The Sports Gene: Inside the Science of Extraordinary Athletic Performance (19 page)

The Jamaican sprint system resembles football in the United States, replete with its own shady boosters. (Several high school coaches at Champs told me that they are now banned from giving refrigerators to parents in an effort to recruit their children.) This island-wide, sprint-talent-spotting-and-capture system has paid off in Olympic gold for Jamaica. None other than Usain Bolt pined to be a cricket star in his youth (his second choice was soccer) until he started blowing away his peers in sprints on sports day and was pushed into track and field as a fourteen-year-old—and even then was renowned for ditching practice—ultimately setting Champs records in the 200 and 400 in 2003. Yohan Blake, Bolt’s training partner who finished second to him in the 100 and 200 at the 2012 London Olympics, also wanted to be a
cricketer, but was identified as a sprinter during sports day at age twelve. Even top American sprinters often come via the Jamaican talent-spotting system. Sanya Richards-Ross, an American who won gold in the 400-meters in London, lived in Jamaica until she was twelve and was plucked by a primary school track coach when, at seven years old, she outstripped older girls in races on sports day. “The coach said, ‘Yep, you’re coming out for the track team,’” Richards-Ross says.

Physiology findings indicate that endurance training can enhance the ability of fast-twitch muscle fibers to resist fatigue, but that sprint training does not increase the speed at which slow-twitch fibers contract. So being endowed with a large proportion of fast-twitch fibers is essential for an elite sprinter. Or, in the dogma of football coaches: “You can’t teach speed.” This is an exaggeration, as speed—and certainly the ability to sustain speed—can be improved. But recall the Netherlands’ Groningen soccer talent studies. No matter the training, the slow kids never catch up to the fast kids in sprint speed. And the words of Justin Durandt, manager of the Discovery High Performance Centre at the Sports Science Institute of South Africa: “We’ve tested over ten thousand boys, and I’ve never seen a boy who was slow become fast.” Slow kids
never
make fast adults. So keeping the swiftest kids in the sprint pipeline is paramount. And in what country other than Jamaica could a boy with blinding speed and who stands 6'4" at the age of fifteen, as Bolt did, end up anywhere but on the basketball or volleyball court or the football field? If he’s born in the United States, Bolt is no doubt ushered toward the path of towering speedsters like Randy Moss (6'4") and Calvin Johnson (6'5"), both large, fast NFL wide receivers who made many millions of dollars. (Johnson’s size and speed helped him land a $132 million contract in 2012.)

The sprint results at Champs are actually comparable to those at state championship meets in big sprinting states, like Texas, and the Champs atmosphere has its fervor in common with Texas high school football. But scores of America’s would-be Olympic sprinters land instead in sports that are more popular in the United States, like
basketball and football. (A Jamaican sportswriter I met at Champs was concerned that the rising popularity of basketball on the island could siphon off track talent.)

Trindon Holliday, an NFL wide receiver, was such an outstanding sprinter at Louisiana State University that he beat Florida State’s Walter Dix—who would take bronze behind Bolt in Beijing—in the 100-meters at the 2007 U.S. national championships, but subsequently gave up his spot on the U.S. world championship team so that he wouldn’t miss a day of preseason practice for LSU football. Xavier Carter, who was at LSU at the same time as Holliday, chose to go pro as a sprinter only after failing to make an impact as a wide receiver in two years with the football team. In Jamaica, a key to world sprint domination is keeping the best sprinters on the track.

It is the island-wide talent-spotting system—in which every kid is made to try sprinting at some point—that Pitsiladis credits with Jamaican sprint success. Not to say that genes don’t matter. “You absolutely must choose your parents correctly to be a world record holder,” he says, rhetorically. “But Jamaica has thousands and thousands sprinting, and you get the best coming through. That’s what accounts for this phenomenon. If you had this in any other country, you would see exactly the same thing.”

When a Scottish publication solicited Pitsiladis’s advice for aspiring United Kingdom athletes, he responded: “Go into sprinting. Don’t worry because you’re white. It’s got nothing to do with the color of your skin.”

His friend and colleague Errol Morrison would heartily disagree.

Malaria and Muscle Fibers

C
ompared with Europeans, Jamaicans have longer legs relative to body height, and more narrow hips. This, Morrison says, is inarguable.

That Jamaicans would have a more linear build than Europeans is no surprise, nor is it specific to Jamaicans. As Allen’s rule of body proportions dictates, men and women with recent ancestry from low latitudes and warm climates generally have proportionally long limbs. Another ecogeographic principle, known as Bergmann’s rule—named for nineteenth-century biologist Carl Bergmann—indicates that humans with recent low latitude ancestry will also tend to be more narrow, with slimmer pelvic bones. Both long legs and narrow hips are advantageous for running and jumping. All other factors being equal, maximum running speed scales with the square root of leg length. But the theory of western African sprint dominance that Morrison coauthored is a thesis entirely apart from these anatomical concerns.

In 2006, Morrison, with Patrick Cooper, proposed in the
West Indian Medical Journal
that rampant malaria along the west coast of Africa, from where slaves were taken, led to specific genetic and metabolic alterations beneficial for sprint and power sports. The hypothesis: that malaria in western Africa forced the proliferation of genes that protect against it, and that those genes, which reduce an individual’s ability to
make energy aerobically, led to a shift to more fast-twitch muscle fibers, which are less dependent upon oxygen for energy production. Morrison helped with the biology details, but the fundamental idea originally came from Cooper, a writer and childhood friend of Morrison’s.

Cooper was a polymath who had professional success in jobs ranging from music recording to writing speeches for Norman Manley, an architect of Jamaica’s independence, and then for his son, Prime Minister Michael Manley. Early in his career, Cooper had been a reporter for
The Gleaner
, Jamaica’s largest newspaper. Working at
The Gleaner
’s sports desk, he first surmised that white athletes had historically dominated sprint and power sports only by systematically excluding or dodging black athletes, like boxing champion Jack Johnson. In later writing, Cooper meticulously documented the fact that athletes with western African heritage become highly overrepresented in sprint and power sports almost immediately once they are allowed a fraction of their white counterparts’ access to sports. Cooper highlighted trends that continue today: At every Olympics after the U.S. boycott of 1980, every single finalist in the men’s Olympic 100-meters, despite homelands that span from Canada to the Netherlands, Portugal, and Nigeria, has his recent ancestry in sub-Saharan West Africa. (The same has been true for women at the last two Olympics, and all but one female winner since the U.S.-boycotted 1980 Games has been of recent western African descent.) And there has not been a white NFL player at cornerback, football’s speediest position, in more than a decade.
*

As a speechwriter during Michael Manley’s combative 1976 reelec
tion campaign, Cooper and his family were under constant threat. Cooper stopped sitting with his back to windows, and when his wife, Juin, was held up at gunpoint, he moved the family away from Jamaica, for good. Living in Houston in the late 1980s, Cooper haunted the library, stalking historical and biological explanations for the dominance of black athletes in sprint sports. Cooper read voraciously from scientific publications in biology, medicine, anthropology, and history in a manner that few ever did prior to the advent of electronic databases that sift scholarly journals with a keystroke.

Cooper found the famous body types study of 1968 Olympians, and he latched on to a curious side note recorded by the scientists. The researchers had been surprised to find that “a sizeable number of Negroid Olympic athletes manifested the sickle-cell trait.” That is, some black Olympians had, in one of two copies of the gene that codes for hemoglobin—the oxygen-carrying molecule in red blood cells—a mutation that causes round red blood cells to curl up in a sickle shape in the absence of oxygen, potentially impairing blood flow through the body during vigorous exercise. The gene variant that causes sickle-cell trait is found most often in people with recent sub-Saharan ancestry in west or central Africa, and scientists had previously believed that the high altitude of the 1968 Mexico City Olympics would prevent athletes with sickle-cell trait from performing well. “Sickle-cell was supposed to be a deterrent,” Morrison says. But it made no difference at the Olympics in events of short duration, like sprints and jumps.

In the decades since, epidemiological studies have found that athletes with sickle-cell trait (they have one copy of the mutant gene and are known as “sickle-cell carriers”) are indeed underrepresented in athletic endeavors that require aerobic endurance. In competitive running, sickle-cell carriers all but disappear in events longer than 800 meters. They are genetically disadvantaged for long-distance sports. In a small number of sickle-cell carriers, blood flow is inhibited to such a degree as to become deadly if they work out too hard for too long. Since 2000, the sudden deaths of nine college football players—all of them
black and in Division I—during training have been tied to sickle-cell trait, and the NCAA now requires screening for the gene variant that causes it. (According to a panel at the 2012 Big East Conference Sports Medicine Society, white college athletes, on the advice of a team doctor, will often sign a waiver to forgo the testing, given the unlikelihood that they carry the sickle-cell gene variant.)

In 1975, the year after the Mexico City Olympics data was published, another study appeared that Cooper would dissect two decades later, this one showing naturally low hemoglobin levels in African Americans. The work was published in the
Journal of the National Medical Association
, run by the Maryland-based National Medical Association, which promotes the interests of physicians and patients of recent African descent. Using data from nearly 30,000 people in ten different states, with ages ranging from the first year to the ninth decade, it reported that African Americans have lower hemoglobin levels at every stage of life than white Americans, even when socioeconomic status and diet are matched. (Errol Morrison’s wife, Fay Whitbourne, formerly head of Jamaica’s National Public Health Laboratory Services, says that hemoglobin levels among Jamaicans are in line with those of African Americans.) Numerous studies, as well as population data from the U.S. National Center for Health Statistics, have replicated this result in the years since, including in athletes. In a colossal 2010 study of 715,000 blood donors across America, researchers wrote that African Americans exhibit a “lower genetic set point for hemoglobin,” regardless of environmental factors like nutrition.
*
Like sickle-cell trait, genetically low hemoglobin—all else being equal—is a genetic
disadvantage
for endurance sports. Runners of recent western African descent are very much underrepresented at high levels of distance running. (The Jamaican record in the 10K would not even have qualified for the 2012 Olympics)

The authors of the
Journal of the National Medical Association
paper
wrote that lower hemoglobin levels raise the possibility that African Americans employ more of some alternate energy pathway to compensate for a relative lack of oxygen-carrying hemoglobin. Two years later, in the same journal, another group of scientists insisted: “some compensatory mechanism must exist to counteract this relative deficiency in hemoglobin, since a significant difference has even been demonstrated in healthy athletes.” Cooper set out to find that compensatory mechanism.

His tireless perusal of medical journals took on greater urgency in 1996, when he was diagnosed with terminal prostate cancer. Cooper and Juin moved to New York City in 2000 so that Cooper could spend every day at the New York Public Library. “My office,” he called it. Weekend trips to Baltimore to visit his daughter doubled as visits to the University of Maryland library.

And then Cooper found just the potential “compensatory mechanism” he was looking for, in a 1986 study from Laval University in Quebec published in the
Journal of Applied Physiology
and coauthored by Claude Bouchard, who would go on to become the most influential figure in the field of exercise genetics, and the leader of the HERITAGE Family Study that documented aerobic trainability differences among families. Bouchard and colleagues took muscle samples from the thighs of two dozen sedentary Laval students, primarily from countries in western Africa, as well as from two dozen sedentary white students, who were identical to the African students in age, height, and weight. The researchers reported that a higher proportion of muscle in the African students was composed of fast-twitch muscle fibers, and a lower proportion was slow-twitch muscle fibers compared with the white students. The African students also had significantly higher activity in the metabolic pathways that rely less on oxygen to create energy and that are engaged during an all-out sprint. The scientists concluded that, relative to the white students, the students from western Africa “are, in terms of skeletal muscle characteristics, well endowed for sport events of short duration.”

The study was small, as usual with biopsy studies that require the surgical removal of a gobbet of muscle tissue. The few similar studies over the years have generally agreed with the Laval findings, but each one has relied on a small number of subjects.
*

In his 2003 book,
Black Superman: A Cultural and Biological History of the People Who Became the World’s Greatest Athletes
, and then in his 2006 paper with Morrison, Cooper first made the argument that West Africans evolved characteristics like a high prevalence of the sickle-cell gene mutation and other gene mutations that cause low hemoglobin for protection from malaria, and that an increase in fast-twitch muscle fibers followed from that, providing more energy production from a pathway that
does not
rely primarily on oxygen, for people who have reduced capacity to produce energy
with
oxygen. The former part of Cooper’s hypothesis—that sickle-cell trait and low hemoglobin are evolutionary adaptations to malaria—now seems undeniable.

In 1954, the same year Sir Roger Bannister broke the four-minute mile, British physician and biochemist Anthony C. Allison, who had been raised on a farm in Kenya, showed that sub-Saharan Africans with sickle-cell trait have far fewer malaria parasites in their blood than inhabitants of the same region who do not have sickle-cell trait. Normally, the sickle-cell gene variant seems like a bad thing to carry. If two people who each have one copy have kids together, one in four of their children will have two copies of the gene and therefore sickle-cell
disease
—also known as sickle-cell anemia—a condition in which sickled blood cells exist even without exercise, and life expectancy is reduced. And yet, this gene mutation has hung
around—proliferated, actually—in the malaria danger zones of sub-Saharan Africa.

That is because people who have one copy of the sickle-cell gene variant are generally healthy, but have red blood cells that sickle when infected with the malaria parasite, which in turn protects the host from the parasite’s devastating effects. (Because sickle-cell disease shortens lives, the sickle-cell gene will never spread through an entire population. Among African Americans who have lived in the malaria-free United States for generations, the sickle-cell gene variant is steadily disappearing.) Today, the sickle-cell balance with malaria resistance is one of biology’s textbook examples of an evolutionary tradeoff, propagating an otherwise harmful gene variant because of an associated protection.

Cooper and Morrison’s suggestion that low hemoglobin in African Americans and Afro-Caribbeans is a second adaptation to malaria has been proven true as well, in a deadly manner.

Even as evidence mounted that low hemoglobin levels in Africans native to malarial zones is at least partly genetic, aid workers in Africa looked upon low hemoglobin as a sign purely of a diet with too little iron. In 2001, the United Nations General Assembly charged the world with reducing iron deficiency among children in developing nations. And so, in a well-intended effort to improve nutrition, health-care providers descended on Africa with iron supplements, which raise the hemoglobin levels of those who consume them. (Hemoglobin is an iron-rich protein, so levels fall if insufficient iron is consumed. Often the first thing elite endurance athletes check for if they start performing poorly is a low iron level.)

The problem was that doctors who studied malarial regions saw increased cases of severe malaria wherever iron supplements were dispensed. Since the 1980s, scientists working in Africa and Asia had documented lower rates of malaria death in people with low hemoglobin levels. In 2006, following a large, randomized, placebo-controlled study in Zanzibar that reported a stark increase in malaria illness and
death among children given iron supplements, the World Health Organization issued a statement backtracking from the earlier UN position and cautioning health workers about giving iron supplements in areas with high malaria risk. Low hemoglobin, like sickle-cell trait, is apparently protective against malaria. And, in keeping with Cooper and Morrison’s hypothesis, many Africans who were forcibly taken to the Caribbean and North America came from the precise parts of the west coast of sub-Saharan Africa that suffer the highest rates of malaria illness and death in the world, as well as the greatest frequency of the sickle-cell gene.

It is the coda of the Cooper and Morrison hypothesis—that fast-twitch muscle fibers moved in as hemoglobin moved out—that is highly speculative.

To the end of his life, Patrick Cooper remained dedicated to his research and writing. Up until the day in 2009 that cancer finally overwhelmed him, Cooper was dictating to Juin from his bed. I had been hoping to meet Cooper on my trip to Jamaica before I learned that he had passed away and hadn’t been living in Jamaica for years anyway. Instead, I met with Morrison and then presented the paper he and Cooper coauthored to five scientists who were not previously familiar with it, and asked their opinions. One insisted that the theory was too speculative to discuss. The other four said that it was a reasonably constructed hypothesis, but also that it had never been directly tested and was not proven. (In 2011, though, scientists from the University of Copenhagen proposed that a high proportion of fast-twitch muscle fibers could account for several physical traits that have been documented in African Americans and Afro-Caribbeans, including low resting and sleeping metabolism, and less metabolism of fat for energy and more of carbohydrates as compared with Europeans.)