The performance of sporting activities like cycling and running is a life style factor that improves health and increases the duration of healthy life [1, 2]. Heavy exercise, such as rowing, cycling, and marathon running at competitive levels, is considered to be healthy, although evidence of the opposite is published from time to time [3, 4]. It is known for quite some time that the hearts of extensive sport athletes develop left ventricular hypertrophy (LVH), known under the name of the “athlete’s heart”. This type of LVH is considered physiological [5–10]. Conditions like hypertensive heart disease lead to pathological LVH [11–15], as it is often associated with perivascular and interstitial fibrosis of left ventricular myocardium [16], diastolic heart failure [17, 18], arrhythmias [19, 20] and mortality [21].

Previous studies from our institution have already addressed the issue of physiological versus pathological LVH [5, 22, 23]. First of all we studied the accuracy of M-mode echocardiography and two different two-dimensional echocardiographic approaches in the assessment of left ventricular mass and volumes in endurance-trained and strength-trained athletes, using cardiovascular magnetic resonance (CMR) imaging as reference standard [23]. It was shown that in general practice the two-dimensional echocardiographic approach was the most accurate estimator of left ventricular mass and volumes in both controls and athletes. For research purposes, however, CMR remains the most accurate and reliable method to assess cardiac anatomy and function [24–27]. In a next study we addressed the question of whether training-induced left ventricular hypertrophy in athletes is a physiological rather than a pathophysiological phenomenon [28]. To that purpose we studied 21 elite cyclists and 12 healthy control subjects. Left ventricular mass, volume, and function were determined by CMR and myocardial high-energy phosphates were examined by 31P magnetic resonance spectroscopy. It was shown that LVH in cyclists was not associated with significant abnormalities of cardiac function or metabolism as assessed by CMR and spectroscopy. These observations suggested that training-induced left ventricular hypertrophy in cyclists is predominantly a physiological phenomenon. Finally in a meta-analysis paper, involving 59 studies and 1,451 athletes, i.e., endurance-trained athletes (long-distance runners), strength-trained athletes (weight lifters, power lifters, bodybuilders, wrestlers, and throwers), and athletes involved in combined forms of dynamic and static training (cyclists and rowers), we confirmed the hypothesis of divergent cardiac adaptations in dynamic and static sports [5]. Overall, the athlete’s heart demonstrated normal systolic and diastolic cardiac functions. However, our meta-analysis concerned relatively young athletes between 18 and 40 years.

Whether individuals older than 50 years engaged in exceptionally extensive sports have LVH and how this LVH relates to their cardiovascular risk factors is addressed by Nassenstein and colleagues in this issue of the International Journal of Cardiovascular Imaging [29]. They investigated 105 clinically healthy male marathon runners aged ≥50 years and determined left ventricular muscle mass (LVMM) and diastolic and systolic left ventricular volumes (LVEDV and LVESV, respectively) by CMR imaging, diastolic and systolic blood pressure by an automatic blood pressure device, coronary artery calcifications (CAC) by electron beam computed tomography, plasma HDL and LDL cholesterol concentrations, smoking habits, and body mass index (BMI). Surprisingly, quite high percentages of individuals in this cohort demonstrated cardiovascular risk factors: 13% hypertension, 9.5% hypercholesterolemia, and 33% a BMI ≥ 25 kg/m2. In the whole cohort LVMM was positively correlated with systolic as well as diastolic blood pressure, thus the hypertensive runners are the ones with the highest LVMM. The authors also demonstrated that the CAC burden was significantly higher (by a factor ≈4) in runners with LVMM ≥ 150 g than in those with LVMM < 150 g. From these results the authors drew the conclusion that in well-trained marathon runners (1) blood pressure contributes to LVH and (2) that LVMM should not be solely interpreted as a physiological adaptation to exercise. So, at least in a substantial percentage of this cohort of well-trained marathon runners aged ≥50 years existing LVH is induced by physiological ánd pathological forces, maybe acting synergistically. As LVMM ≥ 150 g is associated with extensive CAC and given the massive evidence of LVH being a risk factor [30, 31], hypertension in athletes, particularly older athletes, should be considered a reason to stop performing extensive endurance sports and start anti-hypertensive therapy. Consequently, elderly marathon runners should be carefully checked for the presence of hypertension.