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  If this muscle loss continues and accelerates, it puts us at risk for a condition called sarcopenia, or what Shakespeare—keen observer of old age—called the “shrunk shank,” where our limbs basically waste away, putting us at risk for frailty. Loss of muscle due to age is why my surviving dog, Lizzy, now has difficulty jumping up onto the bed or into the car, where she used to clear five-foot fences on the fly. She’s lost her spring. Her haunches, once firm, have gone soft. It’s not just about pole vaulting or fence jumping, either. People (and dogs) with sarcopenia are at greater risk for falling, and in the frail, a simple fall can snowball into a fatal event; this is why muscle wasting is the second-leading cause of institutionalization of the elderly, after Alzheimer’s.

  Nobody knows quite what causes sarcopenia; even its exact definition is controversial among scientists. The cure, too, is a subject of debate. For people like Dr. Life or Suzanne Somers, the answer is easy: Shoot up with testosterone and growth hormone. By this point in the book, you should realize what a bad idea this is. And anyway, while replacing testosterone does increase muscle size, it does not always improve muscle quality, at least not without exercise.

  Half a dozen pharmaceutical companies are developing drugs to fight sarcopenia in the elderly by promoting muscle growth; the drugs are only in early-stage trials, but some of them have already appeared on the black market for athletes and bodybuilders. But there is another, simpler treatment for sarcopenia that science has largely ignored, until recently: staying active. Adults who have exercised for most of their lives keep muscle for longer, as the illustration shows rather dramatically here.

  These drawings are based on MRI images of the upper legs of four different men, similar to those taken in The Blast. Each is a cross-section of someone’s upper thigh. The one on the upper left belongs to a typical fittish forty-year-old, and you can see how it’s mostly muscle, with a small ring of subcutaneous fat on the outside. The one at upper right is a typical sedentary seventy-year-old American man, with the classic signs of sarcopenia: Note how it is nearly all fat, like a slice of pancetta from a very well-fed pig. But the fat has also completely infiltrated his muscle, making it look “marbled” and rendering it weak.

  The bottom two images are just as striking: On the left, a sixty-six-year-old triathlete—looking pretty much the same as the fit forty-year-old. (According to Nathan LeBrasseur, the differences between them would only be visible through a microscope.) But the one on the right belongs to a seventy-six-year-old man who has never done a triathlon or any other sort of running in his life. He’s an English farmer, whose job required him to stay on his feet most of his life, moving around every day. He’s got about the same “muscle age” as the forty-year-old, because his lifestyle is the closest to that of our evolutionary ancestors.

  By pole vaulting and jumping and sprinting into old age, Howard Booth and his fellow senior athletes are not only defying time and gravity, but imitating, in a way, the kinds of things our hunter-gatherer ancestors had to do. Staving off sarcopenia is just a side benefit. They’ll be able to chase their grandkids around on the playground, or even just walk around, say, Paris while on vacation. The sedentary man won’t. Use it or lose it.

  Use It or Lose It even applies to laboratory mice. Traditionally, mice are kept in small plastic cages slightly bigger than shoe boxes, with nearly unlimited access to food but no opportunity to exercise. They live alone, too, because males in captivity have a tendency to fight. About a decade ago, a lab assistant to Tom Kirkwood named Sandy Keith did a small, unpublished experiment where he simply gave his mice bigger cages and more toys to play with, simple things like cardboard toilet-paper tubes. He also played with the mice every day, keeping them socially engaged. One of these “free-range” mice, a male named Charlie, lived an astounding 1,551 days, or four years and three months—which is six months longer than even the longest-lived caloric-restriction mouse. He had a lot more fun, too.

  To this day, Charlie remains one of the longest-lived mice ever—simply because he was given the opportunity to “use it.” The problem is that most older people aren’t expected or encouraged to do much of anything, and it often hurts when they do, so they don’t. “For some generations, exercise has a stigma. You say ‘exercise,’ it turns people off,” says LeBrasseur, whose research center is connected to a senior living community. “The most striking thing to me is how people are building their world around the La-Z-Boy. They have their medication around them, and the TV, and their food. They’ve engineered the physical activity out of life.”

  So it’s not even “exercise,” in the sense of slogging away on the treadmill at the gym, but something closer to “just moving around,” like the English farmer. Recent studies have pinpointed the mere act of sitting, itself, as a potent risk factor for death. An analysis published in the Lancet in 2013 found that inactivity was responsible for more than 5.3 million premature deaths each year worldwide, from causes ranging from heart disease to colon cancer. The authors concluded that eliminating inactivity—perhaps by shackling people to treadmills? Banning televisions?—would reduce the instance of those diseases, as well as Type 2 diabetes and breast cancer, by 6 to 10 percent. Not only that, they concluded it would increase worldwide life expectancy, for the entire human race, by close to nine months.

  Sitting is the new smoking, some scientists believe: a bad habit that leads inevitably to disease. Now go take a walk. Just be sure to hold your breath as you walk past the people who are actually smoking on the sidewalk outside the building.

  At any rate, it’s clear that moving muscle does something far more profound than simply burning up calories. LeBrasseur and his colleagues recently finished a novel experiment that dramatically illustrates the metabolic power of exercise. In the lab, LeBrasseur fed mice a special diet designed specifically to mimic the nutritional content of a fast-food meal: Big Mac, fries, and a Coke. The mice had been genetically modified so that any senescent cells would bind to a special fluorescent marker that would make them glow in the dark. After a few months on the all-fast-food diet, the mice lit up bright green, because they were filled with many more senescent cells than the mice who had been fed a normal diet. But the Big Mac mice that had also exercised had many fewer senescent cells. The exercise had negated the toxic effects of the #1 Combo Meal—either by zapping the resultant senescent cells, or by preventing their formation in the first place.

  “It really highlights the power of exercise,” he says. “You’re pouring this toxic substance into your body, but as long as you’re exercising, it’s not going to be as bad for you.”

  So it’s okay to go to McDonald’s, as long as you jog there. (Or better, jog back.) But what scientists are discovering is that it’s not just that the jogging is cleaning the Special Sauce out of your arteries; it’s that your muscles are somehow communicating with other organs of your body to optimize their function. This we know thanks to innovative experiments in the 1990s with athletes who had been paralyzed due to spinal injuries. When their muscles were stimulated, in a way that mimicked exercise, researchers found that their livers “knew” to send a shot of fuel directly to their muscles. In the past, it was thought that this communication happened via the nervous system and the brain, but the spinal patients got the same burst of fuel; they even experienced a “runner’s high.” How could that be?

  In 2003, biologists Mark Febbraio and Bente Pedersen found that just as fat “talks” to the rest of your body—usually saying terrible things—so does muscle. “We discovered that muscle, when you contract it, is actually an endocrine organ, and it can release factors that can talk to other tissues,” says Febbraio. “So when a muscle contracts, it’s not just an organ of locomotion.”

  The primary signaling factor they identified was a surprising one: our old friend IL-6, the well-known inflammatory cytokine that’s normally associated with bad things like inflammation and early death. Exercise generates huge amounts of IL-6, they found, but in that context it actu
ally has beneficial effects, such as signaling the liver to start converting fat to fuel. “When we made this discovery, people really didn’t believe us, because IL-6 was considered a bad actor in many diseases,” he says. “But the thing is, in exercise it’s anti-inflammatory, actually.”

  The difference had to do with time. Obese and elderly people tend to have constantly elevated levels of IL-6, a sign of chronic inflammation. Normal-weight and younger patients have lower levels—but when they exercised, their IL-6 levels would spike to a very high level, and then dissipate over a few hours. These short bursts of IL-6 were in effect sending messages to other organs, like the liver and the gut, telling them to switch to “exercise” mode.

  Since then, dozens more of these muscle-specific messengers, called myokines, have been identified. Febbraio, a former professional triathlete who describes himself as an “exercise junkie,” believes there are hundreds more yet to be discovered, and that they are largely responsible for the myriad and complex beneficial effects of exercise. Some of them even act on the brain, triggering the release of BDNF, brain-derived neurotrophic factor, which heals and protects neurons.

  In a sense, exercise helps the body clean house. Intense activity triggers a cellular cleaning process called autophagy, from the Greek words for “self-eating.” Autophagy is crucial to our cells’ survival. Without it, our cells would quickly fill up with garbage and become dysfunctional, just like your house would if you quit taking out the trash. “Exercise is an incredibly effective mechanism to drive protein turnover, kind of flushing out the old proteins,” says LeBrasseur. It helps our cells clean house, so they can function better for longer.

  Other myokines appear to work on bone, on the pancreas (which secretes insulin), on the immune system, and on muscle itself, promoting growth and healing. “It seems that muscle is the organ that counteracts fat,” says Pedersen. Literally: One newly discovered myokine even attempts to convert fat to an energy-burning system, like muscle. In 2012, a Harvard-based team identified a hormone called irisin, secreted by muscle during exercise, which tricks plain old white fat, which is most of our fat, into acting like “brown” fat, a far more rare form of fat tissue that is dense with mitochondria and actually burns energy. Bruce Spiegelman, the Harvard scientist who discovered irisin, is now looking for a drug compound that might trigger its release, independent of exercise.

  But Febbraio cautions that “exercise in a pill” is not in the cards: “It’ll never happen,” he says firmly, “because the benefits of exercise are a multifactorial thing. You could never design a drug that would replace exercise.” Just ask Phil Bruno. For him, in fact, exercise wound up replacing the drugs.

  Don and Ron and Bernie and Howard Booth all had one thing in common: They each looked, and acted, much younger than the age on their driver’s license. Yet until recently, mainstream science has insisted that exercise doesn’t really affect the aging process itself; it merely extends healthspan and improves function. In mouse studies (which researchers so love), it only appeared to increase average lifespan, not maximum; that meant it wasn’t actually slowing aging, even if it did help certain individuals live longer than they otherwise would have.

  But some new research is hinting that exercise may have a more profound effect on the aging process than scientists were previously willing to believe. In 2007, Simon Melov was part of a team that found that exercise actually seemed to reverse the effects of aging in a group of older Canadians. The study looked at two groups of people, one older and one younger. The researchers took muscle biopsies from each group, a painful procedure involving a rather large and long needle, and analyzed the “gene expression” patterns in the tissues—which genes were turned on and off. (Over time, different genes are activated in different cells of our bodies, a process called “epigenetic” change.)

  They then placed half of each group on a strict but not-too-demanding resistance-exercise program for six months. At the end of the six months, they took more biopsies and found that the older subjects’ muscles had reverted to a “younger” state—that is, they had had many of the same genes activated as their younger study mates. “We showed you could essentially reverse the gene expression signature of aging with exercise,” says Melov.

  In short, exercise had switched the “young” genes on, and the “old” genes off. Most of those genes had to do with the function of mitochondria, which you surely remember from high school biology class: They’re the little energy plants inside our cells. I like to think of them as tiny little cellular turbines, but their history is what’s really interesting. Mitochondria originally evolved as entirely separate organisms—parasites, really—back in the primordial soup days. Back then, most of the bacteria that made up life on earth were anaerobic: They survived without oxygen. But as the atmosphere slowly became more oxygenated, in this first great episode of global climate change, the anaerobic critters began to die off—unless they had been invaded by the tiny, oxygen-burning parasites that we now know as mitochondria. Now nearly all life depends on oxygen, and mitochondria are found in nearly every living cell. Yet because mitochondria are so ancient and primitive, they still maintain their own small, separate genome, distinct from ours, with just thirteen genes that are both highly important and highly fragile.

  Melov’s coauthor, a researcher and physician named Mark Tarnopolsky at Ontario’s McMaster University, was fascinated by mitochondria, so he picked up where the 2007 study left off. Tarnopolsky had devoted his career to studying rare mitochondrial diseases in children and adults, and he noticed that many of his patients suffered from effects similar to a kind of accelerated aging: They developed premature gray hair, or went blind in their twenties, or lost muscle strength in their forties. Which makes sense, because mitochondrial dysfunction is believed to be one of the primary drivers of aging. “What is it about the aging process which unmasks so many of our disorders?” he asks.

  Tarnopolsky also understood mitochondria on a more functional level, because he was a top-level amateur athlete himself, nationally ranked in cross-country skiing and trail running. As he neared forty, he started wondering about the effects of age on his own mitochondria—and whether exercise would keep those consequences at bay. One theory of aging says that over time, our mitochondria accumulate mutations to their own rather fragile DNA, which causes them to crap out, one by one. As we lose mitochondria with age, we eventually run out of energy, as Luigi Ferrucci observed. Making matters worse is the fact that our mitochondria are the site of some of the most intense chemical reactions in the body, which produce toxic free radicals and other damaging molecules. When enough mitochondria stop functioning, so does the cell—be it a muscle cell, a brain cell, or some other kind of cell.

  Tarnopolsky wanted to try a study of mitochondrial aging in mice, but found himself unable to get funding—because, he thinks, the scientific establishment is biased against exercise studies. “Unfortunately, when you want to study exercise, you are already behind the eight ball,” he says. “People say exercise is ‘dirty,’ because it has so many pathways. We get many of our papers rejected because people say, ‘You haven’t shown the exact mechanism of the pathway of exercise.’ ”

  With no alternative, Tarnopolsky decided to fund the study himself, using more than $100,000 in profits from his medical clinic to pay for a small number of very expensive genetically modified mice. The mice had been programmed to undergo mutations to their mitochondrial DNA at a much greater rate than normal, which caused their mitochondria to conk out more quickly—which, in turn, made them age more rapidly. He then placed some of those mice on a regular treadmill-exercise program, just forty-five minutes three times a week, while letting others stay sedentary in their cages.

  The results were dramatic. As expected, the sedentary mice were prematurely aged: gray, emaciated, and feeble. But the mice that had exercised were still strong, active, and sported lustrous black fur; they literally walked all over their sedentary cousins, despite the fact that th
ey had the same broken mitochondrial DNA. The effects were far more than superficial, too: Autopsies showed that the exercise mice had stronger hearts (of course), but also healthier livers, brains, and even more robust gonads (yay!) than the inactive mice. Exercise had somehow repaired their mitochondrial DNA—in short, it had reversed their aging. Tarnopolsky suspects that in exercise, the mitochondria send some kind of signaling molecules that do the repair work in other organs, not just muscle. He was determined to figure out what those molecules were, because they might lead to drugs that could help his rare-disease patients. For the rest of us, though, exercise is the drug.

  “It’s very simple,” he says. “Get off the couch.”

  I hung around the Senior Games for three days, watching these incredible older athletes run, jump, and throw things. At a certain point, I got used to it, almost numb to the sight of a seventy-year-old lady in a tennis outfit executing a perfect Fosbury Flop. But on the second afternoon, the entire stadium stopped to watch one extraordinary race.

  It was the women’s eight-hundred-meter, two laps around the track, and right from the gun one runner stood out from the rest. She was tall, with long silver hair, and her long legs ate up the distance in long, graceful strides. Where others in her race seemed to struggle, to have lost their spring, she loped around the track with the panache of an Olympian. She finished in 3:28, a new Senior Games record—and a time that few forty-year-olds could equal—and everyone cheered. It was spectacular, even beautiful to watch. I had to find out her secrets.

  Her name is Jeanne Daprano, and she is a seventy-six-year-old former third-grade teacher from outside Atlanta. She is well known in senior track circles, holding multiple world records for her age group. In 2012, she became the only seventy-five-year-old woman ever to run a sub-seven-minute mile; according to the age-grading formulas used in Masters athletics, her 6:58 time translates to a young person running the mile in 4 minutes flat, which no woman has ever done. (The current female world record is 4:12.)