Rower Rob Waddell, Tour de France cyclist Hayden Roulston and triple Olympic champion Sir Peter Snell are other star Kiwi athletes to have developed heart issues.
World champion Australian triathletes Greg Welch and Emma Carney both ended their careers suddenly and had defibrillator pacemakers implanted following repeated severe arrhythmias of the right ventricle - a condition associated with sudden death. Welch raised a possible link with his extreme training regime commenting in a 2006 interview: "I could have pushed myself too hard."
Now emerging scientific studies are finding evidence that appears to support that. "Running too fast, too far and for too many years may speed one's progress towards the finish line of life," concluded a December editorial in British journal, Heart.
Until recently, the cardiac risk of exercise was measured by the incidence of deaths during races. In marathons, that rate was one in 100,000 - a figure that didn't give cause for alarm. But the Heart article authors, citing recent studies, say there is now evidence that years of asking the heart to pump "massive" volumes of blood for hours at a time can lead to long-term damage and reverse the huge health and life expectancy advantages of moderate aerobic exercise.
These include over-stretching heart chambers, thickening of its walls and changes to electrical signalling, which can trigger dangerous heart rhythm problems. Studies have found scarring in the right ventricle of 13 per cent of endurance athletes and estimated veteran athletes may be five times more at risk of atrial fibrillation, Carter's arrhythmia.
Carter, who retired from professional triathlons in 2006, went to the doctor last spring after returning from a light bike ride which became a struggle as he turned off Auckland's Tamaki Drive uphill towards home. "I was just knackered. I felt something was seriously not right."
He had noticed the evening before that his heart felt "jumpy" but said the ride confirmed it. A specialist put Carter on blood thinners to guard against stroke until his heart was shocked back into normal rhythm a month later.
"I've been fine since but you feel in a sort of holding pattern. It might be six months or six years but I'm told it will likely come back. It was a really strange feeling. It would feel like you were suddenly at altitude and you couldn't get enough oxygen. It felt like a real block and I'd have to slow right down."
Carter, who still exercises regularly but much more moderately, thinks he had brief bouts when he was a professional triathlete. "There were phases in races occasionally where I felt flat but would then come right quickly. So, I'm pretty sure I've had it before."
He says years of high intensity training may be a factor, along with a possible inherited susceptibility although no other family member has had it.
"It's overuse, probably bordering on abuse," Carter said of his own past training and racing regime.
"Since I was 13, to when I retired at 34, I have done way too much real intense exercise, day after day after day. I'm not sure it's the healthiest thing to do. I'm pleased to have got out of [elite] sport and still be able to run. Running tends to beat you up after a while."
"It was quite scary to think that there's something wrong with your heart. I'd never really been to hospital before."
The procedure to jolt his heart back into normal rhythm was done when he was unconscious but Carter was told it took two attempts. And then, when it went back to beating normally, his naturally low pulse raised doctors' eyebrows. At 32-36 beats per minute it is half the average normal rate, but not unusual for a highly-trained endurance athlete.
Abnormalities or damage to the heart structure are the most common causes of atrial fibrillation, according to the Mayo Clinic which also lists high blood pressure, heart attacks, congenital defects, overactive thyroid gland, lung diseases and viral infections among possible causes.
The question now is whether extreme training and endurance racing can damage the heart and recent studies have found some evidence it may do.
Researchers headed by Australian heart specialist Dr Andre La Gerche, a marathon runner himself, took blood tests soon after endurance athletes crossed the finish line, which found raised levels of troponin, a marker of injury to the heart muscle. Ultrasound showed the damage predominantly involved the right ventricle, which has been shown to carry maximal load during racing.
About the same time a paper came out in Europe suggesting that athletes presenting with serious arrhythmias had serious right ventricular abnormalities. Of 46 athletes with abnormal rhythms studied, nine died suddenly within five years. Until then scientists thought these right ventricle arrhythmias, even though they looked serious, could never be life-threatening.
The next question was whether exercise had contributed. "We believe that it probably has, but we do not know exactly how and whether it has been in combination with a genetic weakness or because the athletes have trained very hard with an illness such as the flu or even whether drugs have played a role - although I am confident that this is not the explanation for many," La Gerche wrote in a recent article.
While the authors of the Heart article, Drs James O'Keefe and Carl Lavie, say that "chronic extreme exercise appears to cause excessive 'wear and tear' on the heart" and recommend moderate exercise to maximise health and longevity, some scientists say too little research has been done to identify significant risk.
Professor Harvey White, director of coronary care and cardiovascular research at Auckland Hospital, said the scarring is of concern and requires more research. "We are worried that with people doing extreme exercise that these little scars may be sites for life-threatening abnormal rhythms. We don't know - it's a leap. We don't know whether the scars manifest long-term or whether they cause abnormal heart rhythms. But there may be an upper limit as to what exercise humans should do over a long period of time."
Regular aerobic exercise is believed to increase life expectancy by six years and to prevent heart attacks, stroke, diabetes and some cancers and helps with depression, but dosage may be as relevant to exercise as to any other form of medical treatment, particularly given huge and rising participation rates in triathlons and marathons. Though that might seem preposterous, it could prove to be the retrospective "elephant in the room", heart specialist and medical director of the London Marathon Professor Sanjay Sharma said last year when calling for detailed long-term studies of large groups of endurance athletes.
Stress of action
• Rob Waddell, Olympic champion sculler. Famously imploded in his third head-to-head race against Mahe Drysdale before the 2008 Beijing Olympics when his heart went into atrial fibrillation. He has had an operation called an ablation where the tissue triggering the abnormal rate is cauterised. As a result of the condition he gave up rowing, an aerobic sport, but is currently an America's Cup grinder - a strength-based role - for Team New Zealand.
• Hayden Roulston, professional cyclist diagnosed in 2006 with arrhythmogenic right ventricular dysplasia - a condition thought to be inherited, charactised by fibrous fatty tissue build-up, weakness and bulging in one of the four heart chambers. He was advised to stop competing as his condition has been linked to sudden death during sport. After trying an alternative remedy he resumed racing. He won silver at the 2008 Olympics and has competed in the "Grand Tours" of France, Italy and Spain.
• Greg Welch, triathlete, the only winner of his sport's grand-slam of world titles (Olympic, Long-Course and Ironman distances and Duathlon), the Australian quit after his heart surged to 320 beats a minute during the 1999 Hawaii Ironman. He has had nine open-heart operations and has a defibrillator pacemaker under his clavicle.
• Sir Peter Snell, triple Olympic gold-medallist, developed idiopathic dilated cardiomyopathy, a disease of unknown cause that results in an enlarged heart that does not pump properly. It is the most common reason people have a heart transplant.
Snell, an Associate Professor, Department of Internal Medicine, University of Texas, provided this footnote on his condition:
'[It] is mainly caused by advanced coronary artery disease, which leads to small occlusions, which damages the section of the heart downstream - a bad situation. Enlargement of the heart to improve pumping is a response to the this weakness. A stretched heart muscle delivers more force but at the expense of a thinner wall. In my case the heart was always big, with normal wall thickness (in response to athletic training). Damage to the LV wall, possibly by a virus, predisposes me to bouts of ventricular fibrillation during strenuous exercise. This life-threatening condition is controlled by drugs, change of exercise habits & an ICD. Otherwise the heart is ok and I don't ever expect a transplant."
