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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.

OBJECTIVE--To test the hypothesis that the complement system may be activated in patients with type II diabetes and CAD. RESEARCH DESIGN AND METHODS--The plasma C3d concentration was measured in 106 type II diabetic patients and 25 nondiabetic control subjects. The patient group was subdivided according to AER, and the groups were adjusted for age, sex, and known duration of diabetes. For the assignment to a given subgroup, normoalbuminuria was defined as AER < 15 microns/min, microalbuminuria as AER 16-250 micrograms/min, and macroalbuminuria as AER > 250 micrograms/min. The presence or absence of coronary disease was assessed through clinical examination, ECG, and coronary angiography. An RIA system was used for measurement of urinary albumin levels, and the plasma C3d concentrations were measured by ELISA. RESULTS--Within each of the AER-defined subgroups, the plasma C3d levels were significantly higher in patients with IHD than in those without. Thus, in the normoalbuminuric group, plasma C3d levels were 16.3 AU/ml (95% CI 13.9-19) in patients with IHD vs. 11.6 AU/ml (95% CI 10.5-12.7) in those without (P < 0.001). The corresponding data for the microalbuminuric and macroalbuminuric groups were 21.8 (95% CI 18.1-26.3) vs. 13.6 (95% CI 12.3-15.1) and 31.6 (95% CI 24.9-40) vs. 17.5 (13.6-22.6) AU/ml (P < 0.01), respectively. Patients with IHD also had significantly higher plasma C3d levels than normal control subjects, regardless of AER subgroup. A multiple logistic regression analysis demonstrated an association between the plasma C3d concentration and IHD and AER. CONCLUSIONS--Activation of the complement system may play a role in the development of macrovascular disease in type II diabetes.

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