Exercise hypertension: Link to myocardial fibrosis in athletes?

With a series of articles published over the last two years E Tahir and colleagues participate in the debate on potential detrimental consequences for cardiac structure and function related to extensive, strenuous exercis. In order to further study the well-described biological significance of elevated cardiac biomarkers seen after extreme endurance competitions they have investigated triathletes by blood sampling and cardiac magnetic imaging before and after competition (mean race time: 3.3 2.7 h). In the current study published in the European Journal of Preventive Cardiology the authors aimed to assess the predictive value of clinical baseline characteristics of their athletes, for example, training history, maximal exercise capacity and exercise blood pressure during ergometry as well as myocardial dimensions and fibrosis assed by cardiac magnetic resonance imaging (CMR) and correlated these to increases of cardiac biomarkers and impairment of myocardial function or structure during the race. The data imply good and bad news for endurance (elite) athletes. First, it was found that despite the fact that serum cardiac biomarkers such as troponin T and N-terminal pro-brain natriuretic peptide (NT-proBNP) significantly increased immediately after the race, maximal exercise strain during a triathlon race does not induce acute overt myocardial inflammation or oedema as assessed by CMR. In a way, these data exonerate such extreme exercise since others had generally observed discrete morphological alterations of the myocardium after endurance competitions, including an increase of physiological strain of the myocardium during volume overload, particularly of the right ventricle. The bad news is that Tahir and colleagues revealed a positive late gadolinium enhancement (LGE) in CMR as a correlate for myocardial fibrosis in a large portion of their athlete male population (33%), a finding more pronounced than in previous investigations. Explanations for the prevalence of myocardial lesions particularly in male athletes are diverse and include genetic predisposition, gender (females are less affected), risk factors for coronary artery disease and coronary ischaemia itself, acute or reactivated myocarditis, pulmonary artery pressure overload and exercise-induced repetitive micro-injury during prolonged exercise stress. However, most importantly the series of data adds another potential risk factor to the currently discussed ones, the role of exercise blood pressure on myocardial remodelling and determinant for myocardial injury. The current study has revealed that those athletes with positive LGE had a significantly higher maximal exercise blood pressure (30mmHg higher compared with LGE negative athletes) at similar maximal exercise capacities between groups. Also, early adaptation typical for arterial hypertension such as left ventricular hypertrophy and left atrial enlargement was observed in the LGE positive group. Furthermore, in LGE positive athletes post-race values demonstrated increased left atrial strain as indicated by a trend towards higher NT-proBNP values. These findings are supported by the research group’s previous analysis also investigating triathletes, in which peak exercise systolic blood pressure assessed during ergometry before the race and exercise volume during the race were identified as independent predictors of the presence of LGE. Summing up these data may lead to the hypothesis that a repetitive volume overload of the myocardium induced by repetitive endurance training sessions of several hours per day over many years will have an impact on vascular and myocardial physiological adaptation as well as pathological remodelling, resulting in a consecutive pressure overload with increased blood pressures during exercise (Figure 1). Whether this will