Alleman 2016 Am J Physiol Heart Circ Physiol: Difference between revisions
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Revision as of 10:36, 13 September 2016
Alleman RJ, Tsang AM, Ryan TE, Patteson DJ, McClung JM, Spangenburg EE, Shaikh SR, Neufer PD, Brown DA (2016) Exercise-induced protection against reperfusion arrhythmia involves stabilization of mitochondrial energetics. Am J Physiol Heart Circ Physiol 310:H1360-70. |
Alleman RJ, Tsang AM, Ryan TE, Patteson DJ, McClung JM, Spangenburg EE, Shaikh SR, Neufer PD, Brown DA (2016) Am J Physiol Heart Circ Physiol
Abstract: 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 (ฮฮจm) 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 ฮฮจm and ECG. Following ischemia-reperfusion, the collapse of ฮฮจm was commensurate with the onset of arrhythmia. Exercise preserved ฮฮจm 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 ฮฮจm during reoxygenation. Finally, we induced anoxia-reoxygenation in isolated mitochondria using high-resolution respirometry with simultaneous measurement of respiration and H2O2. Ex mitochondria sustained respiration with lower rates of H2O2 emission compared to Sed.
Exercise helps sustain post-ischemic mitochondrial bioenergetics, leading to preserved โฮจm 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 ยฉ 2015, American Journal of Physiology - Heart and Circulatory Physiology. โข Keywords: Arrhythmia, Cardioprotection, Exercise, Membrane potential, Mitochondria
โข O2k-Network Lab: US NC Greenville Neufer PD, US NC Greenville Brown DA
Labels: MiParea: Respiration, mt-Biogenesis;mt-density, mt-Membrane, Exercise physiology;nutrition;life style
Pathology: Cardiovascular
Stress:Ischemia-reperfusion
Organism: Rat
Tissue;cell: Heart
Preparation: Isolated mitochondria
Coupling state: LEAK, OXPHOS
HRR: Oxygraph-2k
2016-05, Amplex Red