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Irregular heartbeats and different forms of ventricular ectopic activity are a common occurrence among elite athletes with high contractile cardiac capacity. At the same time, experiments demonstrated that the electrical stimulation threshold, causing ventricular fibrillation, increases during adaptation to physical exercise, without the increase in the contractile cardiac capacity. The research purpose is to examine the dependence of ventricular fibrillation threshold and contractile cardiac capacity on intensity and duration of swimming sessions, as well as duration of the training period. Female Wistar rats were assigned to five groups: sedentary (S), training 1 (T1, low intensity), training 2 (T2, moderate intensity), training 3 (T3, long-term), training 4 (T4, exhaustive). At the end of the experimental period, the rats were anesthetized and their ventricles irritated with rectangular pulses of 10 ms duration, to determine the minimum current causing ventricular fibrillation. The cardiac capacity was assessed by the maximum pressure in the left ventricle, at full aortic-cross clamping. The ventricular fibrillation threshold was increased by 60% in T1, 57.5% in T2 and 74% in T3, but no difference in T4 was observed, compared with S. The pick pressure in the left ventricle after aortic cross-clamping in T1 and T2 was not enhanced, compared with S; in T3 and T4, however, it was significantly increased. Physical exercise training changed the ventricular fibrillation threshold and cardiac contractile capacity, independently of the intensity of exercise. The rise of the ventricular fibrillation threshold and its contractile capacity can be demonstrated during a long adaptation to moderate-term sessions of aerobic exercises.
We examined whether thyroid hormones affect myocardial -PKC signalling, downstream target substrate, connexin-43 (Cx43) and arrhythmogenesis in non-diabetic and diabetic rats. Diabetes was induced by a single streptozotocin injection (50mg/kg, i.v.). Triiodothyronine (T3) was applied by gavage (1µg/kg of body weight for 10 days) to 4 weeks and 9 weeks diabetic and age-matched non-diabetic rats. Western blot analysis of Cx43 and -PKC, immunofluorescence of Cx43, ultrastructure of cardiomyocytes and myocardial conduction velocity were performed. Isolated perfused heart preparation was used to test ventricular fibrillation susceptibility. T3 significantly decreased -PKC expression in non-diabetic and suppressed in diabetic rat heart ventricles. Decline of -PKC signalling was associated with decrease of Cx43 phosphorylation in diabetic and to a greater extent in non-diabetic rat hearts. However, conduction velocity was significantly decreased in diabetic while enhanced due to T3 and increased in non-diabetic T3-treated rat heart ventricles compared to non-treated. T3-induced down-regulation of Cx43 was associated with increased cardiac propensity to ventricular fibrillation. Findings indicate that activation of -PKC signalling linked with phosphorylation of Cx43 is one of the mechanisms involved in the adaptation of the heart to hyperglycemia. Suppression of -PKC and Cx43 phosphorylation by T3 abolish benefit of adaptation rendering the heart prone to lethal arrhythmias.
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