Because learning changes everything.

Chapter 09

Muscular System
Histology And Physiology
Seeley’s
ANATOMY & PHYSIOLOGY
Thirteenth Edition
Cinnamon VanPutte, Jennifer
Regan, Andrew Russo

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No reproduction or further distribution permitted without the prior written consent of McGraw Hill, LLC.
 Because learning changes everything. ®

1. Differentiate the three types of muscle tissue—

skeletal, cardiac, and smooth—based on
microscopic structure, location, and function.
2. Identify muscle fiber ultrastructures, including
myofibrils, sarcomeres, and associated proteins,
Learning using histological slides and diagrams.

3. Explain the sliding filament mechanism of

Objectives: muscle contraction and describe the roles of

calcium ions, ATP, and regulatory proteins.

4. Analyze the physiological processes involved in

muscle contraction, fatigue, and recovery, and
relate them to human movement.

5. Demonstrate proper laboratory techniques for

preparing, staining, and observing muscle tissue
samples under the microscope, and record
detailed morphological observations.
 Lecture Outline

The hierarchical organization

of a muscle is an excellent
illustration of the relationship
between form and function.

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 9.1 Functions of the Muscular System 1

Types of Muscle Tissue.

• Skeletal.
• Responsible locomotion, facial expressions, posture, respiratory
movements, other types of body movement.
• Voluntary and controlled by the nervous system.
• Smooth.
• Walls of hollow organs, blood vessels, eye, glands, skin.
• Some functions: propel urine, mix food in digestive tract,
dilating/constricting pupils, regulating blood flow.
• In some locations, autorhythmic.
• Controlled involuntarily by endocrine and autonomic nervous systems.
• Cardiac.
• Heart: major source of movement of blood.
• Autorhythmic.
• Controlled involuntarily by endocrine and autonomic nervous systems.

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 Comparison of Muscle Types 1

Skeletal Muscle Smooth Muscle Cardiac Muscle

Location Attached to bones Walls of hollow organs, Heart

blood vessels, eyes,
glands, and skin
Appearance

Ed Reschke Victor P. Eroschenko Ed Reschke

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 Comparison of Muscle Types 2

Skeletal Muscle Smooth Muscle Cardiac Muscle

Cell Shape Very long and Spindle-shaped (15– Cylindrical and

cylindrical (1 mm–4 200 μm in length, 5–8 branched (100–
cm, or as much as 30 μm in diameter 500 μm in length,
cm in length, 10 μm– 12–20 μm in
100 μm in diameter) diameter)

Nucleus Multiple nuclei, Single, centrally Single, centrally

peripherally located located located

Special None Gap junctions join Intercalated disks

Cell-to-Cell some visceral smooth join cells to one
Attachments muscle cells together another

Striations Yes No

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 Comparison of Muscle Types 3

Skeletal Muscle Smooth Muscle Cardiac Muscle

Control Voluntary and Involuntary Involuntary
involuntary (reflexes)
Capable of No Yes (some smooth Yes
Spontaneous muscle)
Contraction

Function Controlling body Moving food through Pumping blood;

movement the digestive tract, contractions
emptying the urinary provide the major
bladder, regulating force for
blood vessel diameter, propelling blood
changing pupil size, through blood
contracting many gland vessels
ducts, moving hair, and
many other functions

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 9.1 Functions of the Muscular System 2

1. Movement of the body.

2. Maintenance of posture.
3. Respiration.
4. Production of body heat.
5. Communication.
6. Constriction of organs and vessels.
7. Contraction of the heart.

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 9.2 General Properties of Muscle Tissue

• Contractility: ability of a muscle to shorten with force.

• Excitability: capacity of muscle to respond to a stimulus

(usually from nerves).

• Extensibility: muscle can be stretched beyond it normal

resting length and still be able to contract.

• Elasticity: ability of muscle to recoil to original resting

length after stretched.

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 9.3 Skeletal Muscle Anatomy

Whole skeletal muscle anatomy.

• Connective tissue coverings:
• Epimysium. C.T. that surrounds a whole muscle (many fascicles).
• Merges with muscular fascia, the layer of C.T. between adjacent muscles
and between muscles and skin.

• Perimysium. Loose C.T. surrounding a group of muscle fibers;

passage for blood vessels and nerves.
• Bundles of muscle cells are called fascicles.

• Endomysium. Loose C.T. separating individual muscle fibers within

each fascicle.
• Collagen from CT layers merge to form tendons or aponeuroses,
which attach muscle to bone.

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 Nerves and Blood Vessels

Motor neurons stimulate skeletal muscle contraction.

• Each motor neuron controls several muscle fibers.
• Each muscle fiber is supplied by a branch of the motor
neuron.
An artery and 1 to 2 veins extend with a nerve through the CT
layers.
Extensive capillary beds surround muscle fibers.

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 Whole Skeletal Muscle Fiber Structure: Connective
Tissue, Innervation, and Blood Supply

(b) Alvin Telser/Science Source; (c) Biophoto Associates/Science Source

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 Skeletal Muscle Fiber Anatomy

Develop from fusion of

myoblasts, resulting in large,
multinucleated muscle cells.
• 1 to 4 mm avg length (can
get up to 1 foot).
• 10 to 100 microns avg
diameter.
Have a striated appearance.
Number of fibers remains
relatively constant after birth;
muscles get larger due to
hypertrophy of muscle
fibers.
Ed Reschke

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 Histology of Muscle Fibers 1

Electrical component structures can respond to and transmit

electrical signals; they include the following:
• Sarcolemma – plasma membrane; surrounds
sarcoplasm (cytoplasm) and other contents of cell.
• Transverse tubules (T tubules) – inward folds of
sarcolemma; project into the interior of muscle cell.
• Sarcoplasmic reticulum (SR) – specialized smooth
endoplasmic reticulum; stores calcium.
• Enlarged portions called terminal cisternae lie adjacent to T
tubules.

• Two terminal cisternae and their associated T tubule form a triad.

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 Structure of the Triad

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 Histology of Muscle Fibers 2

Mechanical component structures allow muscles to contract;

due to:
• Myofibrils – bundles of protein filaments; contain the
protein filaments (myofilaments) that cause contraction.
• Myofilaments:
• Actin (thin) myofilaments.
• Myosin (thick) myofilaments.
• Myofilaments arranged into orderly units called sarcomeres.

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 Structure of a Muscle

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 Sarcomeres 1

Sarcomere: basic functional unit of muscle fiber; smallest

part that can contract.
Z disk: filamentous network of protein. Serves as attachment
for actin myofilaments.
Regions of sarcomere:
• I bands: lighter-staining regions, each containing a Z disk
and extend to ends of myosin myofilaments.
• A bands: central dark-staining region; overlapping actin
and myosin myofilaments (except at center).
• H zone: region in A band where actin and myosin do not
overlap.
• M line: middle of H zone; delicate filaments holding
myosin in place.
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 Sarcomeres 2

• In muscle fibers, A and I bands of parallel myofibrils are

aligned and so produce striated appearance.

• Titin filaments: elastic chains of amino acids; make

muscles extensible and elastic.

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 Organization of Sarcomeres

(a) Don W. Fawcett/Science Source

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 Actin (Thin) Myofilaments

Two strands of fibrous (F) actin form a double helix extending the
length of the myofilament; attached at either end at sarcomere.
• Composed of G actin monomers each of which has an active
site.
• Actin site can bind myosin during muscle contraction.
Tropomyosin: an elongated protein winds along the groove of the
F actin double helix.
Troponin is composed of three subunits: one that binds to actin, a
second that binds to tropomyosin, and a third that binds to calcium
ions. Spaced between the ends of the tropomyosin molecules in
the groove between the F actin strands.
The tropomyosin/troponin complex regulates the interaction
between active sites on G actin and myosin.

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 Myosin (Thick) Myofilament

Many elongated myosin molecules shaped like golf clubs.

Molecule consists of myosin heavy chains wound together
to form a rod portion lying parallel to the myosin
myofilament and two myosin heads that extend laterally.
Myosin heads.
1. Can bind to active sites on the actin molecules to form
cross-bridges.
2. Attached to the rod portion by a hinge region that can
bend and straighten during contraction.
3. Are ATPase enzymes: activity that breaks down
adenosine triphosphate (A TP), releasing energy. Part of
the energy is used to bend the hinge region of the myosin
molecule during contraction.
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 Organization of the Sarcomere: Actin

(e) Ed Reschke/Photolibrary/Getty Images

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 Neuromuscular Junction Structure 1

Motor neurons carry electrical signals called action

potentials, which stimulate muscle fiber action potentials
followed by muscle contraction.
Points of contact between motor neuron and muscle fiber is
the neuromuscular junction, or synapse, consisting of:
• Presynaptic terminal: axon terminal with synaptic
vesicles containing the neurotransmitter acetylcholine
(ACh).
• Neurotransmitters from one cell (for example, motor neuron) can
bind to ligand-gated ion channels on another cell (for example,
muscle fiber).
• Synaptic cleft: space.
• Postsynaptic membrane or motor end-plate.
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 Neuromuscular Junction Structure 2

(a) Don W. Fawcett/Science Source; (e) Ed Reschke/Photolibrary/Getty Images

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 Sliding Filament Model

Actin myofilaments sliding over myosin to shorten

sarcomeres.
• Actin and myosin do not change length.
• Shortening sarcomeres responsible for skeletal muscle
contraction.
During relaxation, sarcomeres lengthen because of some
external force, like contraction of antagonistic muscles.
• Muscles that produce the opposite effect.

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 Sarcomere Shortening

In a relaxed muscle, the actin and myosin

myofilaments overlap slightly, and the H
zone is visible. The sarcomere length is at
its normal resting length. As a muscle
contraction is initiated, actin myofilaments
slide past the myosin myofilaments, the z
disks are brought closer together, and the
sarcomere begins to shorten.
In a contracted muscle, the A bands do not
narrow because the length of the myosin
myofilaments does not change. The ends
of the actin myofilaments are pulled to and
overlap in the center of the sarcomere,
shortening it and the H zone disappears.
(a top image) Don W. Fawcett/ Science Source; (b
top image) Biophoto Associates/Science Source
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 9.4 Skeletal Muscle Fiber Physiology

Nervous system controls muscle contractions through action

potentials.
Resting membrane potentials.
• Membrane voltage difference across membranes
(polarized).
• Inside cell more negative due to accumulation of large protein
molecules. More K + on inside than outside. K + leaks out but not
completely because negative proteins hold some back.
• Outside cell more positive and more Na + on outside than inside.
• Na + /K + pump maintains this situation.

• Must exist for action potential to occur.

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 Review of membrane permeabilities

• Phospholipid bilayer interior of the plasma membrane is

hydrophobic and inhibits the movement of charged
particles, particularly ions, yet ion movement is the basis
for the electrical properties of the plasma membrane.

• Transport proteins play an important role in membrane

permeability and contribute to the electrical properties of
both the resting and the stimulated cell.

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 Ion Channels

Types.
• Ligand-gated. Ligands are molecules that bind to
receptors. Receptor: protein or glycoprotein with a
receptor site.
• Example: neurotransmitters.
• Gate is closed until neurotransmitter attaches to receptor molecule.
When Ach attaches to receptor on muscle cell, Na+ gate opens.
Na+ moves into cell due to concentration gradient.

• Voltage-gated.
• Open and close in response to small voltage changes across
plasma membrane.
Each is specific for certain ions.

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 Measuring the Resting Membrane Potential

1. The concentration gradient for an ion determines whether it will enter or leave
the cell after its ion channel opens. Because Na+ is in higher concentration
outside the cell, when voltage-gated Na+ channels open, Na+ enters the cell.
In a similar fashion, when gated K + channels open, K + leaves the cell.
Excitable cells have many K + leak ion channels. Thus, at rest, K + moves out of
the cell faster than Na+ moves into the cell. In addition, negatively charged
molecules, such as proteins, are “trapped” inside the cell because the plasma
membrane is impermeable to them. For these reasons, the inside of the
plasma membrane is more negatively charged than the outside.
2. Some K + is able to diffuse down the concentration gradient from inside to
just outside the plasma membrane. Because K + is positively charged, its
movement from inside the cell to outside causes the inside of the plasma
membrane to become even more negatively charged compared with the
outside.
Potassium ions diffuse down their concentration gradient only until the
charge difference across the plasma membrane is great enough to prevent
any additional diffusion of K + out of the cell. Therefore, the resting
membrane potential is an equilibrium in which the tendency for K + to diffuse
out of the cell is opposed by the negative charges inside the cell. These
negative charges inside the cell tend to attract the positively charged K +
back into the cell.
3. It is the active transport of Na+ and K + by the sodium-potassium pump that
maintains the uneven distribution of Na + and K + across the plasma membrane (see
chapter 3). In a resting cell, the sodium-potassium pump transports K + from outside
the cell to the inside and transports Na + from inside the cell to the outside.

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 Action Potentials

Phases.
• Depolarization: Inside of plasma membrane
becomes less negative. If change reaches
+
threshold (when voltage-gated Na gates open),
depolarization occurs.
• Repolarization: return of resting membrane
potential. Note that during repolarization, the
membrane potential drops lower than its original
resting potential, then rebounds. This is because
Na + plus K + together are higher, but then Na+ /K +
pump restores the resting potential.
All-or-none principle: If threshold is reached, the cell
will respond completed.
Propagate: Spread from one location to another. Action
potential does not move along the membrane: new
action potential at each successive location.
Frequency: number of action potential produced per
unit of time.
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 Voltage-Gated Ion Channels and the Action Potential 1

+
1. Resting membrane potential. Na voltage-gated channels (red) and
some, but not all, K + channels (purple) are closed. K + diffuses down its
concentration gradient through the open K + channels (leak
channels), making the inside of the cell membrane negatively
charged compared to the outside.

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 Voltage-Gated Ion Channels and the Action Potential 2

2. Depolarization. Na + channels
(ligand-gated and voltage gated)
+
are open. Na diffuses down its
concentration gradient through
the open Na + channels, making
the inside of the cell membrane
positively charged compared to
the outside.
3. Repolarization. Na + channels are
closed, and Na + movement into
the cells stops. More K + channels
open. K + movement out of the cell
increases, making the inside of
the cell membrane negatively
charged compared to the outside,
once again.

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 Summary of Action Potential Generation

1. Before initiation of an action potential, the muscle fiber is in its resting membrane potential.
2. Depolarization occurs upon opening of voltage-gated Na+ channels.
3. Repolarization occurs when the Na+ channels close and the voltage-gated K+ channels open.
4. A period of hyperpolarization, also called the after-potential, occurs because the voltage-gated K+
channels stay open than longer than required to reach resting membrane potential. The Na+/K+
pump restores the resting ion balance.
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 Action Potential Propagation

1. An action potential in a local

area of the plasma membrane
is indicated by the green band.
Note the reversal of charge
across the membrane.
2. The depolarization of the
membrane in one action
potential location triggers the
opening of voltage-gated Na+
channels in the adjacent
plasma membrane.
3. The action potential propagates
along the plasma membrane
(green arrow).

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 Function of the Neuromuscular Junction

1. When an action potential reaches the presynaptic terminal of a

motor neuron, it causes voltage-gated Ca2 + channels in the
2+
presynaptic membrane to open. As a result, Ca diffuse into the
axon terminal.
2. Calcium ions cause s few synaptic vesicles to migrate to the
presynaptic terminal where they fuse with the plasma
membrane.
3. Acetylcholine (Ach) is released into synaptic cleft by exocytosis.
4. ACh diffuses across the synaptic cleft and binds to ligand-gated
Na+ channels on the motor end plate causing them to open.

5. Na+ enters the muscle fiber, causing the postsynaptic membrane

to depolarize. If depolarization passes threshold, an action
potential is generated along the sarcolemma.
6. Ach detaches from the ligand-gated Na+ channels, which then
close.
7. The enzyme, acetylcholinesterase, breaks down the Ach to
acetic acid and choline.
8. Motor neurons actively reabsorb choline into the axon terminal
and is rejoined with acetic acid to make more Ach.
9. Recycling choline molecules required less energy and is more
rapid than continuously synthesizing new Ach. Acetic acid is an
intermediate in the process of glucose metabolism which can
be taken up and used by a variety of cells near the
neuromuscular junction.
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 Excitation-Contraction Coupling

• Links electrical and

mechanical components of
contraction.

• Action potential produced

on sarcolemma →
propagated into T tubules
→ calcium channels on S R
terminal cisternae open →
calcium enters sarcoplasm,
binds troponin → muscle
contraction.

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 Action Potentials and Muscle Contraction

1. Excitation-contraction coupling begins at the

neuromuscular junction with the production of an action
potential in the sarcolemma. The action potential is
propagated along the entire sarcolemma of the muscle
fiber and into the T tubules. The T tubules wrap around
sarcomeres where actin and myosin overlap and carry
action potentials into the interior of the muscle fiber.
2+
2. There, the action potentials cause voltage-gated Ca
channels in the terminal cisternae of the sarcoplasmic
reticulum to open. When the Ca2 + channels open, Ca2 +
rapidly diffuses out of the sarcoplasmic reticulum and into
the sarcoplasm surrounding the myofibrils.
2+
3. Once in the sarcoplasm, Ca binds to the troponin
molecules of the actin myofilaments. The binding of Ca2 +
to troponin causes the tropomyosin to move, which
exposes active sites on the actin myofilaments. The
myosin heads then bind to the exposed active sites on G
actin to form cross-bridges. Muscles contract when cross-
bridges move.

4. Cross-bridge formation.

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 Cross-Bridge Movement 1

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 Cross-Bridge Movement 2

1. The myosin head stores energy from A TP breakdown that

occurred during the previous cycle. The myosin head will
remain in the high-energy position until the muscle fiber is
stimulated by a motor neuron initiating the events of excitation-
contraction coupling.
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 Cross-Bridge Movement 3

2. Once the Ca2+ binds to the troponin and the active sites
on the G actin are exposed, the myosin heads quickly
bind to them.
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 Cross-Bridge Movement 4

3. Binding of the myosin heads to the active sites on the G actin forms the
cross-bridges and triggers a rapid movement of the myosin heads at their
hinged region. The movement of the myosin head is called the power
stroke. Because the myosin head is bound to the G actin, the actin
myofilament is pulled past the myosin myofilament toward the H zone of the
sarcomere. Thus, the two myofilaments are “sliding” past each other.
However, the myosin myofilament doesn’t move, it is the actin myofilament
that moves.
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 Cross-Bridge Movement 5

4. Binding of ATP to the

myosin head causes it to
detach from the G actin.

5. The myosin head breaks

down ATP into ADP and P,
which remain attached to
the myosin heads.

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 Cross-Bridge Movement 6

6. Breakdown of the ATP by the

myosin head supplies the
energy for the recovery
stroke, which returns the
myosin head to its “high-
energy” position from its “low-
energy” position. In the “high-
energy” position, the myosin
myofilament can bind farther
down the actin myofilament to
another active site, and pull
the actin myofilament even
closer to the H zone, further
shortening the sarcomere.
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 Cross-Bridge Movement 7

During a single contraction, each myosin myofilament goes

through the cycle of cross-bridge formation, movement,
release, and return to its original position many times. Many
cycles of power and recovery strokes occur during each
muscle contraction.

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 Summary of Skeletal Muscle Contraction 1

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 Summary of Skeletal Muscle Contraction 2

1. An action potential is propagated along the motor neuron.

2. The action potential in the motor neuron stimulates the opening of voltage-gated Ca2+ channels.
3. The influx of Ca into the motor neuron causes the secretion of acetylcholine.
4. The acetylcholine opens ligand-gated Ca2+ channels in the sarcolemma.
5. The resulting action potential in the muscle fiber travels along the entire sarcolemma.
6. The action potentials also move down the T tubule membranes.
7. The T tubules wrap around sarcomeres, where actin and myosin overlap and carry action potentials
into the interior of the muscle fiber. There, the action potentials cause gated Ca2+ channels in the
terminal cisternae of the sarcoplasmic reticulum to open When the Ca2+ channels open,
rapidly diffuses out of the sarcoplasmic reticulum and into the sarcoplasm surrounding the myofibrils.
8. Once in the sarcoplasm, Ca2+ binds to the troponin molecules of the actin myofilaments. Binding of
Ca2+ to troponin causes the tropomyosin to move, which exposes attachment sites on the actin
myofilaments. The myosin heads then bind to the exposed attachment sites on actin to form cross-
bridges. Muscles contract when cross-bridges move.
9. ATP molecules are broken down into ADP and P, which releases energy needed to move the
myosin heads. The heads of the myosin myofilaments bend, causing the actin to slide past the
myosin. As long as Ca2+ is present, the cycle repeats.

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 Muscle Relaxation

Three major ATP-dependent events are required for muscle relaxation.

1. After an action potential has occurred in the muscle fiber, the sodium-
potassium pump must actively transport Na+ out of the muscle fiber and
K + into the muscle fiber to return to and maintain resting membrane
potential.
2. ATP is required to detach the myosin heads from the active sites for the
recovery stroke.
3. ATP is needed for the active transport of Ca2+ into the sarcoplasmic
reticulum from the sarcoplasm.

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 9.5 Whole Skeletal Muscle Physiology

Muscle twitch
• The response of a muscle fiber to
a single action potential along its
motor neuron.
• Phases.
• Lag or latent – from the stimulus to the
beginning of the contraction.
• Contraction – Ca2+ released and cross-
bridging cycling occurs.
• Relaxation – Ca2+ returns to SR and
muscle fiber returns to precontraction
length.

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 Types of Muscle Contractions

Isometric: no change in length but tension increases.

• Postural muscles of body.

Isotonic: change in length but tension constant.

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 Motor Units

Motor unit: a single motor neuron

and all muscle fibers innervated
by it. An action potential in the
neuron of a motor unit causes all
the muscle fibers of that unit to
contract.
Motor Unit numbers:
• Large muscles have motor
units with many muscle fibers.
• Small muscles that make
delicate movements contain
motor units with few muscle
fibers.
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 Force of Contraction in Individual Muscle Fibers

The strength of muscle contractions varies from weak to

strong. The muscle responds in a graded fashion, depending
on the force generated in the individual muscle fibers.
Increasing the number of cross-bridges allows a fiber to
contract with more force. Factors that increase the number of
cross-bridges are:
• Frequency of stimulation
• Muscle fiber diameter
• Muscle fiber length at the time of contraction

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 Frequency of Stimulation - Treppe
1. The Ca2+ released in response to the first
stimulus is not completely removed by the
sarcoplasmic reticulum before the second
stimulus causes the release of additional Ca2+ ,
even though the muscle relaxes completely
between the muscle twitches.
2. As a consequence, during the next contraction
of the muscle, the Ca2+ , concentration in the
sarcoplasm increases slightly, making
contraction more efficient because of the
increased cross-bridge formation. For athletes,
treppe achieved during warm-up exercises can
contribute to improved muscle efficiency. Factors
such as increased blood flow to the muscle and
increased muscle temperature are probably
involved because higher temperatures cause the
enzymes in the muscle fibers to function more
rapidly. Thus, muscle fibers do not normally
display an all-or-none response to repeated
stimuli.
3. However, after a few contractions, the level of
tension produced by each contraction is equal to
the previous contraction.
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 Wave Summation and Tetanus 1

As the frequency of action potentials increases beyond

treppe, contraction occurs with greater force.
• Wave summation: muscle tension increases as
contraction frequencies increase.
• Incomplete tetanus: muscle fibers partially relax between
contraction.
• Complete tetanus: no relaxation between contractions.
Wave summation and tetanus result because the mechanical
events of muscle twitches take longer than the electrical
events, allowing several action potentials to be generated in
the time it takes for a single twitch.
Calcium ions can not be removed fast enough; the muscle
fiber is unable to relax.
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 Wave Summation and Tetanus 2

1. A single action potential arriving at a

muscle fiber causes twitches that
completely relax before the next action
potential arrives.
2. As the action potential frequency
increases, muscle fibers only partially
relax before the next action potential
arrives and the muscle fiber contracts
again; this results in wave summation.
3. With continued stimulation, incomplete
tetanus is the result.
4. Action potential frequency can increase
to the point where the muscle fiber
does not relax at all before the next
action potential arrives, causing the
muscle fiber to contract continuously;
this results in complete tetanus.
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 Muscle Fiber Diameter

• The greater the muscle fiber diameter, the greater the

force the muscle fiber can generate.

• In general, larger diameter fibers have more myofibrils and

therefore can form more cross-bridges which provides
more force of contraction.

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 Muscle Length at Time of Contraction

Active tension: force applied to an object to be lifted when a

muscle contracts.
Active tension increases or decreases as a muscle fiber
changes in length; active tension curve.
• Stretched too far – fewer cross-bridges can form.
• If not stretched at all – thick filaments touch Z disks and
very little contraction can occur.
Passive tension: tension applied to load when muscle
stretches but is not stimulated.
Total tension: sum of active and passive tension.

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 Muscle Length and Tension

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 Force of Contraction in Whole Muscles

• Strength of contraction is graded: ranges from weak to

strong depending on stimulus strength.
• Multiple motor-unit recruitment: strength of contraction
depends upon recruitment of motor units. A muscle has
many motor units.

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 Recruitment

• Sub-threshold stimulus: no action potential; no

contraction.
• Threshold stimulus: action potential; contraction.
• Submaximal stimuli: stronger stimuli that produce action
potentials in axons of additional motor units.
• Maximal stimulus: action potentials are produced in
axons of all motor units of a muscle. A greater stimulus
(supramaximal stimulus) has no additional effect.

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 The Size Principle

• Size principle: during recruitment, small motor units are

recruited first followed by large motor units.
• Muscle tone: constant tension by muscles for long
periods of time; due to small percentage of all motor units
contracting out of phase with one another.

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 Types of Isotonic Contractions

Isotonic: change in length but tension constant.

• Concentric: overcomes opposing resistance and muscle

shortens.

• Eccentric: tension maintained but the opposing resistance

is great enough to cause the muscle to lengthen.

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 9.6 Muscle Fibers Types

Slow-twitch (type I).

• Contract more slowly, smaller in diameter, better blood supply,
more mitochondria, more fatigue-resistant than fast-twitch, large
amount of myoglobin.
• Postural muscles, more in lower than upper limbs. Dark meat of
chicken.
Fast-twitch (type II).
• Respond rapidly to nervous stimulation, contain myosin that can
break down A TP more rapidly than that in Type I, less blood
supply, fewer and smaller mitochondria than slow-twitch.
• Lower limbs in sprinter, upper limbs of most people. White meat
in chicken.
• Comes in oxidative and glycolytic (anaerobic) forms.
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 Muscle Fiber Types

Most muscles have both types but varies for each

muscle/person. Conversion from one type to the other not
easily done.
Effects of exercise: change in size of muscle fibers.
• Hypertrophy: increase in muscle size.
• Increase in myofibrils.
• Increase in nuclei due to fusion of satellite cells.
• Increase in strength due to better coordination of muscles, increase
in production of metabolic enzymes, better circulation, less
restriction by fat.
• Atrophy: decrease in muscle size.
• Reverse except in severe situations where cells die.
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 Heat Production

• Exercise: metabolic rate and heat production increase.

• Post-exercise: metabolic rate stays high due to oxygen
debt.
• Excess heat lost because of vasodilation and sweating.
• Shivering: uncoordinated contraction of muscle fibers
resulting in shaking and heat production.

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 9.7 Energy Sources for Muscle Contraction 1

Skeletal muscle fibers have three major ATP-dependent

enzymes:
• The myosin head
• The Na + -K + pump to maintain the resting membrane
potential
• The Ca2+ reuptake pump in the sarcoplasmic reticulum
Muscles fibers only have enough stored ATP for 5-6 seconds
of contraction. Need to make more.

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 Energy Sources for Muscle Contraction 2

ATP provides immediate energy for muscle contractions.

Produced through four processes:
1. Conversion of two A DP to one ATP and AMP
• Adenylate kinase
2. Transfer of phosphate from creatine kinase to A DP
to form ATP
• Creatine kinase
3. Anaerobic respiration
• Occurs in absence of oxygen and results in breakdown of glucose
to yield ATP and lactic acid
4. Aerobic respiration
• Requires oxygen and breaks down glucose to produce ATP,
carbon dioxide and water
• More efficient than anaerobic
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 Production of ATP in Skeletal Muscle

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 Muscle Fatigue

Fatigue - decreased capacity to work and reduced efficiency

of performance.
Mechanisms involved:
• Acidosis and ATP depletion due to either an increased A TP
consumption or a decreased A TP production.
• Oxidative stress, which is characterized by the buildup of
excess reactive oxygen species (R OS; free radicals).
• Local inflammatory reactions
• Physiological contracture - state of fatigue where due to lack of ATP
neither contraction nor relaxation can occur.
• Psychological fatigue – most common type; comes from the central
nervous system rather than the muscles.
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 Rigor Mortis and Muscle Soreness

• Rigor mortis: development of rigid muscles several hours

after death. Ca2+ leaks into sarcoplasm and attaches to
myosin heads and crossbridges form. Rigor ends as
tissues start to deteriorate.

• Soreness: due to the influx of inflammatory chemicals into

the muscle fibers because injury has increased the
permeability of the plasma membranes or ruptured them.

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 Oxygen Deficit and Excess Postexercise Oxygen
Consumption

Oxygen deficit: lag time between when a person begins to

exercise and when he or she begins to breathe more heavily.
Excess postexercise oxygen consumption: lag time
before breathing returns to normal once exercise stops.
• Deficit must be repaid.
• Metabolic processes that restore homeostasis
(body temp, ion concentrations, metabolite and hormone
levels).

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 9.8 Smooth Muscle

• Not striated, fibers smaller than those in skeletal muscle.

• Spindle-shaped; single, central nucleus.
• More actin than myosin.
• Caveolae: indentations in sarcolemma; may act like T
tubules.
• Dense bodies instead of Z disks as in skeletal muscle
that actin attached to; also have noncontractile
intermediate filaments.
• Ca2+ required to initiate contractions; binds to calmodulin
which regulates myosin kinase. Cross-bridging occurs.
• Relaxation: caused by enzyme myosin phosphatase.

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 Smooth Muscle Histology

©Victor Eroschenko

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 Actin and Myosin Proteins in a Smooth Muscle Cell

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 Smooth Muscle Contraction 1

1. Smooth muscle contraction is stimulated

both neurally and hormonally. Regardless
of the stimulus source, a G protein
mechanism opens a Ca2 + channel.
2. An α subunit opens the Ca2 + channel in the
plasma membrane, or depolarization
opens Ca2 + channels. Calcium ions diffuse
through the Ca2 + channels and combine
with calmodulin.
3. Calmodulin with a Ca2 + bound to it binds
with myosin kinase and activates it.

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 Smooth Muscle Contraction 2

4. Activated myosin kinase

transfers a phosphate from ATP
to myosin heads to activate the
contractile process.
5. A cycle of cross-bridge
formation, movement,
detachment, and cross-bridge
formation occurs.
6. Relaxation occurs when myosin
phosphatase removes
phosphate from myosin.

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 Smooth Muscle Contraction 3

If the phosphate is removed from myosin while the cross-

bridges are attached to actin, the cross-bridges release very
slowly. This explains how smooth muscle is able to sustain
tension for long periods and without extensive energy
expenditure. This period of sustained tension is often called
the latch state of smooth muscle contraction.

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 Types of Smooth Muscle

Visceral: cells in sheets; function as a unit.

• Numerous gap junctions; waves of contraction.
• Often autorhythmic.
• Synapses are a series of dilations along the branching
axons.

Multiunit: cells or groups of cells act as independent units.

• Sheets (blood vessels); bundles (arrector pili and iris);
single cells (capsule of spleen).
• Fewer gap junctions; synapses similar to skeletal muscle.

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 Electrical Properties of Smooth Muscle

• Slow waves of depolarization and repolarization transferred

from cell to cell.
• Depolarization caused by spontaneous diffusion of Na + and Ca2+
into cell.
• Does not follow all-or-none law.
• May have pacemaker cells.
• Contraction regulated by nervous system and by hormones.

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 Functional Properties of Smooth Muscle

• Some visceral muscle exhibits autorhythmic contractions.

• Tends to contract in response to sudden stretch but not to
slow increase in length.
• Exhibits relatively constant tension: smooth muscle tone.
• Amplitude of contraction remains constant although
muscle length varies

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 Regulation of Smooth Muscle 1

• Innervated by autonomic nervous system (involuntary).

• Neurotransmitters are acetylcholine and
norepinephrine.
• Hormones such as epinephrine and oxytocin.
• Other chemical regulators are histamine, prostaglandins,
and by-products of metabolism.

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 Regulation of Smooth Muscle 2

Receptors present on plasma membrane; which

neurotransmitters or hormones bind determines response.
• Receptor molecules that stimulate smooth muscle often
open either sodium or calcium channels to cause
depolarization.
• Receptor molecules that inhibit smooth muscle often close
sodium and calcium channels or open potassium channels
to cause hyperpolarization.

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 9.9 Cardiac Muscle

• Found only in heart.

• Striated and branched.
• Each cell usually has one nucleus.
• Has intercalated disks and gap junctions.
• Autorhythmic cells.
• Action potentials of longer duration and longer refractory
period.
• Both Na + and Ca2+ influx needed for depolarization, while
Ca2+ regulates contraction.

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 Cardiac Muscle Fibers

(a) Ed Reschke

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 Effects of Aging on Skeletal Muscle

• Reduced muscle mass.

• Increased time for muscle to contract in response to

nervous stimuli.

• Reduced stamina.

• Increased recovery time.

• Loss of muscle fibers, especially fast-twitch.

• Decreased density of capillaries in muscle.

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 Duchenne Muscular Dystrophy

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