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A list of all pages that have property "Has abstract" with value "Mitochondria influence cardiac electrophysiology through energy- and redox-sensitive ion channels in the sarcolemma, with the collapse of energetics believed to be centrally involved in arrhythmogenesis. This study was conducted to determine if preservation of mitochondrial membrane potential (ΔΨm) contributes to the anti-arrhythmic effect of exercise. We determined the effects of exercise on cardiac mitochondria by utilizing a combination of perfused hearts, isolated myocytes, and isolated mitochondria exposed to metabolic challenge. Hearts from sedentary (Sed) and exercised (Ex; 10 days of treadmill running) Sprague Dawley rats were perfused on a two-photon microscope stage for simultaneous measurement of ΔΨm and ECG. Following ischemia-reperfusion, the collapse of ΔΨm was commensurate with the onset of arrhythmia. Exercise preserved ΔΨm and decreased the incidence of fibrillation/tachycardia (P<0.05). Our findings in intact hearts were corroborated in isolated myocytes exposed to ''in vitro'' hypoxia-reoxygenation, with Ex demonstrating enhanced redox control and sustained ΔΨm during reoxygenation. Finally, we induced anoxia-reoxygenation in isolated mitochondria using high-resolution respirometry with simultaneous measurement of respiration and H<sub>2</sub>O<sub>2</sub>. Ex mitochondria sustained respiration with lower rates of H<sub>2</sub>O<sub>2</sub> emission compared to Sed. Exercise helps sustain post-ischemic mitochondrial bioenergetics, leading to preserved ∆Ψm and protection against reperfusion arrhythmia. The reduction of fatal ventricular arrhythmias through exercise-induced mitochondrial adaptations indicates that mitochondrial therapeutics may be an effective target for the treatment of heart disease. Copyright © 2015, American Journal of Physiology - Heart and Circulatory Physiology.". Since there have been only a few results, also nearby values are displayed.

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    • Alleman 2016 Am J Physiol Heart Circ Physiol  + (Mitochondria influence cardiac electrophysMitochondria influence cardiac electrophysiology through energy- and redox-sensitive ion channels in the sarcolemma, with the collapse of energetics believed to be centrally involved in arrhythmogenesis. This study was conducted to determine if preservation of mitochondrial membrane potential (ΔΨm) contributes to the anti-arrhythmic effect of exercise.</br></br>We determined the effects of exercise on cardiac mitochondria by utilizing a combination of perfused hearts, isolated myocytes, and isolated mitochondria exposed to metabolic challenge. Hearts from sedentary (Sed) and exercised (Ex; 10 days of treadmill running) Sprague Dawley rats were perfused on a two-photon microscope stage for simultaneous measurement of ΔΨm and ECG. Following ischemia-reperfusion, the collapse of ΔΨm was commensurate with the onset of arrhythmia. Exercise preserved ΔΨm and decreased the incidence of fibrillation/tachycardia (P<0.05). Our findings in intact hearts were corroborated in isolated myocytes exposed to ''in vitro'' hypoxia-reoxygenation, with Ex demonstrating enhanced redox control and sustained ΔΨm during reoxygenation. Finally, we induced anoxia-reoxygenation in isolated mitochondria using high-resolution respirometry with simultaneous measurement of respiration and H<sub>2</sub>O<sub>2</sub>. Ex mitochondria sustained respiration with lower rates of H<sub>2</sub>O<sub>2</sub> emission compared to Sed.</br></br>Exercise helps sustain post-ischemic mitochondrial bioenergetics, leading to preserved ∆Ψm and protection against reperfusion arrhythmia. The reduction of fatal ventricular arrhythmias through exercise-induced mitochondrial adaptations indicates that mitochondrial therapeutics may be an effective target for the treatment of heart disease.</br></br>Copyright © 2015, American Journal of Physiology - Heart and Circulatory Physiology.isease. Copyright © 2015, American Journal of Physiology - Heart and Circulatory Physiology.)