Razi Journal of Medical Sciences

fa تغییرات سطوح سرمی تروپونین- I و کورتیکوسترون پس از یک دوره تمرین استقامتی و تحریک الکتریکی در موش های صحرایی انفارکته شده Changes in Serum Troponin-I and Corticosterone Levels after a Period of Endurance Training and Electrical Stimulation in Infarcted Rats فیزیولوژی ورزش Exercise Physiology پژوهشي Research زمینه و هدف: بیماری‌های قلبی‌عروقی عامل اصلی حدود یک سوم از کل مرگ و میرها در جهان می‌باشند که بیومارکرها متفاوتی در ایجاد آن دخالت دارند. هدف از این تحقیق تعیین اثرپذیری سطوح تروپونین-I و کورتیکوسترون موش‌های صحرایی القاء شده به انفارکتوس میوکارد پس از یک دورۀ تمرین استقامتی و تحریک الکتریکی حاد بود. روش کار: در این مطالعه تجربی کنترل شده با گروه شاهد50 سر موش صحرایی نژاد ویستار (8 هفته‌ای با وزن30±130 گرم) به‌طور تصادفی به 5 گروه سالم، انفارکته، انفارکته-تمرین استقامتی، انفارکته-تحریک الکتریکی و انفارکته-تحریک الکتریکی-تمرین استقامتی تقسیم شدند. سپس انفارکتوس میوکارد با استفاده از دو تزریق زیرجلدی ایزوپروترونول (150 میلی‌گرم/کیلوگرم) به فاصلۀ 24 ساعت در گروه‌های انفارکته القاء گردید. گروه‌های مداخله برای یک جلسه تحت تحریک الکتریکی (دستگاه فوت شوک برای 5/0 میلی‌آمپر و 20 دقیقه) و تمرین استقامتی (تردمیل با سرعت 20 متر/دقیقه برای 1 ساعت) قرار گرفتند. سپس بلافاصله بعد از مداخله، سطوح سرمی CORT و  cTnIبررسی شدند. برای آنالیز داده‌ها از آزمون آنووآ یکطرفه و تعقیبی توکی در سطح معنی‌داری 05/0>P استفاده شد. یافته‌ها: نتایج نشان داد که انفارکتوس میوکارد موجب افزایش سطوح سرمی CORT و  cTnIمیشود. از طرفی میزان  CORTدر گروه‌های تمرین استقامتی (0008/0P=)، تحریک الکتریکی (032/0P=) و تحریک الکتریکی-تمرین استقامتی (044/0P=) کاهش معنی‌داری نسبت به گروه انفارکتوس میوکارد داشته است. همچنین مقادیر  cTnIتنها در گروه تمرین استقامتی با انفارکتوس میوکارد کاهش معنی‌داری (013/0P=) را نشان داد. نتیجه‌گیری: انجام تمرین استقامتی همراه با تحریک الکتریکی به‌صورت جداگانه و تلفیق آن‌ها منجر به کاهش میزان کورتیکوسترون و cTnI نمونه های انفارکته می‌شود و به‌نظر می‌رسد در بهبود شرایط بیماران مبتلا به انفارکتوس قلبی مؤثر است. Background & Aims: Cardiovascular disease is the leading cause of one-third of all deaths worldwide, and by 2030 it will account for more than 30.5% of all deaths. Myocardial infarction (MI) is one of the most common causes of this disease. Different biomarkers are involved in these diseases, which lead to this complication by causing structural and molecular changes in heart cells and extracellular matrix. Numerous studies have shown an association between stress and cardiovascular disease. Stress increases the secretion of catecholamine’s and corticosteroids from the endocrine glands, and consequently high levels of these hormones potentially increase the risk of cardiovascular disease. MI necrosis stimulates the hypothalamic-pituitary-adrenal axis (HPA) and, as a stressor, increases cortisol (CORT) and catecholamine levels. High elevated CORT levels lead to higher mortality in MI patients. Stress reduces myocardial blood flow by increasing oxygen demand, increasing vascular resistance, and coronary artery contraction, and is a risk factor for cardiovascular patients. On the other hand, exercise has been an effective stimulant on the HPA axis and leads to increased secretion of adrenocorticotropin from the pituitary gland, which is the most important factor in the secretion of CORT. In sports activity studies, it significantly reduces CORT levels. Evidence also suggests that there is a direct relationship between CORT and cardiac troponin-I (cTnI) levels in patients with MI. Troponin is one of the most sensitive proteins in the diagnosis of MI damage. cTnI is more specific than the other two components due to the presence of 31 amino acids in its N-terminus and cTnI levels increase rapidly after the onset of myocardial injury, which can also occur in intense long-term and short-term continuous exercise. This has not been observed in some studies and exercise results in different responses in CORT and cTnI secretion. One of the non-clinical methods along with exercise is the use of electrical stimulation (ES) in the rehabilitation of cardiovascular patients. ES has also been shown to be used as a new and effective modality in the treatment of ischemia. Few studies have been performed on the effect of endurance training and electrical stimulation. On the one hand, little research has been done more on healthy people and so far the effect of endurance training and ES on changes in CORT and cTnI in infarction samples has not been investigated. Therefore, the present study aimed to determine changes in serum levels of troponin-I and CORT after a period of endurance training and electrical stimulation in infarcted rats as a problem can be proposed. The aim of this study was to determine the efficacy of troponin-I and CORT levels in rats induced myocardial infarction after a period of endurance training and acute electrical stimulation. Methods: In this experimental study, 50 Wistar rats (8 weeks old to weighing 130±30 g) purchased from Pasteur Institute were used with the control group. After adaptation to the standard research environment, the animals were randomly divided into 5 groups: healthy, infarction, infarction-endurance training, infarction-electrical stimulation and infarction-electrical stimulation-endurance training. Myocardial infarction was then induced in two infarct groups using two subcutaneous injections of Isoproterenol (150 mg/kg) 24 hours apart. Forty-eight hours after the last injection, several rats from each group were randomly selected and subjected to experimental conditions to ensure induction of infarction. Electrocardiographic changes and increased cardiac enzyme cTnI confirmed the complication of infarction. The intervention groups were exposed to electrical stimulation for one session (foot shock device for 0.5 mA for 20 minutes) and endurance training (treadmill at 20 m/min for 1 hour). Immediately after the protocol, they were anesthetized and killed with a combination of ketamine and xylazine, and blood samples were taken.  Then, serum levels of CORT and cTnI of the samples were evaluated in the laboratory by ELISA method according to the instructions of the manufacturer of kits of Eastbiofarm China. After examining the normal distribution of data, one-way ANOVA and Tukey post hoc tests were used to analyze it at a significance level of P <0.05. Results: The results showed that serum CORT levels in rats had a statistically significant difference between the healthy group and all groups (P=0.0001 with F=15.1). Also, CORT levels showed statistically significant differences between MI and MI.EX (P=0.008 and F= 5.2), MI and MI.ES (P=0.032 and F = 4.4) and MI with MI.EX.ES (P=0.044 and F=4.4). In different circumstances, Tukey test did not show a statistically significant difference between MI.EX and MI.ES groups (P=0.980 and F=0.8) and MI.ES with MI.EX.ES (P=0.982 and  F=0.1). The results showed that cTnI levels in healthy rats were significantly different from all groups (P=0.0001 with F=26.3). Also, cTnI levels were significantly different between MI and MI.EX groups (P=0.013 with F=4.9).  On the other hand, the difference between MI groups with MI.ES (P=0.476 and F=2.3) and MI.EX.ES (P=0.094 and F=3.7) was not significant. Also, Tukey post hoc test did not show significant differences between MI.EX and MI.ES groups (P=0.390 and F=2.5), MI.ES with MI.ES (P=0.911 and F=1.2) and MI.ES with MI.EX.ES (P=0.833 and F=1.3). Conclusion: The results of the present study show that one endurance training session significantly reduces CORT and cTnI levels in infarct specimens. In this regard, Klapersky et al. Showed a significant reduction in serum CORT levels after endurance training. In contrast to the present study, Zhu et al. showed that acute aerobic exercise increases CORT levels in both males and females. The reason for the discrepancy between these studies and the present study was the difference in the intensity of physical activity. In the present study, the intensity of exercise was about 55% VO2max and was of moderate intensity. It has already been shown that moderate and low intensity physical activity does not cause significant changes in CORT, but high intensity physical activity stimulates the HPA axis. It may be followed by an increase in CORT. In this study, a significant decrease in cTnI levels was shown after one endurance training session in infarcted rats. Consistent with the results of the present study, Marefati et al. Showed that moderate-intensity interval training significantly reduced serum cTnI levels in ischemic rats, indicating a protective role of this type of exercise against ischemic injury. In contrast to this study, Nuano et al. showed that exercise significantly increased cTnI levels in rats with myocardial ischemia. The increase in cTnI secretion after intense and prolonged activity has not been accurately identified, but this increase may be due to oxidative stress, hypoxia, unstable secretion due to cytosolic leakage due to ischemia, changes in cell permeability and membrane permeability. Also, the difference in the measurement of cTnI level can be another reason for the contradiction of the mentioned studies with this research. The results of the present study showed that induction of ES in myocardial infarction rats significantly reduced CORT levels. In contrast to the present study, Digit et al. Investigated the acute and chronic effects of ES through death shock (0.8 mA and 20 min) on rats and showed that CORT levels increased significantly. The inconsistency may be due to differences in the intensity and duration of induced electrical stimulation in the study samples. The results of ES intervention on cTnI levels of infarcted rats did not show a significant difference.  Other results of this study showed that the combined effect of endurance training with ES significantly reduced CORT values in all study groups compared to MI. But changes in cTnI in the endurance training group with ES were not significant compared to the MI group. نفارکتوس میوکارد,تحریک الکتریکی, تروپونین-I, تمرین استقامتی, کورتیکوسترون Myocardial Infarction, Electrical Stimulation, Troponin-I, Endurance Exercise, CORT 271 280 http://rjms.iums.ac.ir/browse.php?a_code=A-10-5808-1&slc_lang=fa&sid=1 Mohammad malekipooya محمد ملکی پویا maleki.p@gmail.com 3900319475328460083697 3900319475328460083697 Yes Assistant Professor of Exercise Physiology, Professor Hasabi Branch, Islamic Azad University, Tafresh, Iran استادیار فیزیولوژی ورزش، واحد پرفسور حسابی، دانشگاه آزاد اسلامی، تفرش، ایران Mojtaba Khansooz مجتبی خان سوز Mojtaba.khansooz@gmail.com 3900319475328460083698 3900319475328460083698 No Assistant Professor of Xercise Physiology, Arak Branch, Islamic Azad University, Arak, Iran استادیار فیزیولوژی ورزش، واحد اراک، دانشگاه آزاد اسلامی، اراک، ایران Mohammadreza Palizvan محمدرضا پالیزوان palizvan@yahoo.com 3900319475328460083699 3900319475328460083699 No Professor of Physiology, University of Medical Sciences, Arak, Iran استاد فیزیولوژی، دانشگاه علوم پزشکی، اراک، ایران Abas Saremi عباس صارمی a-saremi@araku.ac.ir 3900319475328460083700 3900319475328460083700 No Associate Professor of Exercise Physiology, Arak University, Arak, Iran دانشیار فیزیولوژی ورزش، دانشگاه اراک، اراک، ایران Bahram Abedi بهرام عابدی abedi_bahram2000@yahoo.com 3900319475328460083701 3900319475328460083701 No Professor of Exercise Physiology, Mahallat Branch, Islamic Azad University, Mahallat, Iran استاد فیزیولوژی ورزش، واحد محلات، دانشگاه آزاد اسلامی، محلات، ایران