Abstract
Introduction
Atrial fibrillation and heart failure share common risk factors and frequently coexist as atrial fibrillation leads to impaired myocardial function. Although regular exercise training is associated with cardiovascular benefits, the increased risk of atrial arrhythmias has been observed, with differences regarding prevalence between genders. While multiple mechanisms are likely, the atrial alterations induced by long-term physical exercise still need to be elucidated.
Purpose
We aimed at investigating exercise-induced atrial remodeling in a rat model of athlete's heart and determining sex-specific differences.
Methods
Age-matched young adult rats were divided into female exercised (FEx), female control (FCo), male exercised (MEx) and male control (MCo) groups. After exercised animals completed a 12-week-long swim training protocol, echocardiography was used to describe atrial alterations. In vivo electrophysiologic investigation was performed by programmed stimulation with an octapolar catheter inserted into the right atrium and atrial gene expression analysis was carried out.
Results
Post-mortem atrial weight data revealed marked atrial hypertrophy (atrial weight to tibial length: 18.6±2.7g/cm FEx, 10.3±1.0g/cm FCo, 23.7±2.2g/cm MEx, 15.8±1.9g/cm MCo pex<0.01), while echocardiography data showed slight atrial dilatation and improved contraction in both exercised groups. Exercise training was associated with bradycardia, P-wave enlargement and prolonged right atrial effective refractory period (RAERP: 45.7±4.3ms FEx, 40.2±5.9ms, FCo, 49.8±4.2ms MEx, 43.1±4.6ms MCo pex<0.01). Sinus node recovery time (SNRT) did not differ between groups and we could not induce significant number of arrhytmias by programmed stimulation (double extrastimulation, burst pacing) in any groups. We found increased atrial gene expression of antioxidant enzymes (e.g. NADPH oxidase 2, superoxide dismutase 2) in both genders. Despite the marked atrial hypertrophy, no gene expression alteration was found regarding markers that describe pathological remodeling (atrial natriuretic factor), proinflammatoric (tumor necrosis factor-α) and profibrotic [e.g. transforming growth factor-β (TGF-β), matrix metalloproteinase-2 (MMP-2)] processes. While exercise training did not affect on the expression of profibrotic markers, female gender was associated with lower TGF-β and MMP-2 expression. We found altered expression of ion channels participating in atrial depolarization and repolarization.
Conclusions
Our data suggests that long-term exercise-induced atrial hypertrophy is not associated with harmful electrical remodeling and no inflammatory or profibrotic response was observed in the atrium of exercised rats.
Acknowledgement/Funding
NKFIH (K 120277), ÚNKP-17-4 (to A.O.), STIA-KF-17 (to A.O.)
A Case of Wide-Complex Tachycardia Due to Atrial Tachycardia Diagnosed by Non-Invasive Programmed Stimulation
