Alleman 2016 Am J Physiol Heart Circ Physiol

From Bioblast
Revision as of 13:03, 7 March 2020 by Gnaiger Erich (talk | contribs)
(diff) ← Older revision | Latest revision (diff) | Newer revision → (diff)
Jump to navigation Jump to search
Publications in the MiPMap
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.

» PMID: 26945082

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 (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 H2O2. Ex mitochondria sustained respiration with lower rates of H2O2 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. Keywords: Arrhythmia, Cardioprotection, Exercise, Membrane potential, Mitochondria

O2k-Network Lab: US NC Greenville Neufer PD, US NC Greenville Brown DA, US VA Blacksburg 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  Pathway: N, NS  HRR: Oxygraph-2k 

2016-05, AmR