CH 09

Human Anatomy and Physiology
Eleventh Edition
Chapter 09
Muscles and Muscle Tissue
PowerPoint® Lectures Slides prepared by Karen Dunbar Kareiva, Ivy Tech Community College
Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved
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9.1 Overview of Muscle Tissue
• Nearly half of body’s mass
• Can transform chemical energy (ATP) into directed mechanical energy, which is capable
of exerting force
• To investigate muscle, we look at:

– Types of muscle tissue
– Characteristics of muscle tissue
– Muscle functions
Types of Muscle Tissue (1 of 4)
• Terminologies: Myo, mys, and sarco are prefixes for muscle
– Example: sarcoplasm: muscle cell cytoplasm
• Three types of muscle tissue

– Skeletal
– Cardiac
– Smooth
• Only skeletal and smooth muscle cells are elongated and referred to as muscle fibers
• Skeletal muscle
– Skeletal muscle tissue is packaged into skeletal muscles: organs that are
attached to bones and skin
– Skeletal muscle fibers are longest of all muscle and have striations (stripes)
– Also called voluntary muscle: can be consciously controlled
– Contract rapidly; tire easily; powerful
– Key words for skeletal muscle: skeletal, striated, and voluntary
• Cardiac muscle
– Cardiac muscle tissue is found only in heart
 Makes up bulk of heart walls
– Striated
– Involuntary: cannot be controlled consciously
 Contracts at steady rate due to heart’s own pacemaker, but nervous system
can increase rate
– Key words for cardiac muscle: cardiac, striated, and involuntary
• Smooth muscle
– Smooth muscle tissue: found in walls of hollow organs
 Examples: stomach, urinary bladder, and airways
– Not striated
– Involuntary: cannot be controlled consciously
– Key words for smooth muscle: visceral, nonstriated and involuntary
Table 9.3-1 Comparison of Skeletal,
Cardiac, and Smooth Muscle
Table 9.3 Comparison of Skeletal, Cardiac, and Smooth Muscle

Characteristics of Muscle Tissue
• All muscles share four main characteristics:
– Excitability (responsiveness): ability to receive and respond to stimuli
– Contractility: ability to shorten forcibly when stimulated
– Extensibility: ability to be stretched
– Elasticity: ability to recoil to resting length
Muscle Functions
• Four important functions
1. Produce movement: responsible for all locomotion and manipulation
 Example: walking, digesting, pumping blood
2. Maintain posture and body position
3. Stabilize joints
4. Generate heat as they contract
Connective Tissue Sheaths of Skeletal Muscle: Epimysium,
Perimysium, and Endomysium (1 of 2)
Epimysium Epimysium
Bone
Perimysium
Tendon
Endomysium
Muscle fiber
in middle of
a fascicle
(b)
Blood vessel
Perimysium wrapping a fascicle
Endomysium
(between individual muscle fibers)
Muscle fiber
Fascicle
(a)
Figure 9.1 Connective tissue sheaths of skeletal muscle: epimysium, perimysium, and endomysium.
Table 9.1-1 Structure and Organizational
Levels of Skeletal Muscle
Table 9.1 Structure and Organizational Levels of Skeletal

Muscle Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved
9.3 Muscle Fiber Microanatomy and Sliding
Filament Model
• Skeletal muscle fibers are long, cylindrical cells that contain multiple nuclei
• Sarcolemma: muscle fiber plasma membrane
• Sarcoplasm: muscle fiber cytoplasm
• Contains many glycosomes for glycogen storage, as well as myoglobin for O2 storage
• Modified organelles
– Myofibrils
– Sarcoplasmic reticulum
– T tubules
Myofibrils (1 of 7)
• Myofibrils are densely packed, rodlike elements
– Single muscle fiber can contain 1000s
– Accounts for ~80% of muscle cell volume
• Myofibril features
– Striations
– Sarcomeres
– Myofilaments
– Molecular composition of myofilaments
Microscopic Anatomy of a Skeletal Muscle
Fiber (1 of 4)
(b) Diagram of part of a

muscle fiber showing
the myofibrils. One
Sarcolemma
myofibril extends from
the cut end of the fiber.
Mitochondrion
Myofibril
Dark A band Light I band Nucleus
Figure 9.2b Microscopic anatomy of a skeletal muscle fiber.

Myofibrils (2 of 7)
• Striations: stripes formed from repeating series of dark and light bands along length of
each myofibril
– A bands: dark regions
 H zone: lighter region in middle of dark A band
– M line: line of protein (myomesin) that bisects H zone vertically
– I bands: lighter regions
 Z disc (line): coin-shaped sheet of proteins on midline of light I band
Fiber (2 of 4)
(a) Photomicrograph of portions Nuclei

of two muscle fibers (700X).
Notice the striations (alternating
dark and light bands).
Dark A band
Light I band
Fiber
Figure 9.2a Microscopic anatomy of a skeletal muscle fiber.

Myofibrils (3 of 7)
• Sarcomere
– Smallest contractile unit (functional unit) of muscle fiber
– Contains A band with half of an I band at each end
 Consists of area between Z discs
– Individual sarcomeres align end to end along myofibril, like boxcars of train
Fiber (3 of 4)
Thin (actin)
filament Z disc H zone Z disc
(c) Small part of one

myofibril enlarged to
show the myofilaments
responsible for the
banding pattern. Each
sarcomere extends from
one Z disc to the next.
Thick (myosin) I band A band I band M line

filament Sarcomere
Figure 9.2c Microscopic anatomy of a skeletal muscle fiber.

Myofibrils (4 of 7)
• Myofilaments
– Orderly arrangement of actin and myosin myofilaments within sarcomere
– Actin myofilaments: thin filaments
 Extend across I band and partway in A band
 Anchored to Z discs
– Myosin myofilaments: thick filaments
 Extend length of A band
 Connected at M line
– Sarcomere cross section shows hexagonal arrangement of one thick filament
surrounded by six thin filaments
Fiber (4 of 4)
Z disc M line Z disc
(d) Enlargement of one Thin (actin)

sarcomere (sectioned filament
lengthwise). Elastic (titin)
filaments
Thick
(myosin)
filament
(e) Cross sections of a Myosin

sarcomere cut through filament
in different locations.
Actin
filament
I band H zone M line Outer edge of A band

thin filaments thick thick filaments linked thick and thin
only filaments by accessory proteins filaments overlap
only
Figure 9.2d, e Microscopic anatomy of a skeletal muscle

fiber. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved
Myofibrils (5 of 7)
• Molecular composition of myofilaments
– Thick filaments: composed of protein myosin that contains two heavy and four light
polypeptide chains
 Heavy chains intertwine to form myosin tail
 Light chains form myosin globular head
– During contraction, heads link thick and thin filaments together, forming
cross bridges
 Myosins are offset from each other, resulting in staggered array of heads at
different points along thick filament
Myofibrils (6 of 7)
• Molecular composition of myofilaments (cont.)
– Thin filaments: composed of fibrous protein actin
 Actin is polypeptide made up of kidney-shaped G actin (globular) subunits
– G actin subunits bears active sites for myosin head attachment during
contraction
 G actin subunits link together to form long, fibrous F actin (filamentous)
 Two F actin strands twist together to form a thin filament
– Tropomyosin and troponin: regulatory proteins bound to actin
Composition of Thick and Thin Filaments
(1 of 4)
Thick filament
Each thick filament consists of many myosin molecules
whose heads protrude at opposite ends of the filament.
Portion of a thick filament
Myosin head
Actin-binding sites
Tail
Heads
ATP-
binding
site Flexible hinge region
Myosin molecule
Figure 9.3 Composition of thick and thin filaments.

Composition of Thick and Thin Filaments
(2 of 4)
Thin filament
A thin filament consists of two strands of actin subunits
twisted into a helix plus two types of regulatory proteins
(troponin and tropomyosin).
Portion of a thin filament
Tropomyosin Troponin Actin
Myosin-
binding sites
Actin subunits
Figure 9.3 Composition of thick and thin filaments.

Relationship of the Sarcoplasmic Reticulum
and T Tubules to Myofibrils of Skeletal
Muscle
Part of a skeletal I band A band I band
muscle fiber (cell)
H zone
Z disc Z disc
M
line
Sarcolemma
Myofibril
Triad:
• T tubule
• Terminal
Sarcolemma cisterns
of the SR (2)
Tubules of
the SR
Myofibrils
Mitochondria
Figure 9.5 Relationship of the sarcoplasmic reticulum and T

tubules to myofibrils of skeletal
Copyright © 2019, 2016,muscle.
2013 Pearson Education, Inc. All Rights Reserved
Sliding Filament Model of Contraction
(1 of 3)
• Contraction: the activation of cross bridges to generate force
• Shortening occurs when tension generated by cross bridges on thin filaments exceeds
forces opposing shortening
• Contraction ends when cross bridges become inactive
(2 of 3)
• In the relaxed state, thin and thick filaments overlap only slightly at ends of A band
• Sliding filament model of contraction states that during contraction, thin filaments
slide past thick filaments, causing actin and myosin to overlap more
– Neither thick nor thin filaments change length, just overlap more
• When nervous system stimulates muscle fiber, myosin heads are allowed to bind to
actin, forming cross bridges, which cause sliding (contraction) process to begin
(3 of 3)
• Cross bridge attachments form and break several times, each time pulling thin filaments
a little closer toward center of sarcome in a ratcheting action
– Causes shortening of muscle fiber
• Z discs are pulled toward M line
• I bands shorten
• Z discs become closer
• H zones disappear
• A bands move closer to each other
(1 of 2)
1 Fully relaxed sarcomere of a muscle fiber
Z H Z
I A I
Figure 9.6-1 Sliding filament model of contraction.

(2 of 2)
2 Fully contracted sarcomere of a

muscle fiber
Z Z
I A I
Figure 9.6-2 Sliding filament model of contraction.

9.4 Muscle Fiber Contraction (2 of 2)
Background and Overview
• Decision to move is activated by brain, signal is transmitted down spinal cord to motor
neurons which then activate muscle fibers
• Neurons and muscle cells are excitable cells capable of action potentials
– Excitable cells are capable of changing resting membrane potential voltages
• AP crosses from neuron to muscle cell via the neurotransmitter acetylcholine (ACh)
Background and Overview (1 of 4)
• Ion Channels
– Play the major role in changing of membrane potentials
– Two classes of ion channels:
 Chemically gated ion channels – opened by chemical messengers such as
neurotransmitters
– Example: ACh receptors on muscle cells
 Voltage-gated ion channels – open or close in response to voltage changes in
membrane potential
“Chemically Gated Ion Channel” and
“Voltage-Gated ion Channel”
Chemical messenger
(e.g., ACh)
Chemically gated ion Voltage-gated ion

channel channel
• Anatomy of Motor Neurons and the Neuromuscular Junction
– Skeletal muscles are stimulated by somatic motor neurons
– Axons (long, threadlike extensions of motor neurons) travel from central nervous
system to skeletal muscle
– Each axon divides into many branches as it enters muscle
– Axon branches end on muscle fiber, forming neuromuscular junction or motor
end plate
 Each muscle fiber has one neuromuscular junction with one motor neuron
Overview of Skeletal Muscle Contraction
(1 of 3)
Brain
Spinal cord Axon of

motor neuron
Motor
neuron:
The neuromuscular junction is the
• Cell body region where the motor neuron
contacts the skeletal muscle. It
• Axon consists of multiple axon terminals
• Axon and the underlying junctional folds
of the sarcolemma.
terminals
Muscle fiber
Figure 9.7 Overview of skeletal muscle contraction.

Overview of Skeletal Muscle Contraction (2 of 3)
Axon of
motor
neuron Axon terminal of
motor neuron
Synaptic
vesicle
with ACh
Synaptic cleft
Cytoplasm
of skeletal
muscle fiber
Junctional
folds of the
sarcolemma
Figure 9.7 Overview of skeletal muscle contraction.

• The Big Picture - Four steps must occur for skeletal muscle to contract:
1. Events at neuromuscular junction
2. Muscle fiber excitation
3. Excitation-contraction coupling
4. Cross bridge cycling
Overview of Skeletal Brain
Muscle Contraction Spinal cord
Motor
Axon of
motor neuron
(3 of 3) neuron:
• Cell body
The neuromuscular junction is the
region where the motor neuron
contacts the skeletal muscle. It
• Axon consists of multiple axon terminals
• Axon and the underlying junctional folds
terminals of the sarcolemma.
Muscle fiber
Sequence of events leading to contraction: Axon of motor

A motor neuron fires an action potential neuron Axon terminal of
(AP) down its axon. motor neuron
Synaptic
vesicle
1 Events at the The motor neuron’s axon terminal with ACh Synaptic cleft
neuromuscular releases acetylcholine (ACh) into the
junction (see synaptic cleft. Cytoplasm
Focus Figure 9.1) of skeletal
muscle fiber
ACh binds receptors on the junctional
folds of the sarcolemma. Junctional
folds of the
sarcolemma
ACh binding causes a local depolarization
called an end plate potential (EPP).
2 Muscle fiber The local depolarization (EPP) triggers an

excitation (see AP in the adjacent sarcolemma.
Figure 9.8)
AP in sarcolemma travels down T tubules.
3 Excitation-
contraction coupling Sarcoplasmic reticulum releases Ca2+.
(see Focus Figure 9.2)
Ca2+ binds to troponin, which shifts

tropomyosin to uncover the myosin-binding
Figure 9.7 Overview sites on actin. Myosin heads bind actin.
of skeletal muscle 4 Cross bridge cycle

(see Focus Figure 9.3)
Contraction occurs via cross bridge cycling.
contraction. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved
Events at the Neuromuscular Junction
1. AP arrives at axon terminal
2. Voltage-gated calcium channels open, calcium enters motor neuron
3. Calcium entry causes release of ACh neurotransmitter into synpatic cleft
4. ACh diffuses across to ACh receptors (Na+ chemical gates) on sarcolemma
5. ACh binding to receptors, opens gates, allowing Na+ to enter resulting in end plate
potential
6. Acetylcholinesterase degrades ACh
When a Nerve Axon of
Action motor neuron
Impulse Reaches a potential (AP) Axon terminal of
neuromuscular
Neuromuscular junction
Sarcolemma of
Junction, the muscle fiber
Acetylcholine (ACh)
is Released (6 of 6) 1 Action potential arrives at axon
terminal of motor neuron.
Ca2+
2 Voltage-gated Ca2+ Ca2+
Synaptic vesicle
channels open. Ca2+ enters the
containing ACh
axon terminal, moving down its
electrochemical gradient. Axon terminal Synaptic cleft
of motor neuron
Fusing synaptic
vesicles
3 Ca2+ entry causes ACh (a
neurotransmitter) to be released by
exocytosis. ACh Junctional
folds of
4 ACh diffuses across the sarcolemma
synaptic cleft and binds to ACh Sarcoplasm of
receptors on the sarcolemma. muscle fiber
5 ACh binding opens chemically gated
Postsynaptic membrane
ion channels that allow simultaneous Na+ K+
passage of Na+ into the muscle fiber and ion channel opens;
K + out of the muscle fiber. More Na + Ions ions pass.
enter than K + ions exit, which produces a
local change in the membrane potential
called the end plate potential.
6 ACh effects are terminated by ACh Degraded ACh

Ion channel closes;
its breakdown in the synaptic Na+
ions cannot pass.
cleft by acetylcholinesterase and
FOCUS FIGURE 9.1 Events diffusion away from the junction.
at the Neuromuscular Acetylcholin-
esterase K+
Junction
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Junction

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Generation of an Action Potential Across the
Sarcolemma (1 of 4)
• Resting sarcolemma is polarized, meaning a voltage exists across membrane
– Inside of cell is negative compared to outside
• Action potential is caused by changes in electrical charges
• Occurs in three steps
1. Generation of end plate potential
2. Depolarization
3. Repolarization
Summary of Events in the Generation and Propagation of an Action
Potential in a Skeletal Muscle Fiber (1 of 3)
ACh-containing
synaptic vesicle Axon terminal of
neuromuscular
junction
Ca2+
Ca2+
Synaptic
cleft
Wave of
depolarization
1 An end plate potential is generated at the

neuromuscular junction (see Focus Figure 9.1).
Figure 9.8 Summary of events in the generation and

propagation of anCopyright
action© potential inPearson
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Education, muscle
Inc. All Rightsfiber.
Reserved
Summary of Events in the Generation and Propagation of an Action
Potential in a Skeletal Muscle Fiber (2 of 3)
ACh-containing Open Na+ Closed K+
synaptic vesicle Axon terminal of channel channel
neuromuscular Na+
junction
Ca2+
Ca2+
Synaptic
cleft
K+
Action potential
2 Depolarization: Generating and propagating an

Wave of action potential.
depolarization
1 An end plate potential is generated at the

neuromuscular junction (see Focus Figure 9.1).
Figure 9.8 Summary of events in the generation and

propagation of anCopyright
action© potential inPearson
2019, 2016, 2013 a skeletal
Education, muscle
Inc. All Rightsfiber.
Reserved
Summary of Events in the Generation and Propagation of an Action Potential in a Skeletal Muscle Fiber (3 of
3)
ACh-containing Open Na+ Closed K+

synaptic vesicle Axon terminal of channel channel
neuromuscular Na+
junction
Ca2+
Ca2+
Synaptic
cleft
K+
Action potential
2 Depolarization: Generating and propagating an

Wave of action potential.
depolarization
1 An end plate potential is generated at the Closed Na+ Open K+

neuromuscular junction (see Focus Figure 9.1). channel channel
Na+
K+
3 Repolarization: Restoring the sarcolemma to its

Figure 9.8 Summary of events in the initial polarized state (negative inside, positive
generation and propagation of an outside).
action potential in a skeletal muscle
fiber.
Excitation-Contraction (E-C) Coupling is the Sequence of Events by Which Transmission of an
Action Potential Along the Sarcolemma Leads to the Sliding of Myofilaments (1 of 3)
Excitation-contraction (E-C) coupling is the sequence of

events by which transmission of an action potential along
the sarcolemma leads to the sliding of myofilaments.
Setting the stage

The events at the neuromuscular junction
(NMJ) set the stage for E-C coupling by
providing excitation. Released acetylcholine
binds to receptor proteins on the sarcolemma
and triggers an action potential in a muscle
fiber.
Axon terminal of
Synaptic
motor neuron at NMJ
cleft
Action potential
is generated
Sarcolemma
T tubule
Terminal
cistern
of SR
Muscle fiber Ca2+
One sarcomere
One myofibril
FOCUS FIGURE 9.2 Excitation-Contraction Coupling

Excitation-Contraction (E-C) Coupling is the Sequence of Events by Which Transmission of an
Action Potential Along the Sarcolemma Leads to the Sliding of Myofilaments (3 of 3)
Steps in E-C Coupling:

Sarcolemma
Voltage-sensitive T tubule 1 The action potential (AP) propagates

tubule protein along the sarcolemma and down the
T tubules.
Ca2+
release
2 Calcium ions are released.
channel
Transmission of the AP along the
T tubules of the triads causes the
Terminal voltage-sensitive tubule proteins to
cistern change shape. This shape change opens
of SR the Ca2+ release channels in the terminal
cisterns of the sarcoplasmic reticulum
(SR), allowing Ca2+ to flow into the
cytosol.
Ca2+
Actin
Troponin Tropomyosin blocking

myosin-binding sites
Myosin
Ca2+
Myosin-binding sites exposed

and ready for myosin binding
Myosin
cross
bridge
The aftermath
When the muscle AP ceases, the voltage-sensitive tubule proteins return to their
original shape, closing the Ca 2+ release channels of the SR. Ca 2+ levels in the
sarcoplasm fall as Ca2+ is continually pumped back into the SR by active transport.
Without Ca2+ , the blocking action of tropomyosin is restored, myosin-actin
interaction is inhibited, and relaxation occurs. Each time an AP arrives at the
neuromuscular junction, the sequence of E-C coupling is repeated.
FOCUS FIGURE 9.2 Excitation-Contraction Coupling

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Muscle Fiber Contraction: Cross Bridge
Cycling (1 of 3)
• At low intracellular Ca2+ concentration:
– Tropomyosin blocks active sites on actin
– Myosin heads cannot attach to actin
– Muscle fiber remains relaxed
• Voltage-sensitive proteins in T tubules change shape, causing sarcoplasmic reticulum

(SR) to release Ca2+ to cytosol
• At higher intracellular Ca2+ concentrations, Ca2+ binds to troponin
• Troponin changes shape and moves tropomyosin away from myosin-binding sites
• Myosin heads is then allowed to bind to actin, forming cross bridge
• Cycling is initiated, causing sarcomere shortening and muscle contraction
• When nervous stimulation ceases, Ca2+ is pumped back into SR, and contraction ends
Muscle Fiber Contraction: Cross Bridge
Cycling (3 of 3)
• Four steps of the cross bridge cycle
1. Cross bridge formation: high-energy myosin head attaches to actin thin filament
active site
2. Working (power) stroke: myosin head pivots and pulls thin filament toward M line
3. Cross bridge detachment: ATP attaches to myosin head, causing cross bridge to
detach
4. Cocking of myosin head: energy from hydrolysis of ATP “cocks” myosin head
into high-energy state
 This energy will be used for power stroke in next cross bridge cycle
The Cross Bridge Cycle is Actin Ca2+ Thin filament
the Series of Events

During Which Myosin ADP
Myosin
Heads Pull Thin Filaments cross bridge Pi
Toward the Center of the Thick filament
Sarcomere (4 of 4)
Myosin
1 Cross bridge formation. Energized

myosin head attaches to an actin myofilament,
forming a cross bridge.
ADP
ADP
ATP Pi
Pi hydrolysis
4 Cocking of the myosin head. As 2 The power (working) stroke. ADP

myosin hydrolyzes ATP to ADP and Pi , the and Pi are released and the myosin head
myosin head returns to its prestroke high- pivots and bends, changing to its bent low-
energy, or “cocked,” position. * energy state. As a result it pulls the actin
filament toward the M line.
In the absence of
ATP, myosin
heads will not
detach, causing
rigor mortis.
ATP ATP
FOCUS FIGURE 9.3 Cross *This cycle will continue as long as ATP is
available and Ca2+ is bound to troponin. If ATP
3 Cross bridge detachment. After ATP
attaches to myosin, the link between myosin and
Bridge Cycle
is not available, the cycle stops between actin weakens, and the myosin head detaches
steps 2 and 3 . (the cross bridge “breaks”).
A&P Flix™: Cross Bridge Cycle

A&P Flix™: Cross Bridge Cycle
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A Motor Unit Consists of One Motor Neuron and All The Muscle Fibers it Innervates
Spinal cord
(cross section) Axon terminals at Branching axon
neuromuscular junctions of motor unit

Motor Motor
unit 1 unit 2
Nerve
Motor neuron
cell body
Motor neuron
axon
Muscle
Muscle
fibers
(b) Branching axon terminals form
neuromuscular junctions, one
per muscle fiber (photomicrograph
330X).
(a) Axons of motor neurons extend from the spinal cord to the muscle. At the muscle, each
axon divides into a number of axon terminals that form neuromuscular junctions with muscle
fibers scattered throughout the muscle.
Figure 9.10 A motor unit consists of one motor neuron and all the muscle fibers it innervates.
Comparison of Energy Sources Used During Short-
Duration Exercise and Prolonged-Duration Exercise
Short-duration, high-intensity exercise Prolonged-duration exercise
6 seconds 10 seconds 30–40 seconds End of exercise Hours
ATP stored in ATP is formed from Glycogen stored in muscles is broken down to glucose, ATP is generated by breakdown
muscles is creatine phosphate which is oxidized to generate ATP (anaerobic pathway). of several nutrient energy fuels by
used first. and ADP (direct aerobic pathway.
phosphorylation).
Figure 9.17 Comparison of energy sources used during

short-duration exercise and prolonged-duration exercise.
Muscle Fatigue (1 of 2)
• Fatigue is the physiological inability to contract despite continued stimulation
• Possible causes include:

– Ionic imbalances can cause fatigue
 Levels of K+, Na+ and Ca2+ can change disrupting membrane potential of
muscle cell
– Increased inorganic phosphage (Pi) from CP and ATP breakdown may interfere with
calcium release from SR or hamper power
– Decreased ATP and increased magnesium
 As ATP levels drop, magnesium levels increase and this can interfere with
voltage sensitive T tubule proteins
– Decreased glycogen
• Lack of ATP is rarely a reason for fatigue, except in severely stressed muscles
Excess Postexercise Oxygen Consumption
• For a muscle to return to its pre-exercise state:
– Oxygen reserves are replenished
– Lactic acid is reconverted to pyruvic acid
– Glycogen stores are replaced
– ATP and creatine phosphate reserves are resynthesized
• All replenishing steps require extra oxygen, so this is referred to as excess

postexercise oxygen consumption (EPOC)
– Formerly referred to as “oxygen debt”
Table 9.2 Structural and Functional
Characteristics of the Three Types of
Skeletal Muscle Fibers
Table 9.2 Structural and Functional Characteristics of the

Three Types of Skeletal
Copyright ©Muscle
2019, 2016, Fibers
2013 Pearson Education, Inc. All Rights Reserved
9.8 Adaptation to Exercise
Aerobic (Endurance) Exercise
• Aerobic (endurance) exercise, such as jogging, swimming, biking leads to increased:

 Muscle capillaries
 Number of mitochondria
 Myoglobin synthesis
– Results in greater endurance, strength, and resistance to fatigue
– May convert fast glycolytic fibers into fast oxidative fibers
• Resistance exercise (typically anaerobic), such as weight lifting or isometric exercises,

leads to
– Muscle hypertrophy
 Due primarily to increase in fiber size
– Increased mitochondria, myofilaments, glycogen stores, and connective tissue
– Increased muscle strength and size
Clinical – Homeostatic Imbalance 9.4
• Muscles must be active to remain healthy
• Disuse atrophy (degeneration and loss of mass)

– Due to immobilization or loss of neural stimulation
– Can begin almost immediately.
• Muscle strength can decline 5% per day
• Paralyzed muscles may atrophy to one-fourth initial size
• Fibrous connective tissue replaces lost muscle tissue
• Rehabilitation is impossible at this point
Table 9.3 Comparison of Skeletal, Cardiac, and Smooth

Muscle

Muscle

Muscle

Muscle
Extracellular fluid (ECF)
Ca2+
Sequence of Events in
Plasma membrane
Excitation-Contraction Cytoplasm
Coupling of Smooth Muscle 1 Calcium ions (Ca )

enter the cytosol from
2+
(5 of 5) the ECF via

voltage-gated or Ca2+
non-voltage-gated
Ca2+ channels, or from
the scant SR.
Sarcoplasmic
2 Ca2+ binds to and reticulum
activates calmodulin.
Ca2+
Inactive calmodulin Activated calmodulin
3 Activated calmodulin
activates the myosin
light chain kinase
enzymes.
Inactive kinase Activated kinase
ATP
4 The activated kinase enzymes
catalyze transfer of phosphate
to myosin, activating the myosin ADP
ATPases.
Pi
Pi
Inactive Activated (phosphorylated)

myosin molecule myosin molecule
5 Activated myosin forms cross

bridges with actin of the thin
filaments. Shortening begins.
Thin
filament
Figure 9.26 Sequence Thick

filament
of events in excitation-
contraction coupling of

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Human Anatomy and Physiology

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• To investigate muscle, we look at:

• Three types of muscle tissue

Table 9.3 Comparison of Skeletal, Cardiac, and Smooth Muscle

– Excitability (responsiveness): ability to receive and respond to stimuli

– Contractility: ability to shorten forcibly when stimulated

– Extensibility: ability to be stretched

– Elasticity: ability to recoil to resting length

Table 9.1 Structure and Organizational Levels of Skeletal

• Sarcolemma: muscle fiber plasma membrane

• Sarcoplasm: muscle fiber cytoplasm

(b) Diagram of part of a

Dark A band Light I band Nucleus

Figure 9.2b Microscopic anatomy of a skeletal muscle fiber.

(a) Photomicrograph of portions Nuclei

Figure 9.2a Microscopic anatomy of a skeletal muscle fiber.

(c) Small part of one

Thick (myosin) I band A band I band M line

Figure 9.2c Microscopic anatomy of a skeletal muscle fiber.

Z disc M line Z disc

(d) Enlargement of one Thin (actin)

(e) Cross sections of a Myosin

I band H zone M line Outer edge of A band

Figure 9.2d, e Microscopic anatomy of a skeletal muscle

Portion of a thick filament

Figure 9.3 Composition of thick and thin filaments.

Tropomyosin Troponin Actin

Figure 9.3 Composition of thick and thin filaments.

Figure 9.5 Relationship of the sarcoplasmic reticulum and T

• Contraction ends when cross bridges become inactive

• Z discs are pulled toward M line

• Z discs become closer

• A bands move closer to each other

1 Fully relaxed sarcomere of a muscle fiber

Figure 9.6-1 Sliding filament model of contraction.

2 Fully contracted sarcomere of a

Figure 9.6-2 Sliding filament model of contraction.

Chemically gated ion Voltage-gated ion

Spinal cord Axon of

Figure 9.7 Overview of skeletal muscle contraction.

Figure 9.7 Overview of skeletal muscle contraction.

Muscle Contraction Spinal cord

Sequence of events leading to contraction: Axon of motor

2 Muscle fiber The local depolarization (EPP) triggers an

AP in sarcolemma travels down T tubules.

Ca2+ binds to troponin, which shifts

Figure 9.7 Overview sites on actin. Myosin heads bind actin.

of skeletal muscle 4 Cross bridge cycle

2. Voltage-gated calcium channels open, calcium enters motor neuron

3. Calcium entry causes release of ACh neurotransmitter into synpatic cleft

4. ACh diffuses across to ACh receptors (Na+ chemical gates) on sarcolemma

6. Acetylcholinesterase degrades ACh

6 ACh effects are terminated by ACh Degraded ACh

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• Action potential is caused by changes in electrical charges

• Occurs in three steps

1. Generation of end plate potential

1 An end plate potential is generated at the

Figure 9.8 Summary of events in the generation and

2 Depolarization: Generating and propagating an

1 An end plate potential is generated at the

Figure 9.8 Summary of events in the generation and