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

Author

Listed:
  • Roozbeh Aschar-Sobbi

    (University of Toronto
    University of Toronto)

  • Farzad Izaddoustdar

    (University of Toronto
    University of Toronto)

  • Adam S. Korogyi

    (University of Toronto
    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
    University of Toronto)

  • Wallace Yang

    (University of Toronto
    University of Toronto)

  • David Dorian

    (University of Toronto)

  • Jeremy A. Simpson

    (University of Guelph)

  • Jari M. Tuomi

    (Western University
    Present Address: Northern Ontario Medical School, Sudbury, Ontario, Canada)

  • Douglas L. Jones

    (Western University)

  • Kumaraswamy Nanthakumar

    (University of Toronto
    Peter Munk Cardiac Centre, University Health Network)

  • Brian Cox

    (University of Toronto
    Program in Developmental and Stem Cell Biology, Hospital for Sick Children Research Institute)

  • Xander H. T. Wehrens

    (Cardiovascular Research Institute, Baylor College of Medicine, One Baylor Plaza)

  • Paul Dorian

    (University of Toronto
    St Michael’s Hospital)

  • Peter H. Backx

    (University of Toronto
    University of Toronto
    Peter Munk Cardiac Centre, University Health Network
    Heart & Stroke Richard Lewar Centre of Excellence, University of Toronto, 1 King's College Cir., Toronto)

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.

Suggested Citation

  • 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 & K, 2015. "Increased atrial arrhythmia susceptibility induced by intense endurance exercise in mice requires TNFα," Nature Communications, Nature, vol. 6(1), pages 1-14, May.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7018
    DOI: 10.1038/ncomms7018
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