Abstract 2619: Sustained Endurance Exercise Training Creates a Substrate for Atrial Fibrillation in Rats
Although regular physical activity has recognized health benefits, recent reports suggest that high-level exercise training (ExT) may promote atrial fibrillation (AF). In this study, we examined the effects of ExT on AF susceptibility, fibrosis-associated gene expression and atrial fibrosis in a rat model.
Methods: Rats subjected to daily 1-hour treadmill training (n=14) for 16 weeks were compared to parallel sedentary (CTL, n=15) rats. At 16 weeks, rats underwent electrophysiological study to assess AF inducibility. If sustained AF (>30 s) was not induced, carbachol (CBC) was given and induction re-attempted. Atrial mRNA expression of fibrosis-related markers (TGF-β, fibronectin, procollagen-I, procollagen-III, MMP-2 and TIMP-1) was evaluated by RT-PCR. Masson trichrome was used for fibrosis assessment.
Results: ExT rats had reduced body weight (BW, 544±29 vs 666±74 g CTL, p<0.001) and increased heart weight/BW ratio (0.31±0.04 vs 0.23±0.02 CTL, p=0.001) vs CTLs. In the absence of CBC, programmed stimulation reproducibly induced sustained AF in 9/14 (64%) ExT vs 3/15 (20%, p=0.02) CTL rats. After CBC administration, sustained AF was induced in all 14 (100%) ExT rats but only 9/15 (60%) CTL rats (p=0.01). All fibrosis-related markers were substantially upregulated in ExT rats (figure A⇓) and atrial fibrosis was seen (B).
Conclusion: In this rat model, chronic endurance exercise increased AF susceptibility, enhanced expression of fibrosis-related genes and promoted atrial fibrosis. Our findings suggest that intensive physical training creates an AF-maintaining substrate. These observations substantiate the link between ExT and AF and point to underlying mechanisms.