{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T19:23:37Z","timestamp":1792005817815,"version":"4.4.0"},"reference-count":71,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2005,12,7]],"date-time":"2005-12-07T00:00:00Z","timestamp":1133913600000},"content-version":"vor","delay-in-days":6,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2005,12]]},"abstract":"<jats:p>This study was conducted to examine the role of myocardial ATP\u2010sensitive potassium (K<jats:sub>ATP<\/jats:sub>) channels in exercise\u2010induced protection from ischaemia\u2013reperfusion (I\u2013R) injury. Female rats were either sedentary (Sed) or exercised for 12 weeks (Tr). Hearts were excised and underwent a 1\u20132 h regional I\u2013R protocol. Prior to ischaemia, hearts were subjected to pharmacological blockade of the sarcolemmal K<jats:sub>ATP<\/jats:sub>channel with HMR 1098 (SedHMR and TrHMR), mitochondrial blockade with 5\u2010hydroxydecanoic acid (5HD; Sed5HD and Tr5HD), or perfused with buffer containing no drug (Sed and Tr). Infarct size was significantly smaller in hearts from Tr animals (35.4 \u00b1 2.3<jats:italic>versus<\/jats:italic>44.7 \u00b1 3.0% of the zone at risk for Tr and Sed, respectively). Mitochondrial K<jats:sub>ATP<\/jats:sub>blockade did not abolish the training\u2010induced infarct size reduction (30.0 \u00b1 3.4<jats:italic>versus<\/jats:italic>38.0 \u00b1 2.6 in Tr5HD and Sed5HD, respectively); however, sarcolemmal K<jats:sub>ATP<\/jats:sub>blockade completely eradicated the training\u2010induced cardioprotection. Infarct size was 71.2 \u00b1 3.3 and 64.0 \u00b1 2.4% of the zone at risk for TrHMR and Sed HMR. The role of sarcolemmal K<jats:sub>ATP<\/jats:sub>channels in Tr\u2010induced protection was also supported by significant increases in both subunits of the sarcolemmal K<jats:sub>ATP<\/jats:sub>channel following training. LV developed pressure was better preserved in hearts from Tr animals, and was not influenced by addition of HMR 1098. 5HD decreased pressure development regardless of training status, from 15 min of ischaemia through the duration of the protocol. This mechanical dysfunction was likely to be due to a 5HD\u2010induced increase in myocardial Ca<jats:sup>2<\/jats:sup><jats:sup>+<\/jats:sup>content following I\u2013R. The major findings of the present study are: (1) unlike all other known forms of delayed cardioprotection, infarct sparing following chronic exercise was not abolished by 5HD; (2) pharmacological blockade of the sarcolemmal K<jats:sub>ATP<\/jats:sub>channel nullified the cardioprotective benefits of exercise training; and (3) increased expression of sarcolemmal K<jats:sub>ATP<\/jats:sub>channels was observed following chronic training.<\/jats:p>","DOI":"10.1113\/jphysiol.2005.095729","type":"journal-article","created":{"date-parts":[[2005,10,14]],"date-time":"2005-10-14T00:14:15Z","timestamp":1129248855000},"page":"913-924","source":"Crossref","is-referenced-by-count":103,"title":["Cardioprotection afforded by chronic exercise is mediated by the sarcolemmal, and not the mitochondrial, isoform of the K<sub>ATP<\/sub>channel in the rat"],"prefix":"10.1113","volume":"569","author":[{"given":"David 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