Fight Aging!

While I was in the "use it or lose it" frame of mind, the latest SAGE Crossroads article caught my eye:

The age-related atrophy of muscle tissue originates within muscle cells themselves. The bundles of contractile fibers that give muscles their stretch begin to vanish. And the fibers that remain start to shrivel and don't produce the power they did in their youth.

But what drives this decline remains a matter of some debate. Biochemist Ewa Prochniewicz of the University of Minnesota, Minneapolis, pins part of the blame on accumulated damage to actin and myosin, the proteins that drive muscle contraction.

...

Another theory for why muscles fizzle with age builds on the "use it or lose it" hypothesis. Muscles contract only after they've received the go-ahead from embedded nerves - nerves that don't fire as vigorously in older adults. Thus, aging muscles receive fewer nerve signals and eventually die from disuse.

Another interesting passage:

But injured muscles can repair themselves by building new fibers, at least in younger people, and some scientists are testing whether aging muscles weaken because they lose this regenerative capacity. Neurogerontologists Jan-Erik Edstrom and Brun Ulfhake of the Karolinska Institute in Stockholm, Sweden, categorized a group of aging rats as either "well-preserved" or "severely affected" based on their performance on standard tests of strength and balance. Surprisingly, they found that the leg muscles from the gimpier rats appeared to have tried harder to mend themselves: They contained larger quantities of proteins that jump-start muscle development than did the better preserved muscles. Why muscles poop out in spite of their apparent potential for restoration remains unclear, Edstrom says.

It is possible that this has something to do with the age-related decline of muscle stem cells; you may recall recent work showing that these aged stem cells can be jolted back into operation with the right biochemical cues, giving old muscle a youthful capacity for regeneration. Given that age-related decline in strength and muscle capacity is a downward spiral - the more you lose, the less able you are to slow further losses with exercise - this sort of research can only be a good thing.

While scientists are pinning down causes, I don't see anybody arguing that exercise is a bad thing or that it doesn't help to slow age-related degeneration. Given the choice between full-speed or slower degeneration while we wait for medical technologies capable of repairing age-related damage, I think I know which option I'll be taking. Here is a final thought from the article:

There's no one drug that could purport to have all the behavioral, psychosocial, and physiological effects of exercise and physical activity.

Yet. But exercise while you're daydreaming about not having to. It'd be a shame to miss out on the benefits of future medical technology because you let things slide today.