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.

Background: Methionine has shown protective effects in experimental models of myocardial infarction and is highly reactive to oxidative compounds produced by polymorphonuclear leukocytes (PMN), which in turn have been associated with myocardial damage. We have investigated the effect of methionine administration on spontaneous leukocyte peroxidative activity in myocardial ischemia and reperfusion. Methods: In anesthetized dogs, with coronary occlusion (90 min) and reperfusion (90 min), PMN activation was measured by flow cytometric determination of H₂O₂ with dihydrorhodamine 123, and correlated to hemodynamic parameters and infarct presence. To assess a possible direct effect of methionine, H₂O₂ and superoxide were measured by flow cytometry in dog leukocyte suspensions following in vitro stimulation with f‐MLP. Results: PMN peroxidative activity in saline‐treated dogs increased significantly after coronary occlusion and after reperfusion. These changes were greater in coronary venous blood than in femoral blood. Methionine administration (150 mg/kg, i.v.) before occlusion totally suppressed PMN activation, both after occlusion and reperfusion. Conclusions: PMN are promptly activated in myocardial ischemia, and methionine administration prevents such activation. However, methionine has no direct effect on spontaneous peroxidative activity, and f‐MLP induced peroxidative activity. These in vivo effects of methionine, may additionally contribute to explain its protective role in experimental myocardial ischemia. Cytometry 37:140–146, 1999.