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| Muscles, Speed, and Lies |
A new study by a group of researchers from the Mayo Clinic, however, examined the effects of aging on muscle in 146 healthy men and women, aged 18 to 89.1 The primary finding was that muscle aging is caused by cumulative damage to muscle DNA, which is required to replicate muscle cells. When DNA is damaged, the cells don’t repair themselves correctly and eventually die. On a grand scale, that means a gradual loss of muscle with each passing year.
The researchers also found that the DNA in muscle mitochondria, where energy is produced in cells, reduces with age. Having fewer mitochondria means less production of adenosine triphosphate (ATP), the source of cellular energy. Without adequate ATP the cell’s “housekeeping” functions shut down, and the cell dies. The loss of muscle mitochondrial DNA manifests such symptoms as age-related weakness, loss of muscle mass and related diseases, such as insulin resistance, diabetes and heart disease.
Now scientists know exactly how the process of muscle aging begins and can design therapies to block the effect. What causes the loss of muscle and mitochondrial DNA is long-term, out-of-control oxidation. Mitochondria are highly prone to oxidation because ATP production releases a lot of oxygen in the cell. That promotes the activity of free radicals, by-products of oxygen metabolism that are the destructive elements in oxidative reactions.
As people age, the built-in antioxidant systems of the body, such as the superoxide dismutase system of enzymes, begin to falter. That sets the stage for the degenerative aspects of oxidation in cells. In fact, that’s a major theory of the aging process. The effect is especially troublesome in sedentary people who don’t exercise. Exercise promotes the body’s built-in antioxidation system. Some scientists think that may be the main value of exercise in helping to forestall the aging process and the degeneration of brain and body.
The scientists who found this elemental cause of muscle aging suggest that the process begins at age 30. The same is true of such other conditions as osteoporosis, a bone-wasting disease more common in women than in men, which begins at about age 30 but doesn’t usually become apparent until after age 60. By then, however, the damage is extensive, resulting in fragile bones and hip fractures.
Can exercise block the loss of mitochondrial DNA in muscle? The Mayo researchers didn’t answer that question, but common sense and observation of people who stay active and continue to exercise as they age indicate that exercise probably helps.
Nutrition also enters the picture. Rats that get fewer calories as they age show little or no degenerative muscle changes. Specifically, old rats fed about 30 percent less than other rats have muscles that appear the equivalent of a quarter their age. That effect is thought to be due to less muscle oxidation, which protects the muscle mitochondria and maintains the energy-producing function of the cell. That in turn maintains muscle repair even though the body is aging.
Reducing total calories by 30 percent isn’t practical for most humans, of course, and it’s unclear whether humans who did that would benefit the way rats do. Another, easier option would be to ingest nutrients that protect the vulnerable mitochondrial DNA from oxidation, such as coenzyme Q10, lipoic acid and acetyl L-carnitine. Research conducted at the University of California, Berkeley, showed that intake of those nutrients led to complete regeneration of muscle mitochondria and protected against further damage. Typical doses would be 30 to 60 milligrams a day of CoQ10, 200 milligrams of lipoic acid and 1,000 milligrams of acetyl L-carnitine.
1 Short, K.R., et al. (2005). Decline in skeletal muscle mitochondrial function with aging in humans. Proced Nat Acd Sci. 102(15):5618-23.
©,2013 Jerry Brainum. Any reprinting in any type of media, including electronic and foreign is expressly prohibited.
