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By Marc Harrison, M.D
New Report Shows:
heart is not spared effects of hard racing
Overtraining
If you are like most triathletes, you understand that you are a little faster, stronger, leaner and healthier than your sedentary friends. By and large, you are probably correct, and your triathlon habit may be a large part of the reason you feel and look better than most people your age.
The triathlon lifestyle of activity and aerobic fitness encourages cessation or diminution of unhealthy habits such as smoking or excessive alcohol consumption. As a result, you are less likely to be obese or have high blood pressure and more likely to hear this voice of concern when you visit the doctor’s office: “Sir, did you know your heart rate is 43? Are you feeling light-headed?”
Sports scientists and physicians recognize that prolonged, strenuous exercise is associated with muscle injury. The reason for muscle breakdown during endurance events is probably a combination of physical trauma and biochemical stress (e.g., free radicals) resulting in “leaky” myocytes. After a physiologic stress such as a marathon, significant elevations of proteins normally found only in muscles may be found in the blood of athletes. Until recently, this injury has been thought to be primarily isolated to the skeletal muscle.
Creatine kinase (CK) is a protein and enzyme found in all muscle cells. CK-MB is a form of the enzyme, which is found primarily in heart muscle and, to a lesser degree, in skeletal muscle. In the absence of skeletal trauma, an elevated CK-MB is a reliable marker for injury to heart muscle. As early as 1981, elevations of CK-MB have been noted in marathon runners. The degree to which elevated CK-MB was released from a cardiac versus a skeletal muscle source has been debatable.
Over the past two decades, studies have consistently shown acute, reversible decreases in function of the left ventricle (the heart chamber that pumps blood to the body) in athletes following bouts of strenuous exercise. The reason for these changes has not been clear and many hypotheses were tendered. In the absence of compelling biochemical evidence of injury to the heart muscle, these changes have been chalked up to “cardiac fatigue.”
Since the early 1990s, physicians and scientists have developed assays for cardiac troponins, a class of proteins found only in cardiac muscle. With the current generation of troponin assays, there is less than 0.005 percent cross-reactivity between skeletal and cardiac troponins. Thus, if an assay is positive, then the source must be injured heart muscle. These assays have been incorporated into diagnosis and risk stratification of myocardial infarction (heart attack) and are in wide clinical use.
Based on the worldwide proliferation of Ironman-distance races, it would seem that current triathlon wisdom is that if a little triathlon is good then a lot of triathlon is even better. However, a recent article in the American Journal of Cardiology by Nader Rifai, Ph.D., an associate professor at Harvard Medical School, suggests that Ironman-distance racing may be associated with myocardial injury and short-term abnormalities in heart function.
Dr Rifai and colleagues looked for biochemical markers of myocardial injury and change in heart function in 23 well-trained amateur athletes who participated in the 1994 Hawaii Ironman. The subjects’ average weekly training consisted of 8K swimming, 330K cycling and 75K running. Subjects were healthy without history of heart disease, hypertension, smoking or other risk factors for cardiac dysfunction.
Blood was obtained from the subjects two days before and within 15 minutes after finishing the Ironman. An echocardiogram (ultrasound image of the heart) was obtained in 12 subjects two to five days prior to the race and immediately after completing the event.
Biochemical markers for skeletal and cardiac muscle were normal for all subjects prior to the race. Plasma CK and CK-MB were markedly elevated post race. Two subjects (nine percent of the total count) had marked increases and four subjects (17 percent) had moderate increases in cardiac troponins following the race. These biochemical findings of cardiac muscle injury were confirmed at the 1995 Ironman using the most recent generation of troponin assay, which has minimal cross-reactivity with skeletal muscle.
Interestingly, cardiac troponins correlated inversely with finishing times — the faster the racer, the higher the plasma concentration of troponins.
Echocardiograms obtained prior to the race were normal in all 12 subjects. After the race, nine subjects (75 percent) had abnormal echocardiograms. The ejection fraction (amount of blood squeezed from the left ventricle per heartbeat) was diminished by 24 percent. Abnormal wall motion correlated strongly with elevated cardiac troponin, suggesting that abnormal heart function is at least partially due to myocardial injury — not “cardiac fatigue.”
Prior studies have demonstrated that wall motion and ejection fraction return to normal within 24 to 48 hours after an Ironman.
Given that the subjects in this study were experienced athletes (one subject had been racing for 17 years) and all had normal pre-race echocardiograms and biochemical profiles, it is possible to infer that cardiac dysfunction associated with Ironman racing is reversible. However, the long-term cardiac effects of ultra-endurance events are not known.
Dr Rifai is not sure why the heart is temporarily injured by extreme exercise. He reminded me that, “The heart is not an invincible muscle. It can be injured by exercise just like skeletal muscle. Care should be taken in recovering from Ironman racing.”
Many of you have followed Greg Welch’s retirement with interest and empathy. I know that I have. Based on my knowledge of his situation, I do not believe that there is a causal link between Welch’s career-ending difficulties with ventricular tachycardia and his repeated super-human race efforts. I have not uncovered any evidence that suggests that the cardiac injury described by Dr. Rifai and discussed in this article leads to the formation of arrhythmogenic foci in the heart.
Certainly, all people with symptoms, risk factors or history of heart disease should be thoroughly evaluated by a well-qualified physician prior to engaging in a training program. Symptoms during exercise should not be ignored. Given Dr. Rifai’s data, I would not rush back into heavy training after an ultra-distance race. I would wait until muscle soreness is completely resolved and motivation has returned before resuming training after an Ironman.
In the final analysis, are my parents, who are convinced that the ultra-distance racing is “not healthy,” right? It is difficult to know how to incorporate this body of literature into one’s overall approach to the sport.
I am in my 19th consecutive season of racing, have completed three Ironman-distance races and would like to do another in the next year or two. Personally, I had an exercise stress test supervised by a cardiologist. I have resolved to listen carefully to my body and to recover completely after hard racing. I hope you will do the same.
Marc Harrison is a pediatric intensive care specialist at the Cleveland Clinic Children's Hospital and an avid age group triathlete. He lives with his perennially supportive wife and three children in Shaker Heights, OH.
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