اثر تمرین مقاومتی و تستوسترون انانتات بر بیان ژنهای Bax ، Bcl2 در بافت قلب موش های صحرایی نر ویستار
محورهای موضوعی : علوم ورزشی و سلامت
ریحانه قانعی
1
,
عبدالعلی بنائی فر
2
,
علی گرزی
3
,
سجاد ارشدی
4
1 - 1. دانشجوی دکتری ، گروه فیزیولوژی ورزش ، واحد تهران جنوب، دانشگاه آزاد اسلامی ، تهران ، ایران.
2 - دانشیار، گروه فیزیولوژی ورزش ، واحد تهران جنوب، دانشگاه آزاد اسلامی ، تهران ، ایران.
3 - گروه فیزیولوژی ورزشی، دانشگاه زنجان، زنجان، ایران
4 - Assistant Professor of Exercise Physiology , South Tehran Branch , Islamic Azad university, Tehran, Iran.
کلید واژه: تمرین مقاومتی , , Bax Bcl2, بافت قلب , تستوسترون انانتات .,
چکیده مقاله :
هدف از پژوهش حاضر مطالعه تاثیر هشت هفته تمرین مقاومتی و مصرف تستوسترون بر برخی شاخص های آپوپتوز بافت قلبی در موشهای صحرایی نر ویستار می باشد. در این پژوهش، 21 سر موش صحرایی نر نژاد ویستار (با سن 8 هفته) با میانگین وزنی 70/11 ± 20/252 گرم انتخاب و به 3 گروه کنترل،تمرین مقاومتی و تمرین مقاومتی+ تستوسترون، تقسیم شدند. پروتکل تمرین مقاومتی پنج روز در هفته (چهار نوبت ششتایی با استراحت 60 الی 90 ثانیه) به صورت صعود از نردبان ۱متری که در آن وزنهها، هفتهی اول 60 درصد وزن بدن و هر هفته 20 درصد وزن بدن موشها، به وزنه ها اضافه میشد. تزریق تستوسترون انانتات با دوزmg/kg20 ، 3 روز در هفته به صورت درون عضلانی انجام شد. جهت تجزیه و تحلیل یافتههای پژوهش از آزمون آنالیز واریانس یک راهه و از آزمون تعقیبی توکی جهت نشان دادن تفاوت بین گروهها استفاده شد (05/0≥p). نتایج نشان داد : بیان Bax و Bcl2 در گروه تمرین نسبت به گروه کنترل تفاوت معنی داری نشان نداد (05/0P≥). لیکن این تغییرات در گروه تمرین + تستوسترون نسبت به گروه کنترل، افزایش معنی داری در بیان Bax (001/0P=) نشان داد. هر چند تغییر معنی داری در بیان Bcl2 ایجاد نشد (05/0P≥). بر اساس نتایج مطالعه حاضر می توان گفت استفاده از دوزهای فوق فیزیولوژیک میتواند توسعه عوامل آپوپتوز در بافت قلب را افزایش دهد و احتمال آسیب میوکارد را بالا ببرد.بنابراین باید آگاهی افراد ورزشکاران افزایش یابد تا از آسیب پیشگیری نماید.
Introduction
Anabolic androgenic steroids (AAS) are derivatives of the hormone testosterone that play a significant role in protein synthesis, muscle growth, and improved athletic performance. Following the abuse of these compounds, serious complications and problems can occur for various tissues, including heart tissue. There have also been reports of sudden cardiac death, myocardial infarction, and cardiomyopathy caused by AAS use during exercise, which has been associated with increased apoptosis and cardiac oxidative stress. Studies have shown that exogenous testosterone administration during exercise causes and changes physiological hypertrophy to pathological cardiac hypertrophy. Chronic AAS abuse leads to different patterns of pathological changes and apoptosis. Bax and Bcl-2 proteins act as the main proteins effective in the mitochondrial apoptosis process. Accordingly, the aim of the present study was to investigate the effect of eight weeks of resistance training and testosterone enanthate consumption on some apoptosis indicators including Bax and Bcl-2 in the cardiac tissue of male Wistar rats.
Materials and methods:
This study was conducted on 21 8-week-old male Wistar rats (weight: 220 ± 15 g). The animals were housed in polycarbonate cages under standard conditions and had free access to food and water. After a week of familiarization, the animals were divided into three groups: control (7 rats), training (7 rats), and training + testosterone (7 rats). Rats in the training and training + testosterone groups performed resistance training for eight weeks, five sessions per week.
This exercise consisted of four sets of six with a rest of 60 to 90 seconds, in the form of climbing a one-meter ladder with 26 steps and tying weights to the tails of the mice, and 20% of body weight was added to the weights each week and continued up to 180% of body weight. Also, the mice in the exercise + testosterone group received 20 mg/kg testosterone enanthate (manufactured by Iran Hormone Company, Iran, serial number 0069) by injection three days a week. 48 hours after the last training session and testosterone administration, the mice were anesthetized with a combination of xylazine (3 to 5 mg/kg) and ketamine (30 to 50 mg/kg). Then, their heart tissue was removed, washed in physiological serum, and immediately transferred to frozen liquid nitrogen. PCR was used to measure the expression of the desired genes, with GAPDH as a control gene. The Shapiro-Wilk test was used to determine the normality of the data, and the one-way analysis of variance and Tukey's post hoc test were used to determine the difference between variables. Ethical standards for working with laboratory animals were followed in accordance with the guidelines of the Ethics Committee with the ID IR.IAU.VARAMIN.REC.1403.032.
Results and findings:
The results of the one-way analysis of variance test showed a significant difference in the mean Bax index between the research groups (P = 0.001), but the results of this test did not show a significant difference between the research groups in relation to the Bcl-2 index (P = 0.989). Also, the results of the Tukey post-hoc test showed that the mean BAX expression in the exercise + testosterone group was significantly different from the control group (P = 0.038) and a significant increase was observed in this group (Figure 1). However, this difference was not significant between the exercise group and the control group and between the exercise group and the exercise + testosterone group (P = 0.948).
Conclusion:
The results obtained from the present study regarding the Bax index showed a significant increase in this index compared to the control group, although very limited studies have been conducted regarding the effect of exercise combined with testosterone consumption on Bax and Bcl-2 indices in heart tissue, but some studies also indicate an increase in apoptosis indices including Bax and Bcl-2 in various tissues due to testosterone consumption along with resistance training. It seems that AAS may change the function of the mitochondrial respiratory chain complex and monooxygenase systems, and as a result, cause an imbalance between the production of free radicals and their subsequent recovery. This can lead to an increase in apoptosis indices including Bax and Bcl-2.
Studies show that apoptosis plays a significant role in the process of testosterone-induced cardiac damage. It seems that anabolic steroids have a pro-apoptotic effect on cardiac myocytes, such that by increasing the release of Ca2+ in the sarcoplasmic reticulum, they increase mitochondrial permeability, which ultimately leads to the release of apoptosis-inducing factors such as cytochrome C, caspase, and consequently apoptosis. The use of AAS can have many undesirable effects, especially with the occurrence of cardiac apoptosis. It can be said that the use of anabolic compounds along with resistance training can provide the basis for the occurrence of cardiac tissue damage. Therefore, increasing awareness about the complications of AAS use among the public, especially athletes, seems necessary. In general, the findings of the present study indicate the effect of testosterone in the development of apoptosis factors in cardiac tissue and the possibility of increasing the occurrence of myocardial damage. It seems that the mechanism of these changes could be related to oxidative stress in the tissue caused by steroid abuse. Considering the use of a dose of 20 mg of the drug in this study, it can be said that the use of supraphysiological doses probably increases the development of apoptosis factors in the heart tissue and can increase the possibility of damage. Therefore, it is suggested to avoid the use of steroid compounds along with resistance training.
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