High-intensity interval training-induced hypertrophy in gastrocnemius muscle via improved IGF-I/Akt/FoxO and myostatin/Smad signaling pathways in rats
Autor: | Farnoosh Mafi, Fatemeh Shabkhiz, Soheil Biglari, Alireza Ghardashi Afousi |
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Rok vydání: | 2020 |
Předmět: |
0303 health sciences
medicine.medical_specialty biology business.industry 030310 physiology FOXO1 Myostatin Interval training Muscle hypertrophy 03 medical and health sciences Gastrocnemius muscle Endocrinology Physiology (medical) Internal medicine biology.protein medicine business Protein kinase B High-intensity interval training Follistatin |
Zdroj: | Physiology International. 107:220-230 |
ISSN: | 2498-602X |
DOI: | 10.1556/2060.2020.00020 |
Popis: | ObjectiveIt has been shown that high-intensity interval training (HIIT) leads to skeletal muscle hypertrophy; however, its mechanisms of cellular and molecular regulation are still unclear. The purpose of this study was to investigate the effect of HIIT on muscle hypertrophy and major signal transduction pathways.Design12 male rats were randomly divided into two groups: control and HIIT. The exercise group performed 30-min HIIT in each session (5 × 4-min intervals running at 85–95% VO2max separated by 2-min active rest at 55–60% VO2max), 3 days/week for 8 weeks. Muscle fiber cross-sectional area (CSA) and the expression of signal transduction pathway proteins were determined in the gastrocnemius muscle.ResultsIn the HIIT group, the expression of IGF-I, IGF-IR Akt, p-Akt, AMPKα, p-AMPKα and follistatin increased significantly, whereas a significant decrease was observed in the expression of FoxO1, p-FoxO1, myostatin, ActRIIB, Smad2/3 and p-Smad2/3 (P < 0.05). However, there were no significant differences between the HIIT and control groups in the expression of mTOR, p-mTOR, P70S6K, and p-P70S6K (P > 0.05). In addition, CSA and gastrocnemius muscle weight increased significantly in the HIIT group (P < 0.05).ConclusionsHIIT induced muscle hypertrophy by improving IGF-I/Akt/FoxO and myostatin/Smad signal transduction pathways. |
Databáze: | OpenAIRE |
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