Another Revealing Study on Exercise

I came across yet another study done on exercise that I wanted to share (am I overdoing this whole exercise study thing here? Please let me know. But I do find these studies endlessly fascinating)

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.

But shiny fur was the least of its benefits. Indeed, in heartening new research published recently 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. ( Just to let you know, mitochondria are microscopic power generators. I learn from these studies too)

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.

After reading a study like this, I always think if they could put exercise in a pill form and sell it, the pill would cost a fortune, due to the benefits it offers. But exercise does not cost anything except our time and energy. Not a bad deal!

The Emerging Field of Epigenetics

How much of our health depends on our family genes? How much can we influence our own lifespan? These are questions that I have discussed with friends and family over the years and are questions that interest me for oomphTV.

I recently came across an article in the LA Times about a rapidly growing field in health called Epigenetics that caught my eye.

We all have an idea of what DNA is and what it does. I just learned there is a kind of secondary code, carried along with the DNA, called the “epigenome.” This code is a set of chemical marks, attached to the genes, that act like the DNA referees. They turn off some genes and let others do their thing.

And although the epigenome is pretty stable, it can change. This means lifestyle choices such as diet, exercise and drug use could have lasting effects on how the body works.

“The thing I love about epigenetics is that you have the potential to alter your destiny,” says Randy Jirtle, who studies epigenetics at Duke University Medical Center in Durham, N.C.

The epigenome is part of what tells different cells in the body which DNA recipes to read and which to ignore. The small chemicals that attach to the DNA may cover up or restrict access to genes that aren’t needed and keep others wide open and readable.

Jirtle compares the system to a computer: The DNA is the hardware – set and unchanging- and the epigenome is the software that tells it when, where and how to work. Some very important stuff here.

Epigenetics might be especially important for pregnant women and infants, because much of the epigenetic code is laid down early in development. Some experts speculate that the time before puberty might also be important, since the genome and epgenome are gearing up to launch new genetic programs.

So why should those of us over 40 care about about epigenetics? Because the epigenome can also be altered in our adulthood. Epigenome may change in response to what you had for breakfast today, or the stress you feel after a tough day.

Genes are not just “on” or “off.” They can be on just a little bit, on a lot and everything in between. So referees, both the short-term and long-term types, turn genes up or down, rather like the dimmer switch for a lamp.

And many genes can be turned up or down by changes in behavior and environment. For example, researchers at the Preventive Medicine Research Institute in Sausalito, Calif., studied 30 men with prostrate cancer. These men declined traditional medical treatment and instead underwent a three-month program that included a healthy diet, moderate exercise and daily stress management.

When the researchers examined gene activity in the men’s prostate biopsy samples, they found that 48 genes were turned up and 453 were turned down, compared with gene activity at the beginning of the study. The authors noted that the study, published in the Proceedings of the National Academy of Sciences in 2008, was small and needs to be repeated to be sure of the effects.

Though the science of epigenetics is young, scientists think there’s good reason to think about how lifestyle choices may affect the epigenome.

So the next time you eat a healthy meal or finish a good round of exercise, think of those little epigenomes. Hopefully you are helping them make good decisions and giving them a little oomph!