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Oscar Wilde once said, ‘Moderation is a fatal thing. Nothing succeeds like excess’. Some would say that, for elite athletes, ignoring this aphorism can only lead to failure. With the stoichiometric rise in the number of veteran athletes taking part in ultra-endurance exercise, it is apparent that a growing number of athletes are adopting Wilde's maxim with some impressive results. The winner of the 2011 Virgin London Marathon male 60–64 year age group clocked 3 h 3 min 25 s, while the 2010 New York Marathon male 70–74 year group winner ran 3 h 18 min 45 s! In support of the endurance obsession, we have recently published a case study of a 68-year-old male runner who had accurately recorded a total distance of 148 561 miles throughout 43 years of daily running.1 While we are assured that moderate intensity, duration and frequency exercise are positive for ciovascular health, can we be sure that running 7 min 30 s repeatedly over 3 h at 70 years of age or 150 000 miles throughout a 70-year lifetime is not damaging to the myocium? In essence, can one have too much of a good thing?
Ageing is associated with changes to the ciovascular system that reduce functional capacity. Regular endurance exercise training appears to slow this progressive decline, however; do such benefits apply to intensive life-long endurance activity in veteran athletes (>50 years)? Compared with age-matched sedentary controls, a higher prevalence of subclinical ciac disease has been reported in veteran athletes that may increase the risk of an exercise-associated ciac event.2 Several case studies have reported an increased prevalence of supraventricular3 and complex ventricular tachyarrhythmias4 in apparently healthy athletes. The aetiology and clinical significance of these arrhythmias remain to be fully elucidated since several similar forms of idiopathic ventricular arrhythmias have been identified in athletes whose hearts show no structural abnormalities.5
In 2008, in this journal, we postulated that in the absence of any other cause, life-long repetitive bouts of uous endurance exercise may result in fibrotic replacement of the myocium in susceptible individuals, resulting in a pathological substrate for the development of arrhythmias.6 A subsequent case report by Bhella et al 7 reported the appearance of late gadolinium enhancement (LGE) on ciac MRI in the inferior insertion of the right ventricle and interventricular septum, with no evidence of decrement in systolic function and undetectable levels of troponin I and T in a male runner attempting the North American transcontinental. In support of this hypothesis, animal studies have documented myocial fibrosis following an exercise intervention. Benito et al8 have recently conditioned male Wistar rats to run vigorously for 16 weeks. The authors observed collagen deposition and a significant increase in messenger RNA and protein expression of fibrotic markers after long-term intensive exercise training, together with changes in ventricular function and increased arrhythmia inducibility. Positively, the authors documented that the cessation of endurance training was able to arrest and even reverse this pathological process.
Within humans, Breuckmann et al9 were the first to investigate whether competitive running history was linked to the prevalence of LGE in male marathon runners. Despite a non-significant difference in the prevalence of LGE (12% vs 4%, p=0.07) between athletes and age-matched controls, the lack of life-long continuous competitive endurance history, and the higher prevalence of former (51.9%) and current smokers (4.6%) in the runners, the higher prevalence of non-CAD (coronary artery disease) patterns of LGE in runners raised the possibility that it was the distance run and not life-long distance running career that may be key to this acquired pathology.
In order to address the dearth of experimental data in high-level healthy athletes, we have recently examined the ciac structure and function of a unique cohort of 12 truly life-long, competitive veteran endurance athletes versus 20 age-matched veteran controls and 17 younger male endurance athletes using ciac MRI with LGE with a view to identifying potential fibrotic infiltrate.10 Our veteran athlete group was unique, with a competitive endurance career spanning 43±6 years (range 35–52), competing in 178±209 marathons (range 20–650) and 65±91 ultra-marathons (range 0–257). We observed evidence of myocial fibrosis in six (50%) athletes (four with LGE of non-specific cause, one with probable previous myocitis and one probable previous silent myocial infarction). Importantly, there was no LGE in the age-matched veteran control group nor in the young athletes, with the prevalence of LGE associated with the number of years spent training (p<0.001), number of competitive marathons (p<0.001) and ultra-endurance (>50 miles) marathons (p<0.007) completed. In support of these data, a recent study of 40 healthy ultra-endurance athletes has found that a small number of athletes (n=5; 13%) exhibited LGE in the interventricular septum together with increased right ventricular remodelling. Importantly, this small cohort had been competing in endurance sports for significantly longer (20+16 vs 8+6 years, p<0.05) than those athletes similar in age, but without LGE.11
One of the problems in examining such a small and unique group of life-long athletes is that it is often difficult to understand the potential mechanisms responsible for the increased incidence of myocial fibrosis. Unlike some inherited ciac conditions, such as hypertrophic ciomyopathy or arrhythmogenic right ventricular ciomyopathy (ARVC), it appears that not all adverse ciac remodelling has a genetic constitution. La Gerche et al12 examined the prevalence of ARVC causing mutations within genes encoding desmosomal proteins in 47 symptomatic endurance athletes with complex right ventricular arrhythmias. The majority of the athletes studied (n=41; 87%) fulfilled Task Force Criteria for definite or suspected ARVC. A total of 10 different heterozygous mutations were identified within five candidate desmosomal genes, however; in only six cases (13%) were these considered to be pathogenic. Individuals who were gene positive (n=6) had worse right ventricular ejection fraction but did not differ from gene negative athletes (n=41) in relation to symptomatic presentation, electrociographical anomalies, therapeutic intervention or subsequent implantable cioverter defibrillator (ICD) discharge. The study adds to the hypothesis that the ARVC phenotype may be acquired through intensive and sustained ciovascular exercise and may not be solely attributed to a genetic predisposition relating to ‘known’ desmosomal proteins. It should be noted that failure to demonstrate a high prevalence of ARVC causing desmosomal mutations in athletes with sinister right ventricular arrhythmias should not automatically lead to an assumption that an acquired form of the disorder is possible, as the yield for ARVC gene mutations in sporadic cases of the disorder is low.
In conclusion, given emerging evidence supporting a potential link between life-long intensive endurance competition and acquired ciac pathology, it is attractive to suggest that excessive life-long exercise may be damaging to the heart. However, in light of the overwhelming evidence promoting the beneficial effects of regular exercise upon long-term ciovascular health in the general population, care is warranted in the delivery of this message. Further well-controlled, large cohort studies are required within veteran athlete populations to ascertain if Oscar Wilde was athletically correct but ciologically wrong.
Competing interests None.
Provenance and peer review Not commissioned; externally peer reviewed.