Long-term exercise training is associated with unique cardiac troponin I phosphorylation pattern and benign myocardial hypertrophy in the right ventricle in an experimental model of exercise-induced myocardial remodelling.

BACKGROUND

Research projects have focused on exercise-induced alterations of the right ventricle (RV) of the heart, because the exercise-associated disproportionate load on the RV might lead to pathological consequences, such as interstitial fibrosis, chamber dilation or pro-arrhytmic remodelling. We aimed at providing a complex characterization of RV alterations induced by regular training in a rat model of exercise-induced cardiac remodelling.

METHODS

Young, adult rats were divided into control (Co) and exercised (Ex) groups. Exercised rats swam 200 min/day for 12 weeks. In vivo cardiac electrophysiological study and in vitro force measurements on isolated permeabilized RV cardiomyocytes were performed to investigate electrical and functional alterations, respectively. Molecular biological and histological investigations were carried out.

RESULTS

Exercise training was associated with mild increased RV hypertrophy (cardiomyocyte diameter: 12.5 ± 0.1 μm Co vs. 13.7 ± 0.2 μm Ex, p < 0.05) and corresponding hyperphosphorylation of protein kinase B (Akt). Absence of pathological remodelling was revealed by unchanged pro-fibrotic and pro-apoptotic markers. We found increased maximal force development (12.1 ± 1.0kN/m2 Co vs. 16.7 ± 1.1 kN/m2 Ex, p < 0.05) and improved calcium sensitivity in the cardiomyocytes of exercised animals. Sarcomere protein investigations revealed marked overall and site-specific (Ser22/23, Ser43 and Thr143) hypophosphorylation of troponinI. We found prolonged QT interval (repolarization) and RV effective refracter period along with decreased gene expression of potassium channels. We could not induce any ventricular arrhythmia by programmed stimulation.

CONCLUSIONS

Regular swim training induced physiological RV hypertrophy that was associated with functional improvement related to unique hypophosphorilation pattern of troponin I. A balanced exercise program without excessive exercise sessions might not be associated with induction of pathological alterations.