Clenbuterol accelerates recovery after immobilization-induced atrophy of rat hindlimb muscle

Suzuki, Hiroyoshi; Yoshikawa, Yuki; Tsujimoto, Hisaya; Kitaura, Takashi; Muraoka, Isao

doi:10.1016/j.acthis.2019.151453

Cited by 12 publications

(8 citation statements)

References 35 publications

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“…Various models of sarcopenia have been previously used, such as denervation, cast immobilization, and hindlimb unloading [38]. Previous studies have shown that hindlimbimmobilization significantly reduced muscle mass, exercise endurance, grip strength, and muscle fiber CSA [43][44][45]. Our study showed similar changes, and, thus, we verified the pathogenesis of sarcopenia by hindlimb immobilization.…”

Section: Discussionsupporting

confidence: 84%

Oyster Hydrolysates Attenuate Muscle Atrophy via Regulating Protein Turnover and Mitochondria Biogenesis in C2C12 Cell and Immobilized Mice

Jeon

Choung

2021

Nutrients

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Sarcopenia, also known as skeletal muscle atrophy, is characterized by significant loss of muscle mass and strength. Oyster (Crassostrea gigas) hydrolysates have anti-cancer, antioxidant, and anti-inflammation properties. However, the anti-sarcopenic effect of oyster hydrolysates remains uninvestigated. Therefore, we prepared two different oyster hydrolysates, namely TGPN and PNY. This study aimed to determine the anti-muscle atrophy efficacy and molecular mechanisms of TGPN and PNY on both C2C12 cell lines and mice. In vitro, the TGPN and PNY recovered the dexamethasone-induced reduction in the myotube diameters. In vivo, TGPN and PNY administration not only improved grip strength and exercise endurance, but also attenuated the loss of muscle mass and muscle fiber cross-sectional area. Mechanistically, TGPN and PNY increased the expression of protein synthesis-related protein levels via phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of the rapamycin pathway, and reduced the expression of protein degradation-related protein levels via the PI3K/Akt/forkhead box O pathway. Also, TGPN and PNY stimulated NAD-dependent deacetylase sirtuin-1(SIRT1), peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α), nuclear respiratory factor 1,2, mitochondrial transcription factor A, along with mitochondrial DNA content via SIRT1/PGC-1α signaling. These findings suggest oyster hydrolysates could be used as a valuable natural material that inhibits skeletal muscle atrophy via regulating protein turnover and mitochondrial biogenesis.

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Section: Discussionsupporting

confidence: 84%

Oyster Hydrolysates Attenuate Muscle Atrophy via Regulating Protein Turnover and Mitochondria Biogenesis in C2C12 Cell and Immobilized Mice

Jeon

Choung

2021

Nutrients

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“…Recent studies showed that immobilization significantly reduced muscle strength, mass, and the CSA of muscle fiber [33,43]. Our findings showed a significant decline in those mentioned above and also total protein content.…”

Section: Discussionsupporting

confidence: 70%

Soluble Whey Protein Hydrolysate Ameliorates Muscle Atrophy Induced by Immobilization via Regulating the PI3K/Akt Pathway in C57BL/6 Mice

Shin

Park²,

Ahn³

et al. 2020

Nutrients

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Sarcopenia, a loss of skeletal muscle mass and function, is prevalent in older people and associated with functional decline and mortality. Protein supplementation is necessary to maintain skeletal muscle mass and whey protein hydrolysates have the best nutrient quality among food proteins. In the first study, C57BL/6 mice were subjected to immobilization for 1 week to induce muscle atrophy. Then, mice were administered with four different whey protein hydrolysates for 2 weeks with continuous immobilization. Among them, soluble whey protein hydrolysate (WP-S) had the greatest increase in grip strength, muscle weight, and cross-sectional area of muscle fiber than other whey protein hydrolysates. To investigate the molecular mechanism, we conducted another experiment with the same experimental design. WP-S significantly promoted the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway and inhibited the PI3K/Akt/forkhead box O (FoxO) pathway. In addition, it increased myosin heavy chain (MyHC) expression in both the soleus and quadriceps and changed MyHC isoform expressions. In conclusion, WP-S attenuated muscle atrophy induced by immobilization by enhancing the net protein content regulating muscle protein synthesis and degradation. Thus, it is a necessary and probable candidate for developing functional food to prevent sarcopenia.

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“…While the misuse of β 2 ‐agonists (including clenbuterol) as an image‐ and performance‐enhancement drug has been documented within the athletic community [45], the mechanisms by which these sympathomimetic agents confer muscle growth and reduce atrophy are ill‐defined [46]. Recent studies have identified increased myonuclear accretion in fast‐twitch muscles of adult male rats [47], as well as elevated cAMP/PKA and Akt2 signaling in resistance‐trained young male adults [48] as putative molecular adaptations. Whether these mechanisms are conserved during the neonatal stage of muscle development must be further investigated to establish concrete insights into β 2 ‐agonists as a potential therapy for reversing muscle wasting in younger patients.…”

Section: Discussionmentioning

confidence: 99%

The role of sympathetic innervation in neonatal muscle growth and neuromuscular contractures

et al. 2023

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Neonatal brachial plexus injury (NBPI), a leading cause of pediatric upper limb paralysis, results in disabling and incurable muscle contractures that are driven by impaired longitudinal growth of denervated muscles. A rare form of NBPI, which maintains both afferent and sympathetic muscle innervation despite motor denervation, protects against contractures. We have previously ruled out a role for NRG/ErbB signaling, the predominant pathway governing antegrade afferent neuromuscular transmission, in modulating the formation of contractures. Our current study therefore investigated the contributions of sympathetic innervation of skeletal muscle in modulating NBPI‐induced contractures. Through chemical sympathectomy and pharmacologic modification with a β2‐adrenergic agonist, we discovered that sympathetic innervation alone is neither required nor sufficient to modulate contracture formation in neonatal mice. Despite this, sympathetic innervation plays an intriguing sex‐specific role in mediating neonatal muscle growth, as the cross‐sectional area (CSA) and volume of normally innervated male muscles were diminished by ablation of sympathetic neurons and increased by β‐adrenergic stimulation. Intriguingly, the robust alterations in CSA occurred with minimal changes to normal longitudinal muscle growth as determined by sarcomere length. Instead, β‐adrenergic stimulation exacerbated sarcomere overstretch in denervated male muscles, indicating potentially discrete regulation of muscle width and length. Future investigations into the mechanistic underpinnings of these distinct aspects of muscle growth are thus essential for improving clinical outcomes in patients affected by muscle disorders in which both length and width are affected.

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Clenbuterol accelerates recovery after immobilization-induced atrophy of rat hindlimb muscle

Cited by 12 publications

References 35 publications

Oyster Hydrolysates Attenuate Muscle Atrophy via Regulating Protein Turnover and Mitochondria Biogenesis in C2C12 Cell and Immobilized Mice

Oyster Hydrolysates Attenuate Muscle Atrophy via Regulating Protein Turnover and Mitochondria Biogenesis in C2C12 Cell and Immobilized Mice

Soluble Whey Protein Hydrolysate Ameliorates Muscle Atrophy Induced by Immobilization via Regulating the PI3K/Akt Pathway in C57BL/6 Mice

The role of sympathetic innervation in neonatal muscle growth and neuromuscular contractures

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