Evidence of functional remodelling of the right and left ventricle in athletes

BACKGROUND: Cardiac remodelling following athletic training manifests as changes in structure and function. Dichotomous remodelling of the left ventricle (LV) in response to strength and endurance training has been suggested by cross-sectional design, purportedly owing to the divergent haemodynamic ‘pressure’ load elicited by static, resistance training and haemodynamic ‘volume’ load caused by dynamic, endurance training. Compared with the LV, the right ventricle (RV) is more sensitive to the acute haemodynamic response, and long-term remodelling of endurance training, which elicits both a volume and pressure load on the RV. The purpose of this thesis was to further the understanding of cardiac adaptation and functional cardiac responses in the athlete’s heart.

METHODS: Meta analyses (Study 1) were performed on RV systolic pressures, at rest and during exercise, and measures of RV function at rest including displacement, velocity and regional longitudinal strain, comparing the weighted mean difference between high-dynamic athletes and non-athletic controls. Using echocardiography, experimental Study 2 examined the RV free wall response to acute plasma volume expansion, achieved via 7 ml·kg-1 intravenous Gelofusine infusion, and subsequent leg raise in endurance-trained (n = 13) and non-trained controls (n = 11). In experimental Study 3 echocardiography was used to compare the LV responses of endurance-trained (n = 15), resistance trained (n = 14) and non-athletic men (n = 13) to (i) progressive isometric leg-press exercise (i.e., pressure load; 20, 40, 60% one-repetition maximum) and (ii) an intravenous Gelofusine infusion (7 ml·kg-1) with and without passive leg-raise (i.e., progressive volume load).

RESULTS: Via meta-analysis (Study 1), it was established that right ventricular systolic pressure was significantly greater in endurance athletes at rest (2.9 mmHg, P = 0.0005) and during exercise (11.0 mmHg, P < 0.0001). Resting RV myocardial displacement (1.8 mm, P < 0.0001) and tissue velocity (0.7 cm/s, P = 0.001) were also greater in endurance athletes.

RV free wall longitudinal strain was similar compared with controls, but apical strain was greater (0.9%, P = 0.03) and basal strain lower (-2.5%, P < 0.0001), in endurance athletes, demonstrating a regional adaptation. Study 2 examined the RV free wall response to acute plasma volume expansion. Both endurance-trained individuals (7 ± 3%) and controls (7 ± 3%) experienced an increase in free wall strain, which was also similar following leg raise (4 ± 3% and 7 ± 3%, respectively; P = 0.793). However, infusion evoked a greater increase in basal longitudinal strain in endurance-trained vs. controls (18 ± 4% vs. 5 ± 5; P = 0.074), which persisted following leg raise (18 ± 3% vs. 1 ± 5%; P = 0.041). In Study 3 resistance-trained participants preserved stroke volume (-3 ± 8%) versus non-athletic controls at 60% 1 repetition maximum (-15 ± 7%, P = 0.001). Time-to-peak longitudinal LV strain was maintained in resistance-trained individuals and delayed in endurance-trained participants (1 vs 12% delay, P = 0.021). Volume infusion caused a similar increase in end-diastolic volume and stroke volume across groups, but leg raise further increased end-diastolic volume only in endurance-trained individuals (5 ± 5% to 8 ± 5, P = 0.018).

CONCLUSIONS: Collectively, this thesis highlights the remodelling capacity of the male athlete’s heart, which extends beyond simply the expression of structural or functional remodelling at rest, and incorporates a training-specific, adaptive response associated with the attendant haemodynamic perturbation.