Exercised: The Science of Physical Activity, Rest and Health

by Daniel E. Lieberman

A study from my lab showed that people’s chances of getting knee osteoarthritis at a given age and weight have doubled over the last two generations as we have become less, not more, active.

The problem is that connective tissues like bones, ligaments, and tendons adapt considerably more slowly than muscles and stamina.

Novice runners, especially first-time marathoners, risk injury because they can increase their mileage or speed (or both) faster than their shins, toe bones, Achilles tendons, IT bands, and other vulnerable tissues can adapt.

Many experts thus advocate increasing mileage only 1...

We use muscles not just to push our bodies forward but also to control movements and reduce loads that can stress and injure tissues.

What happened in Amsterdam bicycle fall

The muscles alongside the hip (termed hip abductors) that prevent the knees from collapsing dangerously inward during every step are a notorious weak link.

Beyond how much we run, another potential way to reduce our chances of injury is how we run.

Running lightly and gently, however, is easier said than done, and in my experience many runners are unaware of their form.

FIGURE 25 Good running form (on right) compared with common poor form (left).

but experienced endurance runners generally take 170–180 steps a minute regardless of speed.

Forefoot and mid-foot strikes usually don’t generate an impact peak on the ground—a rapid, large collisional force that is painful without shoes.

Forefoot and mid-foot strikes also generate rotational forces (torques) that are lower in the knee but higher in the ankle, requiring strong calf muscles and Achilles tendons, which can lead to problems for people trying to transition to this way of running.

If you change how your foot lands, do so gradually and ...

To be sure, shoes may lead to weak feet and encourage you to land hard on your heel, but millions of shod runners do just fine this way.

However, bare feet provide plentiful sensory feedback that is dampened in a shoe.54 If you run far at a moderate speed on a hard surface without shoes, you simply have to run lightly and gently,

Keep in mind that our running ancestors never ran on hard, flat roads in which every step was like the last, and they almost certainly ran less frequently and more slowly than committed runophiles.

One rarely considered parallel between running and dancing is how both can induce altered states. Long periods of vigorous exercise stimulate mood-enhancing chemicals in the brain including opioids, endorphins, and, best of all, endocannabinoids (like the active compound in marijuana). The result is a runner’s or dancer’s high.

they nonetheless built up endurance capabilities for exactly the sort of running people once had to do: long, broken up, and not that fast.

“Men do not quit playing because they grow old; they grow old because they quit playing.”

Chimpanzee mothers, for example, cannot give birth to babies faster than once every five to six years because they forage only enough food every day to sustain their caloric needs plus those of one hungry youngster.

Instead of becoming obsolete, middle-aged and elderly hunter-gatherers bolster their reproductive success by provisioning children and grandchildren, doing child care, processing food, passing on expertise, and otherwise helping younger generations.

Once this novel cooperative strategy—the essence of the hunting and gathering way of life—started to emerge during the Stone Age, natural selection had the chance to select for longevity. According to this theory, hardworking and helpful grandparents who looked out for others and who were blessed with genes that favored a long life had more children and grandchildren, thus passing on those genes.15

there was also selection for genes that repair and maintain our bodies when we are physically active. As a result, many of the mechanisms that slow aging and extend life are turned on by physical activity, especially as we get older. Human health and longevity are thus extended both by and for physical activity.

One of the most reliable measures of age-related fitness is walking speed—a measure that correlates strongly with life expectancy.

The active grandparent hypothesis raises a classic chicken-or-egg question. How much do humans live to old age so they can be active grandparents helping younger generations, or how much does their hard work cause them to live long lives in the first place?

From a Darwinian perspective, the best strategy is to live long and actively and then die fast when you become inactive. An even better strategy, however, would be to avoid any deterioration with age in the first place.

Aging is inexorable, but senescence, the deterioration of function associated with advancing years, correlates much less strongly with age. Instead, senescence is also influenced strongly by environmental factors like diet, physical activity, or radiation, and thus can be slowed, sometimes prevented, and even partly reversed.

The distinction between aging and senescence may seem obvious, but the two processes are frequently confused. Many conditions occur more commonly with advancing age, but only some are actually caused by age.

How and why do certain animals and humans, including those who exercise, tend to senesce more slowly?

At a mechanistic level, we senesce from a multitude of nasty processes that damage cells, tissues, and organs.

How does aging happen?

One worrying source of wear and tear arises from the chemical reactions that keep us alive. The oxygen we breathe generates energy in cells but leaves behind unstable oxygen molecules with free, unpaired electrons. These reactive oxygen species (charmingly also called free radicals) steal electrons indiscriminately from other molecules, thereby “oxidizing” them.

Another self-sabotaging reaction that results from being alive and using energy is browning, technically glycation.

These reactions can damage tissues and produce compounds (advanced glycation end products) that stiffen blood vessels, wrinkle skin, harden the lenses in our eyes, clog up kidneys, and more. These and other kinds of damage then trigger inflammation.

As we have learned, the immune system stimulates inflammation to defend us from pathogens as well as self-inflicted damage caused by physical activity. In short bursts, inflammation is lifesaving, but low levels of inflammation that last for months or years are pernicious because they slowly attack our bodies. Over time, the destructive effects of chronic, simmering inflammation accumulate in cells and tissues from head to toe including neurons in the brain, cartilage in joints, the walls of arteries, and insulin receptors in muscle and fat cells.

Unless we repair these and many other forms of damage, our bodies become more vulnerable to breaking down like cars driven too many miles.

Oxidation, for example, is halted by antioxidants, compounds that bind with reactive oxygen species, thus rendering them harmless.

Why don’t more humans—who we’ve already seen were selected to live longer than most animals—employ them earlier and more often to slow senescence and keep useful grandparents healthier for even longer?

the best explanation by far is that natural selection becomes weaker as we age.

Many other studies confirm the anti-aging benefits of exercise.42 But few of them explain why.

The most common explanation for why exercise slows and sometimes turns back the gradual slide toward poor health is that physical activity prevents or ameliorates bad things that accelerate senescence.

Top of the list is fat. Exercise staves off and sometimes reverses the accumulation of excess fat, especially belly fat, a chief caus...

To understand why physical activity activates dozens of processes that maintain function and repair some of the damage that accumulates with age, we need to explore what I term the costly repair hypothesis.

Instead, her RMR remained slightly elevated for hours in a state technically known as excess post-exercise oxygen consumption (EPOC) but informally called an afterburn. That afterburn may help explain how and why physical activity can help slow senescence.

As her muscles rapidly consumed calories, they pumped out waste compounds that compromised her cells’ functions, and her mitochondria leaked an abundance of harmful reactive oxygen species that damaged DNA and other molecules throughout the body.

If exercise is so destructive, why is it healthy? One explanation is that once she stopped exercising, my wife’s body reacted by repairing whatever harm she caused and, crucially, also repairing some of the damage that she had accumulated beforehand when she wasn’t exercising. As a result, she restored many tissues to their previous state.

Studies show that people’s afterburns can last from two hours to two days depending on the intensity and duration of the physical activity.

While exercise restores most structures (what biologists term homeostasis), in some cases it may make things even better than before (this is termed allostasis).

Among other effects, while physical activity initially stimulates inflammation, especially via muscles, it subsequently causes muscles to produce an even stronger, more lasting, and more widespread anti-inflammatory response whose long-term effect is less inflammation not just in the affected muscle but elsewhere.

All in all, the modest physiological stresses caused by exercise trigger a reparative response yielding a general benefit, a phenomenon sometimes known as hormesis.

physical activity induced plenty of oxidative stress, but those who took antioxidants incurred more oxidative damage because their bodies produced much lower levels of their own antioxidants.