The Man Who Touched His Own Heart

by Rob Dunn

  When West began to consider the general laws of the heart, he did so, as he later would with cities, naively. It was, he said, “like learning about sex on the street.”5 He read up about the heart in a high-school textbook, the only thing lying around. It was enough to get him excited. Then he began to read the older literature on scaling and the body and he became fascinated with the ways in which hearts differ among peoples and species. West found that heart rates varied widely among animals. Yet this variation followed a simple pattern: the larger the animal, the slower its heart.

  This idea is not new. Any hunter knows the hearts of smaller mammals tend to beat faster than those of larger ones. If you catch a mouse and lift it up, you can feel its tiny heart zooming in your hands. If you ride an elephant or a big horse, its heart beats slowly and deliberately against your legs. What is relatively new is the sophistication of the explanation for this pattern and the awareness of its universality. The explanation comes in nested pieces.

  In articles by his intellectual antecedents, such as Max Kleiber, among dozens of others, West read observation after observation about heart rate that appealed to him. Generations of biologists had studied the metabolism of the human body, its energy use, from the perspective of physics. At the most basic level, these biologists noted that the hearts of smaller animals beat faster and each of their individual cells used more energy. Larger animals were like bigger cities: they simply used less energy per capita (where the capita was a cell rather than a person).6 The existence of this relationship had been well explored. It had even been described as a law, the quarter-power scaling law, a reference to the slope of the relationship between body size and metabolism. It is on the basis of this law that drug doses, whether statins, beta blockers, or anything else, are calculated. But its cause remained baffling; many theories had been offered, typically having to do with the relative ease of heating a larger body as opposed to a smaller one, but none of them quite worked. The attempt to explain how and why metabolism, body size, and heart rate related to one another had reached an impasse. West picked it up as if it were an abandoned toy and started playing with it.

  West began with the physics of cells and blood vessels in order to work his way back to the heart (and maybe even to the question of how long an animal like him would live, a question that leaped like a hard-to-catch fish through the marginal waters of his mind). Arteries were like highways, capillaries like back alleys, and blood cells like food trucks, he thought. Their features must relate to the size of an organism, just as their parallel features in a city related to its size. This was not new to the world, just to West, and yet it was compelling. He read as much as he could find about the biology of the body. He met biologists and drained their brains of anything that seemed like it might be of use. When this was not enough, he started collaborating with two of these biologists, Jim Brown and Brian Enquist, then both at the University of New Mexico (and both as ambitious and far-reaching as West). Together, the three began to see patterns they thought others had missed, a kind of underlying mathematics of cells, vessels, and pumps. With these patterns in mind, they used their computers to build a simulated system of blood vessels, a fractal system in which each main branch diverged into ever smaller branches until they arrived at the smallest vessels, the capillaries. The scientists wanted to devise the simplest computer model of blood vessels that could account for the differences among types of organisms. As they started to build this model, they stumbled upon an empirical observation that would prove important, a way in which evolved bodies differed from simulated ones. In theory, a model of the blood vessels could produce infinitely smaller and smaller branches so that a (simulated) big animal could have enough capillaries to get to every cell. But what the trio noticed was that actual human capillaries did not get smaller and smaller. In fact, all of the capillaries in a body are essentially the same size. More than that, capillaries in different animals all seem to be that same size too (just as the size of the smallest vessels are invariant among plants). The capillary’s size is set by the width of a blood cell (capillaries are all one cell wide). This means that the capillaries of a shrew, for example, are much larger relative to its body than the capillaries of, say, a blue whale.

  The sameness of capillaries meant that there were physical limits to blood vessels reaching cells, limits very similar to those present in the streets of cities (which never get narrower than one car wide). As animals get bigger and bigger, their body volumes increase, and the number of capillaries must also increase in relation to that volume. But as it does, something else happens. As the number of capillaries rises, the volume of blood increases, since blood has to get to all of the capillaries. As a result, the heart of a larger animal must pump much more blood. But even though the size of the heart (and its major vessels) can get bigger and bigger, the ability of the heart to get oxygenated blood quickly to every cell in the body decreases. The blood vessels must branch more and more times to meet the demand of the larger volume, and so it takes longer to get the blood throughout the body, and the concentration of oxygen in the farthest capillaries declines. Because it also takes longer for the blood to get back to the heart, the heart rate slows, as does the metabolic rate of each and every cell of the body (which is why larger animals are, all other things being equal, a little cooler than smaller ones). This was, it seemed to West and his new friends, the mechanism lurking behind the ancient relationship between body size and metabolism. Just as in cities, it was a constraint of how roads work; there are relatively few ways of getting from here to there when the width of the path is unalterable.

  Based on an understanding of the capillaries and a model of the fractal connections of blood vessels of larger and larger diameters, West, Enquist, and Brown can predict, in a simulated world, not only the metabolic rate of a mammal but also its number of capillaries, aorta size, and heart rate as a function of its size. What is more, the slopes of the relationships broadly match up with those seen in nature. Add a factor to account for body temperature, and they can predict those same features in birds, reptiles, and frogs too. The same math also seems to hold for plants, at least for their vessels and metabolic rates.7 No animal escapes these associations; no animal escapes the math of West and his colleagues.8 “Sometimes,” West said once, “I look out at nature and think, Everything here is obeying my conjecture.” It’s as though he were the wizard behind the screen, calling each animal into existence.

  Perhaps not surprisingly, West’s laws are subject to great argument among biologists. Some biologists feel they have simpler models that work just as well. Others debate whether he has explained why these patterns among bodies or cities exist; they argue over the extent to which West has sacrificed the interesting details of the living world, the important particulars, in search of, perhaps, overly simplified generalizations. They debate the slopes of relationships. West’s laws are undeniably coarse and sweeping, but it is their sweep that makes them interesting. These laws can even account for changes in our bodies as we age and our bodies get bigger. The hearts of babies beat far faster than those of adults (the heart rate of a newborn is a supercharged 185 beats per minute). The heart must do this to keep the baby’s body warm (within a species, this relationship has its limits. Obese individuals do not have slower hearts, even though it is much easier for obese people to keep themselves warm).

  But West can predict more than how a body works; he can also predict how it will fail to work. This was where cities and bodies diverged; cities fail, sure, but they do not appear to have a natural longevity per se. Not so bodies. Bodies fail on some sort of schedule, and West thinks he can explain when and why. These predictions won’t lead anyone to the fountain of youth, but they may explain why the fountain of youth is desired in the first place. As West put it in John Whitfield’s book In the Beat of a Heart, “If biology is to be a real science, you ought to have a theory that can predict why we live 100 years.” He then proceeded to extend his math and physics and insights
a little further still.

  The life expectancy of mammal species as a function of their resting heart rates. Mammals (and birds, not shown) with high resting heart rates tend to live fewer years than mammals with lower resting heart rates; nearly all mammals get about a billion heartbeats. Historically, humans are no different, but with public health and modern medicine we have escaped these constraints and, in doing so, live out about a billion extra beats.

  We tend to take it for granted that the life expectancies of different organisms are different. We talk about “human years,” for example, as compared to “dog years.” But it is not obvious that longevity should vary. Mammal cells, after all, are essentially the same. Yet, as West found in the literature, with a pen and paper, you can graph the relationship between heart rate and the maximum longevity of a species, or how long individuals under the best of circumstances live. So far, nearly without exception, the longevity of a species is predicted by its heart rate. The relationship is a straight line on a semi-log plot. Species whose hearts beat faster live fewer years. An Etruscan shrew lives one year, a blue whale more than a hundred years. In these lives, their hearts beat about the same number of times: one billion. West thinks this longevity follows from the sizes of bodies, which in turn relates to the rate of hearts. From West’s perspective, the rate of the human heart determines the maximum sustainable metabolic rate and activity level of each cell and, within each cell, each mitochondrion. Indirectly, then, West thinks, body size and heart rate are a measure of how much wear there is on each tiny and large part of the body.9 This wear influences everything, from the buildup of atherosclerosis in arteries to the ability of the body to continue to feed beneficial microbes.

  Ultimately, in accordance with West’s laws, all wild species get a maximum of about a billion heartbeats.10 The only difference is the time over which the beats occur. A shrew uses its heartbeats quickly; a whale savors them, lounging as blood flows from its big muscle out to its brain and its long, long tail. But could our fates, human fates, really be predicated simply on the number of beats of our hearts, and if so, what do such predictions, leveraged from comparisons among species on separate evolutionary trajectories, say about our fates?

  Of course, a truck can hit an animal. Animals can be struck by lightning. They can be eaten. Many calamities befall them (and us), as they always have. Heart rates, though, seem tied to the maximum life span an individual in a population of a species can expect to live if everything goes right. But what about humans? Historically, the life expectancy of a human in a small population was around forty years, somewhere between the shrew’s life span and the whale’s; it falls right where it would be expected to, given the human heart rate and body size. Historically, humans too got about one billion beats.

  If heart rate really does affect an organism’s fate so strongly, one can gin up a few hypotheses in need of testing, particularly if one begins by assuming (as most scientists have) that heartbeats actually use up the body in some way or another, breaking it down in ways it cannot repair. The first, most obvious prediction—if heart rate really influences our longevity—would be that organisms who can slow down their hearts, whether through hibernation or torpor, should live lives longer than would be expected given their average heart rate in their active months. In slowing themselves, they should get a number of days or even years of free ride.

  Animal hearts slow to differing degrees when they need to. Blue-whale heart rates slow when the whales dive (to as few as three beats per minute). Blue-throated-hummingbird hearts beat up to twelve hundred times per minute when they are flying but drop to thirty beats per minute when they are asleep. More conspicuously, the hearts of many mammals slow when they hibernate.

  We tend to think of bears when we think of hibernation, but research has shown that bears are not actually true hibernators.11 They slow their hearts, but their bodies remain warm, so they are somewhat awake the entire winter, ready to take advantage of a good day. Their hearts slow the way yours might if you were practicing yoga. In one study in India in which one group of participants practiced yoga for ten days and another group did not, those who did not saw no change in their resting heart rates, while those who had practiced yoga saw their resting heart rates decline by about eleven beats per minute, even though they had done it for only ten days, and even if they hated yoga.12 Yoga practitioners, in other words, enjoy a sort of permanent hibernation not unlike that which yields sleepy (but testy) bears.13

  Both bears and yogis might be expected to have longer life expectancies than they would if their heart rates were high year-round, but for a more extreme case, we need to turn to the groundhog. Groundhogs (Marmota monax)—also known as whistle pigs or woodchucks—live in grassy areas throughout North America and resemble inflated squirrels.14 Groundhogs are conspicuously fat. They can weigh as much as thirty pounds, and they spend their days walking slowly up hills and down dales, eating.

  Groundhogs have the sort of body type one might imagine could exist only on an island where there were no predators. They remind me of miniature elephants, giant tortoises, and other unfathomable beasts of distant, predator-free lands.15 Groundhogs, though, have an escape plan. They dig deep warrens in the ground into which they plunge at anything remotely resembling danger. Each warren has four or five separate entrances. This is what has saved them from many predators over the several million years of their species’ existence. The predator lunges, runs, or jumps, and the groundhogs dive. The groundhog is one of the silliest-looking mammals in the world, but it proved important in one area of the study of the heart.

  The big challenge for groundhogs is winter, when their food disappears beneath the snow. Larger herbivores deal with such scarcity by moving: caribou migrate and moose stroll and amble and reach higher into the trees. The groundhog has no such luxury; it is chained to the safety of its hole and is too fat to get very far. It must hibernate, and it must hibernate well enough that it is not forced to vacate its safe residence to look for food that is just not around. Hibernation in the style of the bear is relatively easy. Bears eat until they are bulbously round and then camp out in a cave and let the fat burn off. If they get too hungry, they go out and munch something.

  Humans could almost hibernate bear-style, but not groundhog-style. The groundhog goes underground in the late fall and, when it does, turns its body temperature down so far that its core temperature decreases ten degrees centigrade, from 38 degrees C down to 10 degrees C, so far that it doesn’t really need to be that fat to survive the winter, so far that its heartbeat slows dramatically. Its metabolism is 1 percent of normal.16 If the allometricians are right, the groundhog should have a maximum life expectancy that is much longer than might be predicted given its size and normal resting heart rate. It should get bonus years in proportion to the number of heartbeats it saves thanks to its long winter’s rest.

  The summertime heart rate of the groundhog is an ordinary eighty-nine beats a minute, slightly faster than yours or mine. But the wintertime heart rate of the groundhog is just ten beats per minute. And, indeed, the groundhog lives 30 percent longer than we would expect it to based on its summer heart rate. Its winter doze does it good, allowing it to space out its billion beats over a longer period.

  It turns out the groundhog is not alone. All organisms that hibernate add years to their lives, and the more fully they hibernate, the more years they get. This even works when we look at a group of organisms in which some but not all hibernate. Bats that hibernate, for example, live longer than those that do not.

  Nor is hibernation the only slowed-time behavior that has an impact. Hummingbird hearts beat more than a thousand beats per minute when they are flying, but when they land, their heart rates decline to just sixty beats a minute. At night, when they sleep, their hearts nearly stop. As a consequence, hummingbirds live much longer than shrews, even though both of their hearts can beat very, very fast; shrews never slow down. It really does look as though, if you know how many heartbeats a
n animal has—no matter when or in what bursts—you can predict how long it will live. Essentially all tests of this suggest a natural limit to the number of heartbeats an animal gets. All wild animals get about a billion beats; they just get to use them slow (if they are big or hibernate) or fast. Cats may have nine lives, but they too get just the standard number of heartbeats, a billion, give or take, and no more.

  West’s law linking mitochondria, metabolism, body size, heart rate, and longevity has the potential to lead to many insights about the limits of our bodies and hearts. But the idea of studying hibernating mammals and their slow hearts to extend human lives is not totally new. Long before the modern research on heart rate and life expectancy, there was a study on heart rate in groundhogs that yielded what seemed like one of medicine’s most penetrating insights, an insight about the potential to slow our own hearts down and, in doing so, extend our lives.

  In the late 1940s, W. G. Bigelow was a rather ordinary surgeon and researcher at the University of Toronto. He was interested in the heart, but not unusually so. Like many, he wanted to figure out a way to conduct successful heart surgeries. In the 1940s, the chest had been opened and the heart operated on, but there was that limit to what was possible, that old three-minute problem. At about the time that Gibbon went to war, leaving his heart-lung machine at home, Bigelow stumbled on another approach. He had been puzzling over how to better operate on the heart when, fortuitously, a man came into his office suffering from frostbite. Bigelow noted that the man’s heart was beating more slowly than it normally would, and yet he was alive. Seeing this, Bigelow began to think about the ways in which bodies could be cooled, and it led him to the controversial theory that human bodies could be cooled in order to allow heart surgeries to be more easily performed or even, more generally, to extend lives.