As my plane sailed through the night sky 35,000 feet above the Sahara Desert, I looked down through my little plastic window into the immense blackness below and wondered what I’d find when we landed. It was my first trip to Africa, and I was heading to Uganda to study chimpanzee climbing. I was traveling alone in the pre-cell-phone era, my only security blanket a printed sheet of paper—a handful of helpful tips compiled and passed down by other grad students on how to negotiate the trip from the airport in Entebbe to the capital in Kampala by taxi, then onward by bus to Kibale National Park in the heart of the country. I went through the checklists and gear I was carrying once more in my mind, and silently rehearsed the conversation I’d have with the crush of taxi drivers at the airport to negotiate the fare to Kampala. Relax, I reminded myself. You’re prepared.
And for the most part, I was. I was a total noob to rain forest fieldwork, but I’d been prepping for weeks. Rubber boots, long-sleeve shirts and pants, rain gear. Two huge duffel bags full of equipment, most of it from my advisor, who (like all good advisors) used his grad students as mules to transport it to the field. I had gotten the full battery of vaccines and was taking my malaria prophylactics religiously. I got to my hotel in Kampala and then to Kibale without being kidnapped. From the tip sheet, I’d learned how to greet folks in Rutoro, the local language (“Oliota!” for a single person, “Mulimuta!” for groups; the response is always “Kurungi!”). I was even ready for the bugs. The mosquitoes and other buzzing annoyances weren’t as bad as I’d feared. I popped the occasional mango fly larva out of my skin like pimples, thankful they hadn’t found my nether regions. The first time I was swarmed by biting army ants, I ripped off my pants and plucked them from my thighs like an old pro. I even managed to yank a tick from the depths of my nose, way up there practically between my eyes, with a little patience and a long pair of metal Revlon tweezers I borrowed from a helpful (and horrified) fellow researcher.
But I wasn’t prepared for the smell of chimpanzees.
On my first day in the forest with the Kibale Chimpanzee Project research crew, we crested a small knob overlooking an open area and stopped, silent. Just ahead, maybe thirty yards away, a party of chimps sauntered up to an enormous, sprawling fig tree, their bodies a vibrant black against the muted greens and browns of the forest. One by one they scampered up into the canopy and began to eat, lounging in the massive branches and gobbling handfuls of figs like Greek gods. It was my first time ever seeing apes in the wild, and the vision is seared into my memory.
Like all researchers with the Kibale Chimpanzee Project, I knew the rules. We were to observe the chimps quietly and give them their space. We were in their world and needed to respect that. And for the first few days all went according to plan. We’d wake up before dawn, find the chimps, and follow them for as long as we could manage (often until dusk), always keeping a safe distance, twenty yards minimum. It was thrilling, but it still felt a bit like a trip to the zoo. The chimps kept far enough away that I was able to maintain my intellectual distance. They were animals and I was a serious researcher, studiously observing them with academic detachment.
Then, somewhere near the end of my first week, a party of chimpanzees surprised us as we followed them, doubling back and filing past us on the ground just a few feet away, close enough to smell. It was a pungent, woody musk that spoke of a life in damp forest but was still unsettlingly human. That visceral recognition seemed to wake me out of a fog. Suddenly it didn’t feel like I was observing animals anymore. These creatures were something more.
Peter Singer, a moral philosopher at Princeton University, has argued quite powerfully that the boundary we draw around our species is arbitrary, that sentient animals are morally equivalent to humans. Growing up in rural western Pennsylvania, observing animals in forests, pastures, and occasionally through the scope of a hunting rifle, I understood that our species is just one thin twig among millions in the tree of life, but I’d never felt any confusion between human and other. The notion that humans aren’t distinct, that the line between us and them is arbitrary and meaningless, would have seemed absurd to me, the abstract navel-gazing of effete dweebs who had never spent a day in the woods. Now, standing there in the middle of a Ugandan rain forest, I wasn’t sure what I was looking at. The division in my mind between human and animal was still there, but the chimps had crossed over to our side of the fence. I mumbled something to a veteran researcher in our crew. She gave me a knowing look and turned to follow the chimps.
Of course, that uncanny kinship is the reason we find apes so fascinating. We can’t help but see ourselves in them. It’s their inescapable humanness that prompted a young Jane Goodall to break with tradition, giving the chimps of Gombe National Park names like Fifi and Gremlin rather than the inert serial number IDs that previous generations of bird and mammal ecologists had given to their subjects. Ever since Goodall, Dian Fossey, and Biruté Galdikas began their pioneering work with wild apes in the 1960s, we’ve learned just how similar our closest evolutionary relatives are to us in body and behavior (see Figure 4.1). Chimpanzees, bonobos, gorillas, and orangutans have complex social lives and long-lasting friendships. They hunt and use a broad variety of tools, wrestle and play, fight and complain, and seem to grieve when loved ones die. Apes even have something like culture, learning a variety of social norms and foraging tricks from their community.
We share a number of bad habits with our ape cousins as well. As I learned that summer in Kibale, chimpanzees are lazy. True, they are incredibly powerful, able to scale giant trees effortlessly, and the males occasionally thrash one another and display ferociously. But for every dash through the forest or bare-toothed screaming explosion from the alpha male, we’d spend hours watching the chimps just hanging out. Chimpanzees and the other great apes get nine or ten hours of sleep each night and spend another ten hours each day resting, grooming, or eating. They walk less each day than the typical American, and don’t climb as much as you might think. My data from that summer in Kibale showed that chimpanzees climb about 330 feet per day, the energy equivalent of about one mile of walking. It’s the same story for the other apes: they are an impressively indolent bunch.
For us, a life of apelike idleness is a recipe for disaster. Sedentary humans are far more likely to develop cardiometabolic disease, including heart disease and diabetes. Yet, despite their laziness, apes don’t get sick. Diabetes is exceptionally rare among apes, even in zoos. They have naturally high cholesterol levels, but their arteries don’t clog. The primary cause of death in captive apes is cardiomyopathy, a pathology of the heart muscle, the causes of which aren’t entirely known. But they seem to be immune to the kind of heart disease that fells humans. Apes don’t develop hardened vessels or have heart attacks from blocked coronary arteries. They stay lean, too. As my work with Steve Ross, Mary Brown, and others showed (Chapter 1), chimpanzees and bonobos in zoos carry less than 10 percent body fat.
The fact that our closest evolutionary cousins don’t need to be active to stay healthy tells us that exercise isn’t like water or oxygen, some required element that all animals need to survive. Our need to exercise is peculiar. It sets us apart. As our hominin ancestors evolved into hunter-gatherers, the body adapted to the incredible physical demands it entails. No part was left untouched. Muscles, heart, brain, guts—everything was affected. As we discussed in Chapter 4, this transformation fundamentally changed the pace at which our cells work, accelerating our metabolic rates to meet the energetic demands of our high-octane strategy. Those ancient adaptations have consequences for us today: our bodies are built to move. In our modern, industrialized world, free of the daily demands of foraging for our food, we need to exercise for our bodies to function properly. It’s a legacy of our hunter-gatherer past.
Our hunter-gatherer past provides an evolutionary context for exercise, the answer to why exercise is so vital, but it doesn’t tell us anything about how exercise works to keep us healthy. We know from our work with the Hadza and all the other research discussed in Chapter 5 that the standard line—that exercise helps us burn more calories—is wrong. Sadly, a lot of people, when they find out that exercise doesn’t have a big effect on daily energy expenditure or a durable impact on weight, assume that exercise isn’t important. That’s precisely the wrong message to take home! Data from hundreds of studies and hundreds of thousands of subjects over the past several decades are clear: our bodies work better when we exercise. But if exercise isn’t increasing the number of calories we burn each day, what exactly is it doing to keep us healthy?
In this chapter, we’ll delve into the effects that exercise has on our body. Specifically, we’ll look at the impact of exercise on our metabolism. As we’ll see, the metabolic response to exercise—the myriad trade-offs and adaptations that keep daily energy expenditure in check—are a big reason that exercise is so beneficial. Rather than an excuse to avoid exercise, constrained daily energy expenditure is one of the main reasons regular physical activity is so important. Exercise doesn’t change the number of calories you burn each day, but it does change how you spend them—and that makes all the difference.
The benefits of exercise aren’t limited to its effects on energetics. It makes you strong and fit, for one thing, which is a great way to keep the Reaper at bay. One fun example: men who can do more than ten pushups in one go reduce their risk of a heart attack by more than 60 percent compared to men who can’t. (Go on, put the book down and check how you’re doing. I’ll wait.) Aerobic fitness is associated with better cardiometabolic health—and longer, healthier lives as well. The benefits of staying strong are particularly important as we age. One standard measure of fitness for older folks is a 6-minute walk test, wherein a person walks as far as they can in (you guessed it) six minutes. Older adults who can cover at least 1,200 feet in that time have half the risk of dying in the next decade compared to those who can’t make 950.
Vigorous activity, defined as anything demanding 6 METS or more (Chapter 3), has positive effects all over the body. These are activities like jogging, playing soccer or basketball, backpacking, or bicycling that really get your heart rate up. Vigorous exercise gets the blood rushing through your arteries, triggering the release of nitric oxide, which keeps them open and elastic. Pliable vessels keep blood pressure low and are less likely to clog or burst, the catastrophes that cause heart attacks and strokes. Moderate activity (3 to 6 METS, things like a brisk walk, an easy bike ride, or gardening) is great, too. It helps with the trafficking of glucose out of the blood and into cells, and it is known to improve mood, stress, and can even help treat depression. Regular exercise also keeps you sharp mentally, slowing the rate of cognitive decline with age. Running and other aerobic exercise increases blood flow to the brain and causes the release of neurotrophins, molecules that promote the growth and health of brain cells. Dave Raichlen and colleagues have argued that walking and running improve cognitive function by challenging the brain to coordinate a rush of visual and other sensory information to navigate and maintain speed and balance.
Exercise doesn’t stop there. As Dan Lieberman, my PhD advisor at Harvard, details in his book Exercised, physical activity affects every system in the body, from immune response to reproduction. The signaling mechanisms underlying its reach are still being worked out, but the range is staggering. In addition to directly engaging the nervous system and circulatory systems, both of which extend throughout the body, exercising muscles release hundreds of molecules into the bloodstream. We are only beginning to understand all the myriad ways that exercise affects us. No part of our body is untouched.
The fundamental insight from our work with the Hadza and other physically active populations is that our bodies work on a fixed energy budget. This is the constrained model of daily energy expenditure (Chapter 5). Like other animals, our evolved metabolic systems work to keep the total energy burned each day the same, even as demands shift and change. Sure, we’ll experience day-to-day fluctuations in energy expenditure, burning more calories if we exercise and fewer if we don’t. But our bodies adapt to our normal routines, our habitual workload. As you increase the amount of energy burned on physical activity, the energy available for other tasks is diminished (Figure 7.1).
Constrained daily energy expenditure changes the way we think about the role of exercise in our daily energy budget. With a fixed energy budget, everything is a trade-off. Instead of adding to the calories you burn each day, exercise will tend to reduce the energy spent on other activities. You can’t spend the same calorie twice.
While the importance of trade-offs has been understood since Darwin, they’ve been largely ignored in public health. Instead, as we discussed in Chapter 3 and 4, clinicians and researchers in public health have adhered to the armchair engineer’s view of metabolism, that exercise simply increases daily expenditure and doesn’t affect the energy available for other tasks. Only recently, with the growth of doubly labeled water studies of daily expenditure across a wide variety of lifestyles, has the constrained model come to the fore. As a result, we’re only beginning to understand the importance of metabolic trade-offs in exercise and health.
We’ve already seen in the last two chapters just how shrewd our evolved metabolic engines can be. Faced with calorie restriction, our hypothalamus reduces our metabolic rate and cranks up our drive to eat. When excess calories come pouring in, metabolic rates go up, burning off much of the excess intake. Think for a moment about what that means for your organs and all of their various tasks: when energy is scarce, some nonessential metabolic processes are suppressed; when times are good, some nonessential metabolic processes are promoted. The effect of daily physical activity on other metabolic expenditure is illustrated in Figure 7.1.
It should come as no surprise that humans and other animals, as the inheritors of half a billion years of vertebrate evolution, are very clever about which tasks are sacrificed when things get tough and which ones are protected. My favorite example comes from the mouse study out of John Speakman’s lab that I mentioned in Chapter 5. His team subjected adult male mice to different degrees of calorie restriction and measured how their bodies responded as their energy deficit became more and more dire. Metabolic rates and body mass plummeted as expected, but the effects were unevenly distributed across the body. Most organs, like the heart, lungs, and liver, shrank (and burned less energy) as the mice lost weight. Brains were protected, maintaining their size. The stomach and intestines actually grew, in a costly effort to squeeze every last calorie from their food. The best comparison, though, is between the spleen and testes. The spleen, a major organ in the immune system, melted away immediately, shrinking more than other organs. Testes, on the other hand, were protected, changing very little until the energy deficit was truly desperate. I love the study because it lays bare the evolved metabolic strategy of mice: Life is short. Make babies. The immune system is optional.
In a long-lived species like us, the evolved metabolic strategy is different. Sam Urlacher’s work with Shuar kids has shown that children fighting an infection increase the energy spent on immune defense while reducing their growth. Apparently, when times get tough, humans play the long game, allocating energy to maintenance and survival.
When exercise starts to take up a large chunk of the constrained daily energy budget, we see the same sort of prioritization at work. Other functions are squeezed out. Activities that aren’t essential—luxuries to be indulged only when energy is plentiful—are shut down first. Essential activities are protected until the bitter end. As a result, exercise has wide-ranging effects on how our metabolism is managed and where our calories are spent, which has enormous effects on our health.
When your body is under attack from bacteria, viruses, or parasites like the tick that lived deep inside my nose for five days in Kibale, the body’s first line of defense is inflammation. Immune system cells are sent to the site of infection, a ton of signaling molecules called cytokines are released into the bloodstream, and the tissue swells. The inflammation response is energetically costly but essential. It’s the emergency response team, and you need it to deal with invaders.
Big problems arise when inflammation targets the wrong things, attacking our own cells or some harmless grain of pollen rather than a true threat. It’s like the fire department showing up, blasting their hoses and breaking down doors, at a house that’s not on fire. With chronic inflammation, they never leave. The results are destructive. Depending on the tissues involved, inflammation can lead to everything from allergies to arthritis to arterial disease and more. Inflammation can also affect the hypothalamus, promoting overeating and other dysregulation.
We’ve known for decades that regular exercise is an effective way to lower chronic inflammation, and that lower inflammation means less risk of heart disease, diabetes, and other metabolic disease. A constrained daily energy budget helps explain why exercise is so effective at reducing inflammation. When a large portion of the daily energy budget is spent on exercise, the body is forced to be more frugal with the remaining calories at its disposal. Suppressing the inflammation response, limiting it to target real threats rather than sounding the alarm constantly, reduces the energy spent on unnecessary immune system activity.
You need a healthy stress response to deal with the real emergencies that life inevitably throws at you. For our hunter-gatherer ancestors, a surge of adrenaline and cortisol—the hormonal cocktail at the heart of the fight-or-flight response—was essential to escape the occasional leopard. These days, it might be the fuel you need to outrun a mugger or dodge a taxi. But as is true with inflammation, when stress response is triggered incorrectly or never shuts off, the result is chronic stress, which is devastating to our health.
Exercise is well known to reduce stress and improve mood, in part by reducing the magnitude of the stress response. A nice example of this comes from a Swiss study that used public speaking to induce a stress response in two groups of men: endurance athletes and sedentary non-exercisers. The groups were similar in age, height and weight, and general anxiety levels, but their reactions to stress were remarkably different. Both groups showed elevated heart rate and cortisol levels, but the athletes’ response was smaller and dissipated more quickly. Their bodies invested less energy in the stress response, just as the constrained daily energy model would predict.
Another great example of exercise’s healthy, suppressive effects on stress response comes from a study of college-age women with moderate depression. These women enrolled in a four-month trial, with eight weeks of regular jogging and eight weeks without structured exercise. As we’d expect from our evolutionary perspective on metabolism, exercise had no effect on weight (their bodies adjusted to the increased workload perfectly), but it did reduce their stress response. When they were exercising regularly, their bodies produced 30 percent less adrenaline and cortisol each day. Their depression improved, too, demonstrating yet again the expansive reach of exercise on our bodies.
Pop quiz: Who has higher testosterone levels, a Hadza man in the prime of his life or a soft schlub from Boston? Turns out it’s not even close. Testosterone levels among Hadza men are about half those of average U.S. men. It’s not just the men, and it’s not just the Hadza. Around the world, men and women in physically active, small-scale societies like the Hadza, Tsimane, and Shuar have much lower circulating reproductive hormone levels (testosterone, estrogen, and progesterone) than their counterparts in the sedentary industrialized world.
We can be confident that the low reproductive hormone levels in small-scale societies is due to their active lifestyles because they mirror the effects of exercise on hormones in experimental studies. College-age women enrolled in exercise studies routinely show lower levels of estrogen and progesterone, and they’re more likely to have disruptions to their menstrual cycles. The suppressive effects of exercise on the reproductive system are hard to explain with the traditional armchair engineer’s view of energy expenditure, but it makes all the sense in the world from a constrained energy expenditure perspective. With more energy spent on physical activity, less is available for reproduction.
Studies examining reproductive hormone responses to exercise also reveal just how long the process of adjustment can be, as our bodies adapt to different levels of physical activity. Anthony Hackney, an exercise physiologist at the University of North Carolina Chapel Hill, just down the road from me, has been investigating physiological responses to endurance training in men for decades. Comparing testosterone levels in endurance runners to age-matched sedentary men, he found about a 10 percent drop in testosterone, on average, among men who had been training for one year, a 15 percent or so drop for those training for two years, and about a 30 percent drop for those training five years or more, suggesting that it can take years for the body to fully adjust to different levels of exercise. These studies also provide a bridge between exercise physiology in the industrialized world and human ecology with groups like the Hadza. That 30 percent reduction in testosterone among longtime runners is roughly similar to what we see among men in small-scale traditional societies, who have had their entire lives to adjust to their high levels of physical activity.
Suppressing the reproductive system might sound like a bad thing, but in general it’s quite the opposite. Exercise is one of the most effective ways to decrease the risk of cancers of the reproductive system (like breast and prostate cancer), in part because it keeps reproductive hormone levels in check. In fact, reproductive hormone levels in the sedentary industrialized world are likely much higher than they were in our hunter-gatherer past, judging from the levels seen in the Hadza and other physically active, traditional populations.
There is a cost to exercise-induced reproductive suppression, at least in terms of potential family size. In populations like the Hadza, where birth control is nonexistent and people usually want large families, mothers typically have babies every three to four years. In the United States, most mothers who want to can have babies every one to two years, even if they’re breastfeeding. The lower activity levels and easier access to high-calorie foods experienced by women in the U.S. means their bodies can put more energy into reproduction and can recover from the last pregnancy sooner than Hadza moms can, something we’ll discuss again in Chapter 9. The wider birth spacing for Hadza moms is probably closer to the “normal,” evolved physiology for humans.
Taken to the extreme, exercise can begin to cut into normal reproductive system function. At unhealthy workloads, ovulatory cycles can stop completely, libido can evaporate, and sperm count can plummet. And that’s just the beginning of your problems.
Remember the early ’90s, when the sport of cycling was rocked by doping scandals? Of course you don’t, because I’m talking about the 1890s. Using drugs is a human pastime that predates the wheel, so perhaps it’s no surprise that doping was present at the birth of competitive cycling. The modern bicycle was invented in 1885, and in less than a decade, drug use in competition was widespread and generally accepted. People became understandably concerned when riders started dying in the 1890s. Apparently, the preferred performance cocktail at the time—a mix of cocaine, caffeine, strychnine, and heroin—had some nasty side effects.
Still, riders kept at it through the early and middle part of the twentieth century, using stimulants and painkillers to push themselves through grueling multiday races like the Tour de France, which premiered in 1903. After the development and widespread use of amphetamines to turbocharge soldiers on both sides of World War II, athletes started adding those into the mix as well. It wasn’t until 1967 that the International Olympic Committee decided enough was enough and banned the use of stimulants and narcotics. The effect was immediate: cyclists and other athletes stopped admitting that they doped.
The 1960s also saw an expansion of the cyclist’s pharmaceutical palette. They started doping with testosterone and testosterone mimics, powerful hormones that promote muscle growth and aggression. Those were banned by the IOC as well, in 1975, but their use remains widespread. A 2006 investigation by the World Anti-Doping Agency found that testosterone and its synthetic relatives accounted for 45 percent of all doping infractions that year. Later that summer, American cyclist Floyd Landis won the Tour de France, only to be stripped of the victory for failing a drug test. The culprit? Testosterone.
From a purely utilitarian perspective—putting aside the health risks of taking rat poison and narcotics, and the moral failure of cheating—one can understand why athletes might be tempted to take stimulants and painkillers to fuel a race and ignore screaming muscles. But testosterone? Why would cyclists risk their health and careers to take a hormone that their body makes on its own? Sure, testosterone helps grow muscle, which could be helpful during training, months before racing season. It also stokes competitive aggression, which could be good during the race if you weren’t in a competitive mood. But why would a professional athlete in the final stages of his sport’s biggest competition want to grow more muscle or need a chemical spark to push himself?
The answer lies in part with the suppressive effects that exercise has on the body. At the workloads that most of us—even the ambitious exercisers—are likely to experience, the suppressive effects are good for us. They help keep inflammation, stress response, and reproductive hormones at healthy levels. But at extreme workloads, exercise cuts deeper. As we’ll discuss in the next chapter, Tour de France cyclists like Landis burn over 6,000 kcal each day on cycling, and the race lasts nearly a month. They are pushing their bodies to the brink. The consequence is stark: their bodies shut down other functions, cutting into the essential tasks that keep us healthy (Figure 7.1).
This is the dark side of constrained daily energy expenditure, and it helps explain a well-known but poorly understood phenomenon in athletics: overtraining syndrome. We’ve known for decades that too much exercise can be bad for your health. At the workloads that elite athletes often take on during training, their bodies break down. They get sick more often and take longer to recover because their immune system is weakened. Injuries take longer to heal. The cortisol bump that helps them wake up in the mornings is muted and they feel fatigued all the time. The reproductive system goes into hibernation. Libido drops. Women have irregular periods or stop cycling altogether. Men’s sperm counts decline. Testosterone, the hormone that helps maintain muscle and keep their competitive edge, crashes—unless, of course, they can artificially elevate it with a few discreet injections.
Tellingly, giving overtrained athletes more food doesn’t solve the problem (unless there’s an underlying eating disorder—sadly, not uncommon among elite athletes). For example, a 2014 study by Karolina Lagowska and colleagues provided food supplements to thirty-one women endurance athletes (rowers, swimmers, and triathletes) who had irregular ovarian cycles and other symptoms of overtraining. After three months of being plied with extra calories, the women saw their daily energy expenditure increase by a modest amount: they were eating and burning about 10 percent more calories each day, the metabolic effect we’d expect given the body’s usual response to overeating. The women’s weight and body fat didn’t change—they weren’t storing the extra energy, they were using it. Some of those extra calories went to the reproductive system, increasing luteinizing hormone (which stimulates the ovary) by a modest amount. But it wasn’t enough to make a meaningful impact on ovarian function. Daily energy expenditure was still too constrained to take in enough calories to make a difference, and their prodigious exercise regimens were still taking up too much of the energy budget for the reproductive system to function normally.
Interestingly, researchers like Lagowska hit upon the constraints in daily energy expenditure decades ago, from a different angle. They discovered that subtracting the energy burned during exercise from total daily energy expenditure produced a very useful estimate, energy availability, the calories available for non-exercise tasks like immune function and reproduction. As workload increases and an athlete’s energy availability drops below 30 kcal per day for every kilogram of fat-free mass (an ungainly calculation for the recreational athlete, but one must account for body size), the risk of overtraining syndrome climbs. The intuitive treatment is to provide more calories, to try and increase daily energy expenditure. Constrained energy expenditure helps explain why that doesn’t work very well. With daily energy expenditure fixed, the only way to increase energy availability is to decrease training workload.
Rather than some mysterious aberration or a lack of food, overtraining syndrome is just the logical extension of the same energetic trade-offs that make moderate exercise so good for us. As is true with sex, water, bluegrass music, beer, and all other wonderful things, there is such a thing as too much exercise. So how much exercise is enough, and how much leads to trouble?
Finding the sweet spot for daily physical activity should be easy enough. There’s loads of real estate between the chimps idling away the hours in Kibale and the chemically enhanced maniacs racing the Tour de France. Our hunter-gatherer past is, as usual, a good place to start.
Hunting and gathering is hard work, but it’s not the Tour de France. Our research with the Hadza shows that men and women rack up about five hours of physical activity each day. A third of that—around one to two hours—is what physiologists call “moderate and vigorous” activity like fast walking or digging tubers, the kind of exertion that really gets your heart rate up. The rest is “light” activity, like strolling around camp or picking berries. Daily workloads for groups like the Tsimane and Shuar are similar. Living hunter-gatherers and other small-scale societies are culturally diverse, of course, but it’s reasonable to take five hours of physical activity, with one or two hours in the “moderate” or “vigorous” range, as a reasonable guideline for the amount of physical activity our hunter-gatherer ancestors typically got each day. If we want to think of this in terms of steps per day, we’d be well north of 10,000. Hadza men and women average around 16,000 steps per day.
Compare that to the training regimes of elite athletes. Pro cyclists train about five hours each day, mostly at “vigorous” (6+ METS) levels of exertion. Olympic swimmers regularly log five to six hours of swimming each day during training. That’s about three times more exercise than our bodies are evolved to handle, judging by Hadza standards. No wonder professional endurance athletes are tempted to experiment with hormones and other drugs that mask the metabolic consequences of their superhuman training programs.
On the other end of the spectrum, chimpanzees in the wild rack up less than two hours of physical activity each day, and most of it is light. They average around 5,000 steps per day. That’s remarkably similar to the typical U.S. adult, who gets about two hours of light activity (5,000 steps each day), and less than twenty minutes of moderate and vigorous activity. A lazy apelike existence is great for chimps—their bodies have been tuned to it over millions of years. But the human body has evolved to expect more—about three times more, if we use the Hadza and other foragers as a guide. Despite all the fascinating similarities that bind us to our ape relatives, our metabolic engines are fundamentally different. When we act like apes, we get sick.
As a first pass, then, we might aim to be on our feet for around five hours a day, with an hour or so of structured exercise or other activity where we get our heart rates up. That amount of physical activity would land us halfway between our ape cousins and overtrained Olympians, and in the good company of our hunter-gatherer friends. With a little luck, we’ll grow old with strong hearts, fresh legs, and clear minds. Healthy as a Hadza.
That Hadza-approved level of physical activity jibes well with the clinical and epidemiological data. In cultures around the world, daily physical activity is one of the strongest predictors of whether you live well or die young. One large study followed nearly 5,000 U.S. adults for five to eight years to test whether daily activity affected their risk of dying during that period. People who got an hour or more of moderate and vigorous activity each day were 80 percent less likely to die than the most sedentary participants. A similar study of 150,000 Australian adults found that an hour of vigorous exercise each day helped counteract the negative health effects of sitting at a desk job all day. In Denmark, men and women in the famed Copenhagen City Heart Study cut their risk of dying in half if they averaged at least thirty minutes of exercise a day.
My favorite example of finding the sweet spot for daily physical activity comes from a study of postal workers in Glasgow. As you might guess, these men and women walk a lot each day carrying the mail. Mail carriers in the study who clocked 15,000 steps a day (about two hours of walking) were virtually free of heart problems and other metabolic disease. And this is in Scotland, land of the deep-fried Mars bar, with one of the lowest life expectancies in Western Europe. You don’t have to move to the African savanna or cosplay as a hunter-gatherer to get the health benefits of an active lifestyle.
For those of us who spend our days banging away on a keyboard, delivering dank memes instead of the post, a Hadza-sized dose of daily activity can seem out of reach. The U.S. Centers for Disease Control recommend a modest 150 minutes of moderate and vigorous activity per week, and still only 10 percent of Americans meet that goal. Don’t despair. Just try to get moving. Hunt around until you find an activity that you love. Take the stairs. Bike to work. It doesn’t have to be exercise—any physical activity helps regulate your energy expenditure, reducing the calories spent on inflammation and other unhealthy activity.
While we’re at it, we can learn from the Hadza and other hunter-gatherers about the best ways to rest as well. The difference is in quality, not quantity. Even without electric lights or the garden of televised delights that tempt us in the West, Hadza, Tsimane, and other traditional populations sleep about as much as adults in industrialized populations, averaging around seven to eight hours per night. But they keep a regular schedule dictated by the sun. Too many of us in the industrialized world have shifting schedules, and the misalignment between our body’s internal clock and our sleep schedules can reduce daily energy expenditure and increase our risk of cardiometabolic disease. Hadza adults also accumulate the same amount of resting time as Westerners do during the day, hanging out around camp or resting on a foray. But in the industrialized world, we spend far too much of our lives in comfy chairs and sofas that leave our muscles limp. Hadza men and women use more active resting postures, like squatting, that engage the core and leg muscles. That low level of muscle activity helps reduce circulating levels of glucose, cholesterol, and triglycerides.
So how much exercise is best? More is the simple answer. The vast majority of us are far too chimpanzee-like in our daily activity, burning too many calories on nonessential (and potentially harmful) tasks like inflammation instead of exercise. Unless you’re already pushing your physical limits on a regular basis, you really can’t go wrong spending more time in motion, and your body will thank you. We should be cognizant of our inactive behavior as well, avoiding long periods of sitting in chairs and aiming to keep a regular sleep routine. And if you’re one of the few who already spend hours exercising each day, look out for the warning signs of overtraining, like constant fatigue or colds that won’t go away. If you find yourself in a French hotel room injecting synthetic testosterone into your ass, that’s a definite sign to back it off a bit.
With all these metabolic benefits of exercise, is there really no effect on weight? Well, the short answer is still no. Decades of research are very clear. As we discussed in Chapter 5, exercise isn’t effective for weight loss, and being more physically active is poor protection against the real problem in unhealthy weight gain: overeating. But there are two important caveats, curious wrinkles in the way exercise affects our bodies that deserve attention.
The first is that a complete absence of physical activity—sitting on the sofa or at a desk all day, every day—seems to mess up our body’s ability to regulate its metabolic tasks, including the regulation of eating. Exercise gets everywhere, sending hormones and other molecules all over the body. Without those cues and communication, the system doesn’t work right. Similar to what happens with a billionaire recluse who lives for months in the dark without human contact, things get weird. Basic tasks of cellular hygiene, like breaking down lipids in the blood or trafficking glucose into cells, start to fall apart.
Some of the best, early evidence for the dangers of inactivity come from an unlikely place, the Ludlow Jute factory in Chengail, India. In 1956, physiologist Jean Mayer of Harvard teamed up with a dietician and medical officer at the massive factory (at the time, it had more than 7,000 employees on site) to study the effects of daily activity on body weight. They ranked 213 workers by the physical demands of their job, from Stallholders who sat in a stall all day, six days a week, to Carriers, who ferried 190-pound bales of jute around the factory. In general, the amount of daily physical activity had no effect on weight: pencil-pushing clerks weighed the same as hardworking coalmen (Figure 7.2). But the extremely sedentary men were another story. Stallholders, who Mayer describes as having an “extraordinarily inert mode of life,” were fifty pounds heavier than the other men. Supervisors, the second most sedentary group, were thirty pounds heavier. The usual checks and balances that match energy intake to expenditure weren’t working.
The mechanisms that lead to overeating in “extraordinarily inert” people are still being worked out. It’s not as simple as sedentary people having lower daily energy expenditures. If it were, we’d see that daily activity and weight were related for all the men, not just the most sedentary. The lack of correspondence between activity and weight is a widespread phenomenon. A recent study by Lara Dugas, Amy Luke, and colleagues followed nearly two thousand men and women from the United States and four other countries for two years, and showed that daily physical activity, measured by accelerometer, had no effect on weight gain. For the vast majority of people, physical activity and the energy it burns each day has no effect on weight.
A more compelling explanation is that physical activity changes the way the brain regulates hunger and metabolism. Regular exercise seems to help the brain match appetite to caloric needs. Inflammation might play a role here as well. Overconsumption of energy-rich fatty foods can cause inflammation in the hypothalamus, leading to poor regulation of hunger and satiety signals and weight gain, at least in rat studies. It’s speculative, but perhaps chronic inflammation brought on by inactivity has similar ill effects in the brain.
Whatever the mechanism, it’s clear that spending hours each day being inactive is disastrous for your health. As we can see with the jute factory study, extreme inactivity can lead to dysregulated eating and unhealthy weight gain. Time spent sitting each day, either at your desk or watching TV, is a strong predictor of heart disease, diabetes, cancer, and a range of other serious problems. More than five million deaths around the world each year are attributable to sedentary lifestyles. Modernization is pulling us indoors, out of the sun, and into the warm embrace of a computer screen—and the apelike lethargy is killing us.
The second caveat in the relationship between activity and weight is that exercise can also be useful for managing weight once you’re able to lose it. Exercise is a poor tool for achieving weight loss, but it does seem to help people maintain weight loss. A great example of this comes from a study of obese policemen in Boston (not the same men in the testosterone study mentioned above). The men were assigned to one of two weight-loss programs for two months: diet only or diet plus exercise. There was no difference between the groups in the amount of weight lost, just as we’d expect. But once the active weight-loss intervention was over, men who exercised were much more successful in keeping the weight off (Figure 7.3). This was true for both men who exercised during the first two months and those who started in the “diet only” condition. The opposite was true as well: men who didn’t exercise after the weight-loss intervention gained all their weight back.
Some of the best evidence for the role of exercise in maintaining weight loss comes from the National Weight Control Registry, an online group of over ten thousand men and women who have lost at least thirty pounds and kept it off for at least a year. These folks defy the cynical view that meaningful, sustainable weight loss is impossible. The average Registry member has lost over sixty pounds and kept it off for more than four years. They are truly exceptional.
Much of what we know about Registry members comes from surveys, which is worth keeping in mind. People are notoriously unreliable when it comes to discussing their diet, exercise, or body weight. Still, the common threads among these weight-loss success stories are interesting. Nearly all of them (98 percent) report changing their diet to lose weight, which makes sense given how diet can affect the reward and satiety systems in our brain and impact how much we eat (Chapter 6). They report being more physically active, too, and the most common exercise added is walking.
More revealing are the empirical studies done with Registry members, from researchers collecting hard data on their metabolism and lifestyle. A 2018 study compared daily physical activity of Registry members (measured using accelerometers) to two other groups: obese adults who weighed the same as the Registry members did before their weight loss, and normal-weight adults who were never obese and weighed the same as Registry members do today. Just as we might expect from the Boston police study results, Registry members spent nearly an hour more each day engaged in light physical activity (like casual walking) and about forty minutes more in moderate and vigorous physical activity than the obese group. Exercise seemed to help Registry members keep weight off.
Tellingly, the Registry members also racked up more physical activity each day than the normal-weight adults who had never been obese. In other words, the Registry members worked harder than never-obese adults did to maintain the same body weight. A follow-up study that measured daily energy expenditures helps to explain why. Despite their smaller body size and lower BMRs, Registry members had the same daily energy expenditures as obese adults. Their bodies—or more specifically, the weight management systems in their brains—were stuck at their old, pre-weight-loss daily energy expenditures, targeting the same number of calories they burned before their weight loss, when they were a lot bigger. To stay in energy balance and keep the weight off, Registry members had to find a way to burn all those calories. Exercise provided the answer.
The daily energy expenditures of National Weight Control Registry members sheds light on the inner workings of our evolved metabolic engines. For one thing, they suggest that the daily energy intake that our hypothalamus targets doesn’t change much after diet-induced weight loss, even after we’ve maintained a lower weight for years, and even when the starvation response has passed and BMR has returned to normal. Perhaps some deep, distant echo of the starvation response drives the hypothalamus to retain its old target for food intake. Another possibility is that the constraints on daily energy expenditure affect the regulation of energy intake as well, and that the body resists any changes to the calories it brings in. Either way, it’s a problem. As we discussed in Chapter 3, weight loss lowers our daily energy expenditure. If our hypothalamic hunger and satiety systems continue to target our pre-weight-loss intake, we’ll be pushed to eat more calories than we burn. As a result, we’ll slowly gain the weight back, until our body weight and daily energy expenditure are right back where they were before we lost weight. Sound familiar?
Exercise is one way to maintain weight loss in a constrained energy expenditure world, allowing people who’ve lost weight to retain their old, pre-weight-loss daily intakes and expenditures without regaining weight. As we discussed above, exercise also seems to help the brain do a better job matching eating and expenditure. It’s likely that exercise does both for successful weight-loss maintainers, pushing daily energy expenditure back toward pre-weight-loss levels and helping to regulate food intake.
A few years ago, at a conference on metabolism, I found myself at the hotel bar late in the evening, talking to a colleague who has spent his career investigating energy expenditure and obesity. I had given a talk earlier in the day, laying out the evidence that daily energy expenditure is constrained. The details are a little foggy, but the conversation went something like this.
“You might be right,” he said, “that exercise doesn’t do much to increase daily energy expenditure or lose weight. But you have to be careful. Once people find out that exercise won’t help them lose weight, they’ll stop doing it. Avoiding death isn’t a big enough incentive. The only reliable motivation to exercise is vanity.”
It was an unfiltered take on the inherent weakness of the human species from a frustrated scientist who knew the score. I suspect he was right. When it comes to our inner desires, our lazy ape relatives are more of a mirror than we’d care to admit. Deep in our subconscious, we still yearn to lie around all day, eating and grooming. The industrialized human zoos we’ve built ourselves make it all too easy. Of course we’d like to avoid heart disease. But first we’d like to check our phones. Maybe get a snack. Relax a little. If exercise isn’t going to make me look hot, it can wait.
The danger, though, in selling exercise as a way to lose weight is that it doesn’t work. Eventually, people notice the results don’t match the sales pitch. Some will keep with it anyway, hooked by the many other benefits of exercise—improved mood, clearer minds, stronger body—and willing to overlook the bait and switch. But there would be more happy customers if those of us in public health were honest about what we’re selling. Exercise won’t keep you thin, but it will keep you alive.
Exercise does much more than rev our metabolic engines. It’s the rhythm section of our vast internal orchestra, keeping our 37 trillion cells on the same beat. Constrained daily energy expenditure doesn’t diminish the importance of physical activity. To the contrary. The fact that daily energy expenditure is constrained helps explain why exercise has such pervasive effects throughout the body. My lab and others are busy with the painstaking work of unraveling the impact of exercise on our other systems. It’s an exciting time to explore. There is undoubtedly much more to exercise’s impact on metabolism and the rest of our body waiting to be discovered.
Still, the evidence for constrained daily energy expenditure raises other questions. How can we reconcile the idea that energy expenditure is limited with the jaw-dropping workout regimens we see in elite athletes, mountaineers, and Arctic explorers? As we’ll see in the last two chapters, the metabolic machinery that powers an Ironman triathlete, a Tour de France cyclist, or an Arctic trekker is the same that fuels a pregnant mother. And yet those feats, impressive as they are, do not tell the whole story of our ravenous appetite for energy. As our species has evolved, our energy demands have grown beyond what our own bodies can provide. The calories that each of us command today shape the modern world—and threaten our long-term survival.