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

نویسندگان

1 استاد دانشگاه گیلان

2 دانشجوی دکتری فیزیولوژی ورزشی

چکیده

هدف: هدف از این مطالعه بررسی اثر فعالیت هوازی با و بدون محدودیت جریان خون (BFR) بر لاکتات، کورتیزول پلاسما و محتوای پروتئین PGC-1α عضله بود.
روش‌شناسی: پنج مرد سالم تمرین نکرده (با میانگین و خطای معیار سن: 02/1±4/33 سال؛ توده بدن: 69/4±64/79 کیلوگرم؛ قد: 02/9±4/173 سانتی متر؛ چربی بدن: 22/2±97/18 درصد) در دو وهله جداگانه مورد مطالعه قرار گرفتند: (1) فعالیت هوازی به همراه BFR شامل راه رفتن بر روی تردمیل با شدت 40% از توان هوازی بیشینه (VO2max) و (2) راه رفتن در شرایط مشابه بدون BFR (به عنوان کنترل). نمونه های بیوپسی عضلانی قبل و 3 ساعت پس از هر وهله فعالیت از عضله پهن جانبی برای تعیین بیان پروتئین PGC-1α گرفته شد، نمونه های خونی نیز قبل از فعالیت، بلافاصله بعد از فعالیت و 2 ساعت بعد فعالیت جهت بررسی تغییرات لاکتات و کورتیزول خون از سیاهرگ بازویی گرفته شد.  
یافته‌ها: نتایج نشان داد که محتوای پروتئین PGC-1α سه ساعت پس از یک وهله فعالیت هوازی با BFR به طور معنی‌داری در مقایسه با گروه کنترل افزایش می یابد (05/0>P). لاکتات خون و کورتیزول در هیچ یک از نقطه های زمانی در گروه با و بدون محدودیت جریان خون افزایش معنی‌دار نشان ندادند.
نتیجه‌گیری: نتایج نشان داد که در فعالیت هوازی با BFR، تحریک متابولیکی مکانیسمی برای تنظیم شبکه سیگنالی سلول جهت تحریک بایوژنز میتوکندری نیست. همچنین، بایوژنز میتوکندری یکی از مکانیسم‌های احتمالی افزایش در توان هوازی به همراه تمرین با محدودیت جریان خون است.

کلیدواژه‌ها

عنوان مقاله [English]

The effect of aerobic exercise with and without blood flow restriction on lactate, cortisol and PGC-1α response in human skeletal muscle

نویسندگان [English]

  • B Mirzaei 1
  • A barjaste 2
  • F Rahmani-nia 1

1 Professor in Exercise Physiology, University of Guilan

2 PhD Student in Exercise Physiology, University of Guilan

چکیده [English]

Aim: This study aimed to examine the effect of aerobic exercise with and without BFR on blood lactate, cortisol and PGC-1α response in human skeletal muscle.
Method: On two different occasions, five healthy untrained male subjects (mean±SE; age:  33.4±1.02 years, height: 173.9±4.02 cm, body mass: 79.64±4.69 kg), were required to perform (i) a BFR aerobic exercise at an exercise intensity of 40 % of VO2max; and (ii) similar exercise bouts without BFR (Ctrl). For each condition, baseline and 3 h post-exercise muscle biopsy samples (vastus lateralis) were performed for PGC-1α protein expression analysis. Venous blood samples were also collected at pre-exercise, immediately and 2 h post-exercise to measure changes in blood lactate and serum cortisol.
Results: PGC-1α protein content was significantly higher (P < 0.05) at 3-h post-exercise with BFR compared with Ctrl. Blood lactate and serum cortisol did not significantly change from baseline to immediately after exercise and at 2-h post exercise.
Conclusion: Metabolic stimuli are not a mechanism to mediate cell signaling network responsible for mitochondrial biogenesis. However, the addition of blood flow restriction during aerobic exercise induces an increase in PGC-1α to regulate mitochondrial biogenesis.

کلیدواژه‌ها [English]

  • KAATSU
  • Vascular Occlusion
  • Submaximal Exercise
  • Mitochondrial Biogenesis
  • Muscle Biopsy
  • Blood Lactate
  1. Abe T, Fujita S, Nakajima T, Sakamaki M, Ozaki H, Ogasawara R, Ishii N. (2010b). Effects of low-intensity cycle training with restricted leg blood flow on thigh muscle volume and VO2max in young men. Journal of sports science & medicine 9(3): 452.
  2. Abe T, Kearns CF, Sato Y. (2006). Muscle size and strength are increased following walk training with restricted venous blood flow from the leg muscle, Kaatsu-walk training. J Appl Physiol 100: 1460–1466.
  3. Abe T, Sakamaki M, Fujita S, Ozaki H, Sugaya M, Sato Y, Nakajima T. (2010a). Effects of low-intensity walk training with restricted leg blood flow on muscle strength and aerobic capacity in older adults. Journal of geriatric physical therapy, 33(1): 34-40.
  4. Baar K, Wende AR, Jones TE, Marison M, Nolte LA, Chen MA, Kelly DP, Holloszy JO. (2002). Adaptations of skeletal muscle to exercise: rapid increase in the transcriptional coactivator PGC-1. The FASEB journal. 16(14):1879-86.
  5. Bahreinipour M A, Joukar S, Hovanloo F, Najafipour H, Naderi V, Rajiamirhasani A, Esmaeili-Mahani S. (2018). Mild aerobic training with blood flow restriction increases the hypertrophy index and MuSK in both slow and fast muscles of old rats: Role of PGC-1α. Life sciences 202: 103-109.
  6. Conceição MS, Chacon-Mikahil MP, Telles GD, Libardi CA, Junior EM, Vechin FC, DE AA, Gáspari AF, Brum PC, Cavaglieri CR, Serag S. (2016). Attenuated PGC-1α Isoforms following Endurance Exercise with Blood Flow Restriction. Medicine and science in sports and exercise. 48(9): 1699-707.
  7. Egan B, Zierath JR. (2013). Exercise metabolism and the molecular regulation of skeletal muscle adaptation. Cell metabolism 5;17(2):162-84.
  8. Fujita S, Abe T, Drummond M, Cadenas J, Dreyer H, Sato Y, Volpi E, and Rasmussen BB. (2007). Blood flow restriction during lowintensity resistance exercise increases S6K1 phosphorylation and muscle protein synthesis. J Appl Physiol 103: 903–910.
  9. Garber CE, Blissmer B, Deschenes MR, Franklin BA, Lamonte MJ, Lee IM, Swain DP. (2011). Quantity and quality of exercise for developing and maintaining cardiorespiratory, musculoskeletal, and neuromotor fitness in apparently healthy adults: guidance for prescribing exercise. Medicine & Science in Sports & Exercise, 43(7), 1334-1359.

10. Goto KA, Ishii NA, Kizuka TO, Takamatsu KA. (2005). The impact of metabolic stress on hormonal responses and muscular adaptations. Medicine and science in sports and exercise;37(6):955-63.

11. Handschin C, Choi CS, Chin S, Kim S, Kawamori D, Kurpad AJ, Neubauer N, Hu J, Mootha VK, Kim YB, Kulkarni RN. (2007). Abnormal glucose homeostasis in skeletal muscle–specific PGC-1α knockout mice reveals skeletal muscle–pancreatic β cell crosstalk. The Journal of clinical investigation. Nov 1;117(11):3463-74.

12. Handschin C, Spiegelman B M. (2006). Peroxisome proliferator-activated receptor γ coactivator 1 coactivators, energy homeostasis, and metabolism. Endocrine reviews 27(7): 728-735.

13. Hood DA. (2001). Invited review: contractile activity-induced mitochondrial biogenesis in skeletal muscle.  J Appl Physiol 90: 1137–1157.

14. Jäger S, Handschin C, Pierre J S, Spiegelman B M. (2007). AMP-activated protein kinase (AMPK) action in skeletal muscle via direct phosphorylation of PGC-1α. Proceedings of the National Academy of Sciences 104(29): 12017-12022.

15. Kraemer WJ, Marchitelli L, Gordon SE, Harman E, Dziados JE, Mello R, Frykman P, McCurry D, Fleck SJ. (1990). Hormonal and growth factor responses to heavy resistance exercise protocols. Journal of Applied Physiology;69(4):1442-50.

16. Loenneke J P, Thrower A D, Balapur A, Barnes J T, Pujol T J. (2012). Blood flow–restricted walking does not result in an accumulation of metabolites. Clinical physiology and functional imaging, 32(1): 80-82.

17. Olesen J, Kiilerich K, Pilegaard H. (2010). PGC-1α-mediated adaptations in skeletal muscle. Pflügers Archiv-European Journal of Physiology 460(1): 153-162.

18. Park S, Kim JK, Choi HM, Kim HG, Beekley MD, Nho H. (2010). Increase in maximal oxygen uptake following 2-week walk training with blood flow occlusion in athletes. European journal of applied physiology, 109(4), 591-600.

19. Pearson SJ, Hussain SR. (2015). A Review on the Mechanisms of Blood-Flow Restriction Resistance Training-Induced Muscle Hypertrophy.Sports Medicine, 45(2), 187-200.

20. Pierce J, Clark B, PloutzSnyder L, and Kanaley J. (2006). Growth hormone and muscle function response to skeletal muscle ischemia. J Appl Physiol 101: 1588–1595.

21. Pope ZK, Willardson JM, Schoenfeld BJ. (2013). Exercise and blood flow restriction. The Journal of Strength & Conditioning Research, 27(10), 2914-2926.

22. Smiles WJ, Conceição MS, Telles GD, Chacon-Mikahil MP, Cavaglieri CR, Vechin FC, Libardi CA, Hawley JA, Camera DM. (2017). Acute low-intensity cycling with blood-flow restriction has no effect on metabolic signaling in human skeletal muscle compared to traditional exercise. European journal of applied physiology 117(2): 345-58.

23. Takano H, Morita T, Iida H, Asada K, Kato M, Uno K, Hirose K, Matsumoto A, Takenaka K, Hirata Y, Eto F, Nagai R, Sato Y, and Nakajima T. (2005). Hemodynamic and hormonal response to a short-­‐term low-­‐intensity resistance exercise with a reduction in muscle blood flow. Eur J Appl Physiol 95: 65–73.

24. Uth N, Sørensen H, Overgaard K, Pedersen P K. (2004). Estimation of VO2max from the ratio between HRmax and HRrest–the heart rate ratio method. European journal of applied physiology 91(1): 111-115.

25. Wisløff Uو Nes B M, Janszky I, Støylen A, Karlsen T. (2013). Age‐predicted maximal heart rate in healthy subjects: The HUNT Fitness Study. Scandinavian journal of medicine & science in sports 23(6): 697-704.