Preordained Peak Performance

By Editorial Staff · September 2002 · pp. 77-95 · 32 min read

Preordained Peak Performance

FeatureVol. 6, No. 5 (2002)September 200230 min readpp. 77-95

LET’S START with a few safe predictions. All of the sprinters in the men’s 100-meter final at the Athens Olympics in 2004 will trace their ancestry to West Africa. Almost all of the world-class throwers, shot-putters, and weightlifters will be white, mostly of Eurasian ancestry. And distance races, from 800 meters to the marathon, will be dominated by North and East Africans.

Of course there will be exceptions to this pattern, perhaps a breakthrough marathon by an Ecuadorian or a 1,500-meter scamper by a Russian woman. But by and large, don’t place your bets on the long-promised and ever-elusive resurgence of the United States, Britain, or Europe in distance running: won’t happen, can’t happen.

Not too long ago, distance running was dominated by a bloodline of the Flying Finns, the British and Scottish middle-distance contingent of Sebastian Coe, Steve Ovett, Steve Cram, and Peter Elliott, and a potpourri of great Australians and Americans. Today, runners from countries of European stock are invariably the also-rans in a field dominated by Africans. In the world rankings, which combine race results from the 800 meters to the marathon, Kenyan men and women head the list and hold 8 of the top 10 places. Hicham El Guerrouj of Morocco, an undefeated double world champion, and the fastest woman marathoner in history, Catherine Ndereba of Kenya, were named Runner’s World magazine’s male and female Runners of the Year for 2001.

NATURE VERSUS NURTURE

What’s behind this extraordinary phenomenon? There are two conflicting theories. While one is heard in the back of the local pub, sotto voce—we’ll discuss this in a moment—the common wisdom proclaims that the eclipse of the Western runner demonstrates the affliction of affluence and the incredible hard work of desperately poor but ambitious Africans.

There is some—if limited—truth to that. But common sense—and overwhelming scientific evidence—forces one to ask whether hungry athletes can somehow transform themselves into elite competitors through dedication alone? Or, put another way: do hard work and opportunity trump innate capacity?

That’s Sebastian Coe’s belief. “So where is the problem [of the failure of the rest of the world versus the East and North Africans]?” mused Coe shortly before the 2001 World Championships in Edmonton, where African athletes swept two-thirds of the running medals. “The answer, I rather fancy, as Shakespeare said, ‘lies not in the stars but in our hands’—run faster.” Coe exhorted aspiring runners to train with the “brutal” commitment of the Kenyans. “The mental and physical intensity of what was commonplace 20 years ago,” he added modestly.

Here’s a wake-up call, Sebastian: one might as well look to the stars because the epicenter of world distance running has shifted decidedly—and permanently—to East and North Africa. And cultural trends have little to do with it.

“Very many in sports physiology would like to believe that it is training, the environment, what you eat that play the most important role,” states Bengt Saltin, director of the renowned Copenhagen Muscle Research Center, who has outlined his findings in Scientific American. “But we argue based on the data that it is ‘in your genes’ whether or not you are talented or whether you will become talented. The extent of the environment can always be discussed, but it’s less than 20, 25 percent.”

Cultural factors certainly play a role in which sports one might play. There are no great ice curlers or cricket players from Texas—black, white, or Hispanic. But all of the focus and training in the world are unlikely to turn a Texan into a Kenyan-challenging marathoner. Trainers, nutritionists, and coaches are not alchemists. One cannot turn clay into marble.

The driving explanation for African domination of running, it turns out, can be found mostly in the genes. “Africans are naturally, genetically, more likely to have less body fat, which is a critical edge in elite running,” notes Joseph Graves Jr., an African American evolutionary biologist at Arizona State University. “Evolution has shaped body types and in part athletic possibilities. Don’t expect an Eskimo to show up on an NBA court or a Watusi to win the world weightlifting championship. Differences don’t necessarily correlate with skin color but rather with geography and climate. Genes play a major role in this.”

Highly heritable characteristics such as skeletal structure, muscle fiber types, reflex capabilities, metabolic efficiency, and lung capacity are not evenly distributed among populations and cannot be explained by known environmental factors. Though individual success is about opportunity and “fire in the belly,” thousands of years of evolution have left a distinct footprint on the world’s athletic map.

KENYA AND GENES

For decades, the “Flying Finns” were the world’s best distance runners, their wins multiplying in tandem with their growing nationalist tradition of success. The Finns were eventually eclipsed by the great Anglo tradition represented by such runners as Coe. But in the past 15 years, as the door of opportunity creaked opened to less-developed nations, the center of gravity in distance running has shifted to North and East Africa.

According to some, the cycle of history suggests that no population has a lock on distance-running success. Surely, they say, Kenyan dominance will fade, much as it did for the Finns, and the trend will shift once again to another nation? Not so fast. To flesh out this debate, it’s instructive to assess how a small East African country, with a population of less than 30 million, has emerged as the greatest per capita concentration of raw athletic talent in the history of the world.

Kenya’s national sport drives its countrymen to intense public displays of passion. It’s a cultural heritage. The national and occasional African championship events draw tens of thousands of adoring fans to the National Stadium in Nairobi. The best players are icons. The selection process to spot the great stars begins at a very young age. Government coaches comb the countryside to ferret out the next generation of potential stars. The most promising are sent to special schools. It’s not an exaggeration to call Kenya’s most popular sport a kind of national religion.

According to conventional and socially acceptable wisdom, this is a familiar story—the sure cultural explanation for the phenomenal success of Kenyan distance runners. There’s only one problem: the national sport, the hero worship, the adoring fans, the social channeling—all these relate to Kenya’s enduring love affair with soccer, not running! Yet, despite the enormous success of Kenyan runners in the past two decades, running remains a relative afterthought in this soccer-crazed nation.

Passion and cultural traditions go only so far. While Kenyans and other East Africans sweep upward of 60 percent of the world’s distance-running events, they are among the world’s worst soccer players—and sprinters. Despite an expenditure of vast amounts of the country’s sparse sports resources, Kenya has flopped in trying to replicate its wondrous distance-running success (which began for the most part with little state help) in soccer.

Science certainly does not support the popular notion that Kenyans prevail in distance running because they train harder or ran huge distances as kids, myths frequently peddled by the media. For every Kenyan athlete who ran 100 miles a week, there are others who got along on 30 and did not regularly run extraordinary distances as children.

“I lived right next door to school,” laughs Kenyan-born Wilson Kipketer, world 800-meter record holder. “I walked, nice and slow.”

Though individual success is indeed largely about opportunity and “fire in the belly,” when it comes to the patterns that we see in sports, genetic traits proscribe possibility.

As Dr. Saltin has noted, “Kenyans and other East Africans are born with a high number of slow-twitch fibers. More than other populations. That’s a critical factor in their success.” The Great Rift Valley adjacent to Lake Victoria is ground zero of world-class distance running, where evolutionary factors and social conditions reinforce each other in a feedback loop. Runners from the Kenyan highlands that snake along the western edge of the valley have won more than 40 percent of top international events. The Nandi district of 500,000 people—1/12,000 of earth’s population—boasts an unfathomable 20 percent, marking the greatest concentration of raw athletic talent in sports history.

No amount of political correctness can obscure the reality that East Africans and genetically similar populations of mountainous North Africa have a distinct body type and physiology. They are ectomorphs, short and slender, with huge natural lung capacity and a preponderance of slow-twitch muscle fibers, the vital energy system for endurance sports. It’s a perfect biomechanical package for distance running but a disaster for sports—like sprinting and soccer—that require anaerobic bursts of speed.

No amount of hard training can radically change what we are born with. Kenyans, other East Africans, and some local North African populations have an innate capacity, not an innate ability, to thrive in distance running; individual effort and courage separate the pretenders from the stars. Success in sports is a biosocial phenomenon.

“RACE” IS NOT THE ISSUE

This is not an issue of black and white but the consequence of evolving in varying terrains, say anthropologists. East Africans have a very different biomechanical and genetic makeup from blacks who trace their ancestry from West Africa. There is not even one—zero—elite long-distance runner who traces his or her primary ancestry to West Africa (which includes almost all American, British, Canadian, and Caribbean blacks).

In contrast, though dominant in distance running, East Africans are flat-out mediocre in the sprints. While the fastest Kenyan 100-meter run is 10.28 seconds, ranking 5,000 on the all-time list, blacks who trace their ancestry to West Africa hold the top 200 and 494 of the top 500 100-meter times.

Based on genetically proscribed body type differences, we would expect to find that Asian runners (from Japan, China, and Korea) and their ancestral descendants in Mexico and South America (the great Ecuadorian runners, for instance) could be competitive in long-distance races. Their small frames and extra layer of energy-generating body fat, which is otherwise a hindrance in sprinting, is a biomechanical plus in endurance events. Note for instance the incredible success in ultramarathoning by the Tarahumara from Mexico’s Copper Canyon. The few great white male distance runners are almost exclusively from southern Portugal, Spain, and Italy, and share many of the physical and physiological characteristics—and some of the genetic makeup—of North and East Africans.

“Differences among athletes of elite caliber are so small,” notes Robert Malina, a Michigan State University anthropologist and editor of the American Journal of Human Biology, “that physique or the ability to fire muscle fibers more efficiently that might be genetically based . . . it might be very, very significant. The fraction of a second is the difference between the gold medal and fourth place.”

If genetics does matter in athletic performance, then we might expect to find noticeable differences in the ways different population groups sustain anaerobic and aerobic functioning. Timothy Noakes, longtime director of the Sport Science Center at the University of Cape Town Medical School and author of many scholarly books, including Lore of Running, has observed that black South Africans, who share much of their genetic ancestry with East Africans, sweep more than 90 percent of the top places in endurance races held in his country, despite the fact that blacks represent no more than one-quarter of the active running population.

Noakes has attempted to figure out why. In a treadmill study, black marathoners consistently bested whites. Although white runners matched or exceeded the black runners at distances up to 5,000 meters, blacks were “clearly superior at distances greater than 5km.” The fine print in the data was particularly revealing. There was a dramatic difference in the ability of the blacks to run at a higher maximum oxygen capacity. In the case of the marathoners, blacks performed at 89 percent of the maximum oxygen capacity, while whites lagged by nearly 10 percent. The muscles of the African athletes also showed far fewer signs of fatigue as measured by lactic acid.

Noakes notes a link between his findings and the training habits of well-known Kenyan runners who report favoring low-mileage, high-intensity workouts. This presents a nurture/nature conundrum. Does hard training lead to a change in oxidative capacity and fatigue resistance or does it merely reflect a genetically well-endowed athletic machine?

TRAINING VERSUS GENES

The answer can be found in the wild card in performance: muscle efficiency. David Costill, former head of the Human Performance Laboratory at Ball State in Muncie, Indiana, has shown that the adaptability of the muscle fiber for aerobic metabolism—its oxidative potential—is more important than the basic composition of the muscle. More aerobically efficient fibers produce fewer fatigue-producing lactate toxins, resulting in better performance. And although fiber composition is genetically fixed, which effectively limits the pool of possible successful athletes in each event, exercise can help muscles better utilize oxygen.

A team from South Africa and Australia, including Noakes, has found an apparent link among oxidative capacity, resistance to fatigue, and population. The researchers measured “running economy”—the amount of metabolic work (and therefore oxygen consumption) that is required to run at a given speed, much like the fuel economy of a car. Running economy can be affected by a variety of factors, both environmental, such as running technique, and physiological, such as body mass distribution and muscle elasticity.

“We’ve shown that the oxidative enzyme capacity of the [East and South African black] athletes we looked at was one and a half times higher on average than the white runners,” reports Kathy Myburgh, a coauthor of the report and senior lecturer at the University of Stellenbosch in South Africa. Comparing black and white athletes with nearly identical race times, the researchers found that blacks were both more efficient runners and able to utilize a considerably higher percentage of their maximum oxygen potential—a decided advantage if two athletes otherwise have the same capacity.

“Whilst the current study does not elucidate the origins of these differences,” their report concludes, “the findings may partially explain the success of African runners at the elite level.” A subsequent study determined that the superior fatigue resistance during high-intensity endurance exercise is partially related to the higher skeletal muscle oxidative capacity and lower plasma lactate accumulation found more commonly in blacks.

Bengt Saltin has come to the conclusion that certain population groups, including northern Europeans, who are notable endurance runners and cross-country skiers, may also have superior fatigue resistance encoded in their genes. He has found that Scandinavian distance runners, as well as Kenyans and South African blacks, have consistently lower blood lactate levels and perform more efficiently than athletes from other regions, the likely result of their having evolved in mountainous regions. Population genetics—ancestry—is the key determinant.

To further test his findings, Saltin brought a half dozen established Swedish national-class runners to St. Patrick’s School in Iten, Kenya, where coach Colm O’Connell has developed many famous Kenyan runners. He wanted to see how they might match up against up-and-coming East African schoolboys. It was a demoralizing experience for the Swedes.

National champion after national champion was soundly trounced in races from 800 meters to 10 kilometers. Stunned, Saltin estimated that in this one tiny area of the Rift Valley there were at least 500 schoolboys who could best his national champions at 2,000 meters.

In a subsequent study, Saltin brought several groups of Kenyans to the Karolinska labs in Sweden, where he was then working. Muscle fiber distribution was similar for the Kenyans and Swedes. But biopsies of the quadriceps muscles in the thighs indicated that the Kenyans had more blood-carrying capillaries surrounding the muscle fibers and more mitochondria within the fibers. That’s important because mitochondria act a little like power stations, processing the glucose into energy with oxygen brought in by breathing. The Kenyans also were found to have relatively smaller muscle fibers than the Swedes, which Saltin speculated might serve to bring the mitochondria closer to the surrounding capillaries. This process aids in oxidation, bringing more “fuel” to the mitochondria, the engine of the muscles.

The Kenyans also showed little ammonia accumulation in their muscles from protein combustion and less lactic acid buildup. They have more of the muscle enzymes that burn fat, and their glycogen reserves are not burned as quickly, which improves endurance. Most impressive, they are able to take months off from regular training and then regain their old form quickly. When they do train, more than half of their total mileage occurs at heart rates of 90 percent of maximum, far higher than the rate for Europeans or Americans. In general, Saltin reported a 5 to 15 percent greater running economy at far less mileage but at a higher intensity. Saltin has privately suggested that Kenyans appear to be innately efficient, durable, and fast—with the most perfect aerobic potential measured so far on earth.

Could an American, British, or European runner defy the genetic odds and thrash the East and North African contingents in future World Championships or Olympics? Certainly, for genes only circumscribe possibility, and any race opens the door for the roulette wheel of the human spirit. As a result of natural human variation, there will always be great runners from every part of the globe. But don’t expect a return to the past—that is, unless we start tinkering with the genes themselves.

CYBORG ATHLETES

Genetic engineering is one of those concepts, like organic farming or how one feels about big bad Microsoft, that stirs an immediate and powerful gut reaction. Many believe the new age of biogenetics ushers in a wonderful opportunity to target historically incurable diseases. Others fear a cyborg future, where humans are transformed into soul-less machines. Almost always the controversy is projected as a future concern.

That may be true in medicine, for the promise of gene therapies and human cloning remains a distant, if realistic, dream. But in the world of athletics, genetic engineering is the here and now. In fact, there are athletes with genetically enhanced advantages. Unfettered by fears of being caught, they will likely shatter accepted limits of human athletic performance—but at unknown cost to their health.

By the Athens Olympics in 2004, say geneticists and sports physiologists, dozens if not hundreds of athletes will have experimented with a rapidly emerging range of performance-enhancing drugs, such as human growth hormone (HGH) or erythropoietin (EOP), or experimented with gene therapies whose use is utterly undetectable.

“I think genetic engineering may have already started,” says former Norwegian speed-skating champion Johann Olav Koss, a doctor and member of the World Anti-Doping Agency (WADA), an International Olympic Committee organization found to oversee drug testing. “We can’t be naive. We must be realistic.”

There is heated disagreement as to whether genetic manipulation represents sports’ doomsday future or society’s salvation—or both. In recent years, geneticists have made small but measurable strides in gene therapy, which involves injecting the body with artificial genes that produce therapeutic proteins to block diseases, such as hemophilia and cystic fibrosis, or even chronic pain. The technique, while still being tested experimentally on humans, has been used successfully in some cases on animals.

But the caution that shadows medical research is hardly present in the win-at-all-costs world of athletics. There is a huge incentive for athletes to angle for every edge, even illegal ones. Athletes, from running backs who have lost a half step to Kenyan-chasing distance runners, could see their prospects soar if they can find a scientist willing to experiment on them. Athletes will no doubt be the “canary in the mine” in genetic engineering, willing to experiment on themselves in the quest for gold, even recognizing the potentially disastrous consequences.

“It would be risky because of unknown side effects, but the basic genetic advances have been made,” acknowledges Bengt Saltin, who is a key member

of WADA, which met in March to draft guidelines on gene doping. “But if scientists are willing to cooperate, there are athletes who will experiment on themselves.”

Developed to treat dwarfism, synthetic growth hormone has been a favorite among strength athletes for more than a decade. It created hardly a ripple in 1998 when Australian customs inspectors discovered 13 vials of genetically engineered HGH hidden in the luggage of a Chinese swimmer before the 1998 World Swimming Championships.

EPO, a synthetic hormone that increases the production of oxygen-carrying red blood cells, is a favorite among endurance athletes, particularly cyclers. There have been on-again, off-again rumors of Kenyans doping with EPO but with no evidence. While tests are being developed to detect EPO, scientists are one step ahead of the doping police, having already perfected a virtually undetectable, injectable version.

“It’s not rocket science,” says Theodore Friedman, director of the gene therapy program at the University of California at San Diego and a WADA member. “If you asked any student of molecular biology how he would implant genes to change muscle function, he could cite three or four ways to do it.”

“If direct injection is used, the DNA will only be present in that specific muscle,” notes Peter Schjerling, Saltin’s colleague at the Copenhagen research center. “Therefore, a positive test would require a slice of actual muscle tissue. It would have to be at the exact spot of the injection. That’s just not feasible.”

In other words, as soon as a version of EPO now being tested on animals is perfected for use in humans, the insertion of a single gene into a leg muscle could turn the body into an endurance factory for months, with almost no chance of being nabbed. “I have no doubt that if this is being done on mice, humans aren’t far behind,” agrees Dr. Saltin, who is a former competitive runner.

Like ordinary genes, the artificial genes consist of DNA, the basic raw materials of human life. The direct delivery approach entails injecting the DNA into the muscle. The fibers would then take up the DNA and add it to the normal pool of genes. As this method is not yet very efficient, researchers are experimenting with viruses to carry the gene payload into a cell’s nucleus. Unfortunately, in contrast to the direct injection, the genes are also delivered to many other cells, such as those of the blood and liver, in addition to the intended target. A third approach entails removing specific cell types from the patient, adding the artificial gene in the laboratory, and reintroducing the cells into the body. Since the artificial genes would produce proteins that in many cases are identical to the normal proteins, that means you can kiss good-bye any effective policing by sports agencies.

DELICATE BALANCE

Scientists and their athlete guinea pigs are already experimenting with various gene therapies to hasten the healing process after sports-related injuries. The technique involves delivering therapeutic proteins (such as those encoding growth factors or antibiotics) to the injured tissue. Tissue engineering, which may eventually be combined with gene therapy, offers the potential to create tissues for regeneration of defects occurring from trauma. Such therapies may eventually offer wonder treatments to those suffering from cartilage damage, ACL injury, meniscus tears, and severe fractures. Although there have been many successful experimental studies in humans, potential side effects are still an open question.

Several more radical but promising performance-enhancing gene modifications have also been successfully tested on animals. They include generating the growth of explosive, fast-twitch muscle fibers and stimulating the release of growth hormone releasing hormone (GHRH), which can make recipients both stronger and leaner.

The list of genetically engineered drugs that are sure to entice athletes grows daily. Some of the most advanced research would benefit sprinters. Although the fastest muscle fiber types are not found in human skeletal muscle, the potential for developing such fibers is embedded in long-dormant genes. Geneticists have recently developed a protein known as a “transcription factor” called Velociphin, which can activate these genes. Just a few injections of this DNA into the quadriceps, hamstring, and gluteus, and the muscle fibers will start cranking out Velociphin, which will activate the fast myosin gene. In weeks the muscles would burst with energy, which could transform a so-so 100-meter sprinter into a world record holder. There are no visible side effects, and without a muscle biopsy directly into manipulated muscle the genetic modification is undetectable.

But there is a cost, and not just the potential disintegration of sports as we know it. Many drugs have dangerous, or even toxic, side effects. For example, the use of human growth hormone leads to enlarged organs and uncontrollable bone growth in the face and hands. And inserted genes could spin out of control, leading to thickening blood, strokes, heart attacks, and even death. Weightlifters pondering cancellation of their health club memberships should consider that once a gene for a growth factor gets inserted, the muscle nucleus continues churning out elevated quantities—forever.

“In principle, the only thing lacking is a control mechanism to keep a lid on this,” says Schjerling. But, inevitably perhaps, scientists are working on this too. A Stanford University molecular pharmacologist, Helen Blau, has demonstrated that a gene could be introduced to stimulate growth hormone in the bloodstream and then be switched off with the use of an oral antibiotic.

“[Athletes] could be genetically engineered to have a gene which increased their strength as they trained but then was shut off when required,” Blau said. “It could be a future concern for the Olympics.”

Even if control mechanisms are developed, serious problems loom. Imagine an enhanced-in-the-lab distance runner (or thoroughbred horse, since these techniques are being used in horse racing) whose genetically bloated muscles are too powerful for the skeletal system to support. In many sports, genetic enhancements can permanently and perhaps perilously alter the natural human balance.

While many of us naively view the human body as an invincible machine, it is an integrated combination of tendons, cartilage, bones, muscle, and fat. All living creatures are a delicate balance. One small change can have extraordinary and unanticipated consequences. For example, researchers have genetically altered a housefly with muscles 300 percent stronger than normal. That may sound promising, but “the fly actually lost power because it couldn’t make its wings move fast enough” to support the added muscle weight, notes H. Lee Sweeney, a University of Pennsylvania physiologist.

Sweeney is coauthor of the “He-Man” mouse study, which is often cited as a cutting edge example of how genetic engineering might transform sports. Sweeney’s experiments should send shivers down the back of the Maurice Greenes, the Wilson Kipketers, and the Khalid Khannouchis of this world.

He-Man is a mouse running endless, tireless circles in his basement laboratory cage at a University of Pennsylvania laboratory. Four years ago, he was injected with a synthetic version of a gene called insulin-like growth factor 1 (IGF-1), a protein that makes muscles grow and repair themselves. Now deep into old age, the once tiny mouse and his gene-modified brothers and sisters look more like the Turkish weightlifter Naim Suleymanoglu. He-Man can now climb a ladder carrying three times his body weight.

Following up on the He-Man studies, researchers at London’s Royal Free Hospital and University College London Medical School recently tested muscle-building, engineered vaccines on mice. Dubbed mechano-growth factor (MGF), a protein that makes muscles grow and repair themselves, the vaccines were found to increase muscle mass by as much as 60 percent within a month and with no exercise.

“We call them the Schwarzenegger mice,” says Harvard Medical School professor Nadia Rosenthal, who has run similar experiments. “I’d be totally surprised if it was not going on in sports. Those with terminal cancer and AIDS want to know ‘What will keep me alive?’ Athletes want to know ‘What will help me win?'”

IS A SUB-TWO-HOUR MARATHON IN THE FUTURE?

World record running times are made to be broken. Many performances that were world class only 50 years ago are routine now. In 1954 Roger Bannister stunned the world when he broke the four-minute barrier. But within six weeks his improbable record fell. Fast-forward to 1999, and Moroccan Hicham El Guerrouj has lowered the record to 3:43.13.

The potential—indeed, the reality—of gene enhancement and genetic engineering raises the fascinating question of human limits. What keeps athletes from running longer and faster or throwing farther? In our constant striving to better our achievements and set new records, are there limits? Can we ever expect to see a marathoner break the theoretical two-hour barrier?

The steady improvement in records of all sporting events may, at first glance, look like biological evolution at work, but that’s far-fetched. Genetically we are pretty much the same as we’ve been for thousands of years. And the past 100 years represents but an eye blink of evolutionary time. Moreover, any mutation that might crop up and that could be of value for athletic performance (such as enormously large lung capacity for marathoners) would quickly be diffused in the gene pool.

That said, pockets of populations (as distinct from “races”) with body types or physiology particularly well-suited for certain athletic skills do exist. That is part of the explanation for East African success in long-distance running, Eurasian white dominance of weightlifting and the Olympic power events, and Asian success in sports that place a premium on flexibility, such as diving, skating, and gymnastics.

To understand the record-shattering performances of Kenyan runners, it’s important to recognize that, from a genetics perspective, Olympians are at the far end of the bell curve distribution. They are outliers, freaks of nature if you will, no less so than a 180 IQ or seven-foot-tall person. World-class marathoners are generally off the scale according to every parameter one can think of—physiological systems for muscles, enzymes, hormones, bone structure, and body build. Moreover, all of these superlatives have been bolstered by diet, rest, training, and stress management.

These performance freaks are considerably different from athletes who competed in the early days of Olympic and world competition. While talented, many past athletes were a lot closer in ability to the average population. Just look at old basketball newsreels from the 1930s, when short Jewish, Irish, and Italian players dominated the sport. Over time, they ceded the game to athletes who were stronger, taller, and quicker.

In other words, part of the dramatic increase in the performance curve is statistical. By simply opening up sports to more countries, the likelihood increases of having some individual runner who is faster or a better marathoner

than ever before in history. The dramatic improvement in women’s world records can be explained, in large measure, by the surge in the number of participants who have shaken off social taboos limiting female participation in sports. And the great distance-running success of the Finns and Brits in earlier decades occurred in part because East and North African populations did not participate. It’s easier to win when your toughest competitors aren’t in the race.

If there is a physiological maximum to running speed or the endurance of a human being, one would expect that as athletes approached that limit improvements would become both rarer and smaller. That’s been true in some events, such as the 200-meter run. In 1968 the world record stood at 19.83 seconds. In 1996 Michael Johnson lowered it to 19.32 seconds—a half second improvement in 28 years.

However, over the past 100 years in most events, world record running times declined almost linearly, at least until the last decade. Many in sport believe that the record-shattering marks of the 1980s and ’90s are tainted by the use of performance-enhancing drugs. And now, gene therapies and genetic engineering loom.

The biological limits to athletic performance—at least for sports such as cycling, swimming, and long-distance running that require high endurance—lie in the body’s inefficient supply and consumption of energy. According to researchers in Copenhagen, the lungs are not a limiting factor. Even during the most strenuous exercise, when the lungs are inhaling and exhaling 25 times more air than they do when the body is at rest, they are working at only two-thirds their maximum capacity.

Exercise training does not increase the capacity of the lungs, however, whereas training does improve the performance of all the cardiovascular and muscle components. According to tests, as long as muscles get oxygen as fuel for mitochondria, they can produce without limits. The heart is a different kind of muscle, however. In endurance sports such as long-distance running, the heart works at 90 percent of its maximum capacity, which is close to its limit. Performance is limited by the amount of blood that the heart can pump through the body.

Blood doping and the use of genetically engineered EPO could certainly extend what might otherwise be thought of as “natural” performance limits. Also on the horizon is genetic manipulation of mitochondria so as to increase its consumption of oxygen and therefore its production of adenosine triphosphate (ATP), the general-purpose immediate energy source for cells of the body.

IS GENETIC ENGINEERING NECESSARILY EVIL?

What does all this portend for the future of sport—running in particular? The explosive growth of gene doping leaves Dr. Saltin with a recurring nightmare. He imagines a scenario in which a competitive but sub-elite sprinter obsessed with challenging Maurice Greene and the like turns to a renegade geneticist familiar with the latest research on the genetic modification of muscle fiber types. Saltin likes to spin a tale, set in the future, of this desperate athlete’s long-awaited race for Olympic immortality.

BANG! The genetically doped athlete dashes into the lead, extending it with every stride. Then at 65 meters, far out in front of the field, a sudden twinge tickles the hamstring. Saltin picks up the story:

“At 80 meters, the twinge explodes into an overwhelming pain as he pulls his hamstring. A tenth of a second later the patella tendon gives in—because it is no match for the massive forces generated by his quadriceps muscle. The patella tendon pulls out part of the tibia bone, which then snaps, and the entire quadriceps shoots up along the femur bone. The athlete crumples to the ground, his running career over.”

This is not the scenario that generally comes to mind in connection with the words “genetically engineered super athlete,” notes Saltin, but it is very much a part of the reality.

The now-crippled East German and Soviet sports systems are vivid reminders that victory-hungry athletes and their state sponsors will strike Faustian bargains if the stakes are high enough. Fantasies of glory didn’t die with the collapse of communism. In a 1995 survey of aspiring American Olympians, more than half said they would take a banned substance that would guarantee victory in every competition for five years even if would lead to certain death.

With all of these Frankenstein-like scenarios, it would seem an easy decision to ban genetic engineering of athletes on both medical and ethical grounds. Certainly, the IOC president, Jacques Rogge, talks tough. “Genetic manipulation is there to treat people who have ailments, not to treat a healthy person,” he said recently. “I am very clear on this.”

But few scientists see the issue so clearly. There is a hazy and debatable line between “health restoration” and “performance enhancement.” Imagine an athlete using gene modification to help overcome congenital asthma or some such other genetic abnormality. Many argue that even embryonic gene manipulation to create better athletes, which is a decade or more in the future, should not be banned outright.

As the Olympic 100-meter champion, Maurice Greene, has noted, “What if you’re born with something having been done to you?” Should manipulation of an embryo be considered cheating if, as Greene hypothesizes, “you don’t have anything to do with it?” It is problematic to have genetically enhanced athletes compete against nonenhanced athletes, but is it fair to disqualify them if the changes were made before birth, perhaps even to save their lives?

Considering the promising health potential of genetic enhancement, it certainly appears to be more acceptable than drugs, even legal ones. But this debate, both medical and ethical, can expect to rage for decades. The IOC has set up a “gene doping” advisory group but seems befuddled by these complex issues and intimidated by the political fallout that might greet any radical action on their part.

“While the information from genetic science will feed through into better treatments for disease,” says Bruce Lynn, a neurophysiologist at University College London, “it is also going to present the sports industry with a Pandora’s box.”

Wake up, sports world. The Pandora’s box is open. There are cyborg athletes among us.

BIBLIOGRAPHY

Ama, Pierre F. M. et al. “Anaerobic Performances in Black and White Subjects.” Medicine and Science in Sports and Exercise 22 (1990): 508-511.

Anderson, Jesper L., Peter Schjerling, and Bengt Saltin. “Muscle, Genes and Athletic Performance.” Scientific American 283 (September 2000).

Bailey, Ernest, and Matthew M. Binns. “The Horse Gene Map.” Institute for Laboratory Animal Research (ILAR) Journal 39 (1998).

Barton-Davis, E.R., N. Rosenthal, and H.L. Sweeney. “Viral Mediated Expression of IGF-I Keeps Muscles Young and Strong in Old Mice.” Meeting of the American Society for Cell Biology (December 1998).

Behera, N., and V. Nanjundiah. “An Investigation into the Role of Phenotypic Plasticity in Evolution.” Journal of Theoretical Biology 172 (1995): 225-234.

Bigard, X., H. Sanchez, J. Zoll, P. Mateo, V. Rousseau, V. Veksler, and R. Ventura-Clapier. “Calcineurin Co-regulates Contractile and Metabolic Components of Slow Muscle Phenotype.” Journal of Biological Chemistry 275 (2000): 19653-19660.

Bouchard, C. “Genetic Basis of Racial Differences.” Canadian Journal of Sports Science 13 (1988): 104-108.

Bouchard, C., T. Rankinen, Y.C. Chagnon, T. Rice, L. Pérusse, J. Gagnon, I. Borecki, P. An, A.S. Leon, J.S. Skinner, J.H. Wilmore, M. Province, and D.C. Rao. “Genomic Scan for Maximal Oxygen Uptake and Its Response to Training in the Heritage Family Study.” Journal of Applied Physiology 88 (2000): 551-559.

Bouchard, Claude, P. An, T. Rice, J.S. Skinner, J.H. Wilmore, J. Gagnon, L. Pérusse, A.S. Leon, and D.C. Rao. “Familial Aggregation of VO2max Response to Exercise Training: Results from the Heritage Family Study.” Journal of Applied Physiology 87 (1999): 1003-1008.

Bouchard, C., R. Lesage, G. Lortie, J.A. Simoneau, P. Hamel, M.R. Boulay, L. Pérusse, G. Theriault, and C. Leblanc. “Aerobic Performance in Brothers, Dizygotic and Monzygotic Twins.” Medicine and Science in Sports and Exercise 18 (1986): 639-646.

Bouchard, C., R. Malina, and L. Pérusse. Genetics of Fitness and Physical Performance. Champaign, Ill.: Human Kinetics, 1997, 1-400.

Bouchard, C., L. Pérusse, Y.C. Chagnon, C. Warden, and D. Ricquier “Linkage Between Markers in the Vicinity of the Uncoupling Protein 2 Gene and Resting Metabolic Rate in Humans.” Human Molecular Genetics 6 (1997): 1887-1889.

Brown, Guy C. “Speed Limits.” The Sciences (September/October 2000): 32-38.

Carter, J. E. Lindsay. “Ethnic Variations in Human Performance: Morphological and Compositional Characteristics.” American College of Sports Medicine Symposium (May 31, 1991).

Cauley, J. A. et al. “Black-White Differences in Serum Sex Hormones and Bone Mineral Density.” American Journal of Epidemiology 139 (1994): 1035-1046.

Coetzer, Pieter, T. D. Noakes, B. Sanders, M. I. Lambert, A. N. Bosch, T. Wiggins, and S. C. Dennis. “Superior Fatigue Resistance of Elite Black South African Distance Runners.” Journal of Applied Physiology 75 (1993): 1822-1827.

Dionne, France T., L. Turcotte, M.C. Thibault, M.R. Boulay, J.S. Skinner, and C. Bouchard. “Mitochondrial DNA Sequence Polymorphism, VO2max and Reponse to Endurance Training.” Medicine and Science in Sports and Exercise 23 (1991): 177-185.

Ellis, Lee, and Nyborg Helmuth. “Racial/Ethnic Variations in Male Testosterone Levels: A Probable Contributor to Group Differences in Health.” Steroids 57 (1992): 72-75.

Entine, Jon H. Taboo: Why Black Athletes Dominate Sports and Why We’re Afraid To Talk About It. New York: Public Affairs, 2000.

Gayagay, G., B. Yu, B. Hambly, T. Boston, A. Hahn, D.S. Celermajer, and R.J. Trent. “Elite Endurance Athletes and the ACE I Allele—the Role of Genes in Athletic Performance.” Human Genetics 103 (July 1998): 48-50.

Heaney, Robert P. “Bone Mass, the Mechanostat, and Ethnic Differences.” Journal of Clinical Endocrinology and Metabolism 80 (1995): 2289-2290.

Himes, John H. “Racial Variation in Physique and Body Composition.” Canadian Journal of Sports Science 13 (1988): 117-126.

James, William H. “Causes of Racial Differences in Testosterone Levels of Men.” Journal of Clinical Endocrinology and Metabolism 80 (1995): 2289-2290.

Lambrinides, Ted. “VO2max: Questions & Answers.” Presented at the 2000 NCES Health & Fitness Symposium, Chicago, Ill. (October 28, 2000).

Levesque, M., M.R. Boulay, J.A. Simoneau. “Muscle Fiber Type Characteristics in Black African and White Males Before and After 12 Weeks of Sprint Training.” Canadian Journal of Applied Physiology 19 (1994): Supplement 25P.

Liebman, Dan. “Does Genetics Affect Racing Perfomance?” The Blood-Horse CXXIV (March 21, 1998).

Longman, Jere. “Pushing the Limits: Getting the Athletic Edge May Mean Altering Genes.” New York Times, May 11, 2001, C1+.

Malina, Robert M. “Genetics of Motor Development and Performance.” In R.M. Malina and C. Bouchard (eds.), Sport and Human Genetics. Champaign, Ill.: Human Kinetics, 1984, 23-58.

  • Miah, A., “Designer Genes for Sale—Is It Just a Matter of the Price,” Fifth World Congress of Bioethics, International Association of Bioethics, Imperial College, London, September 2000.
  • Miah, Andy. “Genetic Technologies and Sport: The new ethical issue.” Journal of the Philosophy of Sport XXVIII (March, 2001): 32-52.
  • Montgomery, H.E. et al. “A Gene for Human Performance.” Nature 393 (1998): 221-222.
  • Montgomery, Hugh E. et al. “Angiotensin-Converting-Enzyme Gene Insertion/Deletion Polymorphism and Response to Physical Training.” Lancet 353 (1999): 541-545.
  • Nelson, D. A., G. Jacobsen, D. A. Barondess, and A. M. Parfitt. “Ethnic Differences in Regional Bone Density, Hip Axis Length, and Lifestyle Variables Among Healthy Black and White Men.” Human Biology 58 (1986): 379-390.
  • North, Kathryn N. et al. “A Common Nonsense Mutation Results in Apha-actinin-3 Deficiency in the General Population [letter].” Nature Genetics 21 (April 1999): 353-354.
  • Pollitzer, W.S. and J. Anderson. “Ethnic and Genetic Differences in Bone Mass: A Review with a Hereditary vs. Environmental Perspective.” American Journal of Clinical Nutrition 52 (July 1990): 1244-1259.
  • Rankinen, T., J. Gagnon, L. Pérusse, Y.C. Chagnon, T. Rice, A.S. Leon, J.S. Skinner, J.H. Wilmore, D.C. Rao, and C. Bouchard. “AGT M235T and ACE ID Polymorphisms and Exercise Blood Pressure in the Heritage Family Study.” American Journal of Physiology: Heart Circulatory Physiology 279 (2000): H368-H374.
  • Rankinen, Tuomo, L. Pérusse, I. Borecki, Y.C. Chagnon, J. Gagnon, A.S. Leon, J.S. Skinner, J.H. Wilmore, D.C. Rao, and C. Bouchard. “The Na,K-ATPase a2 Gene and Trainability of Cardiorespiratory Endurance in the Heritage Family Study.” Journal of Applied Physiology 88 (2000): 346-351.
  • Rivera, M.A., F.T. Dionne, J.A. Simoneau, L. Pérusse, M. Chagnon, Y. Chagnon, J. Gagnon, A.S. Leon, D.C. Rao, J. Skinner, J.H. Wilmore, and C. Bouchard. “Muscle-Specific Creative Kinase Gene Polymorphism and V̇O2max in the Heritage Family Study.” Medicine and Science in Sports and Exercise (1997): 1311-1317.
  • Rivera M.A., L. Pérusse, J.A. Simoneau, J. Gagnon, F.T. Dionne, A.S. Leon, J.S. Skinner, J.H. Wilmore, M. Province, D.C. Rao, and C. Bouchard. “Linkage Between a Muscle-Specific CK Gene Marker and V̇O2max in the Heritage Family Study.” Medicine and Science in Sports and Exercise 31 (1999): 698-701.
  • Saltin, B., C. K. Kim, N. Terrados, H. Larsen, J. Svedenhag, and C. J. Rolf. “Morphology, Enzyme Activities and Buffer Capacity in Leg Muscles of Kenyan and Scandinavian Runners.” Scandinavian Journal of Medical Science and Sports 5 (1995): 222-230.
  • Saltin, Bengt. “Metabolic Fundamentals in Exercise.” Medicine and Science and Sports 5, 3 (1973): 137-146.
  • Samson, Jacques, and Magdeleine Yerlès. “Racial Differences in Sports Performance.” Canadian Journal of Sports Science 13 (1988): 110-111.
  • Sawka, M.N., M.J. Joyner, D.S. Miles, R.J. Robertson, L.L. Spriet, and A.J. Young. “The Use of Blood Doping as an Ergogenic Aid.” Medical Science Sports and Exercise 28 (June 1996): R1-R8.
  • Simoneau, J.A., C.K. Allah, M. Giroux, M.R. Boulay, P. Lagassé, G. Thériault, and C. Bouchard. “Metabolic Plasticity of Skeletal Muscle in Black and White Males Subjected to High-Intensity Intermittent Training.” Medical Science Sports and Exercise 23 (1991): S149.
  • Simoneau, J. A., and C. Bouchard. “Genetic Determinism of Fiber Type Proportion in Human Skeletal Muscle.” FASEB Journal 9 (1995): 1091-1095.
  • Skinner, James S. “Do Genes Determine Champions?” Sports Science Exchange, 14 (2001): 1-4.
  • Swift, E.M., and Don Yaeger. “Unnatural Selection,” Sports Illustrated, May 14, 2001, 86+.
  • Weston, A., O. Karamizrak, A. Smith, T.D. Noakes, and K.H. Myburgh. “African Distance Runners Exhibit Greater Fatigue Resistance, Lower Lactate Accumulation and Higher Oxidative Enzyme Activity.” Journal of Applied Physiology 86 (March 1999): 915-923.
  • Weston, Adele R., Z. Mbambo, and K. H. Myburgh. “Fractional Utilisation of Maximal Oxygen Uptake and Running Economy in Well-Trained African and Caucasian Distance Runners.” Journal of Applied Physiology (September 1999).
  • Whitfield, John. “Exercising Your Genes.” Nature News Service, December 3, 2001.
  • Williams A.G. et al. “ACE Genotype and Skeletal Muscle Metabolic Efficiency.” Nature 403 (2000): 614.
  • Xia, L., D. Gallagher, J. Wang, Z. Wang, J.C. Thornton, and R.N. Pierson. “Appendicular Skeletal Muscle Mass (ASM) Is Lower in Asian Males (AM) Than in White Males.” FASEB 10 (1996): A733.
  • Zorpette, G. “The Mystery of Muscles.” Scientific American Presents: Men–The Scientific Truth 10 (Summer 1999): 48-55.
  • Zorpette, Glenn. “Muscular Again.” Scientific American Presents: Your Bionic Future 10 (Autumn 1999): 27-31.
Runners illustration accompanying article title
Runners illustration accompanying article title
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This article originally appeared in Marathon & Beyond, Vol. 6, No. 5 (2002).

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