ROS-Mediated Decline in Maximum Ca2+-Activated Force in Rat Skeletal Muscle Fibers following In Vitro and In Vivo Stimulation

We tested the hypothesis that lengthening contractions result in greater injury to skeletal muscle fibers than isometric or shortening contractions. Mice were anesthetized with pentobarbital sodium and secured to a platform maintained at 37 degrees C. The distal tendon of the extensor digitorum longus muscle was attached to a servomotor. A protocol consisting of isometric, shortening, or lengthening contractions was performed. After the contraction protocol the distal tendon was reattached, incisions were closed, and the mice were allowed to recover. The muscles were removed after 1–30 days, and maximum isometric force (Po) was measured in vitro at 37 degrees C. Three days after isometric and shortening contractions and sham operations, histological appearance was not different from control and Po was 80% of the control value. Three days after lengthening contractions, histological sections showed that 37 +/- 4% of muscle fibers degenerated and Po was 22 +/- 3% of the control value. Muscle regeneration, first seen at 4 days, was nearly complete by 30 days, when Po was 84 +/- 3% of the control value. We conclude that, with the protocol used, lengthening, but not isometric or shortening contractions, caused significant injury to muscle fibers.

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Effects of Creatine Supplementation During Resistance Training on Myosin Heavy Chain (MHC) Expression in Rat Skeletal Muscle Fibers

The Journal of Strength and Conditioning Research ◽

10.1519/jsc.0b013e3181aeb103 ◽

2010 ◽

Vol 24 (1) ◽

pp. 88-96 ◽

Cited By ~ 9

Author(s):

Andreo F Aguiar ◽

Danilo H Aguiar ◽

Alan DS Felisberto ◽

Fernanda R Carani ◽

Rachel C Milanezi ◽

...

Keyword(s):

Skeletal Muscle ◽

Resistance Training ◽

Myosin Heavy Chain ◽

Heavy Chain ◽

Muscle Fibers ◽

Creatine Supplementation ◽

Rat Skeletal Muscle ◽

Skeletal Muscle Fibers

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Glycogen Depletion in Rat Skeletal Muscle Fibers During Exercise

Metabolic Adaptation to Prolonged Physical Exercise ◽

10.1007/978-3-0348-5523-5_47 ◽

1975 ◽

pp. 397-401 ◽

Cited By ~ 3

Author(s):

R. B. Armstrong ◽

C. W. Saubert ◽

W. L. Sembrowich ◽

R. E. Shepherd ◽

P. D. Gollnick

Keyword(s):

Skeletal Muscle ◽

Muscle Fibers ◽

Glycogen Depletion ◽

Rat Skeletal Muscle ◽

Skeletal Muscle Fibers

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Rapid dispersal of clustered postsynaptic nuclei following dissociation of skeletal muscle fibers.

Journal of Experimental Biology ◽

10.1242/jeb.199.11.2359 ◽

1996 ◽

Vol 199 (11) ◽

pp. 2359-2367

Author(s):

C Brösamle ◽

D P Kuffler

Keyword(s):

Skeletal Muscle ◽

Synapse Formation ◽

Contractile Activity ◽

Muscle Fibers ◽

Skeletal Muscle Fibers ◽

Synaptic Region ◽

Nuclear Clusters ◽

Specialized Structure

The vertebrate neuromuscular junction is a highly specialized structure containing many unique proteins and an underlying cluster of nuclei. Part of this specialization results from the expression of the genes for these proteins in nuclei clustered in the postsynaptic region. Contractile activity, as well as molecules located in the synaptic extracellular matrix (ECM), have been implicated in the induction of gene expression in these clustered nuclei. The present experiments were aimed at examining whether the presence of the synaptic ECM and presynaptic cells play a role in maintaining the clustering of the nuclei. We describe the normal distribution of nuclei clustered in the synaptic region of intact adult frog, Rana pipiens, skeletal muscle fibers and show that innervation is not required to maintain the nuclear clusters. Even after long-term (4 week) denervation, the clusters remain unchanged. Dissociation of the muscle fibers with proteases that remove ECM, Schwann cells and other satellite cells from the synaptic sites is followed by a rapid (within approximately 1.5 h) and almost complete dispersal of the clustered nuclei. Attempts to recluster the postsynaptic nuclei by the application of ECM components to muscle fibers in vitro were not successful. We propose that a factor or factors, localized in the synaptic ECM as a result of synapse formation and acting via the transmembrane or cytoplasmic domains of their respective receptors, induces the formation of a specialized cytoskeleton in the postsynaptic region that is capable of pulling in or 'trapping' nuclei. The removal of these factors from the ECM by proteases brings about the disorganization of the cytoskeleton and the freeing of the 'trapped' nuclei.

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PEDF-derived peptide promotes skeletal muscle regeneration through its mitogenic effect on muscle progenitor cells

AJP Cell Physiology ◽

10.1152/ajpcell.00344.2014 ◽

2015 ◽

Vol 309 (3) ◽

pp. C159-C168 ◽

Cited By ~ 18

Author(s):

Tsung-Chuan Ho ◽

Yi-Pin Chiang ◽

Chih-Kuang Chuang ◽

Show-Li Chen ◽

Jui-Wen Hsieh ◽

...

Keyword(s):

Skeletal Muscle ◽

Cell Proliferation ◽

Cyclin D1 ◽

Satellite Cell ◽

Muscle Regeneration ◽

Muscle Fibers ◽

Skeletal Muscle Regeneration ◽

Satellite Cell Proliferation

In response injury, intrinsic repair mechanisms are activated in skeletal muscle to replace the damaged muscle fibers with new muscle fibers. The regeneration process starts with the proliferation of satellite cells to give rise to myoblasts, which subsequently differentiate terminally into myofibers. Here, we investigated the promotion effect of pigment epithelial-derived factor (PEDF) on muscle regeneration. We report that PEDF and a synthetic PEDF-derived short peptide (PSP; residues Ser93-Leu112) induce satellite cell proliferation in vitro and promote muscle regeneration in vivo. Extensively, soleus muscle necrosis was induced in rats by bupivacaine, and an injectable alginate gel was used to release the PSP in the injured muscle. PSP delivery was found to stimulate satellite cell proliferation in damaged muscle and enhance the growth of regenerating myofibers, with complete regeneration of normal muscle mass by 2 wk. In cell culture, PEDF/PSP stimulated C2C12 myoblast proliferation, together with a rise in cyclin D1 expression. PEDF induced the phosphorylation of ERK1/2, Akt, and STAT3 in C2C12 myoblasts. Blocking the activity of ERK, Akt, or STAT3 with pharmacological inhibitors attenuated the effects of PEDF/PSP on the induction of C2C12 cell proliferation and cyclin D1 expression. Moreover, 5-bromo-2′-deoxyuridine pulse-labeling demonstrated that PEDF/PSP stimulated primary rat satellite cell proliferation in myofibers in vitro. In summary, we report for the first time that PSP is capable of promoting the regeneration of skeletal muscle. The signaling mechanism involves the ERK, AKT, and STAT3 pathways. These results show the potential utility of this PEDF peptide for muscle regeneration.

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Defective Acetylcholine Receptor Subunit Switch Precedes Atrophy of Slow-Twitch Skeletal Muscle Fibers Lacking ERK1/2 Kinases in Soleus Muscle

Scientific Reports ◽

10.1038/srep38745 ◽

2016 ◽

Vol 6 (1) ◽

Cited By ~ 5

Author(s):

Shuo Wang ◽

Bonnie Seaberg ◽

Ximena Paez-Colasante ◽

Mendell Rimer

Keyword(s):

Skeletal Muscle ◽

Acetylcholine Receptor ◽

Soleus Muscle ◽

Muscle Fibers ◽

Neuromuscular Synapse ◽

Fiber Morphology ◽

Skeletal Muscle Fibers ◽

Slow Twitch

Abstract To test the role of extracellular-signal regulated kinases 1 and 2 (ERK1/2) in slow-twitch, type 1 skeletal muscle fibers, we studied the soleus muscle in mice genetically deficient for myofiber ERK1/2. Young adult mutant soleus was drastically wasted, with highly atrophied type 1 fibers, denervation at most synaptic sites, induction of “fetal” acetylcholine receptor gamma subunit (AChRγ), reduction of “adult” AChRε, and impaired mitochondrial biogenesis and function. In weanlings, fiber morphology and mitochondrial markers were mostly normal, yet AChRγ upregulation and AChRε downregulation were observed. Synaptic sites with fetal AChRs in weanling muscle were ~3% in control and ~40% in mutants, with most of the latter on type 1 fibers. These results suggest that: (1) ERK1/2 are critical for slow-twitch fiber growth; (2) a defective γ/ε-AChR subunit switch, preferentially at synapses on slow fibers, precedes wasting of mutant soleus; (3) denervation is likely to drive this wasting, and (4) the neuromuscular synapse is a primary subcellular target for muscle ERK1/2 function in vivo.

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