ArticleJournal of molecular and cellular cardiology2011
Exercise-induced expression of cardiac ATP-sensitive potassium channels promotes action potential shortening and energy conservation.
Article in Journal of molecular and cellular cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed.
- High-intensity interval training improves mitochondrial function and attenuates cardiomyocytes damage in ischemia-reperfusion.International journal of cardiology. Heart & vasculature · 2025Review
- Performance horses as a model for exercise-associated cardiac arrhythmias and sudden cardiac death.Journal of molecular and cellular cardiology plus · 2025Review
- KArhiv za farmaciju · 2024Article
- Article
- CL-705G: a novel chemical Kir6.2-specific KFrontiers in pharmacology · 2023Article
- Subcellular trafficking and endocytic recycling of KAmerican journal of physiology. Cell physiology · 2022Review
- Short-term exercise-induced protection of cardiovascular function and health: why and how fast does the heart benefit from exercise?The Journal of physiology · 2022Review
- Stop the beat to see the rhythm: excitation-contraction uncoupling in cardiac research.American journal of physiology. Heart and circulatory physiology · 2021Review
- Kir Channel Molecular Physiology, Pharmacology, and Therapeutic Implications.Handbook of experimental pharmacology · 2021Review
- Diazoxide and Exercise Enhance Muscle Contraction during Obesity by Decreasing ROS Levels, Lipid Peroxidation, and Improving Glutathione Redox Status.Antioxidants (Basel, Switzerland) · 2020Article
- Exercise and cardiac health: physiological and molecular insights.Nature metabolism · 2020Review
- Functional characterization of ABCC9 variants identified in sudden unexpected natural death.Forensic science international · 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
- KThe Journal of physiology · 2017Article
- Cardiovascular KPathobiology of aging & age related diseases · 2016Review
- KATP Channels in the Cardiovascular System.Physiological reviews · 2016Review
- Article
- Inhibition of MCU forces extramitochondrial adaptations governing physiological and pathological stress responses in heart.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Disruption of KATP channel expression in skeletal muscle by targeted oligonucleotide delivery promotes activity-linked thermogenesis.Molecular therapy : the journal of the American Society of Gene Therapy · 2015Article
- Mechanisms of exercise-induced cardioprotection.Physiology (Bethesda, Md.) · 2014Review
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Authors and funding
9 authors.
Funding
Abstract
Physical activity is one of the most important determinants of cardiac function. The ability of the heart to increase delivery of oxygen and metabolic fuels relies on an array of adaptive responses necessary to match bodily demand while avoiding exhaustion of cardiac resources. The ATP-sensitive potassium (K(ATP)) channel has the unique ability to adjust cardiac membrane excitability in accordance with ATP and ADP levels, and up-regulation of its expression that occurs in response to exercise could represent a critical element of this adaption. However, the mechanism by which K(ATP) channel expression changes result in a beneficial effect on cardiac excitability and function remains to be established. Here, we demonstrate that an exercise-induced rise in K(ATP) channel expression enhanced the rate and magnitude of action potential shortening in response to heart rate acceleration. This adaptation in membrane excitability promoted significant reduction in cardiac energy consumption under escalating workloads. Genetic disruption of normal K(ATP) channel pore function abolished the exercise-related changes in action potential duration adjustment and caused increased cardiac energy consumption. Thus, an expression-driven enhancement in the K(ATP) channel-dependent membrane response to alterations in cardiac workload represents a previously unrecognized mechanism for adaptation to physical activity and a potential target for cardioprotection.
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