ArticleThe Journal of physiology2005
Cardioprotection afforded by chronic exercise is mediated by the sarcolemmal, and not the mitochondrial, isoform of the KATP channel in the rat.
Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
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Who cites it
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 131 citations in OpenAlex.
- Mechanisms Involved in Exercise-Induced Cardioprotection: A Systematic Review.Arquivos brasileiros de cardiologia · 2015Pooled it
- High-intensity interval training improves mitochondrial function and attenuates cardiomyocytes damage in ischemia-reperfusion.International journal of cardiology. Heart & vasculature · 2025Review
- Exercise-induced cardioprotection: From endogenous to exogenous mechanisms.Sports medicine and health science · 2025Review
- Myokine Musclin Is Critical for Exercise-Induced Cardiac Conditioning.International journal of molecular sciences · 2023Article
- The Effects of Exercise Training on Glucose Homeostasis and Muscle Metabolism in Type 1 Diabetic Female Mice.Metabolites · 2022Article
- Article
- HNO Protects the Myocardium against Reperfusion Injury, Inhibiting the mPTP Opening via PKCε Activation.Antioxidants (Basel, Switzerland) · 2022Article
- Sexual dimorphism in vascular ATP-sensitive KThe Journal of physiology · 2021Article
- Diazoxide and Exercise Enhance Muscle Contraction during Obesity by Decreasing ROS Levels, Lipid Peroxidation, and Improving Glutathione Redox Status.Antioxidants (Basel, Switzerland) · 2020Article
- Vascular ATP-sensitive KThe Journal of physiology · 2020Article
- Role of Oxidative Stress in the Genesis of Ventricular Arrhythmias.International journal of molecular sciences · 2020Review
- Advances in the Protective Mechanism of NO, HFrontiers in cardiovascular medicine · 2020Review
- Hydrogen sulfide-mediated endothelial function and the interaction with eNOS and PDE5A activity in human internal mammary arteries.The Journal of international medical research · 2019Article
- Exercise and Cardioprotection: A Natural Defense Against Lethal Myocardial Ischemia-Reperfusion Injury and Potential Guide to Cardiovascular Prophylaxis.Journal of cardiovascular pharmacology and therapeutics · 2019Review
- 12-Week Exercise Training, Independent of the Type of Exercise, Attenuates Endothelial Ischaemia-Reperfusion Injury in Heart Failure Patients.Frontiers in physiology · 2019Article
- Chronic Remote Ischemic Conditioning May Mimic Regular Exercise:Perspective from Clinical Studies.Aging and disease · 2018Article
- Aerobic exercise protects against pressure overload-induced cardiac dysfunction and hypertrophy via β3-AR-nNOS-NO activation.PloS one · 2017Article
- Functional Role of Mitochondria in Arrhythmogenesis.Advances in experimental medicine and biology · 2017Review
- Exercise-induced protection against reperfusion arrhythmia involves stabilization of mitochondrial energetics.American journal of physiology. Heart and circulatory physiology · 2016Article
- Cardiovascular KPathobiology of aging & age related diseases · 2016Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
This study was conducted to examine the role of myocardial ATP-sensitive potassium (K(ATP)) channels in exercise-induced protection from ischaemia-reperfusion (I-R) injury. Female rats were either sedentary (Sed) or exercised for 12 weeks (Tr). Hearts were excised and underwent a 1-2 h regional I-R protocol. Prior to ischaemia, hearts were subjected to pharmacological blockade of the sarcolemmal K(ATP) channel with HMR 1098 (SedHMR and TrHMR), mitochondrial blockade with 5-hydroxydecanoic 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 +/- 2.3 versus 44.7 +/- 3.0% of the zone at risk for Tr and Sed, respectively). Mitochondrial K(ATP) blockade did not abolish the training-induced infarct size reduction (30.0 +/- 3.4 versus 38.0 +/- 2.6 in Tr5HD and Sed5HD, respectively); however, sarcolemmal K(ATP) blockade completely eradicated the training-induced cardioprotection. Infarct size was 71.2 +/- 3.3 and 64.0 +/- 2.4% of the zone at risk for TrHMR and Sed HMR. The role of sarcolemmal K(ATP) channels in Tr-induced protection was also supported by significant increases in both subunits of the sarcolemmal K(ATP) 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-induced increase in myocardial Ca2+ content following I-R. 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(ATP) channel nullified the cardioprotective benefits of exercise training; and (3) increased expression of sarcolemmal K(ATP) channels was observed following chronic training.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.