Volume 15, Issue 1 (volume 15, number 1 2023)                   IJDO 2023, 15(1): 59-65 | Back to browse issues page


XML Print


Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:

Khaledi N, Soleimani Dehnavi S, Abbasi S. The Effect of High-Intensity Interval Training on Apoptotic-Related Genes in Skeletal Muscle and Serumic TNF-Alpha of Diabetic Rats. IJDO 2023; 15 (1) :59-65
URL: http://ijdo.ssu.ac.ir/article-1-779-en.html
Associate Professor, Department of Exercise Physiology, Faculty of Physical Education, Kharazmi University, Tehran, Iran.
Abstract:   (330 Views)
Objective: Diabetes is characterized by a comprehensive increase in apoptosis, mitochondrial dysfunction, and inflammation in skeletal muscle. Impaired mitochondrial function in skeletal muscle leads to an increase in Cytochrome C and Caspase-9, and muscle performance is reduced consequently. Exercise training through decreasing inflammatory factors and increasing anti-inflammatory elements prevents apoptosis pathways.
Materials and Methods: Forty male Wistar rats (150±10 g, 8 weeks age) were assigned to 4 groups: control (C), diabetes (D), high-intensity interval training (HIIT), and diabetes high-intensity interval training (DHIIT). Diabetes was induced with intraperitoneal injections of Streptozotocin (STZ) and blood sugar higher than 250 was considered diabetic. The effects of six weeks of HIIT on soleus muscles, Cytochrome C, and Caspase-9 gene expression, as well as evaluation of tumor necrosis factor-alpha (TNF-α) in serum were evaluated using Real-Time PCR  and ELISA techniques respectively.
Results: In comparison with C group Diabetes has significantly increased the Cytochrome C (P= 0.001) and caspase-9 (P= 0.003). However, HIIT training in diabetic rats significantly decreased the Cytochrome C (P= 0.001) and caspase-9 (P= 0.008) in comparison of D group. Also, TNFα (P= 0.01) increased in the D group in comparison with C and DHIIT group (P= 0.001). In comparison between DHIIT groups in HIIT groups, has a significant increase in time to exhaustion post test than pretest (P= 0.001).
Conclusion: It seems that HIIT training decreases intrinsic factors of the apoptosis pathway by decreasing inflammatory factors which leads to significant improvement in skeletal muscle function and overall health in diabetic rats.
 
Full-Text [PDF 657 kb]   (210 Downloads)    
Type of Study: Research | Subject: Special
Received: 2022/10/26 | Accepted: 2023/01/10 | Published: 2023/03/19

References
1. Fujimaki S, Kuwabara T. Diabetes-induced dysfunction of mitochondria and stem cells in skeletal muscle and the nervous system. International Journal of Molecular Sciences. 2017;18(10):2147.
2. Heo JW, Yoo SZ, No MH, Park DH, Kang JH, Kim TW, et al. Exercise training attenuates obesity-induced skeletal muscle remodeling and mitochondria-mediated apoptosis in the skeletal muscle. International Journal of Environmental Research and Public Health. 2018;15(10):2301.
3. Skelly LE, Gillen JB, Frankish BP, MacInnis MJ, Godkin FE, Tarnopolsky MA, et al. Human skeletal muscle fiber type-specific responses to sprint interval and moderate-intensity continuous exercise: acute and training-induced changes. Journal of Applied Physiology. 2021;130(4):1001-14.
4. Winkler G, Lakatos P, Nagy Z, Speer G. Elevated serum tumor necrosis factor-(alpha) and endothelin 1 levels correlate with increased C-peptide concentration in android type obesity. Diabetes Care. 1998;21(10):1778.
5. Khalafi M, Symonds ME. The impact of high‐intensity interval training on inflammatory markers in metabolic disorders: A meta‐analysis. Scandinavian journal of medicine & science in sports. 2020;30(11):2020-36.
6. D'arcy MS. Cell death: a review of the major forms of apoptosis, necrosis and autophagy. Cell biology international. 2019;43(6):582-92.
7. Borisov AB, Carlson BM. Cell death in denervated skeletal muscle is distinct from classical apoptosis. The Anatomical Record: An Official Publication of the American Association of Anatomists. 2000;258(3):305-18.https://doi.org/10.1002/(SICI)1097-0185(20000301)258:3<305::AID-AR10>3.0.CO;2-A. [DOI:10.1002/(SICI)1097-0185(20000301)258:33.0.CO;2-A.]
8. Behaein B, Abednatanzi H, Gholami M, Ghazalian F. Apoptotic changes of cardiac tissue after HIIT and thyme honey in type 2 diabetic rats. Journal of Applied Health Studies in Sport Physiology. 2022;9(2):23-36.(in Persian)
9. Yoo SZ, No MH, Heo JW, Chang E, Park DH, Kang JH, et al. Effects of a single bout of exercise on mitochondria-mediated apoptotic signaling in rat cardiac and skeletal muscles. Journal of exercise rehabilitation. 2019;15(4):512.
10. Abbasi S, Khaledi N, Askari H. High intensity interval training increases the expression of hippocampus BDNF gene and decreases the serum tnf-α in Diabetic Rat. Medical Journal of Tabriz University of Medical Sciences. 2020;42(5):591-600.(in Persian)
11. Sishi B, Loos B, Ellis B, Smith W, du Toit EF, Engelbrecht AM. Diet‐induced obesity alters signalling pathways and induces atrophy and apoptosis in skeletal muscle in a prediabetic rat model. Experimental physiology. 2011;96(2):179-93.
12. Molanouri Shamsi M, Hassan ZH, Gharakhanlou R, Quinn LS, Azadmanesh K, Baghersad L, et al. Expression of interleukin-15 and inflammatory cytokines in skeletal muscles of STZ-induced diabetic rats: effect of resistance exercise training. Endocrine. 2014;46:60-9.
13. Songstad NT, Kaspersen KH, Hafstad AD, Basnet P, Ytrehus K, Acharya G. Effects of high intensity interval training on pregnant rats, and the placenta, heart and liver of their fetuses. PloS one. 2015;10(11):e0143095.
14. Yu T, Sungelo MJ, Goldberg IJ, Wang H, Eckel RH. Streptozotocin-treated high fat fed mice: a new type 2 diabetes model used to study canagliflozin-induced alterations in lipids and lipoproteins. Hormone and Metabolic Research. 2017;49(05):400-6.
15. Liu XY, Shi JH, Du WH, Fan YP, Hu XL, Zhang CC, et al. Glucocorticoids decrease body weight and food intake and inhibit appetite regulatory peptide expression in the hypothalamus of rats. Experimental and therapeutic medicine. 2011 ;2(5):977-84.
16. Lv YQ, Yuan L, Sun Y, Dou HW, Su JH, Hou ZP, et al. Long-term hyperglycemia aggravates α-synuclein aggregation and dopaminergic neuronal loss in a Parkinson's disease mouse model. Translational Neurodegeneration. 2022;11(1):14.
17. Roberts CK, Hevener AL, Barnard RJ. Metabolic syndrome and insulin resistance: underlying causes and modification by exercise training. Comprehensive physiology. 2013;3(1):1-58.
18. Ferrannini E, Haffner SM, Mitchell BD, Stern MP. Hyperinsulinaemia: the key feature of a cardiovascular and metabolic syndrome. Diabetologia. 1991;34:416-22.
19. Mirzendedel Z, Attarzadeh H, Bijeh N, Raouf SA. A comparison of the effects of twelve weeks combined training with different ordering on CTRP3, TNF-α, IL6 and insulin resistance in women with type 2 diabetes. Iranian Journal of Endocrinology and Metabolism. 2019;21(4).(in Persian)
20. Hassanpour G, Nikbakht H, Azarbayjani MA, Shakeri N, Natanzi HA. Effect of Interval and Continued Exercises with Crocin on Bax/Bcl-2 in Diabetic Obese Rats. Iranian journal of diabetes and obesity. 2019, 11(3):196-99.
21. Heo JW, No MH, Park DH, Kang JH, Seo DY, Han J, et al. Effects of exercise on obesity-induced mitochondrial dysfunction in skeletal muscle. The Korean Journal of Physiology & Pharmacology. 2017;21(6):567-77.
22. Boutcher SH. High-intensity intermittent exercise and fat loss. Journal of obesity. 2011;2011.

Add your comments about this article : Your username or Email:
CAPTCHA

Rights and permissions
Creative Commons License This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

© 2024 CC BY-NC 4.0 | Iranian Journal of Diabetes and Obesity

Designed & Developed by : Yektaweb