Smooth muscle is unstriated, visceral and involuntary. It is found in the walls of vessels and hollow organs and undergoes peristaltic contractions to move contents. For example the ciliary muscle in the eye.
Cardiac muscle is involuntary, striated and forms most of the walls of the chambers of the heart. It has the intrinsic ability to contract and is resistant to fatigue.
Classification
Muscles can be described by:
The orientation of the muscle fibres
Unipennate
Bipennate
Multipennate
Circular
Strap
Fusiform
Their action
Flexors
Flexor digitorum profundus
Extensors
Extensor radialis longus
Their shape
Deltoid (triangle)
Trapezius (trapezius)
Rhomboids (rhomboid)
Gracilis (gracile: slender)
Their position in the body
Frontalis
External oblique
Tibialis anterior
The number of heads (proximal attachments)
Biceps
Tripeps
Quadriceps
Neuromuscular Compartment
Many limb muscles are organised into compartments. Each compartment usually has its own nerve and blood supply. The muscles in a compartment usually work together to produce movement. Muscle compartments are surrounded by a sleeve of deep fascia, which aids venous return when the muscles contract.
Motor Units and Motor
Neural Firing Patterns
The nervous system provides the body with an internal
network that delivers electrical impulses to muscles, which need an impulse
before they can contract. The nervous system is divided into the Central
Nervous System (CNS) and the Peripheral Nervous System (PNS). The PNS can
further be divided into the sensory portion (afferent fibres that transmit to the CNS) and the motor portion
(efferent fibres that conduct impulses away
from the CNS).
Structure of the
Motor Unit
The functional unit of the nervous system is the neurone.
The motor neurone is involved with muscle movement and conducts impulses
towards muscles.
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The cell body contains the nucleus, which is the centre of
operation for the neurone. The dendrites conduct electrical impulses towards
the cell body. The axon carries the electrical impulse away from the cell body
to another neurone or effector organ such as a muscle.
Axons can vary in length, from just a few mm’s to a metre.
They branch at the end into axon terminals whose tips are dilated in to tiny
bulbs called synaptic knobs. The axons is also covered in an insulating layer
of Schwann cells that contain the fatty substance; myelin. This myelin sheath of
a Schawnn cell is not continuous and exhibits gaps along the length of the
nerve fibre known as Nodes of Ranvier. These gaps allow rapid conduction of
impulses along the length of the axon as they jump from one node to the next
via salutatory conduction. The velocity of a nerve impulse transmission in
large myelinated fibres can approach 120 metres per second, which is the
equivalent of over 250 mph. This is 5 to 50 times faster than in unmyelinated
fibres.
Myelin
Myelin is a dielectric (electrically insulating) material
that is composed of about 80% lipid and 20% protein. Some of these proteins are
myelin basic protein (MBP), myelin oligodendrocyte glycoprotein (MOG) and
proteolipid protein (PLP). Myelin is primarily made up of a glycolipid called
galactocerebroside. Sphingomyelin in the form of hydrocarbon chains intertwines
and strengthens the myelin sheath around the axon.
The main purpose of the myelin sheath is to increase the
speed at which impulses propagate along the axon by saltation. Myelin increases
electrical resistance across the cell membrane and decreases capacitance (store
of charge), therefore preventing the electrical current from leaving the axon.
Demyelination is the loss of the myelin sheath insulating
the nerves and is common amongst some neurodegenerative autoimmune diseases,
including MS (where the immune system attacks the CNS), transverse myelitis
(inflammation of the spinal chord that results in limited ability to send and
receive messages in the spinal chord) and Leukodystrophy (progressive
degeneration of the white matter of the brain). When myelin degrades,
conduction of impulses along the nerve can be impaired of lost until the nerve
eventually withers.
Typical symptoms of demyelination include:
- · Blurriness in the central visual field affecting only one eye
- Pain with eye movement
- Double vision
- · Tingling or numbness (neuropathy) in arms, legs, chest or face.
- · Speech impairment
- · Memory loss
- · Heat sensitivity
- · Balance disorder
- · Difficulty controlling bowel movements or urination
- · Fatigue
Propagation of a
Nerve Impulse
At rest, neurones (like all cells) have a negative charge on
the inside compared to the outside. This negative charge is known as the
resting membrane potential and the neurone is said to be polarised. For an
impulse to travel along the neurone, this resting potential has to be changed.
This change in the resting electrical charge is called
depolarisation and it caused by a stimulus allowing an influx of Na into the inside of the neurone, therefore
making the inside more positively charged than the exterior. If this
depolarisation reaches a threshold, then an action potential is reached and the
impulse will travel down the neurone.
The ‘all or none’ law states that a minimum depolarisation
must be reached in order for an impulse to be propagated, otherwise there will
be no impulse. The impulses will travel the length of the axon without a
decrease in voltage and the resting membrane potential must be returned before
another impulse can be propagated.
Repolarisation is accomplished by K flowing from the inside to the outside of the
cell membrane so that the inside is negatively charged compared to the outside.
Neuromuscular
Junctions
Neurones communicate with other neurones at junctions called
synapses. These functions rely on neurotransmitters to carry the impulse across
the small gap so that the propagation can continue. A motor neurone
communicates with a muscle fibre at a side known as the neuromuscular junction.
The neurotransmitter is secreted by the synaptic vesicles in the synaptic knob, and in motor neurones is called acetylcholine. This allows depolarisation of the motor end plate of the sarcolemma of the muscle cell. The amount of fibres that a neurone innervates is related to the muscle’s particular movement function. For example, neurones may control fewer than ten muscle fibres of the eye muscles for fine complex movements but it may also innervate 3000 fibres in large muscles involved in gross movements, such as the rectus femoris.
In a motor unit, the ‘all or none’ law means that there is
never a strong or weak contraction from a motor unit. Either the impulse is
strong enough to activate a contraction of it is not, so either all the fibres
in the motor unit contract or none do.
The all or none law is the principle that the strength by
which a nerve or muscle fibre responds to a stimulus is not dependant on the
strength of the stimulus. If the stimulus is any strength above the threshold,
the nerve or muscle fibre will give a complete response or otherwise no
response at all. It was first established by the American physiologist Henry
Pickering Bowditch in 1871 for the contraction of the heart muscle.
Controlling Strength
The ‘all or none’ law raises the question of how we can
control the strength of contractions and the length of time for which they are
held. To do so the brain sends more signals to more motor units so that more
are recruited within each muscle, increasing the strength of the contraction.
Another way of increasing the force of contraction is by
wave summation. This is when the brain increases the frequency of impulses so
that the muscle fibres that are being activated do not have time to relax. If
all the motor units of a particular muscle are recruited at once then the force
of contraction will be great, but only for a short time.
To increase the length of time of contraction the motor
units are recruited in a synchronised way so that certain units can relax
whilst others are contracting. This spacing of the recruitment of motor units
is known as spatial summation.
Muscle cell (fibre)
structure
Muscle fibres range from 10 to 80 micrometres in diameter
but may be more than 35cm long. There are many structures that are common to
all cells that are also found in the muscle cell as well as some that are
unique. The cell membrane surrounding the muscle fibre is called the
sarcolemma. Beneath the sarcolemma is the muscle cell cytoplasm called the
sarcoplasm. The sarcoplasm contains glycogen, fats and mitochondria.
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The perimysium is a layer of connective tissue that
encapsulates the whole muscle. Fasciculi are bundles of fibres surrounded by a
layer of connective tissue called the perimysium. Each fibre is also surrounded
by its own sheath of connective tissue called the endomysium. This acts as
insulation for each muscle fibre.
The muscle cell also has its own network of tubules and
membranous channels. The membranous channels are called the sarcoplasmic
reticulum and are an important site for storing calcium ions involved in
muscular contraction. The transverse tubules extend inwards from the sarcolemma
through the muscle cell. They allow the impulses received by the muscle cell
sarcolemma (motor end plate) to be transmitted rapidly to individual
myofibrils. Each muscle fibre contains several hundred to thousand myofibrils,
which are rod-like structures that run the entire length of the muscle fibre.
Myofibrils contain the contractile proteins involved in muscle contraction:
myosin, actin, troponin and tropomyosin. The myofibrils can further be divided
into sarcomeres, which are separated by sheets of protein called the Z-line.
The sarcomere is the functional unit of the muscle cell.
Under a microscope skeletal muscle is striated (striped).
This is due to the myosin (thick protein filaments) and actin (thin protein
filaments) overlapping and giving distinct bands. The lighter area is known as
the I band (only actin filaments are seen) and the A band is dark where both
myosin and actin overlap.
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The Z-line bisects the I band and attaches to the sarcolemma
to give the structure stability. The H band is in the middle of the A band and
is the section where you only see myosin filaments. The sliding of actin over
myosin and the consequent reduction of distance between Z-lines is thought to
be the way in which muscles shorten and hold tension.
Sliding Filament
Theory
The sliding filament theory describes a process used by
muscles to contract.
An impulse arrives at the neuromuscular junction and causes
the release of acetylcholine. This causes depolarisation of the motor end plate
on the sarcolemma of the muscle cell. This depolarisation is transmitted down
the transverse tubules into the muscle fibres, causing calcium ions to be
released from the sarcoplasmic reticulum.
When a muscle is in its resting state, tropomyosin wraps
around the actin filaments, blocking the myosin binding sites. This inhibits
the myosin from binding to actin and therefore causes a chain of events that
lead to muscle relaxation.
Troponin molecules are attached to the tropomyosin. When
calcium enters the muscle fibre, the ions bind to the troponin molecules
(sometimes stated as the troponin-tropomyosin complex as the two types of
molecule are attached in a complex). They change the shape of the troponin, exposing
the active myosin binding sites on the actin to be exposed. Myosin binds to
these sites to form a cross-bridge, which is energised by the breakdown of ATP
(catalysed by the enzyme ATPase) enabling the myosin to pull the actin inwards
and therefore shorten the muscle. This happens to every single sarcomere along
all the myofibrils in the muscle cell that is being innervated. The pulling of
the actin by the myosin is known as the power stroke.
When an ATP molecule binds to the myosin head, it detaches
from the actin. While detached, ATP hydrolysis occurs ‘recharging’ the myosin
head, allowing it to bind again (providing the binding sites are still
available). The contraction cycle can be repeated as long as calcium ions are
available.
When the impulse stops, the contraction cycle is broken. The
calcium ions are pumped back into the sarcoplasmic reticulum, the actin moves
back out and the muscle returns to its relaxed length.
A single power stroke of all the cross bridges in a muscle
results in a shortening of only about 1%. Since contracting muscles may shorten
by up to 35% of their resting length then each myosin cross bridge must attach
and detach many times during a single contraction. It is thought that only half
of the myosin heads are actively exerting a force at the same time whilst the
rest are seeking their next binding site. This alternate use of the myosin
cross bridge is referred to as the ratchet mechanism.
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