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Related Concept Videos

Relaxation of Skeletal Muscles01:29

Relaxation of Skeletal Muscles

The period of muscle contraction primarily influences the duration of stimulation at the neuromuscular junction (NMJ), the presence of free calcium ions in the sarcoplasm, and the availability of energy or ATP to support contractions.
When an action potential reaches the axon terminal, it depolarizes the membrane and opens voltage-gated sodium channels. Sodium ions enter the cell, further depolarizing the presynaptic membrane. This depolarization causes voltage-gated calcium channels to open.
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...
Motor Unit Stimulation01:20

Motor Unit Stimulation

When the neuron of a motor unit fires an action potential, it triggers a series of events, leading to a twitch contraction in the muscle fibers. The process of excitation-contraction coupling is crucial in relaying the action potential to the muscle fibers.
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Satellite Stem Cells and Muscular Dystrophy01:21

Satellite Stem Cells and Muscular Dystrophy

Satellite stem cells or myosatellite cells are quiescent stem cells that Alexander Mauro first identified in 1961. These cells are located between the sarcolemma, the plasma membrane of muscle fibers, and the basal lamina, the connective tissue sheath covering it. These mononucleated cells are activated in response to muscle injury, can transform into myoblasts, and may form or repair muscle fibers. Myosatellite cells can provide additional myonuclei for muscle regeneration or return to a...

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Related Experiment Video

Updated: May 26, 2026

An in vivo Rodent Model of Contraction-induced Injury and Non-invasive Monitoring of Recovery
08:08

An in vivo Rodent Model of Contraction-induced Injury and Non-invasive Monitoring of Recovery

Published on: May 11, 2011

Myonuclear Dynamics After Skeletal Muscle Surgical Injury.

Micah Goeke1, Nathan Serrano1, Pieter Jan Koopmans1,2

  • 1University of Arkansas, Molecular Muscle Mass Regulation Laboratory, Department of Health, Human Performance, and Recreation, Fayetteville, AR, USA.

Biorxiv : the Preprint Server for Biology
|May 25, 2026
PubMed
Summary

Displaced myonuclei in damaged muscle fibers can originate from resident cells, not just satellite cells. This finding challenges existing beliefs and may impact therapeutic strategies for muscle injury repair.

Keywords:
DamageRegenerationSatellite CellsSurgery

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Last Updated: May 26, 2026

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Identification and Analysis of Myogenic Progenitors In Vivo During Acute Skeletal Muscle Injury by High-Dimensional Single-Cell Mass Cytometry
11:02

Identification and Analysis of Myogenic Progenitors In Vivo During Acute Skeletal Muscle Injury by High-Dimensional Single-Cell Mass Cytometry

Published on: December 1, 2023

Area of Science:

  • Muscle physiology
  • Cell biology
  • Regenerative medicine

Background:

  • Displaced myonuclei are a key indicator of skeletal muscle fiber damage.
  • Traditionally, displaced myonuclei have been attributed solely to satellite cell fusion.

Purpose of the Study:

  • To investigate the origin and prevalence of displaced myonuclei following surgical muscle injury.
  • To challenge the dogma that only satellite cells contribute to displaced myonuclei.

Main Methods:

  • Utilized a surgical resection model for muscle injury.
  • Employed in vivo recombination-independent resident myonuclear labeling.
  • Analyzed myosin heavy chain expression and satellite cell populations post-injury.

Main Results:

  • Non-satellite cell-derived (resident) displaced myonuclei were observed 7 days post-injury, in similar proportions to satellite cell-derived ones.
  • A subset of embryonic myosin-expressing fibers contained resident displaced myonuclei.
  • Multiple resident displaced myonuclei were noted in muscle fibers 7 days after injury.
  • Satellite cell numbers did not increase until 7 days post-surgery.

Conclusions:

  • Resident myonuclei contribute to the pool of displaced myonuclei after muscle trauma.
  • The findings suggest that both satellite cell-dependent and independent mechanisms are involved in muscle repair.
  • This research could inform the development of targeted therapies for muscle injury.