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Background   Elucidation of mechanisms underlying continuous training-related atrial fibrillation (AF) may inform formulation of novel therapeutic approaches and training method selection. This study was aimed at assessing mechanisms underlying continuous training-induced AF in an animal model.Methods   Healthy New Zealand rabbits were divided into three groups ( n =8 each), namely, control (C), and moderate intensity (M), and high intensity (H) continuous training according to treadmill speed. Atrial size andintrinsic and resting heart rates were measured by transthoracic echocardiography before, and 8 and 12 weeks after training. Using a Langendorff perfusion system, AF was induced by S1S2 stimulation and the induction rate was recorded. Atrial I K1  and I KAch  ion current densities were recorded using whole-cell patch-clamp technique in isolated atrial myocytes. Changes in atrial Kir2.1, Kir2.2, Kir3.1, and Kir3.4 mRNA expression were assessed by reverse transcriptase-coupled polymerase chain reaction.Results   After 8 and 12 weeks, Groups M and H vs. Group C had greater (all  P  < 0.05) atrial anteroposterior diameter; greater incidence of AF (60% and 90% vs. 45%, respectively;  P  < 0.05, also between Groups H and M); and greater atrial IK Ach  current density. In Group H, Kir2.1 and Kir2.2 mRNA expression in the left and right atria was increased ( P  < 0.05, vs. Groups C and M) as was left atrial Kir3.1 and Kir3.4 mRNA expression ( P  < 0.05, vs. Group C).Conclusion   In a rabbit model, continuous training enlarges atrial diameter leading to atrial structural and electrical remodeling and increased AF incidence.

Influence of Continuous Training on Atrial Myocytes IK1 and IKAch and on Induction of Atrial Fibrillation in a Rabbit Model

Influence of Continuous Training on Atrial Myocytes I_K1 and I_KAch and on Induction of Atrial Fibrillation in a Rabbit Model