- 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 on Thursday.
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- 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.
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- 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.
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- "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.
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- "What we have done is identified
a pathway that will induce muscles to become slow."
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- In other words, they have found how exercise
makes muscles strong, on a biochemical level.
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- "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.
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- He said that pathway can be modified
to either stimulate or reverse what exercise does naturally.
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- "We believe that it is possible
to design a drug which would have this effect," Williams said.
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- Williams's team identified three proteins,
known as calcineurin, NFAT and MEF2 that are part of a pathway that activates
genes.
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- When a muscle is constantly stimulated
by exercise such as jogging, calcium ions build up inside the muscle cell.
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- 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.
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- 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.
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- 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.
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- "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."
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- Unfortunately, any such drug would not
strengthen the heart. The pathway exists only in skeletal muscles -- the
ones that move the limbs.
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- Williams and Bassel-Duby have only worked
in rats so far, but they think their findings will translate into humans.
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