In an unmarked cage in the bowels of the University of Pennsylvania's Department of Physiology crawls the future of sport. It is a genetically altered mouse. We'll call him He-man because a creature of such import should be known by a name, not a number.
Soon after He-man was born, a team of Penn researchers led by Dr. H. Lee Sweeney injected its muscles with a synthetic gene that instructed its muscle cells to produce more IGF-1 (insulin-like growth factor-1). IGF-1 is a protein that, in a nutshell, makes muscles grow and helps them repair themselves when they've been damaged. It is indispensable to the formation and maintenance of strong physiques. For the most part, when those of us under 30 exercise vigorously, our bodies start producing lots of IGF-1. Our muscles get bigger, and we get stronger.
As we age, the muscles stop producing IGF-1 in the quantities we need to keep our muscles looking as they did when we were younger. They sag, and they don't repair themselves as effectively as they used to. We get slower and weaker. "Even if you train," says Sweeney, "you lose speed."
It happened to Carl Lewis, Wayne Gretzky and Jerry Rice, among others. But it hasn't happened to He-man. Because of the gene that was injected two years ago, the mouse grew exceptionally large muscles, and those muscles keep producing IGF-1. He-man, in the throes of mouse old age, remains as mighty as he ever was, an Arnold Schwarzenegger of mice. His muscle mass is 60% greater than that of a normal mouse. He effortlessly climbs a ladder with 120 grams of weights—equal to three times his body weight—strapped on his back.
"We showed that with a onetime injection of this gene we can get bigger muscles in young animals and that, as they get older, the muscles never change," says Sweeney, whose research is funded by the National Institutes of Health. "The muscles maintain their size through the whole life of the animal."
The implications for athletes are not lost on Sweeney. Implant this IGF-1 gene into the proper muscles and Olympic sprint champion Maurice Greene might be as fast at 48 as he is at 24. Randy Moss might still outrun and outjump defensive backs in 2020. Pavel Bure might be skating as fast 30 years from now as he does today.
Fanciful? Don't bet against it. Whether in one year, three years or five years—the last of those being the prediction of most experts—the first genetically engineered athlete will be secretly competing. "It's not rocket science," says Theodore Friedmann, director of the gene-therapy program at UC San Diego and a member of the medical-research committee of the World Anti-Doping Agency (WADA). "If you asked any molecular biologist, or even his students, how he would implant genes to change muscle function, within half an hour he could write down three or four ways to do it. The same would apply if you asked him, How would you improve oxygen transport? How would you change athletes so they could jump higher and run faster? Be taller, stronger, whatever? Because of the whole Human Genome Project [a federally funded effort to identify the estimated 100,000 genes in human DNA], synthetic genes are available, and putting genes into people to express new functions is becoming reality."
"If this is being done on mice and rats, humans aren't far behind," says Bengt Saltin, a Swedish professor of human physiology at the University of Copenhagen and a member of WADA's special committee on gene doping. "The only thing keeping it from happening today is the control problem. For example, you can insert a gene to increase EPO production"—EPO is a hormone some athletes inject to illicitly boost the production of red blood cells, thus enhancing their endurance—"but you can't shut [that production] off when you want to." When the technology is developed that will enable us to turn hormone production on and off at will, says Saltin, we'll "have real problems."
Sweeney believes the IGF-1-inducing gene will slow the muscle deterioration brought on by muscular dystrophy, and he had hoped to have a clinical trial on humans under way by this spring. But he has delayed seeking approval from the Food and Drug Administration (FDA) because of the 1999 death of a patient in a different gene-therapy trial at Penn. If approval is granted, as is expected, and the synthetic IGF-1 gene proves safe in the muscular dystrophy trial, the next step would be to conduct a trial of the gene's ability to maintain a person's muscle strength as that person ages. "All this is being driven by our aging population," Sweeney says. "As people get old, they get weak, and if they have an injury, [the muscle involved] doesn't repair itself, so they lose even more muscle. They lose their mobility. The ability to maintain muscle mass is [hugely important] for an aging society."
"When [Sweeney's work] is done, it will decrease the incidence of hip fractures in the elderly," says Gary Wadler, associate professor at the New York University School of Medicine and an adviser to the White House Office of National Drug Control Policy. "But you'd better start inventorying the genes because athletes will be trying to get them. That's the plain truth. His work has the potential to be misused. It won't be long before someone does a kinesiologic study of a pitcher's motion, say, to determine which muscles should be enhanced for throwing a baseball. Then with the injection of the IGF-1 gene you create a superpitcher. The only way you'll be able to prove an athlete is cheating is through a muscle biopsy, and that's not going to happen."