Intrinsic changes on automatism, conduction, and refractoriness by exercise in isolated rabbit heart

Abstract

We have studied the intrinsic modifications on myocardial automatism, conduction, and refractoriness produced by chronic exercise. Experiments were performed on isolated rabbit hearts. Trained animals were submitted to exercise on a treadmill. The parameters investigated were 1) R-R interval, noncorrected and corrected sinus node recovery time (SNRT) as automatism index; 2) sinoatrial conduction time; 3) Wenckebach cycle length (WCL) and retrograde WCL, as atrioventricular (A-V) and ventriculoatrial conduction index; and 4) effective and functional refractory periods of left ventricle, A-V node, and ventriculoatrial retrograde conduction system. Measurements were also performed on coronary flow, weight of the hearts, and thiobarbituric acid reagent substances and glutathione in myocardium, quadriceps femoris muscle, liver, and kidney, to analyze whether these substances related to oxidative stress were modified by training. The following parameters were larger (P < 0.05) in trained vs. untrained animals: R-R interval (365 +/- 49 vs. 286 +/- 60 ms), WCL (177 +/- 20 vs. 146 +/- 32 ms), and functional refractory period of the left ventricle (172 +/- 27 vs. 141 +/- 5 ms). Corrected SNRT was not different between groups despite the larger noncorrected SNRT obtained in trained animals. Thus training depresses sinus chronotropism, A-V nodal conduction, and increases ventricular refractoriness by intrinsic mechanisms, which do not involve changes in myocardial mass and/or coronary flow.

The training-induced changes on automatism, conduction and myocardial refractoriness are not mediated by parasympathetic postganglionic neurons activity

“…These results are partially in accordance with those previously obtained in human (20,19,6,36,37) and experimental studies (28,27,38,39). Nevertheless, muscarinic receptor blockade with atropine did not modify the negative chronotropic and dromotropic effects produced by physical training.…”

“…However, data presented by several investigations in which sympathetic and parasympathetic blockade was performed after an exercise training period have shown a decrease in the intrinsic heart rate (20,19,27,6,37) and an intrinsic atrioventricular conduction depression (37). Furthermore, similar results have been obtained in experimental models using isolated heart preparations not only on sinus chronotropism (28,38,39) and atrioventricular node conduction (38), but also on ventricular refractoriness, which increased by training (38,39).…”

“…Previous studies carried out by our research team reported that these changes do not seem to be related to heart hypertrophy, lipid peroxidation, and/or coronary flow modifications either (38).…”

“…As it is well known, the release of acetylcholine (ACh) from parasympathetic postganglionic terminals causes a muscarinic receptormediated opening of specific potassium channels (IKACh) and other effects on several pacemaker currents that result in slowing the firing rate of pacemaker cells and a delay in AV conduction (8,35). As the intrinsic cardiac nervous system displays ongoing activity even when it is disconnected from the higher nervous centers (1,2) and can modify cardiac function (18,15), the changes observed by previous studies using a similar experimental model (28,38,39) could have been mediated by intrinsic nervous activity. In view of the present results, intrinsic parasympathetic nervous system activity does not explain the bradycardia and A-V conduction delay in isolated hearts from trained animals.…”

Bradycardia: changes in intrinsic rate rather than cardiac autonomic modulation

“…While HRV changes have been reported to be dependent on exercise training intensity [5] and initial high HRV levels in young healthy adults [2,6], these past and current results point to localised changes within the myocardium as the primary contributor to EIB. Chronic, mechanical stretching of the sino-atrial node [2-4], changes in ionic concentration within the sino-atrial node [7], and localised changes in myocardial conduction [8] appear to play a role in the development of EIB. The current work of Molina [1] adds to that of others previously and further highlights the necessity to examine sino-atrial function as a key mechanism for EIB.…”