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Background & Objective: Apoptosis plays a major role in the process of diabetes-induced heart disease, but the effects of aerobic intermediate exercises on the status of apoptosis in diabetics’ cardiomyocytes are unclear. The aim of this study was to investigate the effect of 4-week aerobic exercise on apoptosis biomarkers in the cardiomyocytes of Streptozotocin-induced diabetic rats. Material&Methods: 40 adult rats were randomly assigned to 4 groups, including: Control, Control¬+¬Diabetes, Exercise and Exercise + Diabetes. To induce diabetes intraperitoneal injection of Streptozotocin (STZ) solution (55mg/kg) was used. 14 days after STZ injection, the level of fasting blood glucose was measured by a glucometer. After confirming diabetes induction, the exercise protocol was performed for 4 weeks. The training groups ran for 4 weeks (5sessions/week) at a speed of 15-18 m/min and 25 to 44 minutes. 48 hours after the last training session, the subjects were anesthetized and the cardiac muscle was removed. The sFas, FasL and Bcl-2 were measured by ELISA. Results: Induction of diabetes in the control group, resulted in a significant increase in sFas and FasL levels and insignificantly increase in sFas/FasL and also insignificantly decrease in Bcl-2 levels (p

Background & Objective: Apoptosis plays a major role in the process of diabetes‐induced heart disease, but the effects of aerobic intermediate exercises on the status of apoptosis in diabetics' cardiomyocytes are unclear. The aim of this study was to investigate the effect of 4‐week aerobic exercise on apoptosis biomarkers in the cardiomyocytes of Streptozotocin‐induced diabetic rats. Material & Methods: 40 adult rats were randomly assigned to 4 groups, including: Control, Control¬+¬Diabetes, Exercise and Exercise + Diabetes. To induce diabetes intraperitoneal injection of Streptozotocin (STZ) solution (55mg/kg) was used. 14 days after STZ injection, the level of fasting blood glucose was measured by a glucometer. After confirming diabetes induction, the exercise protocol was performed for 4 weeks. The training groups ran for 4 weeks (5sessions/week) at a speed of 15‐18 m/min and 25 to 44 minutes. 48 hours after the last training session, the subjects were anesthetized and the cardiac muscle was removed. The sFas, FasL and Bcl‐2 were measured by ELISA. Results: Induction of diabetes in the control group, resulted in a significant increase in sFas and FasL levels and insignificantly increase in sFas/FasL and also insignificantly decrease in Bcl‐2 levels (p<0.05).In non‐diabetic groups, the implementation of 4 weeks of exercise training resulted in a significant decrease in sFas, FasL and a significant reduction of sFas/FasL and a significant increase in Bcl‐2(p<0.05). Performing of 4 weeks of exercise training in diabetic groups also led to a nonsignificant decrease in sFas and sFas/FasL and a significant decrease in FasL and a nonsignificant increase in Bcl‐2. Conclusion: The present study confirms the progressive effect of diabetes‐induced apoptosis on heart. The results suggest that regular aerobic exercises may be used as a non‐pharmacological strategy to reduce the complications of diabetes‐induced apoptosis in the heart tissue of diabetic people. [ABSTRACT FROM AUTHOR]

Abstract: Loss of dopaminergic neurons in the substantia nigra (A9 cells) and ventral tegmental area (VTA) (A10 cells) has been reported in Parkinson''s disease with reference to causing motor and non-motor deficits, although clinical and laboratory animal studies on the degeneration of VTA neurons are less emphasized comparative to the degeneration of substantia nigra neurons. In the present study, we examined the VTA dopaminergic neurons in a chronic mouse model of Parkinson''s disease induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and probenecid at a level showing moderate neurodegeneration and studied the impact of endurance exercise on VTA neurons in this model. In comparison to the normal control animals, the chronic mouse model of Parkinson''s disease with moderate neurodegeneration demonstrated a significant reduction of VTA neurons (52% loss), when these animals were kept sedentary throughout the study. Morphologically, the VTA dopaminergic neurons in this model displayed a decrease in cell volume and showed irregular or disparaging axonal and dendritic projections. When the chronic Parkinsonian mice were exercised on a motorized rodent treadmill up to 15m/min, 40min/day, 5 days/week for 10 and 18 weeks, the total number of VTA dopaminergic neurons were significantly higher than the sedentary Parkinsonian animals. Especially noted with the 18-week exercised Parkinsonian mice, the number of VTA neurons returned to normal range and the cells were densely populated and displayed distinctive axons and dendritic arborization. These results demonstrate that prolonged exercise training is neuroprotective to the dopaminergic neurons in the VTA of the chronic mouse model of Parkinson''s disease with moderate neurodegeneration. [Copyright &y& Elsevier]

Abstract: Physical rehabilitation with endurance exercise for patients with Parkinson’s disease has not been well established, although some clinical and laboratory reports suggest that exercise may produce a neuroprotective effect and restore dopaminergic and motor functions. In this study, we used a chronic mouse model of Parkinsonism, which was induced by injecting male C57BL/6 mice with 10 doses of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (25 mg/kg) and probenecid (250 mg/kg) over 5 weeks. This chronic parkinsonian model displays a severe and persistent loss of nigrostriatal neurons, resulting in robust dopamine depletion and locomotor impairment in mice. Following the induction of Parkinsonism, these mice were able to sustain an exercise training program on a motorized rodent treadmill at a speed of 18 m/min, 0° of inclination, 40 min/day, 5 days/week for 4 weeks. At the end of exercise training, we examined and compared their cardiorespiratory capacity, behavior, and neurochemical changes with that of the probenecid-treated control and sedentary parkinsonian mice. The resting heart rate after 4 weeks of exercise in the chronic parkinsonian mice was significantly lower than the rate before exercise, whereas the resting heart rate at the beginning and 4 weeks afterward in the control or sedentary parkinsonian mice was unchanged. Exercised parkinsonian mice also recovered from elevated electrocardiogram R-wave amplitude that was detected in the parkinsonian mice without exercise for 4 weeks. The values of oxygen consumption, carbon dioxide production, and body heat generation in the exercised parkinsonian mice before and during the Bruce maximal exercise challenge test were all significantly lower than that of their sedentary counterparts. Furthermore, the exercised parkinsonian mice demonstrated a greater mass in the left ventricle of the heart and an increased level of citrate synthase activity in the skeletal muscles. The amphetamine-induced, dopamine release-dependent locomotor activity was markedly inhibited in the sedentary parkinsonian mice and was also inhibited in the exercised parkinsonian mice. Finally, neuronal recovery from the loss of nigrostriatal tyrosine hydroxylase expression and dopamine levels in the severe parkinsonian mice after exercise was not evident. Taken all together, these data suggest that 4 weeks of treadmill exercise promoted physical endurance, resulting in cardiorespiratory and metabolic adaptations in the chronic parkinsonian mice with severe neurodegeneration without demonstrating a restorative potential for the nigrostriatal dopaminergic function. [Copyright &y& Elsevier]