Key result
Chronic endurance exercise increases AF susceptibility to ~64% in rats, driven by dilation and fibrosis.
Why the study?
High-level exercise training promotes AF, but the underlying mechanisms are unclear.
Does chronic endurance exercise increase atrial fibrillation susceptibility in an animal model?
Does chronic endurance exercise increase atrial fibrillation susceptibility in an animal model?
Absolute Event Rate: 64% vs 15%
p-value: p=< 0.01
Chronic endurance exercise promotes atrial fibrillation in an animal model via autonomic changes, atrial dilation, and fibrosis, highlighting vagal enhancement and RGS protein downregulation as key mechanisms.
Should not yet change endurance exercise guidance for athletes; leaves open translation of autonomic and fibrotic mechanisms to human AF.
OBJECTIVES: The goal of this study was to assess mechanisms underlying atrial fibrillation (AF) promotion by exercise training in an animal model. BACKGROUND: High-level exercise training promotes AF, but the underlying mechanisms are unclear. METHODS: AF susceptibility was assessed by programmed stimulation in rats after 8 (Ex8) and 16 (Ex16) weeks of daily 1-h treadmill training, along with 4 and 8 weeks after exercise cessation and time-matched sedentary (Sed) controls. Structural remodeling was evaluated by using serial echocardiography and histopathology, autonomic nervous system with pharmacological tools, acetylcholine-regulated potassium current (IKACh) with patch clamp recording, messenger ribonucleic acid expression with quantitative polymerase chain reaction, and regulators of G protein-signaling (RGS) 4 function in knockout mice. RESULTS: AF inducibility increased after 16 weeks of training (e.g., AF >30 s in 64% of Ex16 rats vs 15% of Sed rats; p < 0.01) and rapidly returned to baseline levels with detraining. Atropine restored sinus rhythm in 5 of 5 Ex rats with AF sustained >15 min. Atrial dilation and fibrosis developed after 16 weeks of training and failed to fully recover with exercise cessation. Parasympathetic tone was increased in Ex16 rats and normalized within 4 weeks of detraining. Baroreflex heart rate responses to phenylephrine-induced blood pressure elevation and IKACh sensitivity to carbachol were enhanced in Ex16 rats, implicating both central and end-organ mechanisms in vagal enhancement. Ex rats showed unchanged cardiac adrenergic and cholinergic receptor and IKACh-subunit gene expression, but significant messenger ribonucleic acid downregulation of IKACh-inhibiting RGS proteins was present at 16 weeks. RGS4 knockout mice showed significantly enhanced sensitivity to AF induction in the presence of carbachol. CONCLUSIONS: Chronic endurance exercise increased AF susceptibility in rats, with autonomic changes, atrial dilation, and fibrosis identified as potential mechanistic contributors. Vagal promotion is particularly important and occurs via augmented baroreflex responsiveness and increased cardiomyocyte sensitivity to cholinergic stimulation, possibly due to RGS protein downregulation.
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Guasch et al. (2013) studied Atrial fibrillation. Endurance exercise (treadmill training) vs. Time-matched sedentary controls was evaluated on AF inducibility (AF >30 s) (p=< 0.01). Chronic endurance exercise (16 weeks) increased AF susceptibility in rats (64% vs 15% in sedentary controls; p < 0.01), driven by autonomic changes, atrial dilation, and fibrosis.
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