IN 2002, Anna Hemmings was at the peak of her athletic prowess: world kayaking champion. A few months later, she had broken down completely - utterly, incurably exhausted, unable to paddle even for 10 minutes.

"I couldn't go on. I no longer had the energy," says Hemmings. "It was strange . . . I looked normal, yet inside my muscles were aching so badly that sometimes I couldn't even hold my hands up to wash my hair in the shower."

Hemmings was diagnosed with chronic fatigue syndrome (CFS): crippling exhaustion which makes even moderate exercise unbearable. The illness, which affects around 20,000 Scots per year, is mysterious and often untreatable. It has a number of possible triggers - viral, stress-related, dietary - which may also indicate an underlying genetic predisposition. But despite countless experiments, the cause of chronic fatigue has remained elusive.

Now, in search of an explanation and a cure, scientists are turning their approach on its head by studying elite athletes who can withstand fatigue better than others.

Dr Paula Robson-Ansley, of the University of Portsmouth, believes endurance athletes may have a specific type of gene that makes them less likely to suffer fatigue.

To test her theory, she travelled to the 2006 Merida TransWales Mountain Bike Race where competitors covered more than 500km over rugged terrain in seven days.

Each day, Robson-Ansley took blood samples from 80 athletes who took part, before and after the race. Separately, she took blood samples from 85 people around the UK who have been diagnosed with CFS.

She is now carrying out a detailed comparison, at the laboratories of Portsmouth's department of sport and nutrition. "The experiment may help explain why some people develop chronic debilitating fatigue for no apparent reason," she says.

Robson-Ansley has a personal interest in the research: her own athletic career was cut short by a bout of chronic fatigue, sometimes described as "unexplained underperformance syndrome" (UPS). She was an Olympic-standard rower, training in preparation for the 1996 games, when her body rebelled.

A five-kilometre run made her feel like she had just done a marathon. Forced to retire from competition, she set her sights on a new goal: understanding the biological roots of UPS and chronic fatigue syndrome.

Robson-Ansley suspects that endurance athletes may carry a different form of a gene, compared with CFS sufferers, a form which protects the athletes from suffering excessive fatigue, during and following endurance exercise.

Her test is focusing on Interleukin-6 (IL-6), a messenger molecule in the body that is released when the body is under stress; for example, during infection or illness or when blood sugar levels get low by sending a "distress signal" to the brain.

During prolonged exercise, IL-6 levels in athletes increase dramatically. One study found IL-6 levels increasing 100-fold in runners following a marathon.

In another, when runners were injected with IL-6 before a 10km trial run, they ran markedly slower.

The molecule seems to be sending a warning message to the brain: "Slow down, conserve energy - the body is fatigued and recovery time is needed."

So, Robson-Ansley wondered, could it be that endurance athletes have a different version of the IL-6 gene than sufferers of chronic fatigue syndrome?

Certainly different versions of IL-6 are known to exist. Previous studies have found that, during infection, people with one variation of the gene - "C-type" - produced less IL-6 during infection than those with the "G-type" version of the gene.

Over the course of the mountain-bike event, blood samples were taken every morning at 6am before the cyclists completed that day's stage of the race.

IL-6 levels did not change over the seven-day mountain-bike event. But as the mountain bikers became more tired, the study found marked increases in the levels of the IL-6 receptor - the receiver molecule that helps send the IL-6 message to the brain.

This "would heighten the athlete's sensitivity to IL-6 when it is produced", says Robson-Ansley. Therefore, "it may be that chronic fatigue sufferers don't necessarily produce more IL-6 but they are more sensitive to its release," she says.

If her theory is correct, it may one day be possible to treat some types of CFS with a drug that can block IL-6 receptors in the brain. The good news is, such a drug already exists: an antibody which binds to the IL-6 receptor in the brain, de-activating it. In tests, when this antibody was injected into exhausted athletes, it eliminated the sensation of fatigue - offering hope that it would work as a therapy.

Another, more worrying scenario, is that unscrupulous athletes might take IL-6 blockers to train harder, by staving off pain. Robson-Ansley admits this is a possibility, "but it would probably be dangerous", she says. Drug cheats who took it as a performance-enhancer could risk damage to the immune system.

The full results of her study into the IL-6 genes are not expected to be released until the middle of this year, but she is confident that she is winning the race to cure chronic fatigue.

"I think we now know that there is a lot more going on in the relationship between the IL-6 receptor and fatigue than previously thought," she says.

"But one has to be cautious in prescribing the role genes might play in athletic performance as it is still very early days. The history of sport is littered with countless examples of athletes who succeed against all kinds of odds, including physical ones."