Muscles

Physiology
WOLLO UNiversity
College of medicinE & health science Department
of Physiology
 Objectives
At the end of this chapter the student will be able to:
1. List the 3 types of muscle.
2. Define characteristics of muscle.
3. Enumerate functions of muscle.
4. Explain the skeletal & smooth muscle types.
5. Compare skeletal, smooth & cardiac muscle.

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 Outlines
 Introduction.
 Function of muscle.
 Types of muscle.
 Characteristics of muscle.
 Skeletal muscle:
 excitation, excitation contraction coupling, contraction,
relaxation.
 muscle metabolism, fiber types.
 Smooth muscle.
 Cardiac muscle.
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 Introduction

 Muscle is one of our 4 tissue types and combined

with nerves, blood vessels, and various connective
tissues is what makes up those muscle organs that
are familiar to us.
 Muscles are quite complex and are a marvel of both
biology and physics.

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 Muscle Functions

1. Produces movement of:

 Body parts
 Blood throughout the body
 Lymph through the lymphatic vessels
 Food through the GI tract
 Bile out of the gallbladder and into the digestive tract
 Urine through the urinary tract
 Semen through the male and female reproductive tracts
 A newborn through the birth canal

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 Muscle Functions…
2. Maintenance of posture
 Muscle contraction is constantly allowing us to remain
upright.
 muscles of your neck are keeping
your head up right now.
 As you stand, your leg muscles
keep you on two feet.
3. Thermogenesis
 Generation of heat, occurs via shivering.
– an involuntary contraction
of skeletal muscle.

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 Muscle Functions…
4. Stabilization of joints
 Muscles keep the tendons that
cross the joint nice and firm.
 This does a wonderful job of
maintaining the integrity of
the joint.

All the things muscles do fall under one of these 4

categories.

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 3 Types of Muscle Tissue

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 Characteristics of Muscle Tissue
1. Excitability
 The ability to receive & respond to a stimulus.
 The stimulus could be:
 In smooth muscle = neurotransmitter, hormone,
stretch, pH, Pco2/Po2.
 In cardiac muscle = NT, hormone, or stretch.
 In skeletal muscle = NT released by a neuron.
 The response is the generation of an electrical
impulse that travels along the plasma membrane of
the muscle cell.

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 Characteristics of Muscle Tissue…

2. Contractility
 The ability to shorten forcibly when adequately
stimulated.
 This is the defining property of muscle tissue.
3. Extensibility
 The ability to be stretched.
4. Elasticity
 The ability to recoil & resume original length
after being stretched or contracted.

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Sarcolemma
 Plasma membrane of
muscle fiber
 Has invaginations that
penetrate through
the cell= transverse
tubules/T tubules.

Sarcoplasm
• Cytoplasm of muscle fiber
• Has lots of mitochondria (why?), lots of glycogen
granules as well as myofibrils & sarcoplasmic
reticuli.
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 Sarcoplasmic Reticulum
 Muscle cell version of
smooth endoplasmic
reticulum.
 Functions as a calcium
storage depot in muscle
cells.
 Loose network of this
membrane bound
organelle surrounds all
the myofibrils in a
muscle fiber.

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 Myofibrils
 Rod like structures
that extend the length
of the muscle fiber.
 Long bundles of
protein structures
called myofilaments:
 responsible for

muscle contraction.

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 Myofilaments
 2 types of myofilaments (thick & thin) make up myofibrils.
 Thick myofilaments are made up of the protein myosin.

A single myosin protein

resembles 2 golf clubs
whose shafts have been
twisted about one another.

About 300 of these

myosin molecules are
joined together to form a
single thick filament

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 Myofilaments…
 Thin filament is made up of 3 different types of protein:
- actin, tropomyosin, troponin.
 Each thin filament consists of a long helical double strand, a
polymer that resembles a string of beads.
 Each “bead” is the globular protein actin. On each actin
subunit, there is a myosin binding site.
 Loosely wrapped around the actin helix & covering the
myosin binding site is the filamentous protein, tropomyosin.
 Bound to both the actin & the tropomyosin is a trio of
proteins collectively known as troponin.

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 Myofilaments…
 Each myofibril is made up 1000’s of repeating
individual units known as sarcomeres.
 Each sarcomere is an ordered arrangement of thick
& thin filaments. Notice that it has regions of:
 thin filaments by themselves (pinkish fibers)
 thick filaments by themselves (purple fibers)

 regions of thick & thin filaments overlapping.

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 Sarcomere
 Is flanked by 2 protein structures known as Z discs.
 The portion of the sarcomere which contains the
thick filament is known as the A band.
 A stands for anisotropic which is a fancy way of saying
that it appears dark under the microscope.
 The A band contains a zone of overlap & H zone which
contains only thick filaments.

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 Sarcomere…

 Portion of the
sarcomere which
does not contain
any thick
filament is known
as the I band.
 I band contains
only thin filament
& is light under
the microscope
(it is isotropic).
 One I band is
 In the middle of H zone is a structure
actually part of
2 sarcomeres called the M line which functions to hold
at once. the thick filaments to one another.

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 T-Tubules & the SR
 Each muscle fiber
has many
T-tubules
 encircling at each
A-I junction.
 At each A-I
junction, the SR
will expand & form
a dilated sac
 terminal cisterna

• Each T-tubule is flanked by a terminal cisterna this forms a so called

triad consisting of 2 terminal cisternae & 1 T-tubule branch.
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 Excitation
 All cells have a voltage difference across their
plasma membrane due to:
1. Outward diffusion of K+ through K+ leak channels.
 ECF is very high in Na+ while ICF is very high in K+.
As a result, K+ is constantly leaking out of the cell.
2. Na+/K+ pump is constantly pumping 3 Na+ ions out
& 2 K+ ions in for every ATP used.
 Thus more positive charge is leaving than entering.
3. Protein anions
 negatively charged proteins within the ICF that
cannot travel through the PM.
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 Excitation…
 This charge separation is
known as a membrane
potential (Vm).
 The value for Vm in
inactive muscle cells is
typically between – 80
and – 90 millivolts.
 Vm can be changed by
influx or efflux of charge.

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 Excitation…
 Plasma membrane has integral proteins that act as
gated ion channels.
 channels that are normally closed, but in response to a
certain signal, they will open & allow specific ions to pass
through them. They are:
 Ligand-gated  the binding of an extracellular molecule

(hormone, NT) causes these channels to open.

 Voltage-gated  V causes these channels to open.
m
 Mechanically-gated  stretch or mechanical pressure

opens these channels.

 When a channel is open, its specific ion(s) will enter or exit
depending on their electrochemical gradient.

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 Mechanism of Excitation…
 Adjacent to the motor end plate, the sarcolemma
contains voltage-gated ion channels.
 In order for these channels to open, the V m must
depolarize from its resting value of –90mV to
approximately –50mV (threshold).
 Vm must become this positive for the voltage-gated
channels to open.
 The degree of depolarization depends on:
 how much Na+ influx occurred
 which in turn depends on how many Na+ channels were
opened by binding ACh.

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 Mechanism of Excitation…
 If the Vm fails to depolarize to threshold, nothing
will happen. The Vm will soon return to normal and no
muscle contraction will occur.
 If the Vm does reach threshold, 2 types of voltage-gated
ion channels will open:
 Fast Na+ channels, Slow K+ channels
 If Vm reaches threshold, fast Na+ channels open and Na+
rushes in causing the Vm to depolarize to +30mV.
 The depolarization stops when the Na+ channels become
inactivated.

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 Mechanism of Excitation…
 At this point, slow K+ channels have opened & K+ efflux
occurs. This returns Vm back to its resting level. This is
repolarization.
 If we were to graph this change in Vm over time, it would
look somewhat like the animation below.
 This is known as an action potential

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 Mechanism of Excitation…
 AP can propagate itself across
the surface of the plasma
membrane.
 The depolarization caused by the
Na+ influx in one particular area of
the sarcolemma causes voltage-
gated channels in the adjacent
membrane to open.
 The resulting ionic influx then
causes voltage-gated channels to
open in the next patch of
membrane and so on and so on.

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 Excitation-Contraction Coupling
1. AP travels along the sarcolemma going in both
directions away from the motor end plate.
2. T-tubules are invaginations of the sarcolemma, the
AP will spread down & through them as well.

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 Excitation-Contraction Coupling…
3. T-tubular sarcolemma contains voltage sensitive
proteins (arrow) that change their conformation in
response to a significant Vm.
4. These are physically linked to Ca2+ channels in
the SR membrane
 Upon Vm, the voltage sensors change their conformation.
This mechanically opens the Ca2+ channels in the SR
membrane.
5. The SR Ca2+ channels are only open briefly, but a
large Ca2+ gradient exists so a large amount of Ca2+
enters the sarcoplasm.
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 Excitation-Contraction Coupling…
6. Ca2+ interacts with the 2 regulatory proteins.
7. The 2 contractile proteins slide one over the other.
8. The sarcomere shorten (muscle contraction).

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 Myasthenia Gravis
(extreme muscle weakness)

My=muscle,
Asthen=weakness,
Gravi=heavy

 Autoimmune disease where antibodies attack the ACh

receptors on NMJs.
 Results in progressive weakening of the skeletal muscles.
Why?
 Treated with anticholinesterases such as neostigmine or
physostigmine. These decrease the activity of
acteylcholinesterase (ACE).
 Why would this help someone with myasthenia gravis?

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 Contraction
 Tropomyosin obstructs the myosin binding site on
the G-actin subunits.
 Ca2+ binds to the troponin-C polypeptide of the
troponin triad.
 This changes the conformation of troponin which changes
the conformation of tropomyosin which exposes the
myosin binding site on actin.

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 Contraction…

 Once actin’s myosin binding site is exposed, myosin will attach to

it. At this point:
1. Myosin has just hydrolyzed ATP into ADP & Pi – however both
molecules are still bound to the myosin.
 the ATP hydrolysis provides the energy for the “cocking” of

the myosin head

2. Once myosin is bound to actin, the myosin head will release the
ADP & Pi which will cause it change conformation.
 This results in the thin filament sliding along the thick filament .

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 Contraction…
3. Myosin then
remains bound
to actin until it
binds to
another ATP.

4. Myosin then
hydrolyzes the
new ATP and
the cycle can
begin again.

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 The cycle of attachment, power stroke, & release continues
as long as calcium & ATP remain available.
 Typically half the myosin molecules at any time are bound
to the actin while the other half are preparing to bind again
(A common analogy is climbing a rope hand over hand).

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 Relaxation
 Ca2+ pumps in the SR membrane
work constantly to get the Ca2+out
of the sarcoplasm & back into the SR.
 They are unable to do this as long as

the muscle is still binding ACh.

 ACh is released by the motor neuron as long as it keeps

being stimulated.
 Note that ACh does not remain bound to AChR for very long.
 It quickly releases & either binds again or more likely is

hydrolyzed by the enzyme acetylcholinesterase which

exists as part of the sarcolemma & free with in the
synaptic cleft.

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Relaxation…
 When the muscle ceases being
stimulated, the Ca2+ pumps
“win” & sarcoplasmic [Ca2+]
drops.
 Ca2+ stops being available for

troponin & tropomyosin

shifts back into its inhibitory
position.
 The muscle then returns back
to its original length via the
elasticity of the connective
tissue elements, plus the This animation shows another
contraction of antagonistic way to induce muscle relaxation.
Does it make sense?
muscles, and gravity.

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 Rigor Mortis
 Upon death, muscle cells
are unable to prevent Ca2+
entry.
 This allows myosin to
bind to actin.
 Since there is no ATP made
postmortem, the myosin
cannot unbind & the body
remains in a state of
muscular rigidity for
almost the next couple days.

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 Muscle Metabolism
 The chemical energy
released by the hydrolysis
of ATP is necessary for both
muscle contraction & muscle
relaxation.
 Muscles typically store
limited amounts of ATP.
 So resting muscles must
have energy stored in
other ways.

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 ATP Use in the Resting Muscle Cell

1) Necessary for cellular housekeeping duties.

2) Powers the combination of glucose monomers (which
have been taken up from the blood stream) into the
storage polymer glycogen.
3) Create another energy storage compound called
creatine phosphate or phosphocreatine:

ATP + Creatine  ADP + Creatine-Phosphate

creatine kinase

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 Working Muscle
 As we begin to exercise, we almost immediately use our
stored ATP.
 For the next 15 seconds or so, we turn to the
phosphagen system, the energy stored in creatine-
phosphate.
Creatine-P + ADP Creatine Kinase
Creatine + ATP
 The ATP is then available to power contraction and
relaxation.
 The phosphagen system dominates in events such as
the 100m rushing movement or lifting weights.

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 Types of Muscle Contractions
 Muscle contraction is said to be isometric when
the muscle does not shorten during contraction.
 Isotonic when it does shorten but the tension
on the muscle remains constant throughout the
contraction.
 Contractions can be:
1. Isometric (iso = same, meter = measure)
2. Isotonic (iso = same, ton = tension)

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 Other Important Terms
1. Flaccid paralysis
 Weakness or loss of muscle tone typically due to
injury or disease of motor neurons.
2. Spastic paralysis
 Sustained involuntary contraction of muscle (s)
with associated loss of function.
 How do flaccid and spastic paralysis differ?

3. Spasm
 A sudden, involuntary smooth/skeletal muscle twitch.
 Can be painful. Often caused by chemical imbalances.

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 Other Important Terms…

4. Cramp
 A prolonged spasm that causes the muscle to become
taut and painful.

5. Fibrosis
 Replacement of normal tissue with heavy fibrous
connective tissue (scar tissue).
 How would fibrosis of skeletal muscles affect muscular
strength?
 How would it affect muscle flexibility?

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 Other Important Terms…
6. Hypertrophy
 Increase in size of a cell, tissue or an organ.
 In muscles, hypertrophy of the organ is always due to
cellular hypertrophy (increase in cell size) rather than
cellular hyperplasia (increase in cell number).
 Muscle hypertrophy occurs due to the synthesis of
more myofibrils and glycolitic enzymes.
7. Atrophy
 Reduction in size of a cell, tissue, or organ
 In muscles, it is often caused by disuse.

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 Smooth
Muscle
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 Smooth Muscle
Smooth Muscle
 Involuntary, non-striated
muscle tissue
 Smaller: 1-5 µm in
diameter & 20-500µm in
length.
 Uninucleate: contain
1 centrally placed
nucleus.
 Lack any visible
striations.
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 Smooth Muscle…
 Lack T-tubules but its analog caveolae.
 Have a scanty sarcoplasmicreticulum.
 Innervated by the autonomic nervous system unlike
skeletal muscle which is innervated by the somatic
nervous system (over which you have control).
 Only the endomysium is present. Nor perimysium
or epimysium.
 Occurs within almost every organ, forming
sheets, bundles, or sheaths around other tissues.

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 Smooth Muscle location…

1. Cardiovascular system:
 Smooth muscle in blood vessels regulates blood
flow through vital organs, also helps regulate
blood pressure.
2. Digestive systems:
 Rings of smooth muscle (sphincters) regulate
movement along internal passageways.
 Smooth muscle lining the passageways alternates
contraction & relaxation to propel matter
through the alimentary canal.

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 Smooth Muscle location…
3. Integumentary system:
 Regulates blood flow to the superficial dermis.

 Allows for piloerection.

4. Respiratory system:
 Alters the diameter of the airways & changes

the resistance to airflow.

5. Urinary system
 Sphincters regulate the passage of urine.

 Smooth muscle contractions move urine into and

out of the urinary bladder.

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 Smooth Muscle location…
6. Reproductive system
 Females

 Assists in the movement of the egg (& of sperm)

through the female reproductive tract.

 Plays a large role in childbirth.

 Males

 Allows for:

 movement of sperm along the male

reproductive tract.
 erection and ejaculation.

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 Physical structure of smooth muscle

 No Z discs, instead thin filaments are attached to protein

structures (dense bodies) which attach to the sarcolemma.
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 Smooth Muscle Contraction
 Begins with the opening of membrane channels:
 ligand-gated (NTs, hormones, metabolites).
 voltage-gated, or mechanically-gated (stretch).
 Channels will allow significant ca+ entry from the ECF.
 Remember smooth muscle has little SR.
 Ca+ binds to regulatory molecule calmodulin &
activates it.
 Activated calmodulin activates an enzyme called Myosin
Light Chain Kinase (MLCK).

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 Smooth Muscle Contraction…
 Activated MLCK will add a
phosphate group to the
myosin of the thick
filament.
 This enables the myosin
to interact with actin.
 Tropomyosin is present

but not blocking actin’s

myosin binding sites
 Troponin is not present

 Contraction then ensues.

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 Smooth muscle Relaxation
 Ca+ is pumped out of the
cell, which ↓the amount of
active calmodulin which
↓the amount of active MLCK
which ↓the number of cross
bridges.
Relaxation can occur
subsequent
to contraction or at any time if
anything causes a ↓in the ca+
permeability of the smooth
muscle cell.
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 Role of the Smooth Muscle
Sarcoplasmic Reticulum
 Sarcoplasmic tubules lie near
the cell membrane in some
larger smooth muscle cells.
 Small invaginations of the
cell membrane (caveolae)
adjacent to the surfaces of
these tubules.
 Caveolae suggest a
rudimentary analog of the
transverse tubule system of
skeletal muscle.

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 Role of the Smooth Muscle SR…
 When an action potential is transmitted into the
caveolae, this is believed to excite ca+ release from
the adjacent sarcoplasmic tubules.
 in the same way that action potentials in skeletal
muscle transverse tubules cause release of
calcium ions from the skeletal muscle longitudinal
sarcoplasmic tubules.
 In general;
 the more extensive the sarcoplasmic reticulum in
the smooth muscle fiber, the more rapidly it
contracts.

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 Types of Smooth Muscle
 Smooth muscle varies widely
from organ to organ in terms of:
1. Physical dimensions

2. Fiber arrangement

- organization into bundles

or sheets
3. Responsiveness to certain

stimuli
4. Characteristics of innervation

5. Function

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 Multi-Unit Smooth Muscle
 No gap junctions.
 Each fiber is independent of
all the others.
 Responsible to neural &
hormonal controls
 No pacemaker cells
 Less common
 Found in:
 large airways to the lungs

 large arteries

 eye

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 Single Unit Smooth Muscle
 More common
 Cells contract as a unit
because they are all
connected by gap
junctions
- protein complexes that span
the PM’s of 2 cells allowing
the passage of ions between
them, i.e., allowing the
depolarization of one to cause
the depolarization of another

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 Single Unit Smooth Muscle…

 Some will contract rhythmically due to pacemaker

cells that have a spontaneous rate of depolarization.
 Not directly innervated.
 diffuse release of neurotransmitters at varicosities
(swellings along an axon).
 Responsive to variety of stimuli including stretch
and concentration changes of various chemicals.

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 Cardiac Muscle

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 Cardiac Muscle
 Striated, involuntary
muscle
 Found in walls of the heart
 Consists of branching chains
of stocky muscle cells.
 Uni or binucleate.
 Has sarcomeres & T-
tubules
 Cardiac muscle cells are
joined by structures called
intercalated discs – which
consist of desmosomes and Notice the branching & the intercalated
gap junctions. disc, indicated by the blue arrow.
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 Comparison of 3 muscle types

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