THE HULK GENE
KING RONNIE At right , we imagine what Ronnie Coleman could ’ ve looked like with inhibited myostatin .
FOR BODYBUILDERS AND STRENGTH ATHLETES , IT COULD MEAN AN ADVANTAGE SO GREAT THAT IT WOULD LEAVE STEROIDS , GROWTH HORMONE , AND INSULIN IN THE DUST .
BEFORE referred to as “ double-muscled .” The half-ton-plus , marathon-runner-lean animals became highly prized for their rich meat .
Gregor Mendel may have become famous as the “ father of genetics ” for his cross-pollination of pea plants , but the cattle breeders were unwittingly conducting a form of genetic research all their own and in many regards as significant as that done by Mendel .
What the Belgian breeders didn ’ t consider at the time , but Lee would confirm two centuries later through gene analysis , was that they ’ d managed to breed cattle that carried a mutated version of the myostatin gene . The result was oversize muscles due to both hyperplasia ( the creation of new muscle cells ) and hypertrophy ( the expansion of existing muscle cells ).
With evidence mounting , it became apparent that the myostatin gene might be the key to unlocking the mysteries of muscle-wasting diseases , such as muscular dystrophy , in humans and may even ofer hope for a day in which muscle degeneration would no longer be an inevitable by-product of the normal aging process . Of special note to researchers is the fact that myostatin suppression shows a dramatic efect on skeletal muscle but little , if any , efect on smooth muscle and cardiac muscle : The internal organs , as well as the hearts , of the transgenic mice , like the cattle ’ s , remained normal in size .
Of course , altering genes in the embryonic stage of development is a technique that can ’ t be applied to MD patients , even if myostatin were found to play the same role in humans that it did in mice . “ ‘ Knocking out ’ the myostatin gene isn ’ t possible for treating patients ,” Lee said in a 2002 interview quoted in Science Daily , “ but blocking the myostatin protein might be .”
THE IGF-1 ANGLE
At around the same time Lee and his co-workers were conducting their experiments , University of Pennsylvania professor H . Lee Sweeney , Ph . D ., was leading a team of researchers investigating a diferent form of gene therapy to increase muscle mass , also in hopes of mitigating the efects of muscular dystrophy . Rather than using a method of subtraction ( myostatin protein ), Sweeney ’ s group focused on increasing the production of a hormone known to influence the production of muscle — insulinlike growth factor-1 ( IGF-1 )— with rats as the test subjects . IGF-1 is secreted by the liver and produced in other tissues , such as muscles , and promotes growth via several diferent means .
The team injected the hind legs of the rats with a modified virus containing a gene that would trigger increased production of IGF-1 . Then the rats were put on an intensive training regimen of ladder climbing to exercise their leg muscles . The result was a 15 – 30 % increase in the size and strength of the rats ’ legs . Even those not put through this experimental rat race displayed a muscle mass increase of 15 – 20 %.
One potential downside to the IGF-1 therapy , however , is that , unlike myostatin , the hormone afects an array of tissues besides skeletal muscle . Although
PREVIOUS SPREAD : MICE REPRINTED FROM CURRENT OPINION IN GENETICS AND DEVELOPMENT , VOL . 9 , S . J . LEE & A . C . MCPHERRON , “ MYOSTATIN AND THE CONTROL OF
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130 MUSCLE & FITNESS FEBRUARY 2016