کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8270239 | 1534972 | 2014 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Lifelong training preserves some redox-regulated adaptive responses after an acute exercise stimulus in aged human skeletal muscle
ترجمه فارسی عنوان
تمرینات طول عمر، برخی از پاسخ های انعطاف پذیر تنظیم مجدد را پس از یک محرک ورزشی حاد در عضلات اسکلت انسان سالم حفظ می کند
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کلمات کلیدی
HSP72HSP27CAT3-NTeNOSnNOSSOD2SOD1Free radicals - رادیکال آزادRedox - ردوکس(اکسایش و کاهش)RONS - رونendothelial nitric oxide synthase - سنتاز اکسید نیتریک اندوتلیالneuronal nitric oxide synthase - سنتاز اکسید نیتریک عصبیsuperoxide dismutase 1 - سوپر اکسید دیسموتاز 1Superoxide dismutase 2 - سوکسوکس دیسموتاز 2Skeletal muscle - عضله اسکلتیexercise - ورزشPeroxiredoxin 5 - پراکسی اوردوکسین 5Heat shock protein 27 - پروتئین شوک حرارت 27Heat shock protein 72 - پروتئین شوک حرارت 72Catalase - کاتالازReactive oxygen and nitrogen species - گونه های اکسیژن و نیتروژن واکنش پذیرReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
چکیده انگلیسی
Several redox-regulated responses to an acute exercise bout fail in aged animal skeletal muscle, including the ability to upregulate the expression of antioxidant defense enzymes and heat shock proteins (HSPs). These findings are generally derived from studies on sedentary rodent models and thus may be related to reduced physical activity and/or intraspecies differences as opposed to aging per se. This study, therefore, aimed to determine the influence of age and training status on the expression of HSPs, antioxidant enzymes, and NO synthase isoenzymes in quiescent and exercised human skeletal muscle. Muscle biopsy samples were obtained from the vastus lateralis before and 3 days after an acute high-intensity-interval exercise bout in young trained, young untrained, old trained, and old untrained subjects. Levels of HSP72, PRX5, and eNOS were significantly higher in quiescent muscle of older compared with younger subjects, irrespective of training status. 3-NT levels were elevated in muscles of the old untrained but not the old trained state, suggesting that lifelong training may reduce age-related macromolecule damage. SOD1, CAT, and HSP27 levels were not significantly different between groups. HSP27 content was upregulated in all groups studied postexercise. HSP72 content was upregulated to a greater extent in muscle of trained compared with untrained subjects postexercise, irrespective of age. In contrast to every other group, old untrained subjects failed to upregulate CAT postexercise. Aging was associated with a failure to upregulate SOD2 and a downregulation of PRX5 in muscle postexercise, irrespective of training status. In conclusion, lifelong training is unable to fully prevent the progression toward a more stressed muscular state as evidenced by increased HSP72, PRX5, and eNOS protein levels in quiescent muscle. Moreover, lifelong training preserves some (e.g., CAT) but not all (e.g., SOD2, HSP72, PRX5) of the adaptive redox-regulated responses after an acute exercise bout. Collectively, these data support many but not all of the findings from previous animal studies and suggest parallel aging effects in humans and mice at rest and after exercise that are not modulated by training status in human skeletal muscle.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 70, May 2014, Pages 23-32
Journal: Free Radical Biology and Medicine - Volume 70, May 2014, Pages 23-32
نویسندگان
J.N. Cobley, G.K. Sakellariou, D.J. Owens, S. Murray, S. Waldron, W. Gregson, W.D. Fraser, J.G. Burniston, L.A. Iwanejko, A. McArdle, J.P. Morton, M.J. Jackson, G.L. Close,