Muscle hypertrophy following blood flow-restricted, low-force isometric electrical stimulation in rat tibialis anterior: role for muscle hypoxia
Low-force exercise training with blood flow restriction (BFR) elicits muscle hypertrophy as seen typically after higher-force exercise. We investigated the effects of microvascular hypoxia [i.e., low microvascular O partial pressures (P mvO )] during contractions on muscle hypertrophic signaling, gr...
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Published in | Journal of applied physiology (1985) Vol. 125; no. 1; pp. 134 - 145 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
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01.07.2018
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Abstract | Low-force exercise training with blood flow restriction (BFR) elicits muscle hypertrophy as seen typically after higher-force exercise. We investigated the effects of microvascular hypoxia [i.e., low microvascular O
partial pressures (P mvO
)] during contractions on muscle hypertrophic signaling, growth response, and key muscle adaptations for increasing exercise capacity. Wistar rats were fitted with a cuff placed around the upper thigh and inflated to restrict limb blood flow. Low-force isometric contractions (30 Hz) were evoked via electrical stimulation of the tibialis anterior (TA) muscle. The P mvO
was determined by phosphorescence quenching. Rats underwent acute and chronic stimulation protocols. Whereas P mvO
decreased transiently with 30 Hz contractions, simultaneous BFR induced severe hypoxia, reducing P mvO
lower than present for maximal (100 Hz) contractions. Low-force electrical stimulation (EXER) induced muscle hypertrophy (6.2%, P < 0.01), whereas control group conditions or BFR alone did not. EXER+BFR also induced an increase in muscle mass (11.0%, P < 0.01) and, unique among conditions studied, significantly increased fiber cross-sectional area in the superficial TA ( P < 0.05). Phosphorylation of ribosomal protein S6 was enhanced by EXER+BFR, as were peroxisome proliferator-activated receptor gamma coactivator-1α and glucose transporter 4 protein levels. Fibronectin type III domain-containing protein 5, cytochrome c oxidase subunit 4, monocarboxylate transporter 1 (MCT1), and cluster of differentiation 147 increased with EXER alone. EXER+BFR significantly increased MCT1 expression more than EXER alone. These data demonstrate that microvascular hypoxia during contractions is not essential for hypertrophy. However, hypoxia induced via BFR may potentiate the muscle hypertrophic response (as evidenced by the increased superficial fiber cross-sectional area) with increased glucose transporter and mitochondrial biogenesis, which contributes to the pleiotropic effects of exercise training with BFR that culminate in an improved capacity for sustained exercise. NEW & NOTEWORTHY We investigated the effects of low microvascular O
partial pressures (P mvO
) during contractions on muscle hypertrophic signaling and key elements in the muscle adaptation for increasing exercise capacity. Although demonstrating that muscle hypoxia is not obligatory for the hypertrophic response to low-force, electrically induced muscle contractions, the reduced P mvO
enhanced ribosomal protein S6 phosphorylation and potentiated the hypertrophic response. Furthermore, contractions with blood flow restriction increased oxidative capacity, glucose transporter, and mitochondrial biogenesis, which are key determinants of the pleiotropic effects of exercise training. |
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AbstractList | Low-force exercise training with blood flow restriction (BFR) elicits muscle hypertrophy as seen typically after higher-force exercise. We investigated the effects of microvascular hypoxia [i.e., low microvascular O
partial pressures (P mvO
)] during contractions on muscle hypertrophic signaling, growth response, and key muscle adaptations for increasing exercise capacity. Wistar rats were fitted with a cuff placed around the upper thigh and inflated to restrict limb blood flow. Low-force isometric contractions (30 Hz) were evoked via electrical stimulation of the tibialis anterior (TA) muscle. The P mvO
was determined by phosphorescence quenching. Rats underwent acute and chronic stimulation protocols. Whereas P mvO
decreased transiently with 30 Hz contractions, simultaneous BFR induced severe hypoxia, reducing P mvO
lower than present for maximal (100 Hz) contractions. Low-force electrical stimulation (EXER) induced muscle hypertrophy (6.2%, P < 0.01), whereas control group conditions or BFR alone did not. EXER+BFR also induced an increase in muscle mass (11.0%, P < 0.01) and, unique among conditions studied, significantly increased fiber cross-sectional area in the superficial TA ( P < 0.05). Phosphorylation of ribosomal protein S6 was enhanced by EXER+BFR, as were peroxisome proliferator-activated receptor gamma coactivator-1α and glucose transporter 4 protein levels. Fibronectin type III domain-containing protein 5, cytochrome c oxidase subunit 4, monocarboxylate transporter 1 (MCT1), and cluster of differentiation 147 increased with EXER alone. EXER+BFR significantly increased MCT1 expression more than EXER alone. These data demonstrate that microvascular hypoxia during contractions is not essential for hypertrophy. However, hypoxia induced via BFR may potentiate the muscle hypertrophic response (as evidenced by the increased superficial fiber cross-sectional area) with increased glucose transporter and mitochondrial biogenesis, which contributes to the pleiotropic effects of exercise training with BFR that culminate in an improved capacity for sustained exercise. NEW & NOTEWORTHY We investigated the effects of low microvascular O
partial pressures (P mvO
) during contractions on muscle hypertrophic signaling and key elements in the muscle adaptation for increasing exercise capacity. Although demonstrating that muscle hypoxia is not obligatory for the hypertrophic response to low-force, electrically induced muscle contractions, the reduced P mvO
enhanced ribosomal protein S6 phosphorylation and potentiated the hypertrophic response. Furthermore, contractions with blood flow restriction increased oxidative capacity, glucose transporter, and mitochondrial biogenesis, which are key determinants of the pleiotropic effects of exercise training. Low-force exercise training with blood flow restriction (BFR) elicits muscle hypertrophy as seen typically after higher-force exercise. We investigated the effects of microvascular hypoxia [i.e., low microvascular O 2 partial pressures (P mvO 2 )] during contractions on muscle hypertrophic signaling, growth response, and key muscle adaptations for increasing exercise capacity. Wistar rats were fitted with a cuff placed around the upper thigh and inflated to restrict limb blood flow. Low-force isometric contractions (30 Hz) were evoked via electrical stimulation of the tibialis anterior (TA) muscle. The P mvO 2 was determined by phosphorescence quenching. Rats underwent acute and chronic stimulation protocols. Whereas P mvO 2 decreased transiently with 30 Hz contractions, simultaneous BFR induced severe hypoxia, reducing P mvO 2 lower than present for maximal (100 Hz) contractions. Low-force electrical stimulation (EXER) induced muscle hypertrophy (6.2%, P < 0.01), whereas control group conditions or BFR alone did not. EXER+BFR also induced an increase in muscle mass (11.0%, P < 0.01) and, unique among conditions studied, significantly increased fiber cross-sectional area in the superficial TA ( P < 0.05). Phosphorylation of ribosomal protein S6 was enhanced by EXER+BFR, as were peroxisome proliferator-activated receptor gamma coactivator-1α and glucose transporter 4 protein levels. Fibronectin type III domain-containing protein 5, cytochrome c oxidase subunit 4, monocarboxylate transporter 1 (MCT1), and cluster of differentiation 147 increased with EXER alone. EXER+BFR significantly increased MCT1 expression more than EXER alone. These data demonstrate that microvascular hypoxia during contractions is not essential for hypertrophy. However, hypoxia induced via BFR may potentiate the muscle hypertrophic response (as evidenced by the increased superficial fiber cross-sectional area) with increased glucose transporter and mitochondrial biogenesis, which contributes to the pleiotropic effects of exercise training with BFR that culminate in an improved capacity for sustained exercise. NEW & NOTEWORTHY We investigated the effects of low microvascular O 2 partial pressures (P mvO 2 ) during contractions on muscle hypertrophic signaling and key elements in the muscle adaptation for increasing exercise capacity. Although demonstrating that muscle hypoxia is not obligatory for the hypertrophic response to low-force, electrically induced muscle contractions, the reduced P mvO 2 enhanced ribosomal protein S6 phosphorylation and potentiated the hypertrophic response. Furthermore, contractions with blood flow restriction increased oxidative capacity, glucose transporter, and mitochondrial biogenesis, which are key determinants of the pleiotropic effects of exercise training. |
Author | Obi, Syotaro Inoue, Teruo Nakajima, Toshiaki Kano, Yutaka Toyoda, Shigeru Nakamura, Fumitaka Yamasoba, Tatsuya Koide, Seiichiro Hasegawa, Takaaki Poole, David C Yasuda, Tomohiro |
Author_xml | – sequence: 1 givenname: Toshiaki surname: Nakajima fullname: Nakajima, Toshiaki organization: Department of Cardiovascular Medicine, Dokkyo Medical University and Heart Center, Dokkyo Medical University Hospital , Tochigi , Japan – sequence: 2 givenname: Seiichiro surname: Koide fullname: Koide, Seiichiro organization: Bioscience and Technology Program, Department of Engineering Science, University of Electro-Communications , Tokyo , Japan – sequence: 3 givenname: Tomohiro surname: Yasuda fullname: Yasuda, Tomohiro organization: School of Nursing, Seirei Christopher University, Shizuoka, Japan – sequence: 4 givenname: Takaaki surname: Hasegawa fullname: Hasegawa, Takaaki organization: Department of Cardiovascular Medicine, Dokkyo Medical University and Heart Center, Dokkyo Medical University Hospital , Tochigi , Japan – sequence: 5 givenname: Tatsuya surname: Yamasoba fullname: Yamasoba, Tatsuya organization: Department of Otolaryngology, University of Tokyo , Tokyo , Japan – sequence: 6 givenname: Syotaro surname: Obi fullname: Obi, Syotaro organization: Department of Cardiovascular Medicine and Research Support Center, Dokkyo Medical University , Tochigi , Japan – sequence: 7 givenname: Shigeru surname: Toyoda fullname: Toyoda, Shigeru organization: Department of Cardiovascular Medicine, Dokkyo Medical University and Heart Center, Dokkyo Medical University Hospital , Tochigi , Japan – sequence: 8 givenname: Fumitaka surname: Nakamura fullname: Nakamura, Fumitaka organization: Third Department of Internal Medicine, Teikyo University Chiba Medical Center , Chiba , Japan – sequence: 9 givenname: Teruo surname: Inoue fullname: Inoue, Teruo organization: Department of Cardiovascular Medicine, Dokkyo Medical University and Heart Center, Dokkyo Medical University Hospital , Tochigi , Japan – sequence: 10 givenname: David C surname: Poole fullname: Poole, David C organization: Department of Anatomy, Physiology and Kinesiology, Kansas State University , Manhattan, Kansas – sequence: 11 givenname: Yutaka surname: Kano fullname: Kano, Yutaka organization: Bioscience and Technology Program, Department of Engineering Science, University of Electro-Communications , Tokyo , Japan |
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Title | Muscle hypertrophy following blood flow-restricted, low-force isometric electrical stimulation in rat tibialis anterior: role for muscle hypoxia |
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