05 Nerve Muscle

Physiology / 2009-10 Dr. Ahmad .S.
Alarabi
Nerve & muscle
Nerve
The neuron is the structural unit of the nervous system. The nervous system of the
human body contains about 1012 (trillion) neurons which are found in many shapes and
sizes. The neuron is composed of:
1- Cell body (soma): it contains the nucleus and the other cell organelles (except the
centriole), so the neurons can’t divide.
2- Cell processes: they include:
A- Dendrites: they are multiple short processes on the outer surface of soma. These
dendrites have receptors on its surface that receives the signals (stimuli) and convey
it as electrical impulse toward the soma.
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Physiology / 2009-10 Dr. Ahmad .S. Alarabi
B- The axon (nerve fiber): it is a

single long process that conducts
the impulses away from the
soma. The 1st part of axon (1st
mm) is called the initial segment,
which is the most excitable part
of axon, because it has high
density of voltage gated Na+
channels. At the end of axon
there are a number of terminal
branches, each branch end in
many synaptic knobs. These
knobs contain vesicles that
contain the neurotransmitter needed for signal transmission.
The length of axon ranges from few mm to more than a meter, and the diameter
ranges from 0.1 to 20 microns. The axon is covered by 2 sheaths:
i- Neurilemmal sheath (outer sheath): it covers the all axons.

ii- Myelin sheath (inner sheath): it is made up of Schwann cells. It covers some
axons [except at its origin and at nodes of ranvier (every 1 mm)]. According to its
presence or absence, the nerve fibers are classified into [myelinated &
unmyelinated].
The neurons are classified by 3 ways:
1- According to the structure into:
• Unipolar: present in spinal afferent neurons.

• Bipolar: present in some sensory organs [e.g. Retina].
• Multipolar: present in the CNS [e.g. alpha motor neurons].
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2- According to the function into:
[Sensory (afferent) / Motor (efferent) / Interneuron]. See the sheet of autonomic.
3- According to diameter and velocity into 3 groups (see the table page ).
The nerve fibers (axon) of the neurons are classified also by two ways:
1- According to the neurotransmitter released at its end (Adrenergic / Cholinergic).

2- According to its nerve fiber into (Myelinated / Unmyelinated).
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Resting membrane potential

(RMP)
or (Polarization)
Definition: it is the electric potential

difference between the inner and
outer surface of the cell membrane
during rest.
• It is present in all cells of the body
with inner surface is (always)
negative relative to the outer surface
of the cell. It differs from cell to cell
[ranges (– 9) to (– 100) m. volt.
• In the medium sized nerves it is

about (– 70 m.v).
• To know the causes of RMP, we have to know the following facts which are applied for
all membranes:
1- All the ions (+cations or – anions) pass through the leak channels in the membrane
with various degrees of permeability [the membrane poorly permeable to chloride and
impermeable to proteins (Anions)].
2- The leak channels are permeable to K+ 50 times > Na+.
3- The concentration difference of K+ between ICF and ECF is about 30 times (> in ICF)
and of Na+ is 10 times (> in ECF) [please see the table (page 8) in introduction sheet].
4- The V – G Na+ channels are fast while those of K+ are slow.
• By knowing these facts, we can understand that:

1- The high difference in concentration of K+ (30 times > inside) and its high
permeability through the leak channels more than any other ion makes it the most
determinant ion in the creation of RMP.
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So, when the K+ efflux outside the cell in attempt to achieve the equilibrium in its
concentration, it changes the charge inside the membrane to the negative.
2- The amount of Na+ ions that influx inside the cell is not enough to overcome that of
effluxed amount of K+, and the Na+ is less permeable than K+ through leak channels.
3- The chloride has minor role in the creation of RMP.
4- The proteins have no role in the creation of RMP.
[We conclude that the RMP is mainly due to K+ efflux (outflow)].

There is another cause that maintains the RMP which is known as Na+ – K+ pump.
Sodium – potassium pump
Definition: it is an active pump presents in the membrane of all body cells. It pumps
3Na+ outside the cell with pumping 2K+ inside the cell.
Functions:
1- Contributes in creation of RMP
[responsible for about (–4 m.v) of
the RMP].
2- Maintain the Na+ & K+

concentration difference across
the cell membrane. Some of the
Na+ enters the cell during rest
and more amounts enter during
action, and this pump returns the
concentrations to normal.
3- If these excess amounts of Na+

were not removed, they well pull increased amounts of water (by osmosis) and the cell
will swell until burst, but this pump prevents that.
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Action potential
Definition: it is the changes in the electrical potential difference between the inner and
outer surface of the membrane that occurs during action (applying a stimulus).
There are some terms that we have to know regarding the action potential process:
1- Stimulus: it is an environmental change that causes the opening of gated Na+

channels → Na+ influx → change of the inside charge from the negative resting charge
(in RMP) to positive charge.
2- Depolarization: it is the change of membrane potential that ↑ from RMP (– 70 m.v)
until reaches a positive potential (+35 m.v) due to the application of suitable stimulus
which will causes Na+ influx.
3- Repolarization: it is the return of membrane potential from (+35) again to its resting
level due to stopping Na+ influx and ↑ K+ permeability (by K+ efflux).
4- Firing level: it is reaching the magnitude of membrane potential to (+55 m.v).
The process of action potential depends on the presence of 2 voltage gated ion channels
[voltage – gated Na+ channels / voltage – gated K+ channels] in contrast to the leak
channels that are involved in the creation of RMP.
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a- Voltage – gated sodium channels:

These channels have 2 gates:
i- Activation gate (at the outer surface):

during RMP (– 70) these channels are
closed. These channels open in
response to depolarization. Some of
them opens at (– 63) but almost all of
these channels open at the firing level
(–55).
ii- Inactivation gate (at inner surface): the closure of these channels occurs slowly
when the membrane potential increases > (– 55 m.v) and almost all of these gates
will close at the end of depolarization at (+35 m.v). These gates will not reopen again
until the membrane repolarizes, so the Na+ channels will not activate again (after
their stimulation) until the membrane repolarizes.
b- Voltage – gated potassium channels:

These channels have only one gate at the inner
surface. These channels are closed during rest.
They start to open (activate) late in
depolarization and becomes completely
opened by the end of depolarization and
continue to be opened during Repolarization.
Description of action potential
If we recorded the electrical changes of AP by 2 microelectrodes one inside and the

other outside the cell, the produce diagram will be in the form of spike & after potential.
The events of this recording will be in the following steps:
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1- Stimulus artifact: it is the time of application of the stimulus.

2- Latent period: it is the time passed between the application of the stimulus and the
recording of action potential. This period depends on the velocity of conduction of the
nerve & the distance between the stimulus and the electrodes.
3- The spike: it is a rapid process (2 m.seco) with high magnitude changes (105 m.v). It
is composed of:
a- Ascending limb: it represents the depolarization [i.e. change of MP from (–70) to

(+35)]. It is due to ↑ Na+ permeability 1000 – 5000 times when the activation gates of
the V – G Na+ channels opens (in response to stimulus) → Na+ influx → ↑ MP toward
(+35).The 1st part of ascending limb (1st 15 m.v) [(-70) to (-55 or firing level)] is slow.
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b- Descending limb: it represents the 1st 70% of Repolarization [i.e. returning of the MP
from (+35) back to near RMP]. It is due to stoppage of Na+ inflow [due to closure of
inactivation gates] and starting of K outflow [due to activation (opening of the gates) of
V – G K+ channels].
4- After depolarization (negative after potential): it represents the last 30% of

Repolarization. It is a slow process because at this time the gates of some of the V – G
K+ channels close. Its duration is 4 m.seconds.
5- After hyperpolarization (positive after potential): it is the reaching of membrane

potential to a level beyond the RMP [(more negative to about (-90)] and gradually
returning back to the RMP.
This is because that many voltage – gated K+ channels remain opened after
Repolarization → excess K+ diffuse out. And due to hyperactivity of Na+ – K+ pump.
Propagation of AP
One of the properties of AP that it can spreads in both directions away from the
stimulated segment. The method of conduction depends on the type of nerve fiber.
1- Conduction in unmyelinated nerve

fibers: it is by local circuit mechanism.
• The resting segment has +ve charge
outside and –ve charge inside, while the
activated segment has –ve charge outside
and +ve charge inside.
• The local circuits occur between a
depolarized segment and adjacent resting
segment.
• The newly depolarized segment
depolarizes its adjacent segment in the
same way and so on till the depolarization wave reach the end of nerve fiber.
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• The propagation of AP (depolarization wav) along the nerve fiber is called nerve
impulse.
2- Conduction in myelinated nerve fibers: it is by saltatory conduction.

• it is a similar to the conduction in unmyelinated nerve fibers, but the local circuits
occurs between the adjacent nodes of ranvier (not the adjacent segments) because
the myelin sheath acts as an insulator of electricity (passage of ions). So the
depolarization wave jumps from node of ranvier to another (saltatory conduction).
• It is 50 times more rapid than conduction in unmyelinated nerve fibers.
• It needs less energy than conduction in unmyelinated nerve fibers.
Excitability
Definition: it is the ability of living tissue to respond to an adequate stimulus. The most
excitable tissues in the body are the nerve and muscle.
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Excitability changes during AP
1- During local response up to the firing level, the excitability is increased.

2- Absolute refractory period: it is the period during which the nerve fiber can’t
respond to any stimulus whatever it was strong. It coincides with ascending limb and 1st
1/3 of descending limb of the spike. This is because the V – G Na+ channels are either:
• Fully activated [the activation gates are open (in ascending limb)].
• Inactivated [the inactivation gates are closed and will never open until the
membrane repolarized (in 1st 1/3 of descending limb)].
3- Relative refractory period: it is the period during which the membrane to be

excited, it needs the strength of the stimulus to be more than normal (stronger
stimulus). It coincides with the remaining 2/3 of descending limb of the spike.
Factors that affects excitability of nerve
1- Factors that decreases excitability (membrane stabilizers):
• High Ca+ in ECF [↓Na+ permeability]. • Local anesthetics [↓Na+ permeability].

• Low K+ in ECF. • Low Na+ in ECF.
• Acidosis. • Hypoxia.
• cooling (hypothermia). • Pressure.
2- Factors that increases excitability:
• Low Ca+ in ECF

• High Na+ & K+ in ECF.
• Alkalosis
• warming (hyperthermia / fever).
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Stimulus
Definition: it is an environmental change that causes starting diffusion of Na+ to inside.
Types: [Electrical / Chemical (hormone or NT) / Mechanical (e.g. pressure) / Thermal

(e.g. cooling or warming) / Electromagnetic (e.g. light rays)].
Effects of stimulus : It depends on:
I- Intensity (strength) of the stimulus:

The stimuli are classified according to their strength into:
Threshold stimulus: it is the minimal stimulus that can cause an action potential
(propagated response) [i.e. can raise the membrane potential (by Na+ inflow) till reach
the firing level (-55)].
Suprathreshold stimulus: it has more intensity than threshold stimulus, but will
produce the same response as threshold (AP with the same magnitude and duration).
Subthreshold stimulus: it has less intensity than threshold stimulus.

Instead of producing propagated AP, the subthreshold stimulus causes one of two
localized changes:
1- Electrotonic potential: it is a mild change in the MP below 7 m.v change (<-63 m.v).
These changes will not cause actual response (AP) [i.e. no opening of Na+ channels].
2- Local response: it is the change in membrane potential between 7 – 14 m.v when

the stimulus is more in strength than that cause electrotonic potential. In this type of
potential there is an actual response, but it can’t propagate (doesn’t produce AP). If
the stimulus strength ↑ to reach the change in MP to 15 m.v (-55 / firing level), this
local potential will become an action potential (and propagate).
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All or none law
It states that either the nerve (tissue) responds maximally or does not respond at all
when applying a stimulus with suitable strength to cause AP (threshold /
suprathreshold). The tissues that obey all or none law are:
1- Single nerve fiber.

2- Single skeletal muscle fiber.
3- Both atria or both ventricles of the heart.
4- Visceral (single unit) type of smooth muscle.
II- Rate of rise of intensity of the stimulus:

If a subthreshold stimulus is applied to the nerve and its intensity is increased slowly,
the nerve will not respond (will not produce AP even if the stimulus becomes threshold)
because of the accommodation of the nerve.
But if the intensity of the subthreshold increased rapidly, the accommodation will not
be observed and this increase in intensity → generation of AP.
III- Duration of the stimulus:

For the stimulus to be effective, it should be applied fro a certain time called excitation
time.
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Types of nerves
Group Example Diameter Velocity Spike Most

in micron in duration susceptible
(µ) meter/se in to
c (m.sec)
A •Almost all of the 2 – 20 10 – 120 0.5 Pressure
Divided somatic [aff & eff]
into
Alpha (α) •Somatic motor 10 – 20 60 – 120

•Proprioception
Beta (β) •Fine touch 5 – 10 30 – 60

•Proprioception
Gamma (γ) •Somatic motor to 3–5 15 – 30

muscle spindle
Delta (δ) •Temperature (cold) 2–3 10 – 5

•Crude touch
B •Myelinated 1–2 5 – 10 1 O2 lack
autonomic pregang. [Hypoxia]
C •Unmyelinated fibers Less than 1 0.5 – 2 2 Local

•Slow pain anesthesia
•Temp (hot)
•Postg. Autonomic
[> ½ sensory fibers in
most peripheral N]
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Skeletal muscle
Physiologic anatomy
Each muscle is composed of a number of ms. fibers arranged parallel to each other.
Each ms. fiber is cylindrical in shape and has:
• Cell membrane (sarcolemma).

• Cytoplasm (sarcoplasm) that contains the nucleus and other cell organelles.
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• Contractile elements (myofibrils).

• Two types of tubules [longitudinal tubules / transverse (T) tubules].
Each myofibril apparently shows alternating bands [light (I) band & dark (A) band].
The I band is bisected by Z-line.
The A band is bisected by H band.
The sarcomere (the unit in the myofibril) is the distance between two successive Z lines.
The presence of dark (A) and light (I) bands gives the skeletal muscle its striated
appearance.
The myofibril is made up two types of finer myofilaments [as they are when fully
relaxed]:
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I- Thin filament (actin filament): it extends from the Z line toward the center of
sarcomere (but not reaching it). This filament is composed of:
1- Actin: it is formed of globular molecules called (G actin molecules) that are arranged
two chains twisted with each other in spiral manner.
Each molecule has on its side an active (binding) site for binding with myosin head
during cross bridging of actin and myosin filaments (during contraction).
2- Regulatory proteins: these proteins include:
Tropomyosin: it is located in the groove between the 2 chains of actin.

It covers the myosin binding site (on actin molecule) so it will inhibit the binding
(action).
Troponin: it is a small globular protein located on every revolution of actin helix (every
0.04 µ). It is composed of 3 loosely bound protein subunits:
a- Troponin T: binds the other

troponin components to
tropomyosin.
b- Troponin I: covers the myosin
binding site on actin molecule
(inhibits their interaction).
c- Troponin C: binds with Ca+
that initiates the contraction.
II- Thick filament (myosin

filament): it is present in the
middle of sarcomere [forming
the (A) band].
There is a small projections
(cross-bridges) arise from this
filament except at its center (H
band).
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Each myosin filament is made up of myosin molecules.
Morphologically, each myosin molecule is composed of:
► 2 myosin heads (side by side): each head has 2 active sites:
• One for binding with actin.

• One has ATP ase activity (splits ATP) to liberate the energy needed for action.
► Arm and Tail.
In each molecule, there are 2 flexible sites (hinges):
• Between the arm and head.

• Between the arm and tail.
The infrastructure of each myosin molecule is made up of 6 polypeptide chains:

• 2 Heavy chains: form the [tail – arm – (2 heads)].
• 4 Light chains: control the function of head during the
contraction process.
In the thick filament, the myosin molecules are arranged as

the following as:
• Side by side (each 6 molecules arranged around the
circumference separated by 60°) with 0.04 µ distance between each 6 molecules.
• End by end (with 1/2 the myosin molecules on the right and ½ on the left).
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Note: the tails of the molecules form the body of the filament, and the arms and heads
form the cross bridges.
Tubular network of the sarcoplasm: the sarcoplasm has 2 types of tubules:

1- Longitudinal tubules:
These tubules form the sarcoplasmic reticulum which runs parallel to the myofibril. At
their ends (near T tubules) they enlarge to from chambers called cisternae.
Function:
store Ca+ in high concentration (10000 folds) in their cisternae because they have Ca+
pumps.
2- Transverse tubules (T – tubules):

They are invaginations (infolds) of the sarcolemma that extends across the interior of
the muscle fiber (penetrate it).
They contain an ECF, and they run parallel to Z lines (each sarcomere has 2 T tubules at
it end near the z lines).
Function: the T – tubules transmit the action potential to the interior of the ms. fiber
(especially to the cisternae).
Neuromuscular junction
(Motor End Plate)
Definition: it is the area of contact between motor nerve fiber and muscle fiber.
Near the ms. fiber, the nerve fiber looses its myelin sheath, and the neurilemma
becomes continuous with sarcolemma. Axon → several branches, each branch →
multiple synaptic knobs.
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The motor end plate (MEP) composes of:
1- Synaptic knob: it contains:
• In its cytoplasm: Multiple synaptic vesicles containing the NT (which is always Ach
in the MEP). Multiple mitochondria [to provide energy for Ach formation].
• In its axolemma: multiple voltage – gated Ca+ channels.
2- Synaptic cleft: it contains the enzyme that destroys the Ach (acetylcholineesterase).
3- Synaptic gutter: an invagination in the sarcolemma that is involved in MEP. It

contains multiple Ach gated ion channels.
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Notes:
1- Motor unit: it means a single motor neuron and the ms. fibers it innervates.
The number of muscle fibers in the motor neuron of muscles that perform fine
movement is small (3 – 6) while that perform gross movement is large (100 – 200).
2- Motor pool: the number of neurons (AHC) that innervate single sk. Muscle.
The motor pool is composed of multiple motor units.
Mechanism of neuromuscular transmission
The crossing of nerve impulse to the supplied muscle occurs in the following steps:
1- When the nerve impulse (AP) reaches the synaptic knob → depolarization of its
membrane.
2- This depolarization (AP) will activates the voltage – gated Ca+ channels → Ca+ influx.
3- The Ca+ inside the knob → release of Ach from its vesicles into synaptic cleft (by
exocytosis).
4- Ach binds to Ach – gated ion channels in the synaptic gutter → its activation (opening)
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5- The opening of Ach – gated ion channels → influx of large amount of Na+ from ECF
into the sarcoplasm at area of MEP → localized partial depolarization at MEP called end
plate potential (EPP).
6- When the EPP reaches the firing level → AP which will propagate all over the
sarcoplasm. This potential called muscle action potential.
7- Once the released Ach binds to its channels and causes the AP, it will be hydrolyzed
by the enzyme cholinesterase. This rapid destruction prevents re-excitation after
recovery from 1st action potential.
Properties of neuromuscular junction
1- Unidirectional conduction [from the nerve to the muscle, not the oppsite].
2- Synaptic delay (about 0.5 m.sec).
3- Fatigue: it is ↓ response of NMJ as a result of rapid repetitive stimulation (Ach
release exceeds the Ach synthesis → its depletion).
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4- Effects of ions:
↑ Ca+ in ECF stimulates the transmission.
↑ Mg+ in ECF inhibits the transmission.
5- Effects of drugs on transmission in NMJ:

stimulants:
Drugs which have Ach like action [e.g. carbacol - methacholine].
Drugs which inactivate the cholinesterase [anticholinesterases (e.g. neostigmin)]
Inhibitors: neuromuscular blockers (e.g. curare).
Myasthenia gravis
Def: it is a hereditary autoimmune disease characterized by weakness in sk. Muscles

due development of antibodies in the body against its own Ach activated ion channels.
This disease is treated by anticholinesterases [e.g. Neostigmin].
Comparison between the electrical events in the muscle and nerve
AP in the (Nerve) AP in the (sk. Muscle)

RMP -70 m.v -90 m.v
Firing level 15 m.v depol. (-55 m.v) 40 m.v depol. (-50 m.v)
Complete depolarization at +35 +40
Magnitude of AP 105 m.v 130 m.v
Duration of spike 0.5 – 2 m.sec 2 – 4 m.sec
After potential Shorter Longer
Velocity of conduction 0.5 – 120 meter/sec 5 meter/sec
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Mechanical response of the muscle
The single adequate stimulus that reaches the muscle fiber it responds by contraction
(shortening) followed by relaxation, this response called simple muscle twitch.
The recording of simple muscle twitch will shows 3 periods:
• Latent period (10 m.sec).

• Contraction period (40 m.sec).
• Relaxation period (50 m.sec).
Mechanism of contraction
(excitation contraction coupling)
It is the process by which the AP that reaches the muscle fiber initiates contraction.
These events start after the arrival of AP to the sarcoplasm at MEP area.
1- The arrived AP is transmitted through the T – tubules to the interior of ms. fiber.
2- The AP crosses from the T tubules to the cisternae. This will lead to opening of the
voltage gated Ca+ channels in its wall → release of Ca+ into the surrounding sarcoplasm.
3- In the m. fiber, the released Ca+ binds to the troponin C → lateral movement of
troponin – tropomyosin complex → uncover the active site of actin.
4- The uncovering of actin sites leads to binding of the myosin head to these sites.
While the myosin head binds, it uses its ATP ase activity to hydrolyze the ATP to liberate
the energy which will be used during the contraction process [ATP → ADP + P (energy)].
5- The attachment of myosin head to its active site will leads to tilting of the myosin
head centrally and dragging the actin with it, this is called power stroke. The energy
used for power stroke is that was liberated on ATP hydrolysis.
6- After this tilting, a new ATP molecule binds to myosin head → detachment of the
myosin head from actin and its returning to the previous untilted position to start new
power strock.
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7- The cycles of attachment, tilting, detachment proceeds until the load on the muscles
exceeds its ability for more shortening.
Relaxation
When the stimulation by motor neurons (AP) stops, the calcium pumps on the cisternal
membrane start to reuptake the Ca+ from the sarcoplasm into the cisternae. This will
lowers the Ca+ concentration → detachment of Ca+ from troponin C → returning of
troponin – tropomyosin complex to cover the actin binding sites → myosin head unable
to attach to actin → relaxation of muscle fiber to its previous resting length.
Types of contraction
The contraction is of 2 types
1- Isotonic contraction: shortening of the muscle during contraction with constant

degree of tension.
2- Isometric contraction: contraction of the muscle fiber without shortening (↓length).
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isotonic Isometric
Tension Constant Rises markedly
Length Decrease Constant
Example Contraction of biceps Contraction of extensors

to left an object of lower limb to support
the body against gravity
Work Done No work
Mechanical efficiency Relatively high Zero
Energy needed More, as ms performs Less

external work
Duration Long, due to inertia & Short

momentum.
Note:
The muscles in the body can contract by the 2 mechanisms.
Most contractions are composed of the 2 types [e.g. when lifting an object, the muscle
first contracts isometrically then isotonically].
Types of muscle fibers
Every muscle in the body composed of 2 types of fibers known as:
Fast (pale)
&
Slow (red)
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Fast (pale) Slow (red)

Function Short rapid ms. contractions Slow prolonged ms. contractions
[e.g. jumping short distance [support of body weight against
eye movement,] gravity]
Fatigue Easily Not easily
Sarcoplasmic Extensive for rapid Ca+ Less extensive

reticulum release
Glycolytic Large amount (for rapid Smaller amount

enzymes release of energy)
Mitochondria Few Increased number
Blood supply Less extensive More extensive
Myoglobin Little amount Large amount

(stores O2)
Factors affecting contractility
1- The type of the muscle fibers [red or fast].
2- Temperature: warming leads to stronger and faster contraction, while the cooling
has opposite effect.
3- Fatigue:
Def: the decrease in response (contraction) of the muscle as result of rapid repetitive
stimulation (prolonged strong contraction).
It is because of:
• ↓ Energy sources [mainly glycogen & ATP].
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• Accumulation of metabolites → depresses contraction & lead to pain sensation.

• Depletion of the Ach at the neuromuscular junction.
4- Initial length of the muscle:

This is represented by the length – tension relationship [starling’s law].
Starling’s law: it states that the strength of contraction (during isometric contraction)
is directly proportional to the initial length of the muscle (length before contraction)
within limits (the length is the resting limit).
5- Load on the muscle (load – velocity relationship):
When the muscle is allowed to shorten (isotonic contraction), the velocity of contraction
(shortening) is inversely related to the load on the muscle.
That is mean, the muscle that bear light weight (or no weight) contracts (shortens)
rapidly; while the muscle that contract against heavy weight contracts more slowly.
Rigor: it is a state of extreme rigidity (contraction) develops in the muscle as a result of

depletion of ATP, because the ATP is needed for separation of cross bridges from actin.
When this condition occurs after death, it is called rigor mortis.
The rigor mortis has medicolegal importance because it helps in determination of time
of death.
Factors responsible for

gradation of ms. activity
The muscles can contract with various degrees of contraction by the following means:
1- The number of discharging motor units [The more motor units discharging the more
power of contraction].
2- The frequency of discharge in individual nerve fiber [the more frequency, the
stronger contraction]. But if the speed of stimulation was very rapid, it may lead to
tetanus [because enough Ca+ is maintained in sarcoplasm between the action
potentials].
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Smooth muscles
The smooth muscles are also called plain muscles because they have no striation.
Types: they are of 2 general types [multiunit / single unit].
Multiunit Single unit

(visceral)
Arrangement of Discrete fibers Adherent to each other
ms. fibers with many gap junctions
Contraction of Each fiber independent The fibers contracts in

fibers on the others (doesn’t functional syncitium
obey all or none law) (obey all or none law)
Controlled by Mainly autonomic N.S Mainly non nervous, e.g.

hormones
Mech. Of Local depola. Caused by Spontaneous
contraction the NT (enough to elicit depolarization
contraction because the [act as pacemaker
fibers are very small) (self excitatory)]
Ability to contract Unable Able
spontaneously [because of its dependence [because some fibers
on nerve supply]. are self excitatory].
Electrophysiology of
the smooth muscle
The RMP of the sm. Muscle is about (-50) to (-60) m.v.

the AP doesn’t occur normally in most multiunit sm. Muscles.
The action potential in single unit sm. Muscles differs from that of sk. Muscles in 3
aspects:
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1- Its phases and its shape during the recording of electrical activity. The AP of visceral
smooth muscles may occur in 3 forms:
a- Spike potential [similar to sk. muscle]: it is a short period of contraction (10 – 50

m.sec) occurs in most single unit sm. Ms.
b- AP with plateau [similar to cardiac

muscle]: it is contractions with longer
period of contraction [hundreds to
thousands of m.seconds] that occurs in
types of muscles that shows prolonged
periods of contraction (e.g. uterus).
c- Slow wave potentials [pacemaker wave]:

this type of AP occurs without extrinsic stimulus (in self excitatory fibers).
2- The AP is mainly due to Ca+ inflow (not Na+) [because the sm. Ms. have more
voltage – gated Ca+ channels & few voltage – gated Na+ channels].
3- The AP in sm. Ms. in all of its 3 forms is slow compared with that of sk. Ms.
Excitation contraction
coupling in sm. Ms
It is nearly similar to that of sk. Ms, but differs from it in 3 aspects:
1- Source of Ca+ that initiates the contraction: it is from ECF through V – G Ca+ channels.
2- Regulation of contraction by Ca+: instead of the troponin, the smooth muscle has
another regulatory protein called calmodulin. it is activated by ↑ Ca+ → activation of
myosin kinase → contraction.
The process of relaxation is mediated by ↓ Ca+ → inhibition of [calmodulin & MK] &
activation of [myosin phosphatase] → relaxation.
3- The frequency of cycling of the cross bridges is less than that of sk. Ms.
30
Comparison of mechanical activity between sk. & sm. Muscles

Skeletal ms Smooth ms
Energy required More energy Less energy [1/10 to
1/300 of that of sk. Ms.]
Onset of cont. Rapid Slow
& relax.
% of shortening 1/3 its stretch length 2/3 its stretch length
during contraction
Force of contraction More powerful Less powerful
2
[6 kg/cm ]. [4 kg/cm2].
31

05 Nerve Muscle

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05 Nerve Muscle

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Physiology / 2009-10 Dr. Ahmad .S.

Nerve & muscle

2- Cell processes: they include:

B- The axon (nerve fiber): it is a

i- Neurilemmal sheath (outer sheath): it covers the all axons.

The neurons are classified by 3 ways:

1- According to the structure into:

• Unipolar: present in spinal afferent neurons.

2- According to the function into:

[Sensory (afferent) / Motor (efferent) / Interneuron]. See the sheet of autonomic.

1- According to the neurotransmitter released at its end (Adrenergic / Cholinergic).

Resting membrane potential

Definition: it is the electric potential

• In the medium sized nerves it is

• By knowing these facts, we can understand that:

[We conclude that the RMP is mainly due to K+ efflux (outflow)].

Sodium – potassium pump

2- Maintain the Na+ & K+

3- If these excess amounts of Na+

1- Stimulus: it is an environmental change that causes the opening of gated Na+

a- Voltage – gated sodium channels:

i- Activation gate (at the outer surface):

b- Voltage – gated potassium channels:

Description of action potential

If we recorded the electrical changes of AP by 2 microelectrodes one inside and the

1- Stimulus artifact: it is the time of application of the stimulus.

a- Ascending limb: it represents the depolarization [i.e. change of MP from (–70) to

4- After depolarization (negative after potential): it represents the last 30% of

5- After hyperpolarization (positive after potential): it is the reaching of membrane

1- Conduction in unmyelinated nerve

2- Conduction in myelinated nerve fibers: it is by saltatory conduction.

Excitability changes during AP

1- During local response up to the firing level, the excitability is increased.

3- Relative refractory period: it is the period during which the membrane to be

Factors that affects excitability of nerve

1- Factors that decreases excitability (membrane stabilizers):

• High Ca+ in ECF [↓Na+ permeability]. • Local anesthetics [↓Na+ permeability].

2- Factors that increases excitability:

• Low Ca+ in ECF

Definition: it is an environmental change that causes starting diffusion of Na+ to inside.

Types: [Electrical / Chemical (hormone or NT) / Mechanical (e.g. pressure) / Thermal

Effects of stimulus : It depends on:

I- Intensity (strength) of the stimulus:

Subthreshold stimulus: it has less intensity than threshold stimulus.

2- Local response: it is the change in membrane potential between 7 – 14 m.v when

All or none law

1- Single nerve fiber.

II- Rate of rise of intensity of the stimulus:

III- Duration of the stimulus:

Group Example Diameter Velocity Spike Most

Alpha (α) •Somatic motor 10 – 20 60 – 120

Beta (β) •Fine touch 5 – 10 30 – 60

Gamma (γ) •Somatic motor to 3–5 15 – 30

Delta (δ) •Temperature (cold) 2–3 10 – 5

C •Unmyelinated fibers Less than 1 0.5 – 2 2 Local

• Cell membrane (sarcolemma).

• Contractile elements (myofibrils).

2- Regulatory proteins: these proteins include:

Tropomyosin: it is located in the groove between the 2 chains of actin.

a- Troponin T: binds the other

II- Thick filament (myosin

Each myosin filament is made up of myosin molecules.

Morphologically, each myosin molecule is composed of:

► 2 myosin heads (side by side): each head has 2 active sites: