May Strenuous Endurance Sports Activity Damage the Cardiovascular System of Healthy Athletes? A Narrative Review

Figure 1. Acute ECG changes reflecting right heart overload. ECG of a top-level competitive athlete the day before (A) and immediately after (B) running a 50 km ultramarathon. After the race, the ECG showed higher P-wave voltages and a rightward shift in the QRS axis. Adapted from D’Ascenzi et al. [10].

Figure 2. Example of two post-run ECG recordings with a portable single-lead electrocardiogram device showing premature ventricular beats (*) that were not present before the race. Reproduced with permission from Zorzi et al. [39].

Figure 3. A case of sport-induced long-QT syndrome. Male, 15-year-old, plays water polo at a competitive level (training >10 h/week). Negative medical and family history. ECG at pre-participation screening: QTc 597 ms, HR 79 bpm (A), with notched morphology of T waves. Detraining was recommended. Genetic testing of the genes associated with LQTS resulted negative. ECG after 3 months of detraining: QTC 394 ms, HR 58 bpm (B).

Figure 4. Representative example of the role of endurance exercise in worsening the arrhythmogenic cardiomyopathy phenotype. A 38-year-old runner received a diagnosis of arrhythmogenic cardiomyopathy after investigating ventricular arrhythmias and ECG abnormalities at preparticipation screening. Genetic testing was positive for plakophilin-2 gene mutation. At the time of diagnosis, cardiac magnetic resonance 4-chamber view on cine sequences found dilatation of the right ventricle with mild dysfunction (A) and diffuse right ventricular late-enhancement on post-contrast sequences (B). Although he was considered not eligible for competitive sports activity according to Italian law, he continued to practice high-intensity endurance training. After 4 years, repeat cardiac magnetic resonance showed a more enlarged right ventricle, an apical aneurysm (arrow), and a moderate right ventricular dysfunction (C). Post-contrast sequences confirmed diffuse right ventricular late enhancement (D). Reproduced with permission from Zorzi et al. [92].

Figure 5. Example of a myocardial scar in an athlete. A competitive hockey player aged 26 at the pre-participation screening during exercise testing showed frequent PVBs with right bundle branch block/superior axis morphology at high workload ((A), red asterisks). Post-contrast sequences on CMR revealed a subepicardial stria of LGE involving the anterior, lateral, and inferior LV walls in their basal and medium portions, with a “ring-like” pattern (green dotted line; (B) 4-chamber view; (C) short-axis view). Increased signal in the correspondent areas of fibrosis in the native T1 mapping short-axis sequence (D). Reproduced with permission from Brunetti et al. [129].

Figure 6. Representative example of coronary calcifications in a 56-year-old endurance athlete without risk factors who underwent coronary computed tomography for investigation of repolarization abnormalities on resting ECG. 3D reconstruction of the coronary artery tree (A). Calcific plaques in left anterior descending (arrows, B) and circumflex (arrow, C) coronary arteries.