Chapter 8

Histology and
Physiology of
Muscles

Skeletal Muscle Fibers

Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

Functions of the Muscular System

1. Body movement (Skeletal Muscle)
2. Maintenance of posture (Skeletal
Muscle)
3. Respiration (Skeletal Muscle)
4. Production of body heat (Skeletal
Muscle)
5. Communication (Skeletal Muscle)
6. Constriction of organs and vessels
(Smooth Muscle)
7. Heartbeat (Cardiac Muscle)

Functional Characteristics of Muscle

1. Contractility: the ability to shorten

forcibly
2. Excitability: the ability to receive and
respond to stimuli
3. Extensibility: the ability to be stretched
or extended
4. Elasticity: the ability to recoil and
resume the original resting length

Types of Muscle Tissue

The three types of muscle tissue are
skeletal, smooth, and cardiac
These types differ in
Structure
Location
Function
Means of activation

Each muscle is a discrete organ

composed of muscle tissue, blood vessels,
nerve fibers, and connective tissue

Types of Muscle Tissue

Skeletal muscles are responsible for most body
movements
Maintain posture, stabilize joints, and generate heat

Smooth muscle is found in the walls of hollow

organs and tubes, and moves substances through
them
Helps maintain blood pressure
Squeezes or propels substances (i.e., food, feces) through
organs

Cardiac muscle is found in the heart and pumps

blood throughout the body

Tab. 8.1

Skeletal Muscle Structure

Skeletal muscle cells are elongated and are
often called skeletal muscle fibers
Each skeletal muscle cell contains several nuclei
located around the periphery of the fiber near
the plasma membrane
Fibers appear striated due to the actin and
myosin myofilaments
A single fiber can extend from one end of a
muscle to the other
Contracts rapidly but tires easily
Is controlled voluntarily (i.e., by conscious
control)

Skeletal Muscle Structure

Fascia is a general term for connective tissue sheets
The three muscular fascia, which separate and
compartmentalize individual muscles or groups of
muscles are:
Epimysium: an overcoat of dense collagenous
connective tissue that surrounds the entire muscle
Perimysium: fibrous connective tissue that surrounds
groups of muscle fibers called fascicles (bundles)
Endomysium: fine sheath of connective tissue
composed of reticular fibers surrounding each muscle
fiber

Skeletal Muscle Structure

The connective tissue
of muscle provides a
pathway for blood
vessels and nerves to
reach muscle fibers

Fig. 8.1

Skeletal Muscle Structure

The connective
tissue of muscle
blends with other
connective tissue
based structures,
such as tendons,
which connect
muscle to bone

Fig. 8.2

Skeletal Muscle Structure

Muscle Fibers
Terminology
Sarcolemma: muscle cell plasma membrane
Sarcoplasm: cytoplasm of a muscle cell
Myo, mys, and sarco: prefixes used to refer to
muscle

Muscle contraction depends on two kinds of

myofilaments: actin and myosin
Myofibrils are densely packed, rod-like contractile
elements
They make up most of the muscle volume

Fig. 8.2

Skeletal Muscle Structure

Actin (thin) myofilaments consist of two helical
polymer strands of F actin (composed of G actin),
tropomyosin, and troponin
The G actin contains the active sites to which
myosin heads attach during contraction
Tropomyosin and troponin are regulatory subunits
bound to actin

Fig. 8.2

Skeletal Muscle Structure

Myosin (thick) myofilaments consist of myosin
molecules
Each myosin molecule has
A head with an ATPase, which breaks down ATP
A hinge region, which enables the head to move
A rod

A cross-bridge is formed when a myosin head binds

to the active site on G actin

Fig. 8.2

Skeletal Muscle Structure

Sarcomeres
The smallest contractile unit of a muscle
Sarcomeres are bound by Z disks that hold actin
myofilaments
Six actin myofilaments surround a myosin myofilament
Myofibrils appear striated because of A bands and I
bands

Fig. 8.2

Skeletal Muscle Structure

Thick filaments: extend the entire length of an A band
Thin filaments: extend across the I band and partway
into the A band
Z-disc: a coin-shaped sheet of proteins (connectins) that
anchors the thin filaments and connects myofibrils to one
another
Thin filaments do not overlap thick filaments in the lighter
H zone
M lines appear darker due to the presence of the protein
desmin
The arrangement of myofibrils within a fiber is so
organized a perfectly aligned repeating series of dark A
bands and light I bands is evident

Fig.
8.3bc

Sliding Filament Model

Actin and myosin myofilaments do not change in length
during contraction
Thin filaments slide past the thick ones so that the actin
and myosin filaments overlap to a greater degree
Upon stimulation, myosin heads bind to actin and sliding begins
Each myosin head binds and detaches several times during
contraction (acting like a ratchet to generate tension and propel
the thin filaments to the center of the sarcomere)

In the relaxed state, thin and thick filaments overlap only

slightly
As this event occurs throughout the sarcomeres, the
muscle shortens
The I band and H zones become narrower during
contraction, and the A band remains constant in length

Fig. 8.4

Sliding Filament Model

Actin and myosin myofilaments in a relaxed
muscle (below) and a contracted muscle are the
same length. Myofilaments do not change
length during muscle contraction

Fig. 8.4

Sliding Filament Model

During contraction, actin myofilaments at each
end of the sarcomere slide past the myosin
myofilaments toward each other. As a result,
the Z disks are brought closer together, and the
sarcomere shortens

Fig. 8.4

Sliding Filament Model

As the actin myofilaments slide over the myosin
myofilaments, the H zones (yellow) and the I
bands (blue) narrow. The A bands, which are
equal to the length of the myosin myofilaments,
do not narrow because the length of the myosin
myofilaments does not change

Fig. 8.4

Sliding Filament Model

In a fully contracted muscle, the ends of
the actin myofilaments overlap at the
center of the sarcomere and the H zone
disappears

Fig. 8.4

Physiology of Skeletal Muscle Fibers

Membrane Potentials
The nervous system stimulates muscles to contract
through electric signals called action potentials
Plasma membranes are polarized, which means there
is a charge difference (resting membrane potential)
across the plasma membrane
The inside of the plasma membrane is negative as
compared to the outside in a resting cell
An action potential is a reversal of the resting
membrane potential so that the inside of the plasma
membrane becomes positive

Physiology of Skeletal Muscle Fibers

Ion Channels
Assist with the production of action potentials
Ligand-gated channels
Voltage-gated channels

Fig. 8.5

Fig. 8.6

Physiology of Skeletal Muscle Fibers

Action Potentials
Depolarization results from an increase in the
permeability of the plasma membrane to Na+
If depolarization reaches threshold, an action
potential is produced
The depolarization phase of the action potential
results from the opening of many Na+ channels

Fig. 8.6

Physiology of Skeletal Muscle Fibers

Action Potentials
The repolarization phase of the action
potential occurs when the Na+ channels close
and K+ channels open briefly

Fig. 8.6

Fig. 8.6

Physiology of Skeletal Muscle Fibers

Action Potentials
Occur in an all-or-none fashion
A stimulus below threshold produces no action
potential
A stimulus at threshold or stronger will produce an
action potential

Propagate (travel) across plasma membranes

Physiology of Skeletal Muscle Fibers

Nerve Stimulus of Skeletal Muscle
Skeletal muscles are stimulated by motor
neurons of the somatic nervous system
Axons of these neurons travel in nerves to
muscle cells
Axons of motor neurons branch profusely as
they enter muscles
Each axonal branch forms a neuromuscular
junction with a single muscle fiber

Physiology of Skeletal Muscle Fibers

The neuromuscular junction is formed from:
Axonal endings
Have small membranous sacs (synaptic vesicles)
Contain the neurotransmitter acetylcholine (ACh)

Motor end plate of a muscle

Specific part of the sarcolemma
Contains ACh receptors

Though exceedingly close, axonal ends and

muscle fibers are always separated by a space
called the synaptic cleft

Fig. 8.7

Neuromuscular Junction Physiology

1. An action potential (orange
arrow) arrives at the
presynaptic terminal and
causes voltage-gated Ca2+
channels in the
presynaptic membrane to
open
2. Calcium ions enter the
presynaptic terminal and
initiate the release of the
neurotransmitter
acetylcholine (ACh) from
synaptic vesicles
3. ACh is released into the
synaptic cleft by exocytosis
Fig. 8.8

Neuromuscular Junction Physiology

1. An action potential (orange
arrow) arrives at the
presynaptic terminal and
causes voltage-gated Ca2+
channels in the
presynaptic membrane to
open
2. Calcium ions enter the
presynaptic terminal and
initiate the release of the
neurotransmitter
acetylcholine (ACh) from
synaptic vesicles
3. ACh is released into the
synaptic cleft by exocytosis
Fig. 8.8

Neuromuscular Junction Physiology

1. An action potential (orange
arrow) arrives at the
presynaptic terminal and
causes voltage-gated Ca2+
channels in the
presynaptic membrane to
open
2. Calcium ions enter the
presynaptic terminal and
initiate the release of the
neurotransmitter
acetylcholine (ACh) from
synaptic vesicles
3. ACh is released into the
synaptic cleft by exocytosis
Fig. 8.8

Neuromuscular Junction Physiology

4. ACh diffuses across the
synaptic cleft and binds to
ligand-gated Na+ channels on
the postsynaptic membrane
5. Ligand-gated Na+ channels
open and Na+ enters the
postsynaptic cell, causing the
postsynaptic membrane to
depolarize. If depolarization
passes threshold, an action
potential is generated along
the postsynaptic membrane
6. ACh is removed from the
ligand-gated Na+ channels,
which then close
Fig. 8.8

Neuromuscular Junction Physiology

4. ACh diffuses across the
synaptic cleft and binds to
ligand-gated Na+ channels on
the postsynaptic membrane
5. Ligand-gated Na+ channels
open and Na+ enters the
postsynaptic cell, causing the
postsynaptic membrane to
depolarize. If depolarization
passes threshold, an action
potential is generated along
the postsynaptic membrane
6. ACh is removed from the
ligand-gated Na+ channels,
which then close
Fig. 8.8

Neuromuscular Junction Physiology

4. ACh diffuses across the
synaptic cleft and binds to
ligand-gated Na+ channels on
the postsynaptic membrane
5. Ligand-gated Na+ channels
open and Na+ enters the
postsynaptic cell, causing the
postsynaptic membrane to
depolarize. If depolarization
passes threshold, an action
potential is generated along
the postsynaptic membrane
6. ACh is removed from the
ligand-gated Na+ channels,
which then close
Fig. 8.8

Neuromuscular Junction Physiology

7. The enzyme acetylcholinesterase,
which is attached to the postsynaptic
membrane, removes acetylcholine
from the synaptic cleft by breaking it
down into acetic acid and choline
8. Choline is symported with Na+ into
the presynaptic terminal, where it
can be recycled to make ACh.
Acetic acid diffuses away from the
synaptic cleft
9. ACh is reformed within the
presynaptic terminal using acetic
acid generated from metabolism and
choline recycled from the synaptic
cleft. ACh is then taken up by the
synaptic vesicles
Fig. 8.8

Neuromuscular Junction Physiology

7. The enzyme acetylcholinesterase,
which is attached to the postsynaptic
membrane, removes acetylcholine
from the synaptic cleft by breaking it
down into acetic acid and choline
8. Choline is symported with Na+ into
the presynaptic terminal, where it
can be recycled to make ACh.
Acetic acid diffuses away from the
synaptic cleft
9. ACh is reformed within the
presynaptic terminal using acetic
acid generated from metabolism and
choline recycled from the synaptic
cleft. ACh is then taken up by the
synaptic vesicles
Fig. 8.8

Neuromuscular Junction Physiology

7. The enzyme acetylcholinesterase,
which is attached to the postsynaptic
membrane, removes acetylcholine
from the synaptic cleft by breaking it
down into acetic acid and choline
8. Choline is symported with Na+ into
the presynaptic terminal, where it
can be recycled to make ACh.
Acetic acid diffuses away from the
synaptic cleft
9. ACh is reformed within the
presynaptic terminal using acetic
acid generated from metabolism and
choline recycled from the synaptic
cleft. ACh is then taken up by the
synaptic vesicles
Fig. 8.8

Fig. 8.8

Excitation-Contraction Coupling
In order to contract, a skeletal muscle
must:
Be stimulated by a nerve ending
Propagate an electrical current, or action
potential, along its sarcolemma
Have a rise in intracellular Ca2+ levels, the
final trigger for contraction

Linking the electrical signal to the

contraction is excitation-contraction
coupling

Excitation-Contraction Coupling
Invaginations of the sarcolemma form T tubules, which
wrap around the sarcomeres and penetrate into the cells
interior at each A band I band junction
Sarcoplasmic reticulum (SR) is
an elaborate, smooth
endoplasmic reticulum that
mostly runs longitudinal and
surrounds each myofibril
Paired terminal cisternae form
perpendicular cross channels
Functions in the regulation of
intracellular calcium levels

A triad is a T tubule and two

terminal cisternae

Fig. 8.9

Excitation-Contraction Coupling
1. An action potential produced at the
presynaptic terminal in the
neuromuscular junction is propagated
along the sarcolemma of the skeletal
muscle. The depolarization also
spreads along the membrane of the T
tubules
2. The depolarization of the T tubule
causes gated Ca2+ channels in the
SR to open, resulting in an increase
in the permeability of the SR to Ca2+,
especially in the terminal cisternae.
Calcium ions then diffuse from the
SR into the sarcoplasm
3. Calcium ions released from the SR
bind to troponin molecules. The
troponin molecules bound to G actin
molecules are released, causing
tropomyosin to move, exposing the
active sites on G actin
4. Once active sites on G actin
molecules are exposed, the heads of
the myosin myofilaments bind to
them to form cross-bridges

Excitation-Contraction Coupling
1. An action potential produced at the
presynaptic terminal in the
neuromuscular junction is propagated
along the sarcolemma of the skeletal
muscle. The depolarization also
spreads along the membrane of the T
tubules
2. The depolarization of the T tubule
causes gated Ca2+ channels in the
SR to open, resulting in an increase
in the permeability of the SR to Ca2+,
especially in the terminal cisternae.
Calcium ions then diffuse from the
SR into the sarcoplasm
3. Calcium ions released from the SR
bind to troponin molecules. The
troponin molecules bound to G actin
molecules are released, causing
tropomyosin to move, exposing the
active sites on G actin
4. Once active sites on G actin
molecules are exposed, the heads of
the myosin myofilaments bind to
them to form cross-bridges

Excitation-Contraction Coupling
1. An action potential produced at the
presynaptic terminal in the
neuromuscular junction is propagated
along the sarcolemma of the skeletal
muscle. The depolarization also
spreads along the membrane of the T
tubules
2. The depolarization of the T tubule
causes gated Ca2+ channels in the
SR to open, resulting in an increase
in the permeability of the SR to Ca2+,
especially in the terminal cisternae.
Calcium ions then diffuse from the
SR into the sarcoplasm
3. Calcium ions released from the SR
bind to troponin molecules. The
troponin molecules bound to G actin
molecules are released, causing
tropomyosin to move, exposing the
active sites on G actin
4. Once active sites on G actin
molecules are exposed, the heads of
the myosin myofilaments bind to
them to form cross-bridges

Excitation-Contraction Coupling
1. An action potential produced at the
presynaptic terminal in the
neuromuscular junction is propagated
along the sarcolemma of the skeletal
muscle. The depolarization also
spreads along the membrane of the T
tubules
2. The depolarization of the T tubule
causes gated Ca2+ channels in the
SR to open, resulting in an increase
in the permeability of the SR to Ca2+,
especially in the terminal cisternae.
Calcium ions then diffuse from the
SR into the sarcoplasm
3. Calcium ions released from the SR
bind to troponin molecules. The
troponin molecules bound to G actin
molecules are released, causing
tropomyosin to move, exposing the
active sites on G actin
4. Once active sites on G actin
molecules are exposed, the heads of
the myosin myofilaments bind to
them to form cross-bridges

Excitation-Contraction Coupling
1. An action potential produced at the
presynaptic terminal in the
neuromuscular junction is propagated
along the sarcolemma of the skeletal
muscle. The depolarization also
spreads along the membrane of the T
tubules
2. The depolarization of the T tubule
causes gated Ca2+ channels in the SR
to open, resulting in an increase in the
permeability of the SR to Ca2+,
especially in the terminal cisternae.
Calcium ions then diffuse from the SR
into the sarcoplasm
3. Calcium ions released from the SR
bind to troponin molecules. The
troponin molecules bound to G actin
molecules are released, causing
tropomyosin to move, exposing the
active sites on G actin
4. Once active sites on G actin
molecules are exposed, the heads of
the myosin myofilaments bind to them
to form cross-bridges

Fig. 8.11

Fig. 8.11

Fig. 8.11

Fig. 8.11

Fig. 8.11

Fig. 8.11

Fig. 8.11

Muscle Relaxation
Calcium ions are transported back into the
sarcoplasmic reticulum
Calcium ions diffuse away from troponin
and tropomyosin moves, preventing
further cross-bridge formation

Muscle Twitch
The contraction of a
muscle as a result of
one or more muscle
fibers contracting
Has lag, contraction,
and relaxation
phases

Table 8.2

Strength of Muscle Contraction

For a given condition, a muscle fiber or motor
unit contracts with a consistent force in response
to each action potential
For a whole muscle, stimuli of increasing
strength result in graded contractions of
increased force as more motor units are
recruited (multiple motor unit summation)
Stimulus of increasing frequency increase the
force of contraction (multiple-wave summation)

Motor Unit

Fig. 8.13

Strength of Muscle Contraction

Incomplete tetanus is partial relaxation between
contractions, and complete tetanus is no
relaxation between contractions
The force of contraction of a whole muscle
increases with increased frequency of
stimulation because of an increasing
concentration of Ca2+ around the myofibrils
Treppe is an increase in the force of contraction
during the first few contractions of a rested
muscle

Multiple Motor Unit Summation in a Muscle

Fig. 8.14

Multiple-Wave Summation

Fig. 8.15

Treppe

Fig. 8.15

Types of Muscle Contraction

Isometric contractions cause a change in muscle
tension but no change in muscle length
Isotonic contractions cause a change in muscle
length but no change in muscle tension
Concentric contractions are isotonic contractions
that cause muscles to shorten
Eccentric contractions are isotonic contractions
that enable muscles to shorten
Muscle tone is the maintenance of a steady
tension for long periods
Asynchronous contractions of motor units
produce smooth, steady muscle contractions

Muscle Length and Tension

Muscle contracts
with less than
maximum force if
its initial length is
shorter or longer
than optimal

Fig. 8.17

Fatigue
The decreased ability to do work
Can be caused by
The central nervous system (psychologic
fatigue)
Depletion of ATP in muscles (muscular
fatigue)

Physiologic contracture (the inability of

muscles to contract or relax) and rigor
mortis (stiff muscles after death) result
from inadequate amounts of ATP

Energy Sources
Creatine phosphate
ATP is synthesized
when ADP reacts
with creatine
phosphate to form
creatine and ATP
ATP from this
source provides
energy for a short
time
Fig. 8.18

Energy Sources
Anaerobic respiration
ATP synthesized provides
energy for a short time at
the beginning of exercise
and during intense
exercise
Produces ATP less
efficiently but more rapidly
than aerobic respiration
Lactic acid levels increase
because of anaerobic
respiration
Fig. 8.18

Energy Sources
Aerobic respiration
Requires oxygen
Produces energy
for muscle
contractions under
resting conditions
or during
endurance exercise

Fig. 8.18

Fig. 8.18

Speed of Contraction
The three main types of skeletal muscle
fibers are
Slow-twitch oxidative (SO) fibers
Fast-twitch glycolytic (FG) fibers
Fast-twitch oxidative glycolytic (FOG) fibers

SO fibers contract more slowly than FG

and FOG fibers because they have slower
myosin ATPases than FG and FOG fibers

Fatigue Resistance
SO fibers are fatigue-resistant and rely on
aerobic respiration
Many mitochondria, a rich blood supply, and
myoglobin

FG fibers are fatigable

Rely on anaerobic respiration and have a high
concentration of glycogen

FOG fibers have fatigue resistance

intermediate between SO and FG fibers
Rely on aerobic and anaerobic respiration

Functions
SO fibers maintain posture and are involved with
prolonged exercise
Long-distance runners have a higher percentage of
SO fibers

FG fibers produce powerful contractions of short

duration
Sprinters have a higher percentage of FG fibers

FOG fibers support moderate-intensity

endurance exercises
Aerobic exercise can result in the conversion of FG
fibers to FOG fibers

Tab. 8.3

Muscular Hypertrophy and Atrophy

Hypertrophy is an increase in the size of
muscles
Due to an increase in the size of muscle fibers
resulting from an increase in the number of myofibrils
in the muscle fibers
Aerobic exercise
Increases the vascularity of muscle
Greater hypertrophy of slow-twitch fibers than fast-twitch fibers

Intense anaerobic exercise

Greater hypertrophy of fast-twitch fibers than slow-twitch

Atrophy is a decrease in the size of muscle

Due to a decrease in the size of muscle fibers or a
loss of muscle fibers

Effects of Aging on Skeletal Muscle

By 80 years of age 50% of the muscle
mass is gone
Due to a loss in muscle fibers
Fast-twitch muscle fibers decrease in number
more rapidly than slow-twitch fibers

Can be dramatically slowed if people

remain physically active

Types of Smooth Muscle

Visceral smooth muscle fibers have many
gap junctions and contract as a single unit
Multiunit smooth muscle fibers have few
gap junctions and function independently
Found in the walls of hollow visceral organs,
such as the stomach, urinary bladder, and
respiratory passages
Forces food and other substances through
internal body channels
It is not striated and is involuntary

Regulation of Smooth Muscle

Contraction is involuntary
Multiunit smooth muscle contracts when
externally stimulated by nerves, hormones, or
other substances
Visceral smooth muscle contracts
autorhythmically or when stimulated externally

Hormones are important in regulating

smooth muscle

Structure of Smooth Muscle Cells

Spindle-shaped with a single nucleus
Have actin and myosin myofilaments
Actin myofilaments are connected to dense bodies
and dense areas

Not striated
No T tubule
system and
most have less
SR than skeletal
muscle
No troponin

Contraction and Relaxation of Smooth Muscle

Calcium ions enter the cell to initiate
contraction
Bind to calmodulin
Activate myosin kinase, which transfers a
phosphate group from ATP to myosin
When phosphate groups are attached to
myosin, cross-bridges form

Relaxation results when myosin

phosphatase removes a phosphate group
from the myosin molecule

Fig. 8.19

Functional Properties of Smooth Muscle

Pacemaker cells are autorhythmic smooth muscle
cells that control the contraction of other smooth
muscle cells
Smooth muscle cells contract more slowly than
skeletal muscle cells
Smooth muscle tone is the ability of smooth muscle
to maintain a steady tension for long periods with
little expenditure of energy
Smooth muscle in the walls of hollow organs
maintain a relatively constant pressure on the
contents of the organ despite changes in content
volume
The force of smooth muscle contraction remains
nearly constant despite changes in muscle length

Cardiac Muscle Cells

Occurs only in the heart
Is striated like skeletal muscle but is not
voluntary
Have a single nucleus
Connected by intercalated disks that allowing
them to function as a single unit
Capable of autorhythmicity
Contracts at a fairly steady rate set by the
hearts pacemaker
Neural controls allow the heart to respond to
changes in bodily needs

Tab. 8.1

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