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Relaxation of Skeletal Muscles

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.

Motor Unit Stimulation

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.
The latent period of contraction marks the onset of excitation-contraction coupling, when the action potential propagates across the sarcolemma, preparing the muscle fibers for contraction. As the fibers enter the contraction phase, the...

Cross-bridge Cycle

Cross-bridge Cycle

As muscle contracts, the overlap between the thin and thick filaments increases, decreasing the length of the sarcomere—the contractile unit of the muscle—using energy in the form of ATP. At the molecular level, this is a cyclic, multistep process that involves binding and hydrolysis of ATP, and movement of actin by myosin.

Muscle Stimulation Frequency

Muscle Stimulation Frequency

The contraction strength of muscles is regulated by motor neurons, which modulate the frequency of action potentials dispatched to the motor units based on the body's requirements. This process of varying the muscle stimulation frequency allows muscles to contract with a force that is precisely tailored to the needs of the moment, whether lifting a feather or a heavy box.
Wave summation
At low firing rates, motor neurons induce individual twitch contractions in muscle fibers. These twitches...

Muscle Recovery and Fatigue

Muscle Recovery and Fatigue

Muscle fatigue refers to the decline in a muscle's ability to maintain the force of contraction after prolonged activity. It primarily stems from changes within muscle fibers. Even before experiencing muscle fatigue, one may feel tired and have the urge to stop the activity. This response, known as central fatigue, occurs due to changes in the central nervous system, namely the brain and spinal cord. While there is no single mechanism that induces fatigue, it may serve as a protective response...

Generation of Action Potential in Skeletal Muscles

Generation of Action Potential in Skeletal Muscles

Every cell in the body maintains a membrane potential due to an uneven distribution of positive and negative charges across its plasma membrane. The membrane potential is measured in millivolts and quantifies the difference in charge across the membrane.
Like neurons, muscle cells are also regarded as excitable due to their capacity to change in response to stimuli, primarily due to voltage-gated ion channels embedded in their plasma membranes, which get activated by alterations in the cell's...

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Related Experiment Video

Updated: Jun 6, 2026

Myo-mechanical Analysis of Isolated Skeletal Muscle

Myo-mechanical Analysis of Isolated Skeletal Muscle

Published on: February 22, 2011

Rapid decrease in active tension generated by C2C12 myotubes after termination of artificial exercise.

Hideaki Fujita¹, Minoru Hirano, Kazunori Shimizu

¹Toyota Central R&D Labs Incorporation, Yokomichi, Nagakute, Aichi, 480-1192, Japan.

Journal of Muscle Research and Cell Motility

|December 2, 2010

Summary

Disuse muscle atrophy in C2C12 myotubes causes rapid decreases in active tension and sarcomere structure decay. Artificial exercise quickly restores tension and structure, highlighting the link between sarcomere integrity and muscle function during disuse.

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Published on: November 3, 2013

Area of Science:

Muscle physiology
Cellular biology
Biochemistry

Background:

Sustained artificial exercise increases C2C12 myotube active tension.
Muscle atrophy is a significant concern in various physiological and pathological conditions.

Purpose of the Study:

To investigate the effects of terminating artificial exercise on C2C12 myotube active tension and structure.
To elucidate the molecular mechanisms underlying disuse muscle atrophy.

Main Methods:

C2C12 myotubes subjected to 1 Hz artificial exercise for ~10 days.
Measurement of active tension before, during, and after exercise cessation.
Analysis of ubiquitinated proteins and gene expression (Real-time RT-PCR).
Assessment of sarcomere structure integrity.

Main Results:

Active tension rapidly decreased within 8 hours of exercise termination, returning to baseline levels.
Increased ubiquitinated proteins and altered expression of atrophy-related genes (Smc6, Vegfa, etc.) were observed.
Sarcomere structure, particularly thin filaments, rapidly decayed upon exercise cessation.
Reapplication of exercise restored active tension and sarcomere structure within 8 hours.

Conclusions:

Termination of artificial exercise induces atrophy-like responses in C2C12 myotubes.
Disassembly of sarcomere structure is a key factor in the rapid decrease of active tension during disuse muscle atrophy.
Sarcomere reformation is crucial for the rapid recovery of muscle tension upon re-exercise.