In this study, we have examined a cohort of veteran endurance athletes and a paired untrained control group to evaluate the consequences of long time practice of intense endurance exercise on myocardial structure to find that:
Morphological and functional parameters
Cardiac adaptation in veteran, high-performance endurance athletes is characterised by balanced increase of LV and RV volumes, increased LV wall thickness and myocardial mass,12 13 leading to what is known as the athlete’s heart. Accordingly, our cohort showed significantly enlarged left and right ventricles compared to control subjects, with no significant differences in the LVEDV-to-RVEDV ratio. Also, athletes showed an increase in absolute wall thickness compared to control subjects. However, in accordance with previous reports,14 values of indexed LV mass are within normal ranges. The present study also proves the preservation of LV and RV ejection fraction in lifelong endurance veteran athletes.
Focal myocardial fibrosis
LGE was observed in three (9%) athletes, all of them showing a non-ischaemic pattern (figure 1A–C). Furthermore, in two of them, delayed-enhancement patterns were highly suggestive of a previous episode of clinically undetected myocarditis (figure 1 B,C).
There is still some controversy regarding on whether repeated extreme endurance exercise might result in MF. Benito et al
6 exercised rats on a treadmill and observed diffuse fibrosis in the atria and right ventricle which resulted in ventricular arrhythmia. CMR studies have also reported an apparently high incidence of focal MF in veteran athletes: Breuckmann et al
7 examined 102 healthy veteran male marathon runners and reported an unexpectedly high prevalence of LGE (12%), although it was not significantly different from that of age-matched control participants (4%, p=0.07). Another study15 found focal MF by LGE in 6 of 12 elite veteran athletes but not in 20 age-matched controls or in 17 young endurance athletes. The presence of LGE in veteran athletes was significantly associated with the training volume, supporting a link between life-long endurance exercise and MF.
More recently, La Gerche et al
16 showed LGE in 5 of 40 (13%) athletes studied which was confined to the interventricular septum in all cases.
In two of the three athletes, we found a LGE pattern highly suggestive of a previous myocarditis as the potential cause. It would be reasonable to believe that continued exercise training may accelerate myocardial damage and MF during silent myocarditis.17
MF in the RV insertion point has been reported in up to 19% of athletes in the literature,18 and it is an important topic of debate. It is speculated that the RV distention during exercise may result in chronic structural changes of the myocardial architecture, mainly in the septal points of insertion of the right ventricular wall. In our study, we found mild LGE in the inferior septal RV insertion in 23% of athletes. However, we did not consider this finding as true reactive MF. In fact, this finding was also observed in 36% of controls (figure 2). We believe that, as previously reported,17
,19 plexiform fibrosis is a normal feature of the insertion-region anatomy that may result in contrast pooling within this area.
Figure 2A 40-year-old man with a training history of 2 hours/week during 6 years (Control group). A mid-ventricular short-axis view shows mild LGE in the inferior RV-LV junction.