Razi Journal of Medical Sciences

fa تاثیر کاهش حجم تمرین با تغذیه پرچرب پس از تمرین با حجم بالا بر فاکتورهای سلولی بیوژنز میتوکندریایی رت‌های ماده The effect of reduced training volume combined with high-fat post-exercise nutrition—following high-volume training on cellular factors of mitochondrial biogenesis in female rats. فیزیولوژی ورزش Exercise Physiology پژوهشي Research <div style="text-align: justify;">زمینه و هدف: افزایش وزن و چاقی از مسیرهای مختلفی باعث ایجاد تغییر در محتوا و عملکرد میتوکندری میشود که این تغییرات نقش مهمی در سلامت سوخت و سازی دارند. هدف از انجام تحقیق حاضر تبیین تاثیر کاهش حجم تمرین با تغذیه پرچرب پس از تمرین با حجم بالا بر فاکتورهای سلولی بیوژنز میتوکندریایی رتهای ماد بود. روش کار: بدین منظور از بین رتهای ماده نژاد اسپارگو-داولی با وزن 300 تا 325 گرم و سن شش هفتهای که در مرکز پرورش حیوانات دانشگاه علوم پزشکی ایران تکثیر شده بودند 20 سر رت بطور تصادفی به عنوان نمونه آماری انتخاب و بطور تصادفی به 4 گروه کنترل 10 هفتهای با تغذیه معمولی، تمرین 6 هفتهای  و 4 هفته تمرین با کاهش حجم با تغذیه معمولی، روه 3: تمرین 6 هفته ای  و 4 هفته تمرین با کاهش حجم با تغذیه پرچرب، تمرین 6 هفته ای به علاوه بی تمرینی 4 هفتهای با تغذیه پرچرب تقسیم شدند. در ادامه رتها جهت آشناسازی به محیط نگهداری، به مدت یک هفته بدون هیچ مداخله‌ای در قفس‌ها مانند. هفته بعد برای آشناسازی با تردمیل به مدت پانزده دقیقه به مدت سه روز روی تردمیل قرار گرفتند. سپس دو جلسه به مدت 10 دقیقه با سرعت بسیار پایین روی تردمیل راه رفتند. گروه کنترل بدون هیچ مداخلهای تا آخر 10 هفته در فقس نگهداری شده و به غذای معمولی دسترسی آزاد داشتند. سایر گروهها به مدت شش هفته با پروتکل تمرینی 1 که با حجم بالا بود، تمرین کرده و با غذای استاندارد معمولی تغذیه شدند. پس از پایان هفته ششم، گروه 2 به مدت چهار هفته، پروتکل تمرینی 2 که تمرین با کاهش حجم بود را ادامه داده و تغذیه معمولی داشتند. گروه3، به مدت 4 هفته پروتکل تمرینی 2 که تمرین با کاهش شدت بود را انجام دادند و همچنین با غذای پرچرب تغذیه شدند. گروه 4 بی تمرین شده و غذای پرچرب دریافت کردند. در نهایت میزان پروتئین PGC-1a و SIRT1 برای سنجش بیوژنز میتوکندریایی در سلولهای میوکارد بررسی گردید. یافتهها: نتایج نشان داد کاهش حجم تمرین با تغذیه پرچرب پس از تمرین با شدت بالا بر میزان پروتئین PGC-1a و SIRT1 در رتهای ماده تاثیر معناداری دارد. نتیجهگیری: با توجه به نتایج استفاده از تمرینات تناوبی جهت تاثیر بر فاکتورهای بیوژنز میتوکندریایی و هایپرتروفی بطن چپ توصیه میشود.</div> <div style="text-align: justify;">Background & Aims: Weight gain and obesity alter mitochondrial content and function through various pathways, and these changes play a significant role in metabolic health. Indeed, a decline in mitochondrial function and biogenesis across various tissues has been confirmed in the context of obesity. While it appears that high-fat diet-induced obesity primarily leads to mitochondrial dysfunction through increased oxidative stress, SIRT1 plays a crucial role in the cardiac response to a high-fat diet. A high-fat diet can lead to a reduction of SIRT1 in cardiomyocytes. This reduction in SIRT1 may contribute to the obesity and insulin resistance induced by a high-fat diet, potentially triggering an inflammatory cellular cascade (4); however, further research is still needed regarding the direct impact of a high-fat diet on mitochondrial biogenesis. Despite studies examining the effects of exercise and a high-fat diet on research variables, changes in proteins and key factors involved in mitochondrial biogenesis during and after a period of detraining have consistently drawn the attention of researchers. While various studies have been conducted in this area, most prior research has defined detraining simply as the cessation of exercise; consequently, information regarding the impact of detraining periods combined with a high-fat diet on the cardiovascular system remains very limited. Methods: This developmental, experimental study was conducted in a laboratory setting using adult female Sprague-Dawley rats. Twenty rats (weighing 300–325 g and aged six weeks) were randomly selected as the statistical sample and assigned to four groups of five: Group 1 (Control): 10 weeks on a standard diet; Group 2: 6 weeks of training followed by 4 weeks of reduced-volume training on a standard diet; Group 3: 6 weeks of training followed by 4 weeks of reduced-volume training on a high-fat diet; and Group 4: 6 weeks of training followed by 4 weeks of detraining on a high-fat diet. Subsequently, to acclimate to the housing environment, the rats remained in their cages for one week without any intervention. The following week, they were placed on the treadmill for fifteen minutes daily over three days to familiarize them with the apparatus, with the motor turned off. They then underwent two 10-minute sessions of walking on the treadmill at a very low speed. Thereafter, the control group was kept in cages without any intervention for the remainder of the 10-week period, with free access to standard food. Groups 2, 3, and 4 trained for six weeks using "Training Protocol 1" (high-volume training) and were fed a standard diet. After the sixth week, Group 2 continued for four weeks with "Training Protocol 2" (reduced-volume training) while maintaining a standard diet. Group 3 performed "Training Protocol 2" (reduced-intensity training) for four weeks and was fed a high-fat diet. Group 4 ceased training and received a high-fat diet. Training protocol 1 consisted of intermittent aerobic exercise performed on a treadmill at a zero-degree incline for six weeks, five days a week, with one 60-minute session per day. The protocol comprised 10 exercise-recovery intervals; the exercise phase of each interval lasted 4 minutes at an intensity of 85–90% of VO2max, while the recovery phase lasted 2 minutes at 50% of VO2max. Training protocol 2 involved a reduction in volume compared to protocol 1, achieved by decreasing the frequency from 5 days per week to 3 days per week. All other parameters of training protocol 2 were identical to those of protocol 1. The high-fat diet consisted of 10% animal fat, 10% egg yolk powder, 2% cholesterol, 0.2% bile salts, 0.2% methyl-oxy-pyrimidine, and 77.6% basal diet. Finally, the rats were anesthetized with chloroform, their hearts were excised, and the levels of PGC-1α and SIRT1 proteins in myocardial cells were assessed using the Western blot method. Statistical analysis was performed using SPSS/21 software at a significance level of α ≤ 0.05; descriptive statistics (mean and standard deviation) were used to describe the research variables, the Shapiro-Wilk test was employed to assess the normality of data distribution, and a one-way ANOVA followed by a Tukey post-hoc test was used for data analysis. Results: The results indicated that reducing training volume combined with high-fat nutrition following high-volume training had a significant effect on PGC-1α levels in female rats (P=0.001, F=14.147). Furthermore, the Scheffé post-hoc test revealed a significant difference between the control group (1) and experimental groups 2 and 3, but no significant difference compared to experimental group 4. Additionally, while no significant difference was found between experimental groups 2 and 3, a significant difference existed between groups 2 and 4. Finally, no significant difference was observed between group 3 and group 4. Another finding of the present study indicated that reducing training volume while consuming a high-fat diet—following a period of high-volume training—had a significant effect on SIRT1 levels in female rats (P=0.001, F=14.027). Furthermore, the Scheffé post-hoc test revealed a significant difference between the control group (1) and experimental groups 2 and 3, but no significant difference compared to experimental group 4. Additionally, while no significant difference was found between experimental groups 2 and 3, a significant difference existed between groups 2 and 4. Finally, no significant difference was observed between group 3 and group 4. Conclusion: The results of the present study demonstrate the effects of 6 weeks of high-volume training—followed by 4 weeks of either reduced-volume training with a standard diet, reduced-volume training with a high-fat diet, or detraining with a high-fat diet—on PGC-1α levels in female rats. Regarding the mechanism of action for these exercises, it can be stated that the repeated contractions and recruitment of fast-twitch fibers during high-intensity intervals—driven by intracellular signaling involving calcium and its binding to calmodulin—increase the expression of mitogen-activated proteins, thereby indirectly enhancing glucose uptake (12); meanwhile, the engagement of slow-twitch fibers during active recovery intervals modulates gene expression (13). This is because the transition to low-intensity activity following high-intensity exercise bouts—which elevate cellular metabolism—triggers the release of vasodilators and subsequently PGC-1α, thereby promoting mitochondrial biogenesis and protecting cardiac structure (14). Another finding of the present study indicated that reducing training volume while consuming a high-fat diet—following a period of high-volume training—significantly affects SIRT1 levels in female rats. It can be stated that obesity resulting from a high-fat diet leads to mitochondrial dysfunction primarily through oxidative stress and impacts mitochondrial biogenesis (4). However, physical exercise enhances mitochondrial biogenesis through the activation of AMPK (5). On the other hand, it should be noted that training volume is a key determinant of mitochondrial content (18); given the reduction in training volume associated with high-intensity training, this factor may offer an additional explanation for the findings of the present study. Nevertheless, high-intensity interval training induces beneficial metabolic adaptations and increases mitochondrial content—particularly in the context of obesity (20)—by promoting mitochondrial biogenesis through an increase in mitochondrial number and improved mitochondrial function (19). </div> حجم تمرین, تغذیه پرچرب, بیوژنز میتوکندریایی, PGC-1a, SIRT1 Training volume, High-fat diet, Mitochondrial biogenesis, PGC-1α, SIRT1 1 10 http://rjms.iums.ac.ir/browse.php?a_code=A-10-8844-1&slc_lang=fa&sid=1 Mohammad Shirali محمد شیرعلی 3900319475328460091698 0009-0009-0417-7560 No Ph.D. Student in Exercise Physiology, Science and Research Branch, Islamic Azad University, Tehran, Iran دانشجوی دکتری تخصصی فیزیولوژی ورزشی، گروه تخصصی تربیت بدنی و علوم ورزشی، واحد علوم و تحقیقات، دانشگاه آزاد اسلامی، تهران، ایران Farshad Ghazalian فرشاد غزالیان phdghazalian@gmail.com 3900319475328460091699 3900319475328460091699 Yes Associate Professor, Department of Physical Education and Sports Sciences, Science and Research Branch, Islamic Azad University, Tehran, Iran دانشیار، گروه تخصصی تربیت بدنی و علوم ورزشی، واحد علوم و تحقیقات، دانشگاه آزاد اسلامی، تهران، ایران Hossein Abed natanzi حسین عابدنطنزی 3900319475328460091700 3900319475328460091700 No Assistant Professor, Department of Physical Education and Sports Sciences, Science and Research Branch, Islamic Azad University, Tehran, Iran استادیار، گروه تخصصی تربیت بدنی و علوم ورزشی، واحد علوم و تحقیقات، دانشگاه آزاد اسلامی، تهران، ایران Shahram Soheili شهرام سهیلی 3900319475328460091701 3900319475328460091701 No Assistant Professor, Department of Physical Education and Sports Sciences, Shahre Qods Branch, Islamic Azad University, Tehran, Iran استادیار،گروه تربیت بدنی و علوم ورزشی، واحد شهرقدس، دانشگاه آزاد اسلامی، تهران، ایران