Razi Journal of Medical Sciences

fa اثر تمرینات تناوبی با شدت زیاد بر اختلالات شناختی و حافظه ناشی از چاقی و دیابت: مطالعه مروری نظام‌مند The Effect of High-Intensity Interval Training on Cognitive and Memory Impairments in Obesity and Diabetes: A Systematic Review Study فیزیولوژی ورزش Exercise Physiology مروري review article زمینه و هدف: بیماری‌های متابولیک از جمله چاقی و دیابت علاوه بر تاثیرات محیطی می‌توانند باعث آلزایمر و اختلالات شناختی شوند. دلیل اصلی ایجاد آلزایمر و اختلالات شناختی رسوب خارج سلولی پلاک‌های بتا آمیلوئید و ظاهر شدن تجمعات پروتئین فسفریله تاو است که در نهایت موجب تخریب نورون‌های هیپوکمپ می‌شود. این آسیب‌ها حتی می‌تواند یک قدم فراتر گذاشته و تهدید کننده زندگی افراد باشد. یکی از روش‌های پیشگیری و درمان این عوارض تمرینات تناوبی با شدت زیاد است که به علت صرفه جویی در زمان بسیار و تاثیر گذاری بیشتری نسبت به انواع دیگر تمرینات مورد توجه قرار گرفته‌اند. هدف از این مطالعه، مرور اثر تمرینات تناوبی با شدت زیاد بر اختلالات شناختی و.... ناشی از چاقی و دیابت می‌باشد. روش کار: بدین منظور پایگاه های Google <a name="_Hlk51056544">Scholar</a>، PubMed، Scopus، SID، نور و مگیران مورد بررسی قرار گرفتند. در این مطالعه مروری، علاوه بر تمرین تناوبی با شدت زیاد حداقل یکی از کلید واژه‌های اختلالات شناختی، هیپوکمپ و آلزایمر باید در عنوان یا کلمات کلیدی مطالعات وجود می‌داشت و مطالعات چاپ شده بین سال‌های 2000 تا 30 جولای 2021 تجزیه و تحلیل شدند. یافته‌ها: در جست و جوی اولیه 152 مطالعه براساس عنوان و کلید واژه های مورد نظر یافت شد و بعد از بررسی‌های اولیه، 84 مطالعه به علت مرتبط نبودن چکیده با مفاهیم مورد نظر حذف شد. از بین مطالعات باقی مانده 38 مورد به علت دارا نبودن حداقل یک ترکیب از سه کلید واژه مورد نظر حذف شد. در مرحله سوم متن کامل 30 مطالعه، بررسی شد و 15 مطالعه به علت مرتبط نبودن متن کامل با مفاهیم مورد نظر حذف شدند و در نهایت اطلاعات 15 مطالعه حیوانی و انسانی به دو زبان فارسی و انگلیسی مورد بررسی قرار گرفت. نتیجه‌گیری: مرور این مطالعات نشان می‌دهد که تمرینات تناوبی با شدت زیاد باعث بهبود اختلالات شناختی و افزایش یادگیری و حافظه می‌شوند. با این حال جهت انتخاب تاثیرگذار ترین پروتکل تمرین بر اساس نقش متغیرهای تمرینی مانند نوع، شدت و حجم تمرین به پژوهش‌های مقایسه‌ای بیشتری نیاز است.   Background & Aims: Nowadays, industrialization has reduced physical activity and lifestyle changes, resulting in the spread of lifestyle-related diseases. A common feature in most diseases associated with the new lifestyle is obesity. Obesity as a multifactorial disease is often associated with other diseases such as hypertension and cardiovascular disease, osteoarthritis and some kinds of cancers. Considering as a global problem, obesity is on the rise in adults, adolescents, and children. In many societies, the prevalence of overweight and obesity has increased over the past two decades. In the United States, the risk of developing overweight and obesity during a person's lifetime is 4% and 6%, respectively. Obesity is associate with many secondary diseases such as diabetes. Diabetes is a group of metabolic diseases that have in common high blood glucose levels. Symptoms often include frequent urination, increased thirst and increased appetite. If left untreated, diabetes can cause many health complications. Acute complications can include diabetic ketoacidosis, hyperosmolar hyperglycemic state, or death. Serious long-term complications include cardiovascular disease, stroke, chronic kidney disease, foot ulcers, damage to the nerves, damage to the eyes and cognitive impairment. Diabetes is due to either the pancreas not producing enough insulin, or the cells of the body not responding properly to the insulin produced. The most common form of diabetes is type 2 diabetes. High blood glucose causes damage to various organs as well as disturbances in their function. The average life expectancy of diabetic patients is 10 years less than their non-diabetic peers. Diabetes is the most common metabolic disease in humans. Along with peripheral insulin resistance, which is present in 90% of patients with type 2 diabetes, research has also shown central insulin resistance, especially in the hippocampus, which causes impaired glucose metabolism, memory and cognitive problems, and eventually Alzheimer's. The hippocampus is part of the limbic system, and plays important roles in the consolidation of information from short-term memory to long-term memory, and in spatial memory that enables navigation. In Alzheimer's disease, the hippocampus is one of the first regions of the brain to suffer damage short-term memory loss and disorientation are included among the early symptoms. As a result, metabolic diseases such as obesity and diabetes, in addition to environmental effects, can cause Alzheimer's and cognitive disorders. Alzheimer's disease (AD) is one of the main and most common diseases of the nervous system. While 10-15% of AD patients have a genetic background, 85-90% have non genetic causes. The main cause of AD and cognitive disorders is extracellular accumulation of beta amyloid. These plaques cause inflammation and oxidative stress, which eventually leads to the destruction of cortical and hippocampal neurons. The presence of tau protein clots in brain tissue is another feature of AD. Since the hippocampus is the main site of memory and learning, the accumulation of tau and beta amyloid plaques in the hippocampus causes memory and learning disorders. Symptoms of AD include memory loss, anxiety, depression, and cognitive impairment. Cognitive impairment is a major problem in AD patients. Cognitive function refers to a set of mental processes that contribute to perception, memory, and reason. Cognitive function begins with the initial processing of data and ends with executive function. Early data processing requires few stimuli and thus shows a limited level of cognitive function. In contrast, executive functions represent more advanced cognitive processes that contribute to purposeful behavior. Disruption of these cognitive processes can go a step further and cause premature or delayed complications of various diseases by disrupting function of most body systems which eventually could lead to death. Exercise has always been considered as a useful intervention in preventing metabolic disorders. Since the most important reason for not exercising is lack of time, high intensity interval training (HIIT) because of less time needed and being more beneficial have replaced traditional training with high volume. HIIT consists of intervals (from 45 seconds to 4 minutes) of high-intensity activity (more than 85% of maximal heart rate) and low-intensity activity (approximately 50% of maximal heart rate). Many studies have shown the therapeutic and even preventive role of HIIT in memory and learning disorders induced by obesity and diabetes. However, some other reported no positive effects. Therefore, the aim of this study was to review the effect of HIIT on memory and learning impairments induced by obesity and diabetes. Hereby, we tried to find out if HIIT could improve memory and learning impairments induced by obesity and diabetes and in this case which HIT protocol would be the most effective. Methods: The protocol of the present study is as follows: a search was conducted on Google Scholar, PubMed, Scopus, SID, Noor and Mgiran databases. Studies between 2000 and July 2021 which meet inclusion criteria (the manuscript considered as valid by http://impactfactor.ir) were included.  In the initial search, 152 studies were found based on the title and keywords. Then, 84 studies were deleted due to the lack of abstract relevance to the field. Of the remaining studies (68 studies), 38 were removed due to not having at least one combination of our keywords (in addition to HIIT, at least one of the words cognitive impairment, hippocampus, and AD should be included in the title or keywords of the study). In the third stage, the full text of 30 studies was reviewed and 15 studies were excluded due to the lack of relevance of the full text to the field. Finally, the full text of 15 studies was thoroughly reviewed, and at the end, due to the relevance of the full text of these articles and their subject matter to the authors of the present study, they were regularly categorized based on the sample used (human, animal) And entered the research. Results: 8 studies (30%) were conducted between 2000-2010 and 19 studies (70%) were conducted between 2021-2011. 18 studies (66%) were long-term (studies with training protocol lasted more than a week) and 9 studies (33%) were short-term (studies with training protocol lasted less than a week). 8 studies (30%) used human participants and 19 studies (70%) used animal. Conclusion: HIIT shows opposite effects to promote cognitive function by promoting mitochondrial functions and reduce neuronal apoptosis in the hippocampus. Preliminary evidence suggests that HIIT can induce structural and functional brain changes in patients with mild cognitive impairment (MCI) and AD, but results are still inconclusive. It also has been suggested that, HIIT could exerts anti-inflammatory effects and improves the brain redox status, thereby ameliorating the pathophysiological hallmarks of AD (e.g., beta amyloid deposition). Also There is evidence suggesting that incorporating HIIT into the school day is not associated with improvements in the executive function skill of inhibition, but rather, HIIT is better related to attention–concentration in the classroom. Studies showed that only four minutes of HIIT between classes can improve selective attention in children. Notably, HIIT is useful in combating a wide range of neurocognitive and neuropsychiatric symptoms in obese and diabetic rodents, including improving learning and memory disorders, reducing depression-like behaviors, and improving uncontrolled appetitive behaviors. Restored neurogenesis, improved synaptic plasticity, and reduced neuroinflammation may altogether contribute to cognitive improvements in obese and diabetic rodents. Furthermore, accumulating evidence has suggested the indisputable role of adipose tissues on cognitive function, metabolic function, and neural plasticity. HIIT can effectively attenuate metabolic syndromes in obesity and diabetes by improving lipid profile, adipose tissue inflammation, and insulin resistance. In sum, this review of these studies shows that performing any type of HIIT can increase improve cognitive function and learning. HIIT could also stimulates neurogenesis in the hippocampus, and prevents hippocampal neurodegeneration induced by diabetes. As a result, HIIT can improve cognitive impairment, increase learning and memory, and ultimately improve AD symptoms.  Also The authors show that HIIT is beneficial to cognitive control and working memory capacity when compared against "a blend of board games, computer games, and trivia quizzes" and that this effect is mediated by the Adipokines polymorphism. That  study "suggests a promising alternative to enhance cognition, via short and potent exercise regimens". A meta-analysis studies showed that HIIT can elicit short term brain improvements. Future studies should examine the effect of HIIT on the molecular basis of AD (e.g., beta-amyloid protein accumulation and tau) in addition to behavioral tests to measure short- and long-term memory in mice and measure their learning. In addition, measuring the stress and anxiety of mice can help us determine an effective training protocol. In addition, to complete the results of the present study, it is better to examine different training protocols. In this regard, the effect of different types of exercise (running, optional exercise, etc.) on cognitive functions and improvement of learning and memory disorders has been investigated. Therefore, the effect of intense swimming on cognitive function has not been studied yet and it is suggested that it be the focus of suture studies.   تمرینات تناوبی با شدت زیاد, اختلالات شناختی, آلزایمر, هیپوکمپ HIIT, Cognitive Impairments, Alzheimer Diseases, Hippocampus 65 76 http://rjms.iums.ac.ir/browse.php?a_code=A-10-6263-1&slc_lang=fa&sid=1 Elham Madadizadeh الهام مددی زاده 3900319475328460064564 3900319475328460064564 No Department of Exercise Physiology, Faculty of Physical Education, Shahid Bahonar University, Kerman, Iran گروه فیزیولوژی ورزشی، دانشکده تربیت بدنی، دانشگاه شهید باهنر، کرمان، ایران Mohsen Aminaei محسن امینایی 3900319475328460064565 3900319475328460064565 No Department of Exercise Physiology, Faculty of Physical Education, Shahid Bahonar University, Kerman, Iran گروه فیزیولوژی ورزشی، دانشکده تربیت بدنی، دانشگاه شهید باهنر، کرمان، ایران Keyvan Khorami pour کیوان خرمی پور k.khoramipour@kmu.ac.ir 3900319475328460064566 3900319475328460064566 Yes Department of Physiology and Pharmacology, Faculty of Medical Sciences, Kerman University of Medical Sciences, Kerman, Iran گروه فیزیولوژی و فارماکوژی، دانشکده علوم پزشکی، دانشگاه علوم پزشکی کرمان، کرمان، ایران