تأثیر مصرف الکل بر هایپرتروفی عضلانی ناشی از تمرین مقاومتی و کاردیومیوپاتی الکلی

نوع مقاله : مقاله مروری

نویسندگان

گروه علوم زیستی ورزش، دانشکده علوم ورزشی و تندرستی، دانشگاه شهید بهشتی، تهران، ایران

چکیده

فعالیت‌های مقاومتی به تحریک سنتز پروتئین عضلانی منجر شده که از آن به‌عنوان هایپرتروفی عضلانی حاصل از فعالیت ورزشی یاد می‌شود. عوامل متعدد هورمونی و تغذیه‌ای، به‌صورت مستقیم و یا با تأثیر بر آبشارهای سلولی فعال‌شده به‌واسطۀ فعالیت ورزشی، بر میزان سنتز پروتئین عضلانی اثرگذارند. در این بین مصرف حاد و مزمن الکل به‌عنوان عامل منفی اثرگذار، عوامل متعدد درگیر در تعادل بین سازوکارهای آنابولیک و کاتابولیک را دچار اختلال می‌کند و در فرایندی متفاوت بر عضلات و فعالیت قلبی تأثیر می‌گذارد. با این حال، هنوز در زمینۀ سازوکارهای مربوطۀ بحث وجود دارد. در مقالۀ مروری نظام‌مند حاضر، در خصوص تأثیرات مصرف الکل بر سنتز و تجزیۀ پروتئین عضلانی با تأکید بر مسیر هایپرتروفی mTOR و هورمون‌ها که به‌عنوان مسیرهای متابولیکی غالب در سنتز پروتئین عضلانی ناشی از فعالیت ورزشی در نظر گرفته شده‌اند، بحث شده است. بر این اساس جست‌وجو در پایگاه‌های Pubmed، Google scholar، web of science در خصوص تأثیر مصرف الکل بر فرایندهای سنتز پروتئین با تأکید بر مسیر mTOR در عضلۀ اسکلتی و در پی ورزش مقاومتی در بازۀ زمانی سال‌های 2010 تا 2024 صورت گرفت. در عنوان و کلیدواژه‌ها، واژه‌های Protein synthesis، Alcohol، Ethanol، Skeletal muscle، mTOR signaling، Resistance exercise و Hypertrophy جست‌وجو شد. در نهایت پس از مرور و بررسی مقالات، 71 مقاله برای انجام پژوهش حاضر در نظر گرفته شد. به‌طور کلی تحقیقات حاکی از کاهش مقدار هورمون رشد، تستوسترون و عامل رشد شبه‌انسولینی و اثر منفی بر mTOR همراه با مصرف حاد الکل است که در نهایت به کاهش هایپرتروفی منجر می‌شود. پس از مصرف الکل، در عضلۀ اسکلتی کاهش سنتز پروتئین پایه که بیشتر در تارهای نوع II به‌ویژه تارهای نوع  IIxکه بیشترین پاسخ را به هایپرتروفی عضلانی حاصل از ورزش نشان می‌دهند، مشاهده شده است. همچنین مصرف مزمن الکل با افزایش مقدار کورتیزول و فعال شدن مسیر یوبی کوئیتین پروتئوزوم موجب فعال شدن مسیرهای آتروفی و در پی آن کاهش تودۀ عضلانی می‌شود، به‌طوری‌که سوء مصرف الکل با شیوع 50 درصدی میوپاتی عضلانی مرتبط است، این در حالی است که در قلب موجب هایپرتروفی غیرطبیعی و اختلال عملکرد دیاستولی بطن چپ می‌شود. مصرف افراطی یا مزمن الکل موجب کاردیو مایوپاتی یا ناهنجاری‌های ساختاری و عملکردی عضلۀ قلبی می‌شود. با توجه به اینکه الکل حتی تا یک روز پس از مصرف هم آثار منفی بر سنتز پروتئین عضلانی می‌گذارد و مسیرهای سیگنالینگ هایپرتروفی را مختل می‌کند، می‌تواند سلامت قلبی-عروقی را تحت تأثیر قرار دهد و لازم است ورزشکاران از آثار مخرب و پیامدهای آن مطلع شوند. درک آثار منفی الکل بر فرایندهای فیزیولوژیکی برای ترویج سبک زندگی سالم و بهینه‌سازی نتایج تمرین برای سلامت و در ورزش قهرمانی بسیار اساسی است.

کلیدواژه‌ها

موضوعات

عنوان مقاله [English]

The impact of alcohol consumption on resistance training-induced muscle hypertrophy and alcohol-induced cardiomyopathy

نویسندگان [English]

  • Maryam Nourshahi
  • Samira Rostami
  • Nastaran Nazari
Department of Sports Biological Sciences, Faculty of Sports and Health Sciences, Shahid Beheshti University, Tehran, Iran
چکیده [English]

Resistance exercise leads to the stimulation of muscle protein synthesis, known as exercise-induced muscle hypertrophy. Several hormonal and nutritional factors, directly or indirectly impacting cellular pathways activated by exercise, influence muscle protein synthesis. Among these, acute and chronic alcohol consumption disrupts the balance between anabolic and catabolic mechanisms and affects muscles and heart activity in a different process. However, there is uncertainty regarding the precise mechanisms involved. This systematic review discusses the effects of alcohol consumption on muscle protein synthesis and degradation with emphasis on the hypertrophy pathway of mTOR and hormones involved in exercise-induced muscle protein synthesis. For this purpose, comprehensive searches were performed in Pubmed, Google Scholar, and Web of Science regarding the impact of alcohol consumption on protein synthesis processes, with an emphasis on the mTOR pathway in skeletal muscle following resistance exercise, in the time frame of 2010 to 2024. The following keywords were used to search in the title and keywords: protein synthesis, alcohol, ethanol, skeletal muscle, mTOR signaling, resistance exercise, and hypertrophy. After reviewing the articles, a total of 71 articles were selected for the current review. Previous studies indicate a decrease in growth hormone, testosterone, and insulin-like growth factor along with a negative effect on mTOR due to acute alcohol consumption, which ultimately leading to reduced hypertrophy. 15-20% decrease in basal protein synthesis in skeletal muscle is observed twenty-four hours after alcohol consumption, mostly in type II fibers, and particularly in type IIx fibers, which provide the greatest response to muscular hypertrophy after regular exercise. Chronic alcohol consumption also increases cortisol levels and activates the ubiquitin-proteasome pathway, leading to the activation of atrophic pathways and subsequent muscle mass reduction. Over consumption of alcohol is associated with a 50% prevalence of alcoholic myopathy, which also causes abnormal hypertrophy and diastolic dysfunction in the left ventricle of the heart. Chronic alcohol consumption leads to cardiomyopathy or structural and functional abnormalities of the cardiac muscle. Therefore, considering that alcohol can have negative effects on muscle protein synthesis even up to one day after consumption and disrupt hypertrophic signaling pathways, can have an effect on cardiovascular health, and athletes need to be aware of the detrimental effects and consequences. Understanding the negative effects of alcohol on these physiological processes is crucial for promoting a healthy lifestyle and optimizing exercise outcomes in health and sports.

کلیدواژه‌ها [English]

  • Ethanol
  • mTOR
  • Hypertrophy
  • Resistance Training

مراجع

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  • تاریخ دریافت: 28 فروردین 1403
  • تاریخ بازنگری: 20 خرداد 1403
  • تاریخ پذیرش: 24 خرداد 1403
  • تاریخ اولین انتشار: 24 خرداد 1403
  • تاریخ انتشار: 01 تیر 1403

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