Lecture 4 - Muscle

CH.
MUSCLE
PHYSIOLOGY
Biol340 - Mammalian Physiology
UNIT OUTLINE:
I.
INTRODUCTION
i.
ii.
General Functions of Muscular System

Types of Muscle Overview
II. LEVELS OF ORGANIZATION

i.
Structural Organization of Skeletal Muscle
III. STRUCTURE & FUNCTION

i. Excitation-Contraction Coupling
ii. Cross-bridge Cycle
iii. Sliding Filament Model
IV. HOMEOSTASIS
i.
ii.
Development of Force
Fatigue
V. INTEGRATION
i.
ii.
Exercise
Clinical
Remember that these Learning Outcomes make for a great basis for your studying. (Try turning the statements into questions.)
UNIT LEARNING OUTCOMES:
Student will be able to

1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
Distinguish between thick and thin filaments.

Describe the steps in excitation-contraction coupling.
Summarize the changes that occur within a sarcomere during contraction.
Explain the relationship of skeletal muscle elasticity and muscle relaxation.
Explain the length-tension relationship in skeletal muscle contraction.
Describe what occurs in a muscle during a single twitch, and relate each event to a graph of a
twitch.
Distinguish between isometric and isotonic contractions, and give examples of both.
Explain the events that occur in motor unit recruitment as the intensity of stimulation is
increased.
Distinguish between treppe, wave summation, incomplete tetany, and tetany that occur with
an increase in frequency of stimulation.
Define muscle fatigue, and explain some of its causes.
Explain the two primary criteria used to classify skeletal muscle fiber types.
Compare and contrast the three muscle fiber types.
Compare and contrast the changes in skeletal muscle that occur as a result of an exercise
program or from the lack of exercise.
I. INTRODUCTION:
Functions of Muscle
Body movement
due to contraction of muscles attached to bones
produces highly coordinated and localized movements
Maintenance of posture
stabilizes joints and helps maintain the bodys posture
Protection and support
muscles arranged along the walls of abdominal and pelvic cavity
protect the internal organs and support normal position
Storage and movement of materials
sphincters, circular muscle bands
contract and relax to regulate passage of material
allow voluntary expulsion of feces and urine
Heat production
produced by energy required for muscle contraction
continuously generate heat to maintain body temperature
shiver when cold to generate heat
I. INTRODUCTION:
Characteristics
Excitability
responsive to nervous system stimulation
neurons secreting neurotransmitters that bind to muscle cells
Conductivity
electrical change traveling along plasma membrane
initiated in response to neurotransmitter binding
Contractility
contractile proteins within muscle cells
slide past each other
tension used to pull on bones of skeleton
Elasticity
due to protein fibers acting like compressed coils
when contraction ended, tension in proteins released
muscle returns to original length
Extensibility
lengthening of a muscle cell
e.g., extension of the triceps brachii when flex elbow joint
I. INTRODUCTION:
TYPES OF MUSCLE
I. INTRODUCTION:

General Topics
i. Structural Organization of Skeletal Muscle
i. Macroscopic
ii. Microscopic

STRUCTURAL ORGANIZATION OF SKELETAL MUSCLE
Composed of thousands of muscle cells

Typically as long as the entire muscle
Often referred to as muscle fibers
Organized into bundles, termed fascicles
Three concentric layers of connective tissue:
epimysium, perimysium, endomysium
Artery
Vein
Provide
Nerve
protection
sites for blood vessel and nerve distribution
means of attachment to skeleton or other
structures
Tendon
Deep fascia
Epimysium
Skeletal muscle
Perimysium
Fascicle
Endomysium
Muscle fiber

MICROSCOPIC ANATOMY
Multinucleated cell
Elongated cells extending length of
muscle
Myoblasts
embryonic cells which fuse
form single skeletal muscle fibers
during development
each contributing a nucleus to total
nuclei
Thus fibers are multinucleated cells
Satellite cells
myoblasts remaining, unfused, in
adult skeletal tissue
may be stimulated to differentiate if
tissue injured
Myoblasts
Myoblasts fuse
to form a skeletal
muscle fiber.
Muscle fiber
Satellite cell
Muscle fiber
Satellite cell
Nuclei
10
Muscle fibers and myofibrils

Myofibrils
long cylindrical structures
extend length of muscle fiber
compose 80% of volume of muscle fiber
each fiber with hundreds to thousands
Myofilaments
Muscle
Fascicle
Muscle fiber
Sarcoplasmic
reticulum
Triad
T-tubule
Terminal
cisternae
bundles of protein filaments

takes many to extend length of myofibril
two types: thick and thin
Sarcolemma
Nucleus
Myofibrils
Sarcomere
Myofilaments
Openings into
T-tubules
Nucleus
Sarcoplasm
Nucleus
Mitochondrion
11

General Topics
i. Excitation-Contraction Coupling
ii. Cross-Bridge Cycle
iii. Sliding Filament Model
12
OVERVIEW OF EVENTS IN SKELETAL MUSCLE CONTRACTION

Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
NEUROMUSCULAR JUNCTION: EXCITATION OF A SKELETAL MUSCLE FIBER
Release of neurotransmitter acetycholine (ACh) from synaptic vesicles and

subsequent binding of Ach to Ach receptors.
Neuromuscular
junction
Synaptic vesicle (contains ACh)

Action potential
1
Muscle
fiber
ACh
T-tubule
Ach receptor
SARCOLEMMA, T-TUBULES, AND SARCOPLASMIC

RETICULUM: EXCITATION-CONTRACTION COUPLING
ACh binding triggers propagation of an action potential

along the sarcolemma and T-tubules to the sarcoplasmic
reticulum, which is stimulated to release Ca2+.
Terminal
cisterna
of SR
Sarcoplasmic
reticulum
Ca2+
Sarcolemma
Sarcomere
Ca2+
Thin filament
Ca2+
SARCOMERE: CROSSBRIDGE CYCLING
Ca2+ binding to troponin triggers sliding of thin

filaments past thick filaments of sarcomeres;
sarcomeres shorten, causing muscle contraction.
Thick filament
13

1a Ca2+ entry at synaptic knob

A nerve signal is propagated down a motor axon and triggers
the entry of Ca2+ into the synaptic knob.
Nerve signal
Ca2+ binds to proteins in synaptic vesicle membrane.

Voltage-gated
Ca2+ channel
Synaptic knob
1a
Ca2+
Synaptic vesicles
(contain ACh)
Interstitial
fluid
Synaptic cleft
Ca2+
Synaptic
vesicle
ACh
1b
1b Release of ACh from synaptic knob

Calcium binding triggers synaptic vesicles to merge
with the synaptic knob plasma membrane and ACh
is exocytosed into the synaptic cleft.
ACh
1c
1c Binding of ACh to ACh receptor at motor end plate
ACh receptor
ACh diffuses across the fluid-filled synaptic cleft in the

motor end plate to bind with ACh receptors.
Motor end plate
14
SKELETAL MUSCLE FIBER: EXCITATION-CONTRACTION COUPLING

2b Initiation and propagation of an action potential along sarcolemma and T-tubules
An action potential is propagated along the sarcolemma & T-tubules. First, voltage-gated Na+ channels
open, and Na+ moves in to cause depolarization. Second, voltage-gated K+ channels open, and K+ moves out
to cause repolarization.
2 SARCOLEMMA, T-TUBULES, AND SARCOPLASMIC RETICULUM:

EXCITATION-CONTRACTION COUPLING
Sarcolemma
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
+
2c
+
+
+
+
+
+
Terminal cisterna
The result is a reversal in the electrical charge difference across the

membrane of a muscle fiber at the motor end plate, which is called
an end-plate potential (EPP). (The inside which was negative is now
positive.)
Binding of ACh to ACh receptors in the motor end plate triggers
the opening of these chemically gated ion channels. Na+ rapidly
diffuses into and K+ slowly diffuses out of the muscle fiber.
Ca2+
Development of an end-plate potential (EPP) at the motor
Motor end plate
2a end plate
Ca2+
+
+
+
+
+
+
+
+
K+
T-tubule
Voltage-gated
Ca2+ channels
Sarcoplasm
2a
+
+
ACh
Na+
+
+
EPP
ACh
receptor
2b
+
+
+
Synaptic
cleft
Voltage-gated
K+ channel
Voltage-gated
Na+ channel
Terminal cisterna
of sarcoplasmic
reticulum
Sarcolemma
Interstitial fluid
2c Release of Ca2+ from the sarcoplasmic reticulum
When the action potential reaches the sarcoplasmic

reticulum, it triggers the opening of voltage-gated Ca2+
channels located in the terminal cisternae of the
sarcoplasmic reticulum. Ca2+ diffuses out of the cisternae
sarcoplasmic reticulum into the sarcoplasm.
15
ACTION POTENTIALS AND CONTRACTION
16
QUESTION
Thick filaments in skeletal muscle are composed of
A.Actin
B.Myosin
C.Troponin
D.Calmodulin
E.Tropomyosin
17

Thick filaments
Assembled from bundles of protein molecules, myosin
each myosin protein with two intertwined strands
each strand with a globular head and elongated tail
tails pointing toward center of thick filaments
heads pointing toward edges of thick filaments
head with a binding site for actin (thin filaments)
head with site where ATP attaches and is split

Myosin molecule
Tail
Heads
Actin binding site
ATP and ATPase binding site
Myosin heads
18

Thin filaments
Primarily composed of two strands of protein, actin
Two strands twisted around each other
Many small spherical molecules, globular actin
Connected to form a fibrous strand, filamentous actin
Globular actin with myosin binding site
where myosin head attaches during contraction

Tropomyosin
Troponin
twistedstringlike protein
globular protein attached to tropomyosin
cover small bands of the actin strands
binding site for Ca2+
covers myosin binding sites in a noncontracting
together form troponin-tropomyosin complex
muscle
Troponin
Tropomyosin
G-actin
F-actin
Myosin binding site
Ca2+ binding site
19
ROLES OF TROPONIN, TROPOMYOSIN, AND CA2+ IN CONTRACTION
20
Crossbridge cycling
Four repeating steps

1) Crossbridge formation
myosin heads in the ready position
attach to exposed myosin binding sites on actin
results in formation of a crossbridge between thick and thin filament

2)
Power stroke
swiveling of the myosin head, termed power stroke
pulls thin filaments a small distance past thick filaments
ADP and Pi released

3)
Release of myosin head
binding of ATP to binding site of myosin head
causes release of myosin head from actin

4)
Reset myosin head
ATP split into ADP and Pi by ATPase
enzyme on myosin head
provides energy to cock the myosin head
21
SARCOMERE: CROSSBRIDGE CYCLING

2+
3a Ca binds to troponin in muscle thin filaments, causing a
conformational change in troponin. Troponin changes shape and the
entire troponin-tropomyosin complex is movedthus, tropomyosin
no longer covers the myosin binding site on actin.
Myosin binding
Ca2+
sites exposed
Troponin
Thin
Tropomyosin
filament Actin
Relaxed sarcomere
(prior to Ca2+ release)
SARCOMERE:
SKELETAL
MUSCLE
CONTRACTION
Thick
filament
Myosin
Attach
3e ATP is split into ADP and Pi by myosin

ATPase. This provides the energy to reset
the myosin head.
Thin
filament
Myosin head
ADP
Pi
Crossbridge cycling:
Reset myosin head
(reset)
Release of myosin head

(release)
3d ATP binds to the ATP binding site on the
myosin head, which causes the release of
the myosin head from the binding site on
actin.
Thin
filament
Myosin head
ATP
3b Myosin heads, which are in the

cocked position, bind to the exposed
myosin binding site on actin forming a
crossbridge between
Actin myosin and actin.
Thin
filament
ADP
Crossbridge
Pi
Myosin head
Multiple repetitions of attach,

pull, release, and reset lead to
fully contracted sarcomere.
Power stroke (pull)
3c The myosin head swivels toward the
center of the sarcomere, pulling along the

attached thin filament. This motion is
called a power stroke. ADP and Pi are
released during this process.
Thin
filament
Myosin
ADP head
Pi
22
QUESTION
Rigor mortis occurs in a dead person because
A.ATP, which is necessary for the detachment of cross bridges, is not
being formed
B.ATP, which is necessary for the formation of cross bridges, is not being
formed
C.Calcium, which is necessary for the formation of cross bridges, is not
being formed
D.Deterioration of muscle proteins prevents detachment of cross bridges
E.None of the choices are correct
23

I bands
Muscle fiber
region containing only thin filaments

extend from both directions of Z disc
bisected by Z disc
appear light under a microscope
disappear at maximal muscle contraction
A band
central region of sarcomere
contains entire thick filament
contains partially overlapping thin filaments
appears dark under a microscope
Sarcomeres
I band
A band
I band
Z disc
H zone
Z disc
Myofibril
Myofilaments
M line
STRUCTURE OF A SARCOMERE
(a)
H zone
central portion of A band

thick filaments only present; no thin
filament overlap
disappears during maximal muscle
contraction
Sarcomere
M line
protein meshwork structure at center of

H zone
attachment site for thick filaments
24
Transverse
sectional plane
M line
H zone
Thick filaments
Thick filaments
& accessory proteins
A band
Thick filaments
Thin filaments
I band
Thin filaments
Connectin
Z disc
Thin filaments
Connectin
& accessory proteins
25
Sarcomere
Z disc
Thick filament
Thin filament
Connectin
M line
I band
(b)
H zone
A band
Z disc
Thin filament
I band
26
SLIDING FILAMENT
MECHANISM
27

Relaxed sarcomere
Z disc
Thick filament
Z disc
Connectin
Thin filament
Thin filament
M line
H zone
A band
I band
I band
Relaxed sarcomere
Z disc
Z disc
M line
I band
H zone
A band
I band
(a) Relaxed skeletal muscle

Contraction
Z disc
Contraction
M line
Z disc
A band
(b) Fully contracted skeletal muscle
Fully contracted
sarcomere
a, b(right): Dr. H. E. Huxley
Z disc
M line
A band
Fully contracted
sarcomere
Z disc
28
29
QUESTION
During skeletal-muscle contraction, the I band and H zone
shorten but the A band stays the same.
A. True
B. False
30

Events in muscle relaxation
Termination of the nerve signal in the motor neuron
Prevents further release of ACh
Continual hydrolysis of ACh from receptor by acetylcholinesterase
Closure of ACh receptor
Ceasing of end plate potential
No further action potential generated
Closure of voltage-gated calcium channels in SR
Already released calcium continuously returned by calcium pumps
Remaining calcium transported back into storage
Return of troponin to its original shape
Tropomyosin now moving over myosin binding sites on actin
prevents crossbridge formation
Returns to original relaxed position
through natural elasticity of muscle fiber
31

MECHANICS OF SINGLE-FIBER CONTRACTIONS
A muscle fiber generates force called tension in order to
oppose a force called the load, which is exerted on the muscle
by an object.
The mechanical response of a muscle fiber to a single action
potential is known as a twitch.
32
MUSCLE TWITCH
Weight
Voltage
Frequency
Latent
period
Muscle tension
Hardware
Muscle
detecting change
Electrodes
of length of muscle
Pivot
Muscle Twitch
Contraction
period
Relaxation
period
Stimulus
Time (msec)
Latent period
Relaxation period
period after stimulus before contraction begins
begins with release of cross-bridges
no change in fiber length
decreasing muscle tension
time needed to initiate tension in fiber
Contraction period
begins as power strokes pull thin filaments
increasing muscle tension
shorter duration than relaxation period
33
Isometric contraction
Muscle tension insufficient to overcome resistance
Contraction of muscle and increased tension
Muscle length the same
E.g., pushing on a wall
E.g., holding a weight while arm doesnt move
34
Isotonic contraction
Muscle tension able to overcome resistance

Results in movement
Tone same but length changes
E.g., swinging a tennis racket
Concentric contraction, subtype

muscle shortens as it contracts
e.g., in the biceps brachii when lifting a load
Eccentric contraction, subtype
muscle lengthens as it contracts
e.g., in the biceps brachii when lowering a load
35
IV. HOMEOSTASIS
General Topics
i. Development of Force
i. Length-Tension
ii. Load & Velocity
iii. Motor Units
iv. Recruitment
ii. Fatigue
36
IV. HOMEOSTASIS
LENGTH-TENSION RELATIONSHIP
The amount of active tension a muscle fiber
develops during contraction can also be altered
by changing the length of the fiber. If you
stretch a muscle fiber to various lengths and
tetanically stimulate it at each length, the
magnitude of the active tension will vary with
length. The length at which the fiber develops
the greatest isometric active tension is termed
the optimal length, L0.
When a quarterback throws a pass, he
must first bring his arm back. This
slightly stretches the triceps and allows
for a more forceful throw. Explain the
physiology behind the increase in force
of muscle contraction.
37
IV. HOMEOSTASIS
QUESTION
THE MAXIMAL FORCE WILL BE DEVELOPED BY A MUSCLE AT ITS
A. shortest length.
B.
intermediate length.
C. maximal length.
38
IV. HOMEOSTASIS
LOAD-SHORTENING RELATIONSHIP
39
39
IV. HOMEOSTASIS
WHOLE-MUSCLE CONTRACTION
40
40
IV. HOMEOSTASIS
MOTOR UNITS
A motor unit is defined as the motor neuron
and the skeletal muscle fibers it innervates.
One motor neuron innervates many
muscle fibers, but one muscle fiber is
innervated by only one motor neuron.
Within a whole muscle there are many motor
units.
The number of fibers innervated depends on

the muscle, fine motor movements (like
typing) rely on motor units with relatively few
fibers in contrast to those in the leg muscles,
for example.
41
IV. HOMEOSTASIS
Recruitment
Helps explain how muscles can exert varying levels of force
Do this in spite of the all-or-none law
muscle fiber contracts maximally or not at all
Difference in force and precision
varied by changing number of motor units
reduced number of motor unit activated
less force exerted
greater number of motor units activated
more force exerted
42
IV. HOMEOSTASIS
Muscle tension
Maximum contractions
3
4
5
6
7
Voltage increments (mV)
43
Experiments with
increased stimulation
frequency
Frequency of less than 10
per second
muscle contracting and
completely relaxing
before next simulation
each tension same
Muscle tension
IV. HOMEOSTASIS
Stimulus
Muscle tension
Frequency
(less than 10 stimuli per second)
(a) Twitch
44
Frequency between 10 and 20 per

second
allows for complete relaxation
tension increasing
insufficient time to remove all Ca2+
more cross-bridges with
subsequent stimulation
heat also increasing enzyme
efficiency
stepwise increase in contraction
strength, treppe
Muscle tension
IV. HOMEOSTASIS
Experiments with increased
stimulation frequency
Frequency
(1020 stimuli per second)
(b) Treppe
45
Experiments with increased stimulation

frequency (continued)
Frequency between 20 and 40 per second
relaxation not occurring
summation of contractile forces
called wave summation or temporal summation
with further increases less time for relaxation
tension tracing increasing
incomplete tetany
At 40 to 50 per second
contractions fused to form continuous contraction
called tetany
if continues, muscle reaches fatigue
decrease in muscle tension from repetitive
stimulation
In human body, stimulation < 25 stimuli per second

no tetany occurs
sustained contraction in the body due to stimulation of
different motor units in same muscle
Muscle tension
IV. HOMEOSTASIS
Incomplete
tetany
Wave
summation
Tetany
Fatigue
Frequency
(2050 stimuli per second)
(c) Wave summation, incomplete tetany, and tetany
46
IV. HOMEOSTASIS
MUSCLE FATIGUE
When a skeletal muscle
fiber is repeatedly
stimulated, the tension the
fiber develops eventually
decreases even though the
stimulation continues.
This decline in muscle

tension as a result of
previous contractile activity
is known as muscle fatigue.
47
IV. HOMEOSTASIS
MUSCLE FATIGUE CAUSES
Many factors can contribute to the fatigue of skeletal muscle. Acute fatigue from highintensity, short-duration exercise is thought to involve:
decrease in ATP concentration.
increase in concentrations of ADP, Pi, Mg2+ , H+ and oxygen free radicals.
These have been shown to:
decrease the rate of Ca2+ release, reuptake and storage by the endoplasmic reticulum.
decrease the sensitivity of the thin filament proteins to activation by Ca2+ release.
directly inhibit the binding and power-stroke motion of the myosin cross-bridges.
Central Command Fatigue
Another type of fatigue quite different from muscle fatigue occurs when the appropriate
regions of the cerebral cortex fail to send excitatory signals to the motor neurons.
48
IV. HOMEOSTASIS
TYPES OF SKELETAL MUSCLE FIBERS

All skeletal muscle fibers do not all have the same mechanical and metabolic
characteristics. Fibers are classified on the basis of:
1.Their maximal velocities of shortening (fast or slow)
Fast and slow fibers contain forms of myosin that differ in the maximal rates at which they use ATP.
This determines the maximal rate of cross-bridge cycling and thus the maximal shortening velocity.
2.The major pathway they use to form ATPoxidative or glycolytic

Oxidative: Most of the ATP such fibers produce is dependent upon blood flow to deliver oxygen and
fuel molecules to the muscle and contain myoglobin. These fibers appear darker and muscles
containing many of these are used for long term contractions (like standing).
Glycolytic: In contrast, these fibers have few mitochondria but possess a high concentration of
glycolytic enzymes and a large store of glycogen. This allows for quick bursts of activity.
49
IV. HOMEOSTASIS
QUESTION
MUSCLE FIBERS THAT RELY ON ANAEROBIC GLYCOLYSIS FOR THEIR
ATP _____.
A. are able to create more force
B. fatigue more easily
C. have more myoglobin
D. have many mitochondria
50
IV. HOMEOSTASIS
Type of contraction generated

Fiber-types
Fast-twitch fibers
have fast variant of myosin ATPase
initiate contraction more quickly following stimulation
produce contraction of shorter duration
produce a strong contraction
greater power and speed than slow-twitch fibers
Slow-twitch fibers
have slow variant of myosin ATPase
51
IV. HOMEOSTASIS
Means for supplying ATP

Oxidative versus glycolytic fibers
Oxidative fibers
use aerobic cellular respiration
have features that support this
extensive capillaries
large numbers of mitochondria
large supply of myoglobin (impart red appearance)
allow to continue contracting for long periods

also called fatigue-resistant
52
IV. HOMEOSTASIS
Means for supplying ATP

Oxidative versus glycolytic fibers (continued)
Glycolytic fibers
use anaerobic cellular respiration
have fewer structures needed for aerobic cellular respiration
white appearance due to lack of myoglobin
large glycogen reserves for anaerobic respiration

tire easily after short time of sustained activity
also termed fatigable
53
IV. HOMEOSTASIS
Type I
On the basis of these two characteristics, three principal types of

skeletal muscle fibers can be distinguished:
Note that the fourth theoretical possibilityslow-glycolytic fibers
is not found.
Type IIa
54
Type IIb
54
IV. HOMEOSTASIS
Mixture of muscle fiber types in skeletal muscle

Variation in relative percentage of muscle fibers
Most muscles with a mixture of all types
E.g., in eye, high percentage of fast glycolytic fibers
requires swift, brief contractions
E.g., in postural muscles, high percentage of slow oxidative fibers
need to contract continually to help maintain posture
55
IV. HOMEOSTASIS
Variation of muscle
fiber types in
individuals
Long distance runners

higher proportion of
slow-oxidative fibers in
legs
Sprinters
higher percentage of
fast-glycolytic fibers
Determined primarily by
genes
Determined partially by
training
SO
FO
FO
FO
FG
FG
SO
FO
FG
SO
FO
SO
FG
Gladden Willis/ Visuals Unlimited
56
IV. HOMEOSTASIS
COMPARISON OF SKELETAL FIBER TYPES
57
IV. HOMEOSTASIS
CONTROL OF MUSCLE TENSION
58
V. INTEGRATION
General Topics
i. Exercise
ii. Clinical Applications
59
V. INTEGRATION
EFFECTS OF EXERCISE ON SKELETAL MUSCLE
Changes in muscle from a sustained exercise program
Hypertrophy
increase in skeletal muscle size
results from repetitive stimulation of fibers
results in
more mitochondria
larger glycogen reserves
increased ability to produce ATP
more myofibrils that contain larger number of myofilaments
Hyperplasia
increase in the number of muscle fibers
may occur in a limited way with exercise
60
V. INTEGRATION
EFFECTS OF EXERCISE ON SKELETAL MUSCLE
Changes in muscle from lack of exercise
Atrophy
decreasing muscle fiber size
results from lack of exercise
can arise from temporary reduction in muscle use
e.g., individuals in a cast
causes decrease in muscle tone and power
initially reversible, but dead fibers not replaced
with extreme atrophy, loss of muscle function permanent
muscle replaced with connective tissue
61
V. INTEGRATION
SKELETAL MUSCLE DISORDERS

A number of conditions and diseases can affect the contraction of skeletal muscle.
Many of them are caused by defects in the parts of the nervous system that control
contraction of the muscle fibers rather than by defects in the muscle fibers themselves.
For example, poliomyelitis is a viral disease that destroys motor neurons, leading to the
paralysis of skeletal muscle, and may result in death due to respiratory failure.
62
V. INTEGRATION
SKELETAL MUSCLE DISORDERS
Myasthenia Gravis Autoimmune disorder where the nAChR has
antibodies generated against it, causing receptor destruction.
How would this cause a motor deficit?
How would you treat it?
Muscular Dystrophy Defect in the protein dystrophin, which connects the
Z-disc to the muscle cell membrane.
How would this cause a motor deficit?
Muscle Cramps Involuntary tetanic contraction of muscles due to
electrolyte imbalances.
Hypocalcemic Tetany Involuntary tetanic contraction of muscles due to
low calcium.
63
V. INTEGRATION
QUESTION
When you attempt to shovel a load of snow that is too heavy, what
sort of muscle contraction are you using?
A. Isometric Contraction
B. Isotonic Contraction
64

Lecture 4 - Muscle

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CH.

General Functions of Muscular System

II. LEVELS OF ORGANIZATION

Structural Organization of Skeletal Muscle

III. STRUCTURE & FUNCTION

Biol340 - Mammalian Physiology

UNIT LEARNING OUTCOMES:

Student will be able to

Distinguish between thick and thin filaments.

Biol340 - Mammalian Physiology

Biol340 - Mammalian Physiology

II. LEVELS OF ORGANIZATION

Biol340 - Mammalian Physiology

II. LEVELS OF ORGANIZATION

Composed of thousands of muscle cells

Biol340 - Mammalian Physiology

II. LEVELS OF ORGANIZATION

II. LEVELS OF ORGANIZATION

Muscle fibers and myofibrils

bundles of protein filaments

Biol340 - Mammalian Physiology

III. STRUCTURE & FUNCTION

Biol340 - Mammalian Physiology

III. STRUCTURE & FUNCTION

OVERVIEW OF EVENTS IN SKELETAL MUSCLE CONTRACTION

NEUROMUSCULAR JUNCTION: EXCITATION OF A SKELETAL MUSCLE FIBER

Release of neurotransmitter acetycholine (ACh) from synaptic vesicles and

Synaptic vesicle (contains ACh)

SARCOLEMMA, T-TUBULES, AND SARCOPLASMIC

ACh binding triggers propagation of an action potential

Biol340 - Mammalian Physiology

SARCOMERE: CROSSBRIDGE CYCLING

Ca2+ binding to troponin triggers sliding of thin

III. STRUCTURE & FUNCTION

NEUROMUSCULAR JUNCTION: EXCITATION OF A SKELETAL MUSCLE FIBER

NEUROMUSCULAR JUNCTION: EXCITATION OF A SKELETAL MUSCLE FIBER

1a Ca2+ entry at synaptic knob

Ca2+ binds to proteins in synaptic vesicle membrane.

1b Release of ACh from synaptic knob

1c Binding of ACh to ACh receptor at motor end plate

ACh diffuses across the fluid-filled synaptic cleft in the

Biol340 - Mammalian Physiology

III. STRUCTURE & FUNCTION

SKELETAL MUSCLE FIBER: EXCITATION-CONTRACTION COUPLING

2 SARCOLEMMA, T-TUBULES, AND SARCOPLASMIC RETICULUM:

Biol340 - Mammalian Physiology

The result is a reversal in the electrical charge difference across the

Development of an end-plate potential (EPP) at the motor

Motor end plate

2c Release of Ca2+ from the sarcoplasmic reticulum

When the action potential reaches the sarcoplasmic

III. STRUCTURE & FUNCTION

ACTION POTENTIALS AND CONTRACTION

Biol340 - Mammalian Physiology

III. STRUCTURE & FUNCTION

Biol340 - Mammalian Physiology

III. STRUCTURE & FUNCTION

Assembled from bundles of protein molecules, myosin

each myosin protein with two intertwined strands

each strand with a globular head and elongated tail

tails pointing toward center of thick filaments

heads pointing toward edges of thick filaments

head with a binding site for actin (thin filaments)

head with site where ATP attaches and is split