Increased atrial arrhythmia susceptibility induced by intense endurance exercise in mice requires TNFα

Roozbeh Aschar-Sobbi, Farzad Izaddoustdar, Adam S. Korogyi, Qiongling Wang, Gerrie P. Farman, FengHua Yang, Wallace Yang, David Dorian, Jeremy A. Simpson, Jari M. Tuomi, Douglas L. Jones, Kumaraswamy Nanthakumar, Brian Cox, Xander H. T. Wehrens, Paul Dorian and Peter H. Backx ()
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Roozbeh Aschar-Sobbi: University of Toronto
Farzad Izaddoustdar: University of Toronto
Adam S. Korogyi: University of Toronto
Qiongling Wang: Cardiovascular Research Institute, Baylor College of Medicine, One Baylor Plaza
Gerrie P. Farman: Boston University
FengHua Yang: University of Toronto
Wallace Yang: University of Toronto
David Dorian: University of Toronto
Jeremy A. Simpson: University of Guelph
Jari M. Tuomi: Western University
Douglas L. Jones: Western University
Kumaraswamy Nanthakumar: University of Toronto
Brian Cox: University of Toronto
Xander H. T. Wehrens: Cardiovascular Research Institute, Baylor College of Medicine, One Baylor Plaza
Paul Dorian: University of Toronto
Peter H. Backx: University of Toronto

Nature Communications, 2015, vol. 6, issue 1, 1-14

Abstract: Abstract Atrial fibrillation (AF) is the most common supraventricular arrhythmia that, for unknown reasons, is linked to intense endurance exercise. Our studies reveal that 6 weeks of swimming or treadmill exercise improves heart pump function and reduces heart-rates. Exercise also increases vulnerability to AF in association with inflammation, fibrosis, increased vagal tone, slowed conduction velocity, prolonged cardiomyocyte action potentials and RyR2 phosphorylation (CamKII-dependent S2814) in the atria, without corresponding alterations in the ventricles. Microarray results suggest the involvement of the inflammatory cytokine, TNFα, in exercised-induced atrial remodelling. Accordingly, exercise induces TNFα-dependent activation of both NFκB and p38MAPK, while TNFα inhibition (with etanercept), TNFα gene ablation, or p38 inhibition, prevents atrial structural remodelling and AF vulnerability in response to exercise, without affecting the beneficial physiological changes. Our results identify TNFα as a key factor in the pathology of intense exercise-induced AF.

Date: 2015
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DOI: 10.1038/ncomms7018

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