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
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130 MUSCLE & FITNESS FEBRUARY 2016