WASHINGTON (Reuters) -- Drugs that mimic the effects of exercise might be possible someday, thanks to the discovery of a genetic switch that controls muscles, researchers said Thursday.

It is not the answer to a couch potato's prayer, but a team at the University of Texas Southwestern Medical Center in Dallas said it might be possible to restore the muscles of people who wasted away due to disease such as heart failure or diabetes.

Writing in the journal Genes and Development, they said they had identified the molecular pathway in rats that controls whether a muscle fiber acts to provide fast strength or endurance.

"You have two types of muscles. There is slow twitch muscle and fast twitch muscle," Rhonda Bassel-Duby, a molecular biologist who worked on the study, said in a telephone interview.

"What we have done is identified a pathway that will induce muscles to become slow."

In other words, they have found how exercise makes muscles strong, on a biochemical level.

"When people go jogging, molecular events happen in the muscles they are exercising that both enhance their capability to exercise further and improve their health," Dr. R. Sanders Williams, who led the study, said in a statement.

He said that pathway can be modified to either stimulate or reverse what exercise does naturally.

"We believe that it is possible to design a drug which would have this effect," Williams said.

Hopes that exercise-gene research will apply to humans

Williams's team identified three proteins, known as calcineurin, NFAT and MEF2 that are part of a pathway that activates genes.

When a muscle is constantly stimulated by exercise such as jogging, calcium ions build up inside the muscle cell.

When this has gone on for a while the protein calcineurin is turned on. This in turn causes NFAT to move into the nucleus of the cell and team up with MEF2 to turn on the genes that will make new muscle cells form fibers that burn energy slowly, giving sustained energy for endurance.

This turns a "fast" muscle -- one designed for strength needed for sprinting or weightlifting -- into the slow-release aerobic muscle type needed for sustained exercise.

The team is now doing tests to see if this pathway is the same one used in humans and if so, if it could be activated by a drug. What they hope is that unused muscle, which is in a state similar to the "fast" twitch state, can be stimulated by this pathway.

"In patients that are lying in bed or are immobilized, they don't have slow muscle," Bassel-Duby said. "Our ultimate goal is to be able to design a drug that will convert their fast muscle to slow. It's not an exercise pill."

Unfortunately, any such drug would not strengthen the heart. The pathway exists only in skeletal muscles -- the ones that move the limbs.

Williams and Bassel-Duby have only worked in rats so far, but they think their findings will translate into humans.

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