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Insulin-like Growth Factor Helps Slow Down Sarcopenia

Dear Friend and Fellow Athlete,

For quite a few years now, bodybuilders and athletes have known about the anabolic properties of insulin-like growth factor 1 (IGF-I). When injected locally, IGF-1 increases protein-based tissue in muscles, muscle DNA, and satellite cell activity. It is so anabolic that it even promotes localized muscle growth without strength training. And when combined with strength training, the results can be remarkable.

But, as athletes who have experimented with IGF-1 know, it is prohibitively expensive, and the benefits are largely temporary in nature - slowly ending when administration ends. However, this may soon change. The University of Pennsylvania School of Medicine has developed a method to deliver IGF-1 into skeletal muscle using a virus. This revolutionary viral deliver method has enabled the insertion of IGF-1 genes directly into the muscle cell allowing them to produce their own growth factor indefinitely. The implications for bodybuilders and athletes are extraordinary.

If you're 30 to 40, although you feel healthy, you have started to lose skeletal muscle, the tissue that provides your strength and mobility, and the muscles we covet as bodybuilders. This process-known as sarcopenia, or literally vanishing flesh, transforms even the fittest of individuals into the weakest of elderly as we lose about 30% of our muscle mass between the ages of 30 to 80. In fact, the body hides its loss by subtly padding affected areas with extra fat. We know that resistance exercise slows the loss of strength that accompanies age related wasting, but until now, there has been no way to completely halt the muscle wasting that occurs even in healthy individuals who engage in regular exercise. New drug research now suggests that this unrelenting process may be stoppable.

Our skeletal muscles are surrounded by a large group of satellite cells. Their function is limited until a muscle needs to grow or experiences damage--such as a bruise or those minor rips that cause aches the day after exercise. Then the satellite cells spring into action, migrating to where they are needed. Some multiply and turn into new muscle, which eventually fuses to the old muscle. Others return to their quiet state to await the next crisis.

We understand that the performance of satellite cells wanes with age. In rats for example, muscle damage in a 3- to 6-month-old "young adult" rat completely disappears. But when an elderly 24- to 28-month-old animal sustains the same damage, the satellite cells' repair proceeds much more slowly and often incompletely. The problem may not be with the satellite cells themselves but rather with the body's difficulty in communicating with them as it ages. For example, research has shown that when a muscle and its satellite cells are transplanted from an old animal into a young one, the muscle again heals rapidly.

Insulin like growth factors appear to be the key to controlling satellite cell function. And preliminary evidence suggests that satellite cells from older animals mount a less robust IGF response following injury - suggesting that as we age, production of IGF becomes impaired. And as it becomes impaired, satellite cells function sub-optimally, muscle growth and repair becomes more difficult, and age related atrophy takes place.

Age-related neurological changes may also play a pivotal role in sarcopenia.

As we age, the body loses nerves, including those that branch out from the spinal cord into skeletal muscle throughout the body. As one of these nerves dies, a neighbor sends out branches to rescue the muscle fibers that were abandoned. Without a new nerve connection, that muscle would eventually shrink and die.

But, according to studies by neurologist Jan Lexell of Lund University Hospital in Sweden there is a limit to how much a nerve can grow and the limit decreases as we age. Lexell says, "It's somewhere around two to three times its original size … So it can double the number of muscle fibers that it innervates" but probably no more. When surviving nerves are no longer numerous enough to rescue all of the abandoned muscle fibers, he says, wasting becomes inevitable.

Studies to quantify the loss of these muscle-innervating nerves find that somewhere between one-quarter and one-half of them die between the ages of 25 and 75. Moreover, Lexell observes, the rate of nerve loss accelerates dramatically after age 60.

Lexell's studies indicate that the first muscle fibers to go are those used the least --rapidly contracting fibers that serve as a sort of muscular overdrive. The body calls on them to execute the most intense and rapid activities, such as heavy lifting and sprinting. The progressive loss of different types of muscle "accounts for part of the slowing of our movements with age," he says, and much of the frailty.

We have a good idea of what's taking place as we age, but other than weight lifting and anabolics, until recently, there has been nothing to reverse the process, only ways to slow it. In his study at the University of Pennsylvania School of Medicine, Dr. H. Lee Sweeney, professor of physiology, was able to prevent in mice the age-related decrease of muscle size and strength.

Mice, like humans experience a similar loss of 30% of their muscle mass as they age. Normally, when muscle is damaged, satellite cells within the muscle are activated to do their repair work by insulin-like growth factor-1 (IGF-1) and other signaling proteins. In elderly humans and animals, the ability of muscle to activate satellite cells to repair muscle mass diminishes. In the case of muscular dystrophy, muscle damage occurs at such a high rate that the body's intrinsic repair system can't keep up.

Sweeney said, "I felt the simplest way to do something about the weakened repair system was to put back into the muscle a chronic signal that would keep the satellite cells activated to be more responsive and repair damage more completely."

Sweeney and his team started with an adeno-associated virus, or AAV, which is adept at introducing its genetic material into the cells it infects. They stripped the AAV of its own genetic material and replaced it with a naturally occurring gene for IGF-1. They also inserted a "promoter" to drive production of the growth factor. This re-engineered virus was then injected into the muscles of the mice.

The promoter they chose, the myosin light chain promoter, is specific to muscle tissue so that IGF-1 production would be limited to the muscle. The researchers did not want any IGF-1 that may have accidentally leaked outside of the muscle to proliferate and stimulate growth of other organs.

The research team studied two main questions: Can a vector be developed - in this case, a virus - that can be used to specifically deliver genetic material to skeletal muscle or have the genetic material expressed solely and continuously in skeletal muscle? And, can it deliver the genetic material in such a way so as to have a positive effect and no noticeable or serious negative effect?

The study showed that in fact, both could be done.

In the experiment by Sweeney's team and researchers at Massachusetts General Hospital, each mouse served as its own control. The viral IGF-1 was injected into one leg, while the other was left untouched for comparison. The injections were tested in mice that were 2 months, 18 months, and 24 months old - the equivalents of adolescent, 55-year-old, and 70-year-old humans.

After several months, the adolescent mice showed a 15 percent increase in muscle mass in the injected legs compared to the control legs. Both groups of older mice experienced a 19 percent increase in muscle mass. The injection completely prevented the normal decrease of muscle mass associated with aging. Even better, according to the researchers, was the 27 percent boost in muscle strength experienced by the older mice and the preservation of the fastest muscle fiber types. Both mass and function were restored to their youthful levels. Muscle regeneration continued until it reached a steady state and lasted throughout the lives of the treated mice. But their life spans are usually just a couple of years. So it's not known how long the effects might be maintained in humans, or if there could be as yet unknown long-term side effects.

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