Abstract
A study has been made of the effect of chronic exercise on myocardial electrophysiological heterogeneity and stability, as well as of the role of cholinergic neurons in these changes. Determinations in hearts from untrained and trained rabbits on a treadmill were performed. The hearts were isolated and perfused. A pacing electrode and a recording multielectrode were located in the left ventricle. The parameters determined during induced VF, before and after atropine (1μM), were: fibrillatory cycle length (VV), ventricular functional refractory period (FRPVF), normalized energy (NE) of the fibrillatory signal and its coefficient of variation (CV), and electrical ventricular activation complexity, as an approach to myocardial heterogeneity and stability. The VV interval was longer in the trained group than in the control group both prior to atropine (78±10 vs. 68±10 ms) and after atropine (76±8 vs. 67±10 ms). Likewise, FRPVF was longer in the trained group than in the control group both prior to and after atropine (53±8 vs. 42±7 ms and 50±6 vs. 40±6 ms, respectively), and atropine did not modify FRPVF. The CV of FRPVF was lower in the trained group than in the control group prior to atropine (12.5±1.5% vs. 15.1±3.8%) and, decreased after atropine (15.1±3.8% vs. 12.2±2.4%) in the control group. The trained group showed higher NE values before (0.40±0.04 vs. 0.36±0.05) and after atropine (0.37±0.04 vs. 0.34±0.06; p = 0.08). Training decreased the CV of NE both before (23.3±2% vs. 25.2±4%; p = 0.08) and after parasympathetic blockade (22.6±1% vs. 26.1±5%). Cholinergic blockade did not modify these parameters within the control and trained groups. Activation complexity was lower in the trained than in the control animals before atropine (34±8 vs. 41±5), and increased after atropine in the control group (41±5 vs. 48±9, respectively). Thus, training decreases the intrinsic heterogeneity of the myocardium, increases electrophysiological stability, and prevents some modifications due to muscarinic block.
Highlights
It has been reported that aerobic physical exercise can protect against cardiac sudden death, which in most cases is produced by ventricular fibrillation (VF) [1,2], and experimental studies have evidenced that exercise leads to reduced VF [3]
The FRPVF was longer in the trained group than in the control group prior to atropine administration (53 ± 8 vs. 42 ± 7 ms, respectively)
The coefficient of variation (CV) of FRPVF was higher in the control group than in the trained group prior to atropine administration (15.1 ± 3.8% vs. 12.5 ± 1.5%), but not after atropine (12.2 ± 2.4% vs. 10.8 ± 2.1%)
Summary
It has been reported that aerobic physical exercise can protect against cardiac sudden death, which in most cases is produced by ventricular fibrillation (VF) [1,2], and experimental studies have evidenced that exercise leads to reduced VF [3]. The exact underlying cardiovascular protective mechanisms are not fully known [4,5]. In this regard, research has been conducted to elucidate whether electrophysiological modifications produced by training could represent a possible protective mechanism. Reports have shown that training increases ventricular electrical stability [6], decreases electrophysiological heterogeneity in in vivo canine models [7], and increases the VF threshold during coronary occlusion in isolated rat hearts [8]. Myocardial heterogeneity is a well known proarrhythmic factor [12]
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