Part of the TeachMe Series

Skeletal Muscle

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Original Author(s): Harriet Virely
Last updated: 22nd November 2020
Revisions: 6

Original Author(s): Harriet Virely
Last updated: 22nd November 2020
Revisions: 6

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Skeletal muscle is one of the three types of muscle tissue, alongside cardiac and smooth muscle. It is classified as a striated muscle tissue, which functions to contract and permit movements under voluntary control. This article will discuss the structure of skeletal muscle tissue, its mode of contraction and relevant clinical conditions.

Structure of Skeletal Muscle

Skeletal muscle is composed of bundles of elongated muscle fibres which are cylindrical and multinucleated. Fibres show a characteristic banding pattern with cross-striations of alternating light and dark bands. The light bands are divided by a Z disc (dark transverse line). The functional subunit is known as the sarcomere, and this extends between two Z discs.

Figure 1 – Structure of skeletal muscle

Muscle fibres are surrounded by supportive layers of connective tissue:

  • Endomysium – surrounds individual muscle fibres
  • Perimysium – surrounds a bundle of muscle fibres, forming a fascicle (functional unit)
  • Epimysium – surrounds the entire muscle

Skeletal Muscle Fibre Types

Skeletal muscle fibres differ in the speed at which they contract, the amount of force that they generate, how they produce ATP to meet their energy requirements and their susceptibility to fatigue.

There are three main types of skeletal muscle fibre. Most muscles are composed of a mixture of all three of varying proportions.

Type I

(Slow oxidative)

Type IIa

(Fast oxidative)

Type IIx

(Fast glycolytic)

Fibre size Small Large Very large
Contraction speed Slow Fast Very fast
Force generated Low High Very high
Susceptibility to fatigue Low Medium High
Type of metabolism Oxidative (high mitochondria content) Primarily oxidative, but can switch to glycolysis Anaerobic glycolysis
Role Low intensity, high duration contraction, e.g. postural muscles Short, high intensity contraction, e.g. repeatedly lifting a weight Very short, maximal intensity contraction, e.g. short sprint

 

The Motor Unit

Skeletal muscle is innervated by α-motor neurons, which stimulate its fibres to contract. The cell bodies of α-motor neurons are located in either the ventral horn of the spinal cord (for limbs and trunk muscles) or in the motor nuclei of the brainstem (for head and face muscles).

A motor unit is defined as an α-motor neuron and the group of individual muscle fibres that it innervates. A single muscle fibre is only innervated by one α-motor neuron, but each α-motor neuron can innervate a variable number of muscle fibres, depending on the muscle type.

Skeletal Muscle Contraction

The neuromuscular junction is a specialised synapse connecting an α-motor neuron and a skeletal muscle fibre.

Skeletal muscle contraction is triggered by an action potential arriving at the neuromuscular junction, causing opening of voltage-gated calcium ion channels. The resulting increase in intracellular Ca2+ causes vesicles containing acetylcholine (ACh) to release their contents into the synaptic cleft.

ACh activates nicotinic ACh receptors (a type of ligand gated ion channel) in the muscle fibres’ plasma membrane, resulting in an influx of sodium ions and depolarisation of the muscle fibre membrane potential. This local depolarisation activates voltage-sensitive sodium channels, resulting in generation of an action potential in the skeletal muscle fibre.

Figure 2 – Diagram of a neuromuscular junction

ACh is then rapidly broken down (hydrolysed) in the synaptic cleft by the enzyme acetylcholinesterase to terminate signal transmission and allow membrane repolarisation.

Excitation-Contraction Coupling

Excitation-contraction coupling describes the process whereby an action potential triggers a skeletal muscle fibre to contract.

  1. Action potentials generated at the neuromuscular junction travel along the sarcolemma and down into the transverse tubule (T-tubule) system to depolarise the cell membrane.
  2. Depolarisation of the sarcolemma triggers opening of voltage-gated L-type Ca2+ channels (also known as dihydropyridine receptors), allowing calcium to enter into the cell.
  3. Calcium influx leads to activation of ryanodine receptors located in the sarcoplasmic reticulum (intracellular calcium store), which allows calcium to flow from the sarcoplasmic reticulum into the cytoplasm and further increases intracellular calcium concentration.
  4. Calcium binds to troponin-c, inducing a conformational change which reveals a binding site on actin for the myosin head.
  5. This binding results in ATP hydrolysis, providing energy for the actin and myosin filaments to slide past each other and shorten the sarcomere length, thereby initiating muscle contraction.

Figure 3 – Diagram of excitation-contraction coupling

Relaxation of the muscle fibre is facilitated by calcium being pumped back into the sarcoplasmic reticulum by the sarco/endoplasmic reticulum Ca2+-ATPase (SERCA), reversing the conformational change in the tropomyosin complex and restoring sarcomere length.

Myasthenia gravis

Myasthenia gravis is a neuromuscular disorder characterised by progressive skeletal muscle weakness during sustained activity, which improves following rest. The most commonly affected muscles are those of the eyes and face, resulting in diplopia, ptosis and dysphagia.

It results from production of auto-antibodies blocking or destroying the nicotinic acetylcholine receptors (nAChRs), preventing transmission of the action potential across the neuromuscular junction. Therefore, there is failure of the skeletal muscles to contract.

Figure 4 – Image of right partial ptosis resulting from myasthenia gravis

Myasthenia gravis can be treated using acetylcholinesterase inhibitors such as neostigmine, which prolong the level and duration of ACh signalling at the neuromuscular junction, thereby increasing neuromuscular transmission.