The most significant factor appears to be how hardcore these specific athletes were.
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People involved in some of the world's most extreme endurance sports may be at risk of damaging their hearts, according to a new German study of triathletes. The harder the athletes pushed themselves in the past, the greater the likelihood they showed signs of myocardial fibrosis, the scarring of the heart’s ventricles, which has been linked to heart disease.
"The cause and development mechanism of these [heart damages] in competitive athletes remains speculative,” says Jitka Starekova, the author of the study, which will be presented at the Radiological Society of North America’s annual meeting next week. “We hypothesized that the presence of myocardial fibrosis correlates with the amount of cumulative lifetime exercise.”
Starekova and her colleagues at the radiology department of the University Medical Center Hamburg-Eppendorf in Germany gathered 55 men and 30 women who were triathlon competitors and trained at least ten hours a week. They ranged in age from 18 to 55; the men averaged 44 and the women 43. The researchers injected gadolinium, a contrast agent, into their bloodstreams. Gadolinium is taken up by both normal and scarred heart muscle tissue, but normal cardiovascular tissue washes it out more quickly than scarred. This is a common detection method for myocardial fibrosis.
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The study revealed myocardial fibrosis in the left ventricle (the heart's main pumping chamber) in ten of the men (18 percent) and none of the women. Starekova said she did not know if gender was a factor: “It is possible that testosterone has a relevant impact,” she says.
But it seems like the most significant factor in the development of myocardial fibrosis was how hardcore the athletes were. These ten men were some of the most dedicated triathletes in the study. They had completed significantly more Ironman-style competitions than the people whose hearts pumped out the contrast agent in normal measures. These same athletes also had higher levels of peak exercise systolic blood pressure than others in the group, meaning their hearts were pumping blood more quickly—perhaps another result of the extreme conditioning they had endured.
Starekova is careful to state that researchers “cannot prove the exact mechanisms.” She and her colleagues have planned long-term follow-up studies to see if cardiac events or heart problems occur in the triathletes who had evidence of myocardial fibrosis.
It might be that conditioning and endurance sports may have costs, endured by the heart, if done to the extreme. “There appears to be a safe upper limit, beyond which exercise may result in myocardial fibrosis,” she says. “In other words, ‘athlete’s heart’ may not be a benign physiological adaptation to systemic training in all triathletes, and cumulative repetition of extreme athletic activity may put the hearts of athletes in risk.”
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