Cardiac arrhythmogenic remodeling in a rat model of long-term intensive exercise training
Open accessAbstract
Background—: Recent clinical studies suggest that endurance sports may promote cardiac arrhythmias. The aim of this study was to use an animal model to evaluate whether sustained intensive exercise training induces potentially adverse myocardial remodeling and thus creates a potential substrate for arrhythmias. Methods and Results—: Male Wistar rats were conditioned to run vigorously for 4, 8, and 16 weeks; time-matched sedentary rats served as controls. Serial echocardiograms and in vivo electrophysiological studies at 16 weeks were obtained in both groups. After euthanasia, ventricular collagen deposition was quantified by histological and biochemical studies, and messenger RNA and protein expression of transforming growth factor-β1, fibronectin-1, matrix metalloproteinase-2, tissue inhibitor of metalloproteinase-1, procollagen-I, and procollagen-III was evaluated in all 4 cardiac chambers. At 16 weeks, exercise rats developed eccentric hypertrophy and diastolic dysfunction, together with atrial dilation. In addition, collagen deposition in the right ventricle and messenger RNA and protein expression of fibrosis markers in both atria and right ventricle were significantly greater in exercise than in sedentary rats at 16 weeks. Ventricular tachycardia could be induced in 5 of 12 exercise rats (42%) and only 1 of 16 sedentary rats (6%; P =0.05). The fibrotic changes caused by 16 weeks of intensive exercise were reversed after an 8-week exercise cessation. Conclusions—: In this animal model, we documented cardiac fibrosis after long-term intensive exercise training, together with changes in ventricular function and increased arrhythmia inducibility. If our findings are confirmed in humans, the results would support the notion that long-term vigorous endurance exercise training may in some cases promote adverse remodeling and produce a substrate for cardiac arrhythmias.
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Intense endurance exercise promoted RV-specific fibrosis in rats, which increased vulnerability to ventricular tachycardia following programmed stimulation.
“Benito et al. 15 recently documented that intense endurance exercise promoted RV-specific fibrosis in rats which increased vulnerability to ventricular tachycardia following programmed stimulation.”
From Exercise-induced right ventricular dysfunction and structural remodelling in endurance athletes (2012) · cites this paper as [15]
The chamber-specific remodeling section reports right-ventricular fibrosis after intensive training, with no observed left-ventricular difference. The ventricular-arrhythmia section reports greater inducibility during programmed stimulation in exercise rats (42% versus 6%). But the discussion says fibrosis *could play a role* in that susceptibility; it does not establish that the fibrosis caused the increase. (LLM, conf=0.87)
Experimental — accuracy not yet measuredRecent data suggest that exercise-induced proarrhythmic substrates may develop in the RV while sparing the LV.
“Studies focussing on the LV of athletes have failed to provide these mechanistic insights, 4 but recent data have suggested that exercise-induced proarrhythmic substrates may develop in the RV while sparing the LV.12,13,15”
From Exercise-induced right ventricular dysfunction and structural remodelling in endurance athletes (2012) · cites this paper as [15]
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- Authors
- Benito, B., Gay-Jordi, G., Serrano-Mollar, A., Guasch, E., Shi, Y., Tardif, J.-C., Brugada, J., Nattel, S., & Mont, L.
- Affiliations
- Montreal Heart Institute (CA)
- From the Thorax Institute, Hospital Clinic, Universitat de Barcelona, Barcelona, Catalonia, Spain (B.B., E.G., J.B., L.M.); Institut d'Investigacions Biomèdiques August Pi Sunyer, Barcelona, Catalonia, Spain (B.B., G.G.-J., A.S.-M., E.G., J.B., L.M.); Research Center, Montreal Heart Institute and Université de Montréal, Montreal, Quebec, Canada (B.B., Y.S., J.-C.T., S.N.); and Department of Experimental Pathology, Institut d'Investigacions Biomèdiques de Barcelona, Barcelona, Catalonia, Spain (G.G....
- Venue
- Circulation
- Published
- 2011-01
- Volume
- 123
- Issue
- 1
- Pages
- 13-22
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W1974266173
- Cited by
- 478
- References
- 10
- Citations by year
- 2026: 18 · 2025: 22 · 2024: 21 · 2023: 28 · 2022: 33 · 2021: 21 · 2020: 29 · 2019: 23 · 2018: 32 · 2017: 35 · 2016: 41 · 2015: 42 · 2014: 41 · 2013: 35 · 2012: 33
- FWCI
- 19.77
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Circulation (publishedVersion)
- PubMed (publishedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion, other-oa)
- Funders
- Sociedad Española de Cardiología
- Fondation Leducq
- Canadian Institutes of Health Research (MGP6957)
- Instituto de Salud Carlos III
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Effects of Exercise
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- cardiac arrhythmias, exercise-induced cardiac remodeling, endurance training, myocardial fibrosis, ventricular tachycardia, eccentric hypertrophy, diastolic dysfunction, atrial dilatation, collagen deposition, exercise cessation, fibrosis biomarkers, rat model
- MeSH terms
- Animals, Arrhythmias, Cardiac, Male, Physical Conditioning, Animal, Physical Endurance, Random Allocation, Time Factors, Rats, Wistar, Ventricular Remodeling, Models, Animal, Rats
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