie restricted diet extends life span by as much as 35 per cent, but they have now found that it also maintains muscle function.

Apparently the diet appears to help the aging rats rebuild and replace muscle and Hepple says it is unclear why.

He suggests restricted-calorie diets preserve the function of mitochondria which provide the body's cells with energy as the animals grow old.

Despite evidence that reducing calories had a profound impact on rat muscles, Hepple is not suggesting that people follow suit and cut their food intake by 40 per cent.

His advice is instead that humans eat a healthy diet, refrain from overindulging and remain active to maintain their muscles.

A similar diet for humans would be drastic and possibly destructive to muscle, especially if the calories came from protein.

Hepple and his research team now plan to carry out further studies with antioxidants, exercise and gene therapy to see if factors other than fewer calories can lead to younger muscles in old age.

The study is published in the Journal of Gerontology: Biological Sciences.

Specifically, Woo's team investigated myocardial regeneration by initiating heart cell division and replication. They did this by expressing the cell-cycle regulator, a protein called cyclin A2. It is unique in its control at two major transitions of the cell cycle and is the only cyclin that is completely silenced after birth in mice, rats and humans. This approach -- using cyclin A2 expression via gene transfer -- yielded improved myocardial function.

"Penn is the first to do this kind of research with damaged heart tissue, by ramping up the body's native reparative system," states Woo. "We are examining the potential role of this regenerative strategy as a future therapy for heart failure. Someday, this could lead to less surgery and perhaps even less medicine in treating heart disease." Woo cautions that this research work has not yet been done on humans and that we may still be years away from that accomplishment.

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