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Excitation-Contraction Coupling in Skeletal Muscles

Excitation-Contraction Coupling in Skeletal Muscles

Excitation-contraction coupling is a series of events that occur between generating an action potential and initiating a muscle contraction. It occurs at the triad, a structure found in skeletal muscle fibers that comprise a T-tubule and terminal cisternae of the sarcoplasmic reticulum on each side. These triads are visible in longitudinally sectioned muscle fibers. They are typically located at the A-I junction — the junction between the A and I bands of the sarcomere.
When an action...

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...

Smooth Muscle Contraction

Smooth Muscle Contraction

Smooth muscle contraction is a complex process vital for various bodily functions, from maintaining blood vessel tension to facilitating the movement of food through the digestive tract. Unlike striated muscles, smooth muscle contraction begins more slowly and lasts longer.
The onset of contraction is triggered by an increase in calcium ions within the sarcoplasm, similar to the process in striated muscle. However, smooth muscles have a relatively smaller reservoir of the sarcoplasmic...

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 Contraction

Muscle Contraction

In skeletal muscles, acetylcholine is released by nerve terminals at the motor endplate—the point of synaptic communication between motor neurons and muscle fibers. The binding of acetylcholine to its receptors on the sarcolemma allows entry of sodium ions into the cell and triggers an action potential in the muscle cell. Thus, electrical signals from the brain are transmitted to the muscle. Subsequently, the enzyme acetylcholinesterase breaks down acetylcholine to prevent excessive...

Muscle Contraction

Muscle Contraction

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Related Experiment Video

Updated: Jan 5, 2026

Assessment of Myofilament Ca2+ Sensitivity Underlying Cardiac Excitation-contraction Coupling

Assessment of Myofilament Ca2+ Sensitivity Underlying Cardiac Excitation-contraction Coupling

Published on: August 1, 2016

Evolution of Excitation-Contraction Coupling.

John James Mackrill¹, Holly Alice Shiels²

¹Department of Physiology, School of Medicine, University College Cork, Cork, Ireland. J.Mackrill@ucc.ie.

Advances in Experimental Medicine and Biology

|October 25, 2019

Summary

Calcium-induced calcium-release (CICR) is an ancient mechanism, while depolarization-induced calcium-release (DICR) evolved in vertebrates. Gene duplications and losses shaped these excitation-contraction coupling components across vertebrate evolution.

Keywords:

Evolution Excitation-contraction coupling Junctophilin Ryanodine receptor Voltage-gated Ca2+ channel Whole-genome duplication

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Last Updated: Jan 5, 2026

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Area of Science:

Evolutionary biology
Molecular biology
Physiology

Background:

Mammalian cardiomyocytes use Ca2+-induced Ca2+-release (CICR) via L-type voltage-gated Ca2+ channels (VGCCs) and ryanodine receptors (RyR2).
Mammalian skeletal muscles use depolarization-induced Ca2+-release (DICR) via VGCCs and RyR1 channels.

Purpose of the Study:

To explore the evolutionary history of genes encoding VGCCs, RyRs, and junctophilins (JPHs), key proteins in excitation-contraction coupling (ECC).
To determine the evolutionary origins of CICR and DICR mechanisms.

Main Methods:

Genome-wide survey of genes encoding VGCCs, RyRs, and JPHs in animals and their relatives.
Comparative analysis of protein features related to DICR across different taxonomic groups.

Main Results:

Non-vertebrate eukaryotes possess single or no homologues of VGCCs, RyRs, and JPHs.
Molecular features for DICR are unique to vertebrates, suggesting DICR is a vertebrate innovation.
Vertebrates exhibit multiple homologues of ECC proteins, arising from whole genome duplication events, with subsequent diversification across clades.

Conclusions:

CICR represents the ancestral form of ECC, with DICR emerging as a vertebrate-specific adaptation.
Evolutionary processes, including gene duplication and loss, have shaped the diversity of ECC components in vertebrates.
Teleost fish display a highly derived form of DICR, with CaV1.1 VGCCs lacking channel activity.