Sports Competition for Adults Over 40: A Participants Guide to 27 Sports
Sports Competition for Adults Over 40: A Participants Guide to 27 Sports
Sports Competition for Adults Over 40: A Participants Guide to 27 Sports

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A Perspective on Aging

When Phidias, the architect of the Parthenon, was born he could have expected to live to somewhere in his mid-30s. He actually made it past 40, barely. Over the next 24 centuries, life expectancy remained in the 30 to 40 range. As you might expect, the wealthy and powerful lived longer than average - Shakespeare died at 52, George Washington at 67, and Queen Victoria at 82. The poor and disenfranchised, of course, died much younger, keeping their average well below 40.

Then in the 20th century, life expectancy at birth jumped from age 40 to age 78, a stunning increase of 63 percent. This dramatic prolonging of life in the past century has been brought about primarily because of improvements in sanitation and medical science. And life expectancy is still increasing. In developing countries, it is estimated to be growing by about five hours every day. This suggests that aging is not fixed or programmed. It is a mutable process governed by a multitude of factors. So why can's we achieve immortality?

We know that many of these "longevity" factors operate at the cellular level. All cells are subject to a variety of injuries and insults: free radicals disrupt cell membranes, DNA mutates, disease may wreak havoc on delicate cell processes, and so on. Cells are in the business of maintaining life, as well as copying and translating genetic data. Although the mechanisms for accomplishing this are amazing, they are not perfect. So cells change and die.

A recent article by Thomas Kirkwood(1) provide a provocative new perspective on aging. It presents a summary of current genontological research on aging and, I believe, offers some implications for the (potential) competitive athlete.

Kirkwood points out that there are some cells that are immortal. These are germ cells, the sperm or egg that is necessary for reproduction. For those having children these germ cells are passed down from generation to generation. In a subsequent article(2) Kirkwood argues that women may live longer than men because a woman's good health is more critical to producing and nurturing a sound offspring than a man's health.

But how do germ cells achieve their immortality? Why don't they die out? He offers three reasons. First, germ cells have an especially sophisticated system of maintenance and repair. But still, it is not perfect. Second, the body produces many more germ cells than are necessary. Thousands of sperm cells are produced, but only one is required for fertilization. Similarly, many eggs are created, but only a relatively few ovulate. This allows the body to discard germ cells that are damaged or imperfect. Finally, natural selection encourages only the fittest individuals to transmit their germ cells to future generations. So why don't we have enough germ cells to make us immortal. Actually, there are a few creatures that do attain a kind of immortality. For example, the freshwater Hydra does not appear to age or die. In fact, if it is cut into pieces, the Hydra can reproduce itself from a single fragment. How can it do this? Because most of its cells are germ cells.

However, in humans, the vast majority of cells - all but the germ cells - will eventually die. These mortal cells are called "soma." Why do humans, and most other multi-cellular organisms, have mortal soma? Kirkwood answers this question with a "disposal soma theory."

While germ cells in humans are confined to the gonads, soma cells can go all other the place, specializing to become brain cells,muscles, nerves, and liver cells. In other words, soma cells produce complex organisms, such as humans. So that's the choice. Be a simple and immortal freshwater Hydra or a very complex and mortal human being.

The finite amount of energy taken in each day by a complex organism, such as a human, a mouse, or a whale, have to accomplish many purposes. Some of the energy is used to grow the individual; some used for physical work and movement; some for reproduction; some stored as fat to protect against famine; some used to clear away molecular debris; and, of course, much of it used to repair damaged cells. So the body must make trade-offs to survive. For example, a species in a hostile environment, such as a field mouse, may require a great deal of physical work to stay alive long enough to reproduce. On the other hand, species that can dominate their environment, such as a whale or an elephant, will use energy for growth and cell maintenance, and achieve a much longer life than a field mouse. In general, dominant species will sacrifice cell maintenance to invest more energy in growth and reproduction. Result: their body that will not last forever. So aging is driven by the lifelong accumulation of diverse forms of unrepaired molecular and cellular damage.

However, things are not quite that simple. Current research suggests that certain genes can influence how long we live. These genes appear to extend life by altering the organism's metabolism.

The amount of food we consume can also ratchet the metabolism up or down. Since the 1930s evidence has shown that underfeeding laboratory mice will, paradoxically, lengthen their lives. Eat less and live longer. However, caloric restriction which appears to work well with mice may not be work as well in humans because humans may not the flexibility to alter their metabolic control. Only many hungry years of caloric restriction will demonstrate whether or not it actually impacts human longevity, much less an improved quality of life.

Aging is complicated, occurring because cell damage accumulates, breaking down the healthy functions of the body. Damaged cells may react in several ways. One reaction to cell damage is suicide, called apoptosis. The cell actually kills itself. On the one hand, if apoptosis is wide-spread in an older organ, it can result in the death of that organ and eventually the death of the entire body. On the other hand, limited apoptosis can be a survival mechanism protecting the larger body of uninjured cells from potential trouble. So, apoptosis is both good and bad.

A second reaction of damaged cells is that they simply stop dividing, known as replicative senescence. Recent research has tied this phenomenon to erosion of the caps that protect the ends of the chromosomes, called telomeres. If the telomeres are shorted or damaged, cell replication and health are compromised. The deterioration of telomeres has also been tied to cancer. But that is another, longer story.

How does all this related to the aging athlete? Well, if a long, high-quality life is your goal, then, as Kirkwood points out, it is uncertain if caloric restriction, at least in humans, is the road to longevity. Starving yourself is a questionable way to live long and strong. Finally, it is important to bolster the body's cell maintenance and repair functions, such as eating wisely, exercising regularly, and getting adequate rest. Good advice for any human.

(1) "Why Can't We Live Forever?" Thomas Kirkwood, Scientific American September 2010
(2) "Why Women Live Longer" Thomas Kirkwood, Scientific American November 2010


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