Thursday, March 10, 2011

exercise keeps you young?

most of us have been told at some point or another that exercise keeps you young. it's been part of our motivation to start and maintain a regular exercise regimen and follow an active lifestyle. for some of us, we've also made it a premise and a mantra that we recite to get others around us to become physically fit.

except that we've never really been clear as to whether this is true. we're not entirely sure how or why it does so. sure, we can see and feel that the invigoration of fitness in ways encompassing all facets of our lives (i.e., physical, mental, spiritual). but we are not entirely sure as to the biological (i.e., scientific) mechanisms that enable the beneficial results of fitness.

well, here's an article that helps explain why:
the article presents to a lay audience the findings of recent research. for your convenience, i've put the full text of the article at the end of this post. the article refers to the following scholarly research paper (those of you who are academics can probably locate it for free off your school library electronic resources):
essentially, the findings of the research indicate that regular physical exercise seems to improve or prolong the operation of mitochondria. mitochondria are the components of cells responsible for generating energy, and in the human body operate to drive oxygen and nutrients through the biochemical reactions that release energy necessary for cells to function.

as most athletes with any level of scientific curiousity know, mitochondrial health is a key element of cellular health, and cellular health is a building block of overall health. without healthy mitochondria, cells decay, and on a sufficient scale in sufficient magnitude this leads to overall physical breakdown, with all the symptoms that we typically associate with severe aging: weakness (deterioration in muscle and connective tissue), loss of coordination (deterioration in neural pathways), shallow breathing (deterioration in cardiovascular systems), lack of energy (deterioration in ability to process oxygen and food into energy), difficulty thinking or remembering (deterioration in brain activity).

athletes know of the concept of overtraining, where too much training can lead to a physical state of prolonged exhaustion and continued weakness. this arises from physical activity that overwhelms the mitochondrial systems of cells beyond their ability to repair themselves. that "worn out" or "being ground into the ground" feeling is literally the mitochondria in cells being worn out and ground into oblivion.

what's interesting about the research here is that it shows that proper physical exercise somehow sustains mitochondria. in fact, in some ways, it actually makes them resistant to decay. as a result, it shows that there is a link between physical fitness and the avoidance of physical deterioration. of course, this leaves the question as to why exercise serves to preserve mitochondria, and so sets the direction for subsequent study.

something to note here is what kind of physical exercise is appropriate to stay young. sports science knows that overtraining is bad for mitochondria, and it is clear from the research that a sedentary or easy lifestyle is also bad for mitochondria. the journal comments that it involved the study of aerobic strenuous activity--the kind of activity that in most sports forms the foundation of athletic conditioning, and which is endemic to endurance sports. the journal observes that further research is warranted to see if other kinds of physical activity can have the same result, but its findings show that at the very least we need to be engaged in 1) aerobic and 2) strenuous physical exercise to sustain mitochondria and thereby forestall the effects of aging.

it's interesting to compare the research findings here with the commentaries of other sources available on-line:
as these links show, on a general level, we've all believed for some time that exercise keeps us young. but now at least there's research that provides us with some scientific understanding as to why. this provides with more assurance that an active lifestyle is a good thing for us and our acquaintances. so get to it!

Can Exercise Keep You Young?
Gretchen Reynolds
New York Times
March 2, 2011

We all know that physical activity is beneficial in countless ways, but even so, Dr. Mark Tarnopolsky, a professor of pediatrics at McMaster University in Hamilton, Ontario, was startled to discover that exercise kept a strain of mice from becoming gray prematurely.
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But shiny fur was the least of its benefits. Indeed, in heartening new research published last week in The Proceedings of the National Academy of Sciences, exercise reduced or eliminated almost every detrimental effect of aging in mice that had been genetically programmed to grow old at an accelerated pace.

In the experiment, Dr. Tarnopolsky and his colleagues used lab rodents that carry a genetic mutation affecting how well their bodies repair malfunctioning mitochondria, which are tiny organelles within cells. Mitochondria combine oxygen and nutrients to create fuel for the cells — they are microscopic power generators.

Mitochrondria have their own DNA, distinct from the cell’s own genetic material, and they multiply on their own. But in the process, mitochondria can accumulate small genetic mutations, which under normal circumstances are corrected by specialized repair systems within the cell. Over time, as we age, the number of mutations begins to outstrip the system’s ability to make repairs, and mitochondria start malfunctioning and dying.

Many scientists consider the loss of healthy mitochondria to be an important underlying cause of aging in mammals. As resident mitochondria falter, the cells they fuel wither or die. Muscles shrink, brain volume drops, hair falls out or loses its pigmentation, and soon enough we are, in appearance and beneath the surface, old.

The mice that Dr. Tarnopolsky and his colleagues used lacked the primary mitochondrial repair mechanism, so they developed malfunctioning mitochondria early in their lives, as early as 3 months of age, the human equivalent of age 20. By the time they reached 8 months, or their early 60s in human terms, the animals were extremely frail and decrepit, with spindly muscles, shrunken brains, enlarged hearts, shriveled gonads and patchy, graying fur. Listless, they barely moved around their cages. All were dead before reaching a year of age.

Except the mice that exercised.

Half of the mice were allowed to run on a wheel for 45 minutes three times a week, beginning at 3 months. These rodent runners were required to maintain a fairly brisk pace, Dr. Tarnopolsky said: “It was about like a person running a 50- or 55-minute 10K.” (A 10K race is 6.2 miles.) The mice continued this regimen for five months.

At 8 months, when their sedentary lab mates were bald, frail and dying, the running rats remained youthful. They had full pelts of dark fur, no salt-and-pepper shadings. They also had maintained almost all of their muscle mass and brain volume. Their gonads were normal, as were their hearts. They could balance on narrow rods, the showoffs.

But perhaps most remarkable, although they still harbored the mutation that should have affected mitochondrial repair, they had more mitochondria over all and far fewer with mutations than the sedentary mice had. At 1 year, none of the exercising mice had died of natural causes. (Some were sacrificed to compare their cellular health to that of the unexercised mice, all of whom were, by that age, dead.)

The researchers were surprised by the magnitude of the impact that exercise had on the animals’ aging process, Dr. Tarnopolsky said. He and his colleagues had expected to find that exercise would affect mitochondrial health in muscles, including the heart, since past research had shown a connection. They had not expected that it would affect every tissue and bodily system studied.

Other studies, including a number from Dr. Tarnopolsky’s own lab, have also found that exercise affects the course of aging, but none has shown such a comprehensive effect. And precisely how exercise alters the aging process remains unknown. In this experiment, running resulted in an upsurge in the rodents’ production of a protein known as PGC-1alpha, which regulates genes involved in metabolism and energy creation, including mitochondrial function. Exercise also sparked the repair of malfunctioning mitochondria through a mechanism outside the known repair pathway; in these mutant mice, that pathway didn’t exist, but their mitochondria were nonetheless being repaired.

Dr. Tarnopolsky is currently overseeing a number of experiments that he expects will help to elucidate the specific physiological mechanisms. But for now, he said, the lesson of his experiment and dozens like it is unambiguous. “Exercise alters the course of aging,” he said.

Although in this experiment, the activity was aerobic and strenuous, Dr. Tarnopolsky is not convinced that either is absolutely necessary for benefits. Studies of older humans have shown that weightlifting can improve mitochondrial health, he said, as can moderate endurance exercise. Although there is probably a threshold amount of exercise that is necessary to affect physiological aging, Dr. Tarnopolsky said, “anything is better than nothing.” If you haven’t been active in the past, he continued, start walking five minutes a day, then begin to increase your activity level.

The potential benefits have attractions even for the young. While Dr. Tarnopolsky, a lifelong athlete, noted with satisfaction that active, aged mice kept their hair, his younger graduate students were far more interested in the animals’ robust gonads. Their testicles and ovaries hadn’t shrunk, unlike those of sedentary elderly mice.

Dr. Tarnopolsky’s students were impressed. “I think they all exercise now,” he said.

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