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By Maggie Fox, Health and Science Correspondent
WASHINGTON20 (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.
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.