Role of satellite cells in skeletal muscle plasticity: Beyond muscle regeneration

Tamura, Kozo; Furuichi, Yukio; Manabe, Yasuko; Fujii, Nobuharu

doi:10.7600/jpfsm.6.89

Cited by 2 publications

(2 citation statements)

References 41 publications

(45 reference statements)

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“…The satellite cell, an astrocyte-like stem cell, is thought to have a functional role in muscle plasticity. Tamura et al [ 88 , 89 , 90 ] noted in animal studies that aerobic exercise increased the number of satellite cells, but the proliferation was uncoupled from fusion. When the depletion of satellite cells in wheel running was investigated in genetically altered mice (Pax7/DTA) with tamoxifen administration, it was found that voluntary running performance was decreased and proprioception was impaired, possibly due to disruption of muscle spindle fibers [ 91 ].…”

Section: Cox-1 Cox-2 Pge2 Gdnf Ngf and Glutamate Signaling Patmentioning

confidence: 99%

Delayed Onset Muscle Soreness (DOMS): The Repeated Bout Effect and Chemotherapy-Induced Axonopathy May Help Explain the Dying-Back Mechanism in Amyotrophic Lateral Sclerosis and Other Neurodegenerative Diseases

Sonkodi

2021

Brain Sciences

138

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Delayed onset muscle soreness (DOMS) is hypothesized to be caused by glutamate excitotoxicity-induced acute compression axonopathy of the sensory afferents in the muscle spindle. Degeneration of the same sensory afferents is implicated in the disease onset and progression of amyotrophic lateral sclerosis (ALS). A series of “silent” acute compression proprioceptive axonopathies with underlying genetic/environmental factors, damaging eccentric contractions and the non-resolving neuroinflammatory process of aging could lead to ALS disease progression. Since the sensory terminals in the muscle spindle could not regenerate from the micro-damage in ALS, unlike in DOMS, the induced protective microcircuits and their long-term functional plasticity (the equivalent of the repeated bout effect in DOMS) will be dysfunctional. The acute stress invoking osteocalcin, bradykinin, COX1, COX2, GDNF, PGE2, NGF, glutamate and N-methyl-D-aspartate (NMDA) receptors are suggested to be the critical signalers of this theory. The repeated bout effect of DOMS and the dysfunctional microcircuits in ALS are suggested to involve several dimensions of memory and learning, like pain memory, inflammation, working and episodic memory. The spatial encoding of these memory dimensions is compromised in ALS due to blunt position sense from the degenerating proprioceptive axon terminals of the affected muscle spindles. Dysfunctional microcircuits progressively and irreversibly interfere with postural control, with motor command and locomotor circuits, deplete the neuroenergetic system, and ultimately interfere with life-sustaining central pattern generators in ALS. The activated NMDA receptor is suggested to serve the “gate control” function in DOMS and ALS in line with the gate control theory of pain. Circumvention of muscle spindle-loading could be a choice of exercise therapy in muscle spindle-affected neurodegenerative diseases.

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Section: Cox-1 Cox-2 Pge2 Gdnf Ngf and Glutamate Signaling Patmentioning

confidence: 99%

Delayed Onset Muscle Soreness (DOMS): The Repeated Bout Effect and Chemotherapy-Induced Axonopathy May Help Explain the Dying-Back Mechanism in Amyotrophic Lateral Sclerosis and Other Neurodegenerative Diseases

Sonkodi

2021

Brain Sciences

138

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“…Satellite cells are muscle stem cells that play a crucial role in muscle growth during hypertrophy and regeneration process (Tamura et al, 2017). Different growth factors and cellular events regulate the activation of muscle satellite cells during skeletal muscle regeneration that occurs following a myofibril damage, including the proliferation of satellite cells (Bazgir et al, 2017).…”

Section: Skeletal Muscle Plasticitymentioning

confidence: 99%

Myostatin and plasticity of skeletal muscle tissue

Pagliara¹,

Nasso²,

Arillo³

et al. 2019

Journal of Human Sport and Exercise - 2019 - Summer Conferences of Sports Science

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Skeletal muscle is an extremely plastic tissue for its ability to respond to different stimuli such as physiological variation and external stress. Muscle hypertrophy involves an increase in muscle mass, changes in myofibril composition and adaptation of metabolic pathways. Plasticity of skeletal muscle in response to exercise training is also caused by proliferation and differentiation of the satellite muscle stem cells in response to various growth and differentiation factors. This process is mainly mediated by myokines secreted during skeletal muscle contraction. Myokines are proteins that act as hormones both locally in the muscle and/or in an endocrine manner in other organs, mainly liver, brain and adipose tissue. Myostatin, known as growth differentiation factor-8, a myokine member of transforming growth factor-b (TGF-b) superfamily, can act on muscle cells in an autocrine manner leading to inhibition of muscle myogenesis. Muscle myostatin expression and its plasma concentration are downregulated after acute and long-term physical exercise thus allowing muscle hypertrophy. In addition, myostatin is correlated to obesity and insulin resistance for its ability to affect energy metabolism and insulin-sensitivity in muscle cells, respectively. These findings reveal that myostatin may have potential therapeutic applications to treat muscle atrophy diseases in humans. Even in sports, drugs able to inhibit myostatin expression can lead athletes to increase their sport performance. Here, we present a brief overview of myostatin and its role in biological mechanisms involved in exercise-induced plasticity of skeletal muscle.

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Role of satellite cells in skeletal muscle plasticity: Beyond muscle regeneration

Cited by 2 publications

References 41 publications

Delayed Onset Muscle Soreness (DOMS): The Repeated Bout Effect and Chemotherapy-Induced Axonopathy May Help Explain the Dying-Back Mechanism in Amyotrophic Lateral Sclerosis and Other Neurodegenerative Diseases

Delayed Onset Muscle Soreness (DOMS): The Repeated Bout Effect and Chemotherapy-Induced Axonopathy May Help Explain the Dying-Back Mechanism in Amyotrophic Lateral Sclerosis and Other Neurodegenerative Diseases

Myostatin and plasticity of skeletal muscle tissue

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