The relationship between left ventricular structure and function in the elite rugby football league athlete as determined by conventional echocardiography and myocardial strain imaging
Introduction
Athletes' Heart (AH) describes the physiological adaptation from chronic exposure to exercise training [1]. The magnitude and type of adaptation is heterogeneous, being dependent on factors including age, body size, gender, ethnicity, training status and sporting discipline [2]. Recent studies have demonstrated changes in left ventricular (LV) geometry [3,4] alongside functional adaptation [5] across sporting disciplines. Pre-participation cardiac screening (PCS) in Rugby Football League (RFL) is mandatory for all male players competing in the professional RFL Super-League. Although Sudden Cardiac Death (SCD) in an athlete is rare [6], the impact is devastating for the family and the broader sporting community which often results with increased calls for more vigorous screening of athletes [7]. RFL is a high intensity sport, with moderate static (10–20%) and moderate dynamic (50–75%) components [8] and PCS aims to identify athletes at risk of SCD by detecting previously undiagnosed cardiac conditions. It is appropriate that screening strategies should be tailored to the population being screened [7] and it is therefore pertinent to establish the LV phenotype in RFL athletes. Echocardiography is routinely used in this setting with newer techniques, including strain (ɛ) and strain rate (SR) imaging now being implemented to describe chamber mechanics [9]. Previous data on LV mechanics is variable due to heterogeneous study design, methods and/or athlete populations with differentiation from inherited conditions often being based on a ‘one size fits all’ interpretation of echocardiographic derived measures and with little consideration of body size.
The relationships between LV geometry and ejection fraction (EF) have been extensively investigated in pathological hypertrophy [10,11] whilst the association in a physiological model, such as the AH, remains incompletely understood. Since the interrelationship between ventricular wall thickness, cavity dimension and EF is complicated, a better comprehension of the relationship between the thickness of the LV wall, EF and myocardial ɛ has been aided using mathematical modelling [10,12]. Using intuition alone to assess the effects of multiple changes in structure and geometry may lead to incorrect interpretations. Mathematical modelling helps as it eliminates confounding factors and quantifies the individual effects of geometric and physiological changes. The understanding provided by modelling studies has now been applied to hypertensive hypertrophic ventricular disease [11]. It has been shown that using mathematical modelling [10] and confirmed observational clinical data, that increasing LV wall thickness and/or myocardial ɛ independently leads to increased EF [11]. Similar findings have been seen in hypertrophic cardiomyopathy where the combination of reduced myocardial ɛ and increased wall thickness results in a normal or even increased EF [13]. In contrast, athletes tend to have greater wall thickness and dimensions yet have similar EF compared with controls [14].
This study focusses on the LV to provide an in-depth assessment of the structural and functional characteristics of this chamber in the elite RFL athlete to aid PCS and differential diagnosis where the LV is implicated. The primary aims of this study are to (1) establish the LV phenotype in elite male RFL athletes using standard 2D, Doppler, tissue Doppler, ɛ and SR speckle tracking echocardiography (STE), and (2) mathematically model the association between LV size, EF and ɛ in a physiological model of hypertrophy.
Section snippets
Study population and design
Following ethical approval by the ethics committee of Liverpool John Moores University, 139 elite, RFL Super-League athletes aged 24 ± 4 years (range 19–34) and 52 sedentary control subjects 22 ± 3 years (range 20–35) provided written informed consent to participate in the study. Athlete data was collected as part of mandatory PCS. Athletes participated in >10 h structured exercise training per week and healthy controls engaged in <3 h recreational activity per week. Participants completed a
Results
Athletes were significantly older (P = 0.001) than controls (24 ± 4 and 22 ± 3 years). Height (1.82 ± 0.06 and 1.78 ± 0.06 m), weight (96 ± 11 and 78 ± 9 kg) and BSA (2.20 ± 0.15 and 1.96 ± 0.13 m2) were all significantly (P < 0.001) higher in the athlete group whilst HR was significantly (P < 0.001) lower in the athlete group (56 ± 10 and 69 ± 9 beats min−1). Blood pressure (BP) was 131/69 and 129/74 mmHg in the athlete and control groups respectively. There was no significant difference in
Discussion
The main findings of this study are: (1) Absolute and scaled values for LV chamber size and wall thickness are increased in RFL athletes whilst indexed TDI, SR, apical rotation and twist are lower in RFL athletes compared to sedentary controls, (2) EF is maintained which is likely due to the interaction of divergent effects of LVIDd and MWT on LV function.
Absolute and indexed LV structural parameters are increased in elite RFL athletes consistent with previous studies [1,3]. Utomi et al. [14]
Limitations
From this cross sectional study we cannot determine the timing of exercise induced changes in LV structure and function. The athletes were selected according to sporting discipline and whilst physiological adaptation of the nature observed in RFL athletes is likely similar to athletes of other sports of this type, further application of the model is warranted in athletes involved in a range of sporting disciplines. Genetic factors and seasonal variation should also be considered during cardiac
Conclusion
Despite an increased LV size, there is a predominance for normal LV geometry in RFL athletes, who undertake mixed resistance and endurance based training. Despite normal EF and global ɛ, global SR is lower and there is significant regional ɛ and SR heterogeneity compared to controls. Apical rotation and twist are also significantly lower and it is likely that lower SR and twist mechanics are part of the normal physiological cardiac adaptation in RFL athletes. Normal EF and therefore ɛ, observed
Conflict of interest
The authors report no relationships that could be construed as a conflict of interest.
Acknowledgements
This research received funding from the charitable organisation Cardiac Risk in the Young (CRY).
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