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Del Rio CL, Clymer BD, Billman GE. Myocardial electrotonic response to submaximal exercise in dogs with healed myocardial infarctions: evidence for β-adrenoceptor mediated enhanced coupling during exercise testing. Front Physiol. 2015;6:25doi: 10.3389/fphys.2015.00025.
Del Rio, C. L., Clymer, B. D., & Billman, G. E. (2015). Myocardial electrotonic response to submaximal exercise in dogs with healed myocardial infarctions: evidence for β-adrenoceptor mediated enhanced coupling during exercise testing. Frontiers in physiology, 625. https://doi.org/10.3389/fphys.2015.00025
Del Rio, Carlos L, et al. "Myocardial electrotonic response to submaximal exercise in dogs with healed myocardial infarctions: evidence for β-adrenoceptor mediated enhanced coupling during exercise testing." Frontiers in physiology vol. 6 (2015): 25. doi: https://doi.org/10.3389/fphys.2015.00025
Del Rio CL, Clymer BD, Billman GE. Myocardial electrotonic response to submaximal exercise in dogs with healed myocardial infarctions: evidence for β-adrenoceptor mediated enhanced coupling during exercise testing. Front Physiol. 2015 Feb 05;6:25. doi: 10.3389/fphys.2015.00025. eCollection 2015. PMID: 25698976; PMCID: PMC4318283.
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Front Physiol. 2015 Feb 05;6:25. doi: 10.3389/fphys.2015.00025. eCollection 2015.

Myocardial electrotonic response to submaximal exercise in dogs with healed myocardial infarctions: evidence for β-adrenoceptor mediated enhanced coupling during exercise testing.

Frontiers in physiology

Carlos L Del Rio, Bradley D Clymer, George E Billman

Affiliations

  1. Department of Physiology and Cell Biology, The Ohio State University Columbus, OH, USA ; Department of Electrical and Computer Engineering, The Ohio State University Columbus, OH, USA ; Safety Pharmacology, QTest Labs Columbus, OH, USA.
  2. Department of Electrical and Computer Engineering, The Ohio State University Columbus, OH, USA ; Biomedical Engineering, The Ohio State University Columbus, OH, USA.
  3. Department of Physiology and Cell Biology, The Ohio State University Columbus, OH, USA ; Davis Heart and Lung Research Institute, The Ohio State University Columbus, OH, USA.

PMID: 25698976 PMCID: PMC4318283 DOI: 10.3389/fphys.2015.00025

Abstract

INTRODUCTION: Autonomic neural activation during cardiac stress testing is an established risk-stratification tool in post-myocardial infarction (MI) patients. However, autonomic activation can also modulate myocardial electrotonic coupling, a known factor to contribute to the genesis of arrhythmias. The present study tested the hypothesis that exercise-induced autonomic neural activation modulates electrotonic coupling (as measured by myocardial electrical impedance, MEI) in post-MI animals shown to be susceptible or resistant to ventricular fibrillation (VF).

METHODS: Dogs (n = 25) with healed MI instrumented for MEI measurements were trained to run on a treadmill and classified based on their susceptibility to VF (12 susceptible, 9 resistant). MEI and ECGs were recorded during 6-stage exercise tests (18 min/test; peak: 6.4 km/h @ 16%) performed under control conditions, and following complete β-adrenoceptor (β-AR) blockade (propranolol); MEI was also measured at rest during escalating β-AR stimulation (isoproterenol) or overdrive-pacing.

RESULTS: Exercise progressively increased heart rate (HR) and reduced heart rate variability (HRV). In parallel, MEI decreased gradually (enhanced electrotonic coupling) with exercise; at peak exercise, MEI was reduced by 5.3 ± 0.4% (or -23 ± 1.8Ω, P < 0.001). Notably, exercise-mediated electrotonic changes were linearly predicted by the degree of autonomic activation, as indicated by changes in either HR or in HRV (P < 0.001). Indeed, β-AR blockade attenuated the MEI response to exercise while direct β-AR stimulation (at rest) triggered MEI decreases comparable to those observed during exercise; ventricular pacing had no significant effects on MEI. Finally, animals prone to VF had a significantly larger MEI response to exercise.

CONCLUSIONS: These data suggest that β-AR activation during exercise can acutely enhance electrotonic coupling in the myocardium, particularly in dogs susceptible to ischemia-induced VF.

Keywords: arrhythmic risk; electrotonic coupling; exercise; myocardial infarction; β-adrenoceptor stimulation

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