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

Abstract EN

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 IK1 and IKAch 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 IKAch 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.