{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T18:29:33Z","timestamp":1787077773864,"version":"build-2736575974"},"reference-count":52,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circ: Arrhythmia and Electrophysiology"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>Exercise training improves contractile function and can reduce arrhythmia burden after a myocardial infarction (MI). How exercise modifies the proarrhythmic status is uncertain.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>In this study, rats 6 weeks post-MI were randomized to an 8-week high-intensity exercise program (MI-EX) or to a sedentary control group (MI-SED) and compared with a sedentary sham group (Sham-SED). After the exercise program, in vivo and ex vivo programmed electrical stimulation was performed on the rat hearts. Subsequently, optical mapping was conducted to electrophysiologically characterize the MI hearts.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>\n                      Exercise significantly improved maximal oxygen uptake (\n                      <jats:italic toggle=\"yes\">V<\/jats:italic>\n                      O\n                      <jats:sub>2max<\/jats:sub>\n                      ; MI-EX, 67 mL\u00b7min\n                      <jats:sup>\u22121<\/jats:sup>\n                      \u00b7kg\n                      <jats:sup>\u2212<\/jats:sup>\n                      <jats:sup>0.75<\/jats:sup>\n                      versus MI-SED, 47 mL\u00b7min\n                      <jats:sup>\u2212<\/jats:sup>\n                      <jats:sup>1<\/jats:sup>\n                      \u00b7kg\n                      <jats:sup>\u2212<\/jats:sup>\n                      <jats:sup>0.75<\/jats:sup>\n                      ). In vivo cardiac stimulation protocols indicated reduced inducibility of ventricular arrhythmias in MI-EX compared with MI-SED. This anti-arrhythmic effect was retained ex vivo in Langendorff-perfused hearts. Optical mapping of the noninfarcted left ventricle indicated a prolonged average action potential (AP) duration at 4.5 Hz pacing frequency in both MI groups compared with Sham-SED. As pacing frequency increased (6.5 Hz and \u22488 Hz), AP duration remained significantly longer in the MI-SED group but decreased in the MI-EX group, demonstrating a negative frequency dependency. Spatial heterogeneity of AP duration in the noninfarcted left ventricle area was increased post-MI but was significantly reduced following exercise. Optical AP recorded from the remnant myocardium within the scar showed similar AP duration characteristics at low stimulation frequencies, but AP upstroke time was shorter in the MI-EX group compared with MI-SED.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>Post-MI exercise was associated with electrophysiological changes in both the noninfarcted region and the remnant myocardium within the scar. These changes suggest a mechanism for the anti-arrhythmic effects of exercise following MI.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/circep.125.014248","type":"journal-article","created":{"date-parts":[[2026,7,2]],"date-time":"2026-07-02T09:00:27Z","timestamp":1782982827000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["Effect of Exercise Training on Myocardial and Residual Scar Electrophysiology in Post-MI Rats"],"prefix":"10.1161","volume":"19","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2190-9948","authenticated-orcid":true,"given":"Tomas O.","family":"St\u00f8len","sequence":"first","affiliation":[{"name":"Department of Circulation and Medical Imaging, NTNU (T.O.S., M.N., K.G., J.P.L., A.B.J.)."},{"name":"Clinic of Cardiology, St. Olavs University Hospital, Trondheim, Norway (T.O.S., M.N., 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University of Glasgow, United Kingdom (F.L.B., G.L.S.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0492-3286","authenticated-orcid":true,"given":"Jan P\u00e5l","family":"Loennechen","sequence":"additional","affiliation":[{"name":"Department of Circulation and Medical Imaging, NTNU (T.O.S., M.N., K.G., J.P.L., A.B.J.)."},{"name":"Clinic of Cardiology, St. Olavs University Hospital, Trondheim, Norway (T.O.S., M.N., J.P.L.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4821-9741","authenticated-orcid":true,"given":"Godfrey L.","family":"Smith","sequence":"additional","affiliation":[{"name":"School of Cardiovascular &amp; Metabolic Health, University of Glasgow, United Kingdom (F.L.B., G.L.S.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anne B.","family":"Johnsen","sequence":"additional","affiliation":[{"name":"Department of Circulation and Medical Imaging, NTNU 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