ورزش هوازی: رویکردی برای تنظیم استرس اکسیداتیو در بافت قلب رت‌های دیابتی

نوع مقاله : مقاله پژوهشی Released under (CC BY-NC 4.0) license I Open Access I

نویسندگان

1 گروه فیزیولوژی ورزشی ، دانشکده تربیت بدنی و علوم ورزشی، دانشگاه تبریز، تبریز، ایران

2 دانشجوی دکتری فیزیولوژی ورزشی، دانشکدۀ تربیت بدنی و علوم ورزشی، دانشگاه تبریز، تبریز، ایران

چکیده

هدف: دیابت تولید رادیکال‌های آزاد و عوامل التهابی را در بافت قلب افزایش می‌دهد. تمرین در بهبود بیماری‌های قلبی عروقی و فعالیت آنتی‌اکسیدانی و سطح استرس اکسیداتیو نقش دارد. بنابراین، این مطالعه با هدف بررسی تاثیر تمرین هوازی برSOD ،GPX ،TAC  و MDA در بافت قلب رت‌های مبتلا به دیابت نوع دو انجام شد. روش‌شناسی: 24 سر موش صحرایی نر نژاد (وزن 20±200 گرم) و (سن هشت هفته‌) بصورت تصادفی به چهار گروه شامل: 1) کنترل سالم، 2) کنترل دیابتی، 3) تمرین سالم و 4) تمرین دیابتی تقسیم شدند. پروتکل تمرین دویدن روی تردمیل پنج روز در هفته با رعایت اصل اضافه بار در هفته اول با سرعت 10-5 متر در دقیقه به مدت 15-10 دقیقه و در هفته هشتم با سرعت 24-18 متر در دقیقه به مدت 60 دقیقه به دست آمد. سطوحSOD ،GPX ،TAC  و MDA در بافت قلب اندازه‌گیری شد. از آزمون‌های آماری واریانس یک­راهه و تعقیبی توکی در سطح معنی­داری 0.05 P< استفاده شد. یافته‌ها: یافته‌ها نشان داد که هشت هفته دیابت باعث کاهش معنی‌داری در سطوح SOD، GPX و TAC و افزایش سطح گلوکز و MDA (001/0=P)‌ گردید. همچنین در هر دو گروه تمرین سالم (001/0=P) و تمرین دیابت (05/0P<) نسبت به کنترل دیابت، به طور معنی‌داری افزایش در سطوح SOD، GPX و TAC و کاهش سطح گلوکز و MDA مشاهده شد. نتیجه‌گیری: تمرین هوازی می‌تواند سطح گلوکز و MDA را در بافت قلب موش‌های دیابتی کاهش و فعالیت‌های SOD، GPX و TAC را افزایش ‌دهد. علاوه بر این، تمرین هوازی ممکن است به عنوان یک ابزار مفید برای کاهش استرس اکسیداتیو در دیابت در نظر گرفته شود.

کلیدواژه‌ها

موضوعات

عنوان مقاله [English]

Aerobic training: an approach to regulate oxidative stress in heart tissue of diabetic rats

نویسندگان [English]

  • Elaheh Piralaiy 1
  • Badrkhan Rashwan Ismael 2
1 Assistant Professor, Department of Exercise Physiology, Faculty of Physical Education and Sports Sciences, Tabriz University, Tabriz, Iran; epiralaiy@yahoo.com
2 Ph.D student, Exercise physiology, Department of Exercise Physiology, Faculty of Physical Education and Sports Sciences, University of Tabriz, Tabriz, Iran.
چکیده [English]

Aim:  Diabetes increases the production of free radicals and inflammatory agents in the heart tissue. Training plays a role in improving cardiovascular disease, antioxidant activity, and oxidative stress levels. Therefore, this study aimed to investigate the effect of aerobic training on SOD, GPX, TAC, and MDA in the heart tissue of rats with type 2 diabetes. Methods: 24 male rats (weighing 200±20 gr) and (age eight weeks) were randomly divided into four groups: 1) healthy control, 2) diabetic control, 3) healthy training, and 4) diabetic training.   The training protocol was obtained on the treadmill five days per week with the principle of overload in the first week at a speed of 5-10 m/min for 10-15 minutes and in the eighth week at a speed of 18-24 m/min for 60 minutes. The levels of SOD, GPX, TAC, and MDA were measured in heart tissue. One-way ANOVA and Tukey post hoc tests were used at the significance level of P<0.05. Results:  The findings showed that eight weeks of diabetes caused a significant decrease in SOD, GPX, and TAC levels and an increase in glucose and MDA levels (P=0.001). Also, in both healthy training groups (P=0.001) and diabetic training groups (P<0.05) compared to diabetes control, a significant increase in SOD, GPX, and TAC levels and a decrease in glucose and MDA levels were observed. Conclusions:   Aerobic training can reduce the level of glucose and MDA in the heart tissue of diabetic rats and increase SOD, GPX, and TAC activities. In addition, aerobic training may be considered a useful tool for reducing oxidative stress in diabetes.

کلیدواژه‌ها [English]

  • Aerobic exercise
  • Type 2 diabetes
  • Oxidative stress
  • Antioxidant defense system

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مطالعات کاربردی تندرستی در فیزیولوژی ورزش
دوره 11، شماره 2
مهر 1403
صفحه 128-140

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  • تاریخ دریافت: 25 اسفند 1402
  • تاریخ بازنگری: 23 اردیبهشت 1403
  • تاریخ پذیرش: 09 خرداد 1403

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