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Pulmonary vein isolation (PVI) is effective in this group, implicating pulmonary vein (PV) remodelling, but underlying mechanisms are unclear. This study investigated if endurance training remodels PV sleeves and the PV\u2013left atrial (LA) junction to promote PV triggers and a permissive peri-antral substrate for AF.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>In canine and murine endurance-running models, in vivo PV\u2013LA mapping, ex vivo PV electrophysiology, intracellular action potential (AP) profiling with machine learning classification, histology, bulk RNA-seq, and subcellular-resolution spatial transcriptomics of PV\u2013LA tissue were performed. These findings were incorporated into biophysically detailed computer models of human PV cardiomyocytes and a 3D human LA.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Training produced an athlete\u2019s heart phenotype and increased AF inducibility. In vivo, trained animals showed PV\u2013LA conduction slowing and increased rotational activity. Ex vivo, trained PVs showed enhanced \u03b2-adrenergically evoked firing, prolonged burst activity, and a higher proportion of pacemaker-like APs. Spatial transcriptomics revealed discrete PV myocyte subpopulations with training upregulated Hcn4, Cacna1d, and Cacna1g (enhancing automaticity), downregulated Scn5a and Gja1 (slowing conduction), and enriched profibrotic\/inflammatory signalling (Tnf\u03b1, Il6) alongside fibroblast expansion and extracellular matrix deposition. In silico, these changes reproduced faster spontaneous PV firing and sustained re-entry.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Endurance training drives coupled electrical, structural, and inflammatory PV\u2013LA remodelling that provides both trigger and substrate for AF. These data support why PV-targeted strategies can be effective in athletic AF and nominate modifiable pathways including HCN4-linked automaticity and TNF\u03b1-associated signalling.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/eurheartj\/ehag358","type":"journal-article","created":{"date-parts":[[2026,4,24]],"date-time":"2026-04-24T11:42:55Z","timestamp":1777030975000},"source":"Crossref","is-referenced-by-count":1,"title":["Endurance exercise remodels pulmonary vein sleeve myocytes and promotes a proarrhythmic atrial substrate"],"prefix":"10.1093","author":[{"given":"Luca","family":"Soattin","sequence":"first","affiliation":[{"name":"Department of Biomedical Sciences, University of Copenhagen , Copenhagen ,","place":["Denmark"]},{"name":"Division of Cardiovascular Sciences, University of Manchester , Manchester ,","place":["UK"]},{"name":"Department of Pharmacology and Pharmacotherapy, University of Szeged , Szeged 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