Cellular adaptations in soleus muscle during recovery after hindlimb unloading

Oishi, Yasuharu; Ogata, Toru; Yamamoto, Kazumi; Terada, Masahiro; Ohira, Takashi; Ohira, Yoshinobu; Taniguchi, Kohachi; Roy, Roland R.

doi:10.1111/j.1748-1716.2007.01747.x

Cited by 87 publications

(79 citation statements)

References 58 publications

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“…Others using dytrophin staining have also described myonuclear apoptosis and/or loss of myonuclei during atrophy (DupontVersteegden et al, 2006;Guo et al, 2012;Leeuwenburgh et al, 2005;Oishi et al, 2008;Zhu et al, 2013). However, they reported a >30% higher number of defined myonuclei (>2.2 myonuclei per fibre) on 6-10 µm cross-sections (Dupont-Versteegden et al, 2006;Leeuwenburgh et al, 2005;Oishi et al, 2008), suggesting that the population of nuclei included was considerably less selective than in our studies.…”

Section: Are Myonuclei Lost During Atrophy?contrasting

confidence: 49%

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Muscle memory and a new cellular model for muscle atrophy and hypertrophy

Gundersen

2016

Journal of Experimental Biology

134

128

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Memory is a process in which information is encoded, stored, and retrieved. For vertebrates, the modern view has been that it occurs only in the brain. This review describes a cellular memory in skeletal muscle in which hypertrophy is 'remembered' such that a fibre that has previously been large, but subsequently lost its mass, can regain mass faster than naive fibres. A new cell biological model based on the literature, with the most reliable methods for identifying myonuclei, can explain this phenomenon. According to this model, previously untrained fibres recruit myonuclei from activated satellite cells before hypertrophic growth. Even if subsequently subjected to grave atrophy, the higher number of myonuclei is retained, and the myonuclei seem to be protected against the elevated apoptotic activity observed in atrophying muscle tissue. Fibres that have acquired a higher number of myonuclei grow faster when subjected to overload exercise, thus the nuclei represent a functionally important 'memory' of previous strength. This memory might be very long lasting in humans, as myonuclei are stable for at least 15 years and might even be permanent. However, myonuclei are harder to recruit in the elderly, and if the long-lasting muscle memory also exists in humans, one should consider early strength training as a public health advice. In addition, myonuclei are recruited during steroid use and encode a muscle memory, at least in rodents. Thus, extending the exclusion time for doping offenders should be considered.

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Section: Are Myonuclei Lost During Atrophy?contrasting

confidence: 49%

“…However, they reported a >30% higher number of defined myonuclei (>2.2 myonuclei per fibre) on 6-10 µm cross-sections (Dupont-Versteegden et al, 2006;Leeuwenburgh et al, 2005;Oishi et al, 2008), suggesting that the population of nuclei included was considerably less selective than in our studies.…”

Section: Are Myonuclei Lost During Atrophy?contrasting

confidence: 42%

Muscle memory and a new cellular model for muscle atrophy and hypertrophy

Gundersen

2016

Journal of Experimental Biology

134

128

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“…Among several experimental models inducing disuse muscle atrophy, the hindlimb suspension model is a well-designed animal model [5,6,19]. Atrogin-1 and MuRF1 are up-regulated up to 3 fold in hindlimb suspension, immobilization and denervation [4,17].…”

mentioning

confidence: 99%

Protective effect of branched chain amino acids on hindlimb suspension-induced muscle atrophy in growing rats

Jang¹,

Yun²,

Park³

et al. 2015

J. Exerc. Nutr, Biochem.

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Protective effect of branched chain amino acids on hindlimb suspension-induced muscle atrophy in growing rats. JENB., Vol. 19, No. 3, pp.183-189, 2015 [Purpose] The effect of BCAA (branched chain amino acid) administration on muscle atrophy during growth phases is not well known. We investigated whether BCAA administration can prevent the muscle atrophy induced by hindlimb suspension in growing male rats. [Methods] Male Wistar rats were assigned to 1 of 2 groups (n = 7/group): hindlimb suspension and hindlimb suspension with oral BCAA administration (600 mg·kg -1 ·day -1

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“…Probably, pathways related to translational regulation and the apoptotic process could be involved in the soleus muscle adaptation. According to Oishi et al 36 , the apoptotic response could be a key factor that induces atrophy in the soleus muscle.…”

Section: Muscle Response To Joint Inflammationmentioning

confidence: 99%

Effect of tibiotarsal joint inflammation on gene expression and cross-sectional area in rat soleus muscle

Ramírez¹,

Russo²,

Delfino³

et al. 2013

Braz. J. Phys. Ther.

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| Background: Joint inflammation is a common clinical problem in patients treated by physical therapists. The hypothesis of this study is that joint inflammation induces molecular and structural changes in the soleus muscle, which is composed mainly of slow-twitch muscle fibers. Objective: To study the effect of tibiotarsal joint inflammation on muscle fiber cross-sectional area (CSA), gene expression levels (atrogin-1, MuRF1, MyoD, myostatin, p38MAPK, NFκB, TNF-alpha), and TNF-alpha protein in the soleus muscle. Method: Wistar rats were randomly divided into 3 periods (2, 7 and 15 days) and assigned to 4 groups (control, sham, inflammation, and immobilization). Results: In the inflammation group at 2 days, MuRF1 and p38MAPK expression had increased, and NFκB mRNA levels had decreased. At 7 days, myostatin expression had decreased. At 7 and 15 days, this group had muscle fiber CSA reduction. At 2 days, the immobilization group showed increased atrogin-1, MuRF1, NFκB, MyoD, and p38MAPK expressions and reduced muscle fiber CSA. At 7 and 15 days, myostatin mRNA levels had increased, and the CSA had decreased. The sham group showed increased p38MAPK and myostatin expressions at 2 and 7 days, respectively. No changes occurred in TNF-alpha gene or protein expression. Conclusion: Acute joint inflammation induces gene expression related to the proteolytic pathway without reduction in muscle fiber CSA. Chronic joint inflammation induced muscle atrophy without up-regulation of important genes belonging to the proteolytic pathway. Thus, muscle adaptation may differ according to the stage of joint inflammation, which suggests that the therapeutic modalities used by physical therapists at each stage should also be different.Keywords: skeletal muscle; joint disease; gene expression; muscle plasticity; physical therapy; rehabilitation. HOW TO CITE THIS ARTICLERamírez C, Russo TL, Delfino G, Peviani SM, Alcântara C, Salvini TF. Effect of tibiotarsal joint inflammation on gene expression and cross-sectional area in rat soleus muscle. Braz J Phys Ther. 2013 May-June; 17(3):244-254. http://dx

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Cellular adaptations in soleus muscle during recovery after hindlimb unloading

Abstract: Our results indicate that apoptotic mechanisms are involved in the modulation of myonuclear number during chronic unloading and subsequent reloading. Furthermore, it appears that CaN is related to fibre size and phenotype adaptations, but not to apoptotic responses.

Cited by 87 publications

References 58 publications

Muscle memory and a new cellular model for muscle atrophy and hypertrophy

Muscle memory and a new cellular model for muscle atrophy and hypertrophy

Protective effect of branched chain amino acids on hindlimb suspension-induced muscle atrophy in growing rats

Effect of tibiotarsal joint inflammation on gene expression and cross-sectional area in rat soleus muscle

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