Transcript Chapter 10: Muscle Tissue

Chapter 10:
Muscle Tissue
1
Muscle Tissue
• A primary tissue type, divided into:
– skeletal muscle
• Voluntary striated muscle, controlled by
nerves of the central nervous system
– cardiac muscle
• Involuntary striated muscle
– smooth muscle
• Involuntary nonstriated muscle
2
Characteristics of all Muscle Tissues
1. Specialized Cells:
- elongated, high density of myofilaments =
cytoplasmic microfilaments of actin and myosin
2. Excitability/Irritability:
- receive and respond to stimulus
3. Contractility:
- shorten and produce force upon stimulation
4. Extensibility:
- can be stretched
5. Elasticity:
- recoil after stretch
3
Skeletal Muscle Tissue
• Skeletal muscles make up 44% of body
mass
• Skeletal muscle = an organ
– composed of:
• skeletal muscle cells (fibers) and CT
• nerves and blood vessels
4
Functions of Skeletal Muscles
1.
2.
3.
4.
5.
Produce skeletal movement
Maintain posture and upright position
Support soft tissues
Guard entrances and exits
Maintain body temperature by
generating heat
6. Stabilize joints
5
Muscle Tissue Organized at the
Tissue Level
6
Formation of
Skeletal Muscle Fibers
• Skeletal muscle cells are called fibers
7
Figure 10–2
Skeletal Muscle Anatomy
• Each muscle is innervated by one nerve:
– Nerve must branch and contact each skeletal
muscle fiber (cell)
• One artery, branches into extensive
capillaries around each fiber:
– supply oxygen
– supply nutrients
– remove wastes.
8
Organization of Connective Tissues
9
Figure 10–1
Organization of Connective Tissues
• Muscles have 3 layers of connective tissues
that hold the muscle together:
1. Epimysium
- covers the muscle (exterior collagen layer),
separates muscle from other tissues, composed of
collagen, connects to deep fascia
2. Perimysium
- composed of collagen and elastin, has associated
blood vessels and nerves, bundles muscle fibers into
groups called fascicles
- perimysium covers a fascicle
3. Endomysium
- composed of reticular fibers, contains capillaries,
nerve fibers and satellite cells (= stem cells 
10
repair), surrounds individual muscle fibers
Muscle Attachments
• Endomysium, perimysium, and
epimysium come together:
– at ends of muscles
– to form connective tissue attachment to
bone matrix
– Tendon = cord-like bundles
– Aponeurosis = sheet-like
11
How would severing the tendon attached
to a muscle affect the muscle’s ability to
move a body part?
A. Uncontrolled movement would
result from a severed tendon.
B. Movement would be greatly
exaggerated with no tendon.
C. No movement is possible without a
muscle to bone connection.
D. Limited movement would result.
12
Muscle
13
Skeletal Muscle Fibers
• Huge cells:
– up to 100 µm diameter, 30 cm long
• Multinucleate
• Formed by fusion of 100s of myoblasts
• Nuclei of each myoblast retained to provide
enough mRNA for protein synthesis in large
fiber
• Unfused myoblasts in adult = satellite cells
• Satellite cells are capable of division and
fusion to existing fibers for repair but
14
cannot generate new fibers
Organization of
Skeletal Muscle Fibers
15
Figure 10–3
Skeletal Muscle Fibers
• Cell membrane = sarcolemma
• Sarcolemma maintains separation of electrical
charges resulting in a transmembrane potential
• Na+ pumped out of the cell creating positive charge
on the outside of the membrane
• Negative charge from proteins on inside give
muscle fibers a resting potential of -85mV
• If permeability of the membrane is altered, Na+ will
flow in causing a change in membrane potential
• Change in potential will signal the muscle to
contract
16
Transverse Tubules
• Tubes of sarcolemma called transverse
tubules (T tubules) reach deep inside
the cell to transmit changes in
transmembrane potential to structures
inside the cell
• Transmit action potential through cell
• Allow entire muscle fiber to contract
simulataneously
17
Skeletal Muscle Fibers
• Cytoplasm = sarcoplasm:
– rich in glycosomes (glycogen granules) and
myoglobin (binds oxygen)
• Fiber is filled with myofibrils extending the
whole length of the cell
• Myofibrils consist of bundles of
myofilaments
• Myofilaments are responsible for muscle
contraction
– made of actin and myosin proteins
• 80% of cell volume
18
Organization of
Skeletal Muscle Fibers
19
Figure 10–3
Skeletal Muscle Fibers
• Actin:
– makes up the thin filament
• Myosin:
– makes up the thick filament
• When thick and thin filaments interact,
contraction occurs
20
Skeletal Muscle Fibers
Sarcoplasm contains networks of SER called
sarcoplasmic reticulum (SR)
• Sarcoplasmic Reticulum:
– A membranous structure surrounding each myofibril
– Function:
• store calcium and help transmit action potential to
myofibril
– SR forms chambers (terminal cisternae) attached to
T-tubules
– Cisternae
• Concentrate Ca2+ (via ion pumps)
• Release Ca2+ into sarcomeres to begin muscle
contraction
• All calcium is actively pumped from sarcoplasm21to
SR (SR has 1000X more Ca2+ than sarcoplasm)
Skeletal Muscle Fibers
• Triads are located repeated along the length
of myofilaments
– Triads = T-tubule wrapped around a myofibril
sandwiched between two terminal cisternae of
SR
• Formed by 1 T tubule and 2 terminal cisternae of SR
• Triads are located on both ends of a
sarcomere
– Sarcomere = smallest functional unit of a
myofibril
22
Sarcomere
23
• Each muscle = ~ 100 fascicles
• Each fascicle = ~ 100 muscle
fibers
• Each fiber (cell) = ~ 1 thousand
myofibrils
• Each myofibril = ~ 10 thousand
sarcomeres
24
The structural components of
a sarcomere.
25
Sarcomeres
• The contractile units of muscle
• Structural units of myofibrils
• Form visible patterns within myofibrils
26
Sarcomeres
Composed of:
1. Thick filaments – myosin
2. Thin filaments – actin
3. Stabilizing proteins:
-hold thick and thin
filaments in place
4. Regulatory proteins:
- control interactions of
thick and thin filaments
Organization of the proteins in
sarcomere causes striated
appearance of the muscle fiber
27
Figure 10–4
Muscle Striations
• A striped or striated pattern within
myofibrils:
– alternating dark, thick filaments (A bands)
and light, thin filaments (I bands)
28
Regions of the Sarcomere
1. A-band:
- whole width of thick filaments, looks dark
microscopically
2. M line: at midline of sarcomere
- Center of each thick filament, middle of A-band
- Attaches neighboring thick filaments
3. H-zone:
- Light region on either side of the M line
- Contains thick filaments only
4. Zone of overlap:
- ends of A-bands
- place where thin filaments intercalate between thick
filaments (triads encircle zones of overlap)
29
Regions of the Sarcomere
3.
4.
I-band:
- Contains thin filaments outside zone of overlap
- Not whole width of thin filaments
Z lines/disc:
- the centers of the I bands
- constructed of Actinins
Anchor thin filaments and bind neighboring
sarcomeres
- Constructed of Titin Proteins
Bind thick filaments to Z-line, stabilize the
filament
30
31
Why does skeletal muscle appear striated
when viewed through a microscope?
A. Z lines and myosin filaments align
within the tissue.
B. Glycogen reserves are linearly
arranged.
C. Capillaries regularly intersect the
myofibers.
D. Actin filaments repel stain,
appearing banded.
32
• Sarcomere Function
– Transverse tubules encircle the sarcomere
near zones of overlap
– Ca2+ released by SR causes thin and thick
filaments to interact
• Muscle Contraction
– Is caused by interactions of thick and thin
filaments
– Structures of protein molecules determine
interactions
33
Thin Filament
34
Figure 10–7a
Thin Filaments (5-6 nm diameter)
• Made of 4 proteins:
1. Actin
2. Nebulin
-
Holds F actin strands together
F-actin (filamentous) consists of rows of G-actin
(globular)
-
Each G-actin has an active site that can bind to myosin
3. Tropomyosin
- Covers the active sites on G actin to prevent actin–
myosin binding
4. Troponin: holds tropomyosin on the G-actin
-
Also has receptor for Ca2+:
-
when Ca2+ binds to the troponin-tropomyosin complex it
causes the release of actin allowing it to bind to myosin
35
Troponin and Tropomyosin
36
Figure 10–7b
Initiating Contraction
• Ca2+ binds to receptor on troponin
molecule
• Troponin–tropomyosin complex changes
• Exposes active site of F actin
37
Thick Filament
38
Figure 10–7c
Thick Filaments (10-12 nm diameter)
• Composed of:
– bundled myosin molecules
– titin strands that recoil after stretching
• Each Myosin has three parts
1. Tail:
- tails bundled together to make length of
thick filament
- all point toward M-line
2. Hinge:
- flexible region, allows movement for
contraction
39
Thick Filaments (10-12 nm diameter)
3. Head:
- hangs off tail by hinge, will bind actin at active
site.
- No heads in H-zone
- also contains core of titin:
- elastic protein that attaches thick
filaments to Z-line
- Titin holds thick filament in place and aid
elastic recoil of muscle after stretching
- Each thick filament is surrounded by a
hexagonal arrangement of thin filaments with
which it will interact
40
The Myosin Molecule
41
Figure 10–7d
Myosin Action
• During contraction, myosin heads:
– interact with actin filaments, forming
cross-bridges
– pivot, producing motion
42
Sliding Filaments
43
Figure 10–8
Sliding Filament Theory
Contraction of skeletal muscle is due to thick filaments and thin
filament sliding past each other
–
not compression of the filaments
1. H-zones and I-bands decrease width during contraction
2. Zones of overlap increase width
3. Z-lines move closer together
4. A-band remains constant
Sliding causes shortening of every sarcomere in every myofibril in
every fiber
Overall result = shortening of whole skeletal muscle
44
The components
of the neuromuscular
junction, and the events
involved in the neural control
of skeletal muscles.
45
Skeletal Muscle Contraction
1. Excitation
2. Excitation-Contraction
Coupling
3. Contraction
4. Relaxation
46
Figure 10–9 (Navigator)
1. Excitation and the
Neuromuscular Junction
• Excitation of muscle fiber is controlled
by the nervous system at the
neuromuscular junction using
neurotransmitter
47
The Neuromuscular Junction
• Is the location of neural stimulation
• Action potential (electrical signal):
– travels along nerve axon
– ends at synaptic terminal
48
Components of Neuromuscular Junction
Neuromuscular Junction:
- where a nerve terminal interfaces with a muscle fiber at
the motor end plate
- one junction per fiber: control of fiber from one neuron
1. Synaptic Terminal:
- expanded end of the axon, contains vesicles of
neurotransmitters  Acetylcholine (Ach)
2. Motor End Plate:
- specialized sarcolemma that contains Ach receptors
and the enzyme acetylcholinesterase (AchE)
3. Synaptic Cleft:
- space between the synaptic terminal and motor end
plate where neurotransmitters are released
49
Skeletal Muscle:
Neuromuscular Junction
50
Figure 10–10a, b (Navigator)
51
2. Skeletal Muscle Excitation
52
Figure 10–10c
The Neurotransmitter
• Acetylcholine or ACh:
– travels across the synaptic cleft
– binds to membrane receptors on
sarcolemma (motor end plate)
– causes sodium–ion rush into sarcoplasm
– is quickly broken down by enzyme
(acetylcholinesterase or AChE)
53
Action Potential
• Generated by increase in sodium ions
in sarcolemma
• Travels along the T tubules
• Leads to excitation–contraction
coupling
54
The Process of Contraction
• Neural stimulation of sarcolemma:
– causes excitation–contraction coupling
• Cisternae of SR release Ca2+:
– which triggers interaction of thick and
thin filaments
– consuming ATP and producing tension
55
3. Excitation–Contraction Coupling
• Action potential reaches a triad:
– releasing Ca2+
– triggering contraction
• Requires myosin heads to be in
“cocked” position:
– loaded by ATP energy
56
The key steps involved in the
contraction of a skeletal
muscle fiber.
57
Exposing the Active Site
1. The action potential of
the transverse tubules
reaches a triad and
causes the release of
calcium ions from the
cisternae of the SR into
the sarcoplasm around
the zones of overlap of
the sarcomeres
2. Calcium binds to
troponin on the thin
filaments
3. Troponin pulls
tropomyosin off the
active sites of the actin
so that cross bridges can
form.
58
Figure 10–11
The Contraction Cycle
59
Figure 10–12 (1 of 4)
5 Steps of the Contraction Cycle
1.
2.
3.
4.
5.
Exposure of active sites
Formation of cross-bridges
Pivoting of myosin heads
Detachment of cross-bridges
Reactivation of myosin
60
The Contraction Cycle
1. Actin, free of
tropomyosin, binds to
myosin via its active site
2. Cross bridges are formed
* Actin active sites are
bound to myosin heads61
Figure 10–12 (2 of 4)
The Contraction Cycle
3. Myosin heads have been
pre-primed for
movement via ATP
energy prior to cross
bridge formation and are
pointed away from the
M line.
Upon actin binding, the
myosin heads pivot
toward the M line in an
event called the power
stroke, which pulls the
thick filament along the
thin filament Figure 10–12 (362of 4)
The Contraction Cycle
• Myosin ATPase uses
ATP to break the
cross bridges
releasing the myosin
head from the actin
active site, and
resets the myosin
head pointed away
from the M-line
63
The Contraction Cycle
• The myosin head is
now primed to
interact with a new
active site on actin
• Myosin can carry out
5 power strokes per
second while
calcium and ATP are
available.
• Each power stroke
shortens the
sarcomere by 1%
64
Figure 10–12 (Navigator) (4 of 4)
Fiber Shortening
• As sarcomeres shorten, muscle pulls
together, producing tension
65
Figure 10–13
Contraction Duration
• Depends on:
– duration of neural stimulus
– number of free calcium ions in sarcoplasm
– availability of ATP
66
4. Relaxation
1. Ca2+ reabsorbed by sarcoplasmic reticulum
2. Ca2+ ions detach from troponin
3. Troponin, without Ca2+, pivots tropomyosin
back onto active sites on actin, no cross
bridges can form
4. Sarcomeres stretch back out:
-
Gravity
Opposing muscle contractions
Elastic recoil of titin protein
Result: Muscle returns to Resting Length
67
A Review of Muscle Contraction
68
Table 10–1 (1 of 2)
A Review of Muscle Contraction
69
Table 10–1 (2 of 2)
Rigor Mortis
• A fixed muscular contraction after death
• Caused when:
– SR can not absorb Ca2+ :
• ion pumps cease to function
• calcium builds up in the sarcoplasm
– Ca2+ bind troponin
– Tropomyosin frees actin
– Cross bridges from
– No ATP to detach myosin head because ATP is already all
used up
• fixed cross bridge
• Contractions occur until necrosis releases lysosomal
enzymes which digest cross bridges
70
Disease of Muscle Contraction
1. Botulism/Botox:
-
Bacteria Clostridium botulinum (grows in improperly
canned foods) produces botulinum toxin
-
Toxin prevents the release of Ach at the neuromuscular
junction
- Results in flaccid paralysis
2. Tetanus:
-
Bacteria Clostridium tetani (grows in soil) produces
tenanus toxin:
-
Toxin causes over stimulation of motor neurons
- Results in spastic paralysis
3. Myasthenia gravis:
-
Autoimmune disease
Causes loss of Ach receptors  muscles become
non-responsive
71
KEY CONCEPT
• Skeletal muscle fibers shorten as thin filaments
slide between thick filaments
• Free Ca2+ in the sarcoplasm triggers contraction
• SR releases Ca2+ when a motor neuron stimulates
the muscle fiber
• Contraction is an active process
• Relaxation and return to resting length is passive
72
Where would you expect the greatest
concentration of Ca2+ in resting skeletal
muscle to be?
A.
B.
C.
D.
T tubules
surrounding the mitochondria
within sarcomeres
cisternae of the sarcoplasmic
reticulum
73
How would a drug that interferes with
cross-bridge formation affect muscle
contraction?
A.
B.
C.
D.
interferes with contraction
slows contraction
speeds contraction
increases strength of contraction
74
Predict what would happen to a muscle if
the motor end plate failed to produce
acetylcholinesterase.
A. Muscle would lose strength.
B. Muscle would be unable to
contract.
C. Muscle would lock in a state of
contraction.
D. Muscle would contract
repeatedly.
75
What would you expect to happen to a
resting skeletal muscle if the sarcolemma
suddenly became very permeable to Ca2+?
A.
B.
C.
D.
increased strength of contraction
decreased cross bridge formation
decreased ability to relax
both A and C
76
The mechanism responsible for
tension production in a muscle
fiber, and the factors that
determine the peak tension
developed during a
contraction.
77
Tension Production
• Muscle tension:
– Force exerted by contracting muscle
– Force is applied to a load
• Load = weight of the object being acted upon
• For a single muscle fiber contraction is
all–or–none:
– as a whole, a muscle fiber is either
contracted or relaxed
78
Tension of a Single Muscle Fiber
• Once contracting tension depends on:
1. The number of pivoting cross-bridges
2. The fiber’s resting length at the time of
stimulation
3. The frequency of stimulation
79
Resting Length
• Greatest tension produced at optimal resting length
– Optimal resting length = Optimum overlap
– Overlap determines the number of pivoting cross-bridges
• Enough overlap, so that myosin can bind actin, not so
much that thick filaments crash into Z-lines
80
Figure 10–14
Why is it difficult to contract a muscle
that has been overstretched?
A. Myosin filaments break.
B. Crossbridges can not be formed.
C. Z lines are unable to sustain
contractile forces.
D. Tendons lose elasticity.
81
Frequency of Stimulation
• Twitch = single contraction due to a single
neural stimulation, 3 phases:
1. Latent period: post stimulation but no tension
-
Action potential moves across the sarcolemma
Ca2+ is released
2. Contraction phase: peak tension production
-
Ca2+ bind
Active cross bridge formation
3. Relaxation phase: decline in tension
-
Ca2+ is reabsorbed
Cross bridges decline
82
Myogram
• A graph of twitch tension development
83
Twitch
•
Single twitch will not produce normal
movement
–
requires many cumulative twitches
•
Repeat stimulation will result in higher tension
due to Ca2+ not being fully absorbed
- Ca2+  more cross bridges
• Types of Frequency Stimulation
1. Treppe
2. Wave summation
a. Incomplete Tetanus
b. Complete Tetanus
84
Treppe
• Stepping up of tension production to max
level with repeat stimulation of the same
fiber following relaxation phase
• Repeated stimulations immediately after
relaxation phase:
– stimulus frequency < 50/second
• Causes a series of contractions with
increasing tension
85
Treppe
• A stair-step increase in twitch tension
86
Figure 10–16a
Wave Summation
• Repeat stimulation before relaxation phase ends
resulting in more tension production than max
treppe
– stimulus frequency > 50/second
• Typical muscle contraction
• Increasing tension or summation of twitches
87
Figure 10–16b
Incomplete Tetanus
• Rapid cycles of contraction and
relaxation produces max tension
• Twitches reach maximum tension
Cardiac muscle 
incomplete tetanus
Only to prevent seizure
of heart
88
Figure 10–16c
Complete Tetanus
• Relaxation eliminated, continuous contraction
• Fiber is in prolonged state of contraction
– Produces 4x more tension than maximum treppe
– Quick to fatigue
Most Skeletal muscle 
complete tetanus when
contracting
89
Figure 10–16d
During treppe, why does tension in a muscle
gradually increase even though the strength
and frequency of the stimulus are constant?
A. Increased blood flow improves
contraction.
B. Sarcomeres shorten with each
contraction.
C. Calcium ion concentration
increases with successive stimuli.
D. Generated heat improves
contraction.
90
The factors that affect peak
tension production during the
contraction of an entire
skeletal muscle, and the
significance of the motor unit
in this process.
91
Tension Produced by
Whole Skeletal Muscles
• Depends on:
1. Internal tension produced by sarcomeres
-
Not all the tension is transferred to the load,
some of it is lost due to the elasticity of muscle
tissues
2. External tension exerted by muscle fibers on
elastic extracellular fibers
-
Tension applied to the load
3. Total number of muscle fibers stimulated
92
Total Number of Muscle Fibers Stimulated
• Each skeletal muscle has thousands of fibers
organized into motor units
• Motor units = all fibers controlled by a single
motor neuron
– Axon branches to contact each fiber
• Number of fibers in a motor unit depends on the
function
– Fine control: 4/unit (e.g. eye muscles)
– Gross control: 2000/unit (e.g. leg muscles)
• Fibers from different units are intermingled in
the muscle so that the activation of one unit
will produce equal tension across the whole
muscle
93
Motor Units in a Skeletal Muscle
94
Figure 10–17
Recruitment (Multiple
Motor Unit Summation)
• In a whole muscle or group of muscles,
smooth motion and increasing tension is
produced by slowly increasing size or number
of motor units stimulated
• Recruitment = order of activation of a motor
unit
– Slower weaker units are activated first
– Strong units are added to produce steady
increases in tension
95
Contraction Skeletal Muscle
• During sustained contraction of a muscle
– Some units rest while others contract to avoid fatigue
• For maximum tension, all units in complete tetanus
– Leads to rapid fatigue
• Muscle tone = maintaining shape/definition of the
muscle
– Some units are always contracting
– Exercise = Increase # of units contraction 
Increase in metabolic rate 
Increase in speed of recruitment (better tone)
96
KEY CONCEPT
• Voluntary muscle contractions involve
sustained, tetanic contractions of
skeletal muscle fibers
• Force is increased by increasing the
number of stimulated motor units
(recruitment)
97
The types of
muscle contractions.
98
Contraction Skeletal Muscle
• All contractions produce tension but
not always movement
1. Isotonic Contractions:
-
Muscle length changes resulting in
movement
2. Isometric Contractions
-
Tension is produced with no movement
99
Isotonic Contraction
• If muscle tension > resistance:
– muscle shortens (concentric contraction)
• If muscle tension < resistance:
– muscle lengthens (eccentric contraction)
100
Figure 10–18a, b
Isometric Contraction
• Skeletal muscle develops tension, but is
prevented from changing length
Note: Iso = same, metric = measure
101
Figure 10–18c, d
Return to Resting Length
• Expansion via:
1. Elastic recoil after contraction
-
-
The pull of elastic elements (tendons and
ligaments)
Expands the sarcomeres to resting length
2. Opposing muscle contractions
-
Reverse the direction of the original motion
3. Gravity
-
Opposes muscle contraction to return a muscle to
its resting state
102
Can a skeletal muscle contract without
shortening? Explain.
A. Yes; isotonic contractions
produce no movement.
B. No; resistance is always less than
force generated.
C. Yes; concentric contractions are
common.
D. No; contraction implies
movement.
103
The mechanisms by which
muscle fibers obtain energy to
power contractions.
104
Muscle Metabolism
•
•
•
•
•
1 fiber ~15 million thick filaments
1 thick filament ~ 2500 ATP/sec
1 glucose (aerobic respiration) = 36 ATP
Each fiber needs 1x1012 glucose/sec to contract
ATP unstable, muscles store respiration energy
on creatine as Creatine Phosphate (CP)
• Creatine phosphokinase transfers P from CP at
ADP when ATP is needed to reset myosin for
next contraction
• Each cell as only ~20 sec of energy reserved
105
ATP and CP
• Adenosine triphosphate (ATP):
– the active energy molecule
• Creatine phosphate (CP):
– the storage molecule for excess ATP energy
in resting muscle
• Energy recharges ADP to ATP:
– using the enzyme creatine phosphokinase
(CPK)
• When CP is used up, other mechanisms
generate ATP
106
Muscle Metabolism
• At Rest:
– Use glucose and fatty acids with O2 (from blood)
 aerobic respiration
• Resulting ATP is used to CP reserves
• Excess glucose is stored as glycogen
• Moderate Activity:
– CP used up
– Glucose and fatty acids with O2 (from blood) are
used to generate ATP (aerobic respiration)
107
Muscle Metabolism
• High Activity:
– O2 not delivered adequately
– Glucose from glycogen reserves are used for
ATP via fermentation (glycolysis only)
• Pyruvic acid is converted to lactic acid
• Excess lactic acid production leads to
muscle cramps
108
ATP Generation
• Cells produce ATP in 2 ways:
– aerobic metabolism of fatty acids in the
mitochondria (At rest and Moderate activity)
• Is the primary energy source of resting muscles
• Breaks down fatty acids
• Produces 34 ATP molecules per glucose molecule
– anaerobic glycolysis (fermentation) in the
cytoplasm (High activity)
• Is the primary energy source for peak muscular
activity
• Produces 2 ATP molecules per molecule of glucose
• Breaks down glucose from glycogen stored in skeletal
109
muscles
Muscle Metabolism
110
Figure 10–20a
Muscle Metabolism
111
Figure 10–20b
Muscle Metabolism
112
Figure 10–20c
Muscle Metabolism
113
Figure 10–20 (Navigator)
Factors that contribute to
muscle fatigue, and the stages
and mechanisms involved in
muscle recovery.
114
Muscle Fatigue
•
When muscles can no longer perform a
required activity (contraction), they are
fatigued
1. Depletion of reserves
-
glycogen, ATP, CP
2. Decreased pH due to:
-
lactic acid production
3. Damage to sarcolemma and sarcoplasmic
reticulum
4. Muscle exhaustion and pain
115
To restore function, cell need:
1. Intracellular energy reserves
-
Glycogen and CP
2. Good Circulation
-
Nutrients in, wastes out
3. Normal O2 levels
4. Normal pH
-
Lactic Acid Disposal
116
Normal pH
Lactic Acid Disposal
- Lactic acid diffuses into the blood
- Filtered out by the liver
- Converted back to glucose through the
Cori Cycle
- Returned to blood for use by cells
- When O2 returns
- Remaining lactic acid in the muscle is
converted to glucose and used in aerobic
cellular respiration
117
KEY CONCEPT
• Skeletal muscles at rest metabolize fatty
acids and store glycogen
• During light activity, muscles generate
ATP through aerobic breakdown of
carbohydrates, lipids or amino acids
• At peak activity, energy is provided by
anaerobic reactions that generate lactic
acid as a byproduct
118
Muscle fibers and physical
conditioning that relate to
muscle performance.
119
Muscle Performance
• Power:
–
the maximum amount of tension produced
• Endurance:
–
the amount of time an activity can be
sustained
• Power and endurance depend on:
1. Types of muscle fibers
A. Fast Glycolytic Fibers (fast twitch)
B. Slow Oxidative Fibers (slow twitch)
C. Intermediate/Fast Oxidative Fibers
2. Physical conditioning
A. Aerobic Exercise
B. Resistance Exercise
120
Fiber Types
• Types of fibers in a muscle are genetically
determined and mixed
1. Fast glycolytic Fibers (fast twitch)
-
Myosin ATPase work quickly
Anaerobic ATP production: glycolysis only
Large diameter fibers
More myofilaments and glycogen
Few mitochondria
Fast to act, powerful, but quick to fatigue
Catabolize glucose only
121
Fiber Types
2. Slow Oxidative Fibers (slow twitch)
-
Myosin ATPases work slowly
Specialized for aerobic respiration
-
-
Many mitochondria
Extensive blood supply
Myoglobin (red pigment, binds oxygen)
Smaller fibers for better diffusion
Slow to contract, weaker tension, but resist
fatigue
Catabolize glucose, lipids, and amino acids
122
Fiber Types
3. Intermediate/Fast Oxidative Fibers
-
Qualities of both fast glycolytic and slow
oxidative fibers
Fast acting but perform aerobic
respiration so to resist fatigue
Physical conditioning can convert some
fast fibers into intermediate fibers for
stamina
123
Fast versus Slow Fibers
124
Figure 10–21
Comparing Skeletal Muscle Fibers
125
Table 10–3
Muscles and Fiber Types
• White muscle:
– mostly fast fibers
– pale (e.g., chicken breast)
• Red muscle:
– mostly slow fibers
– dark (e.g., chicken legs)
• Most human muscles:
– mixed fibers
– pink
126
Physical Conditioning
1. Aerobic Exercise:
- Increase Capillary Density
- Increase Mitochondria and myoglobin
Both then:
- Increase efficiency of muscle metabolism
- Increase strength and stamina
- Decrease fatigue
2. Resistance Exercise:
-
Results in Hypertrophy:
- fibers increase in diameter but not number
Increase glycogen, myofibrils, and myofilaments
results in increase tension production
127
Physical Conditioning
• Growth Hormone (pituitary) and
Testosterone (male sex hormone)
– Stimulate synthesis of contractile proteins
• Results in Muscle Enlargement
• Epinephrine
– Stimulates increase muscle metabolism
• Results in increase force of contraction
• Without stimulation muscles will atrophy
– Fibers shrink due to loss of myofilament
proteins
– Loss: up to ~5%/day
128
KEY CONCEPT
• What you don’t use, you loose
• Muscle tone indicates base activity in motor
units of skeletal muscles
• Muscles become flaccid when inactive for
days or weeks
• Muscle fibers break down proteins, become
smaller and weaker
• With prolonged inactivity, fibrous tissue may
replace muscle fibers
129
Why would a sprinter experience muscle
fatigue before a marathon runner would?
A. Sprinters cannot utilize ATP for
long periods of time.
B. Sprinters’ muscles are most
efficient aerobically.
C. Sprinters’ muscles are most
efficient anaerobically.
D. Sprinters’ muscles are weaker.
130
Which activity would be more likely
to create an oxygen debt: swimming
laps or lifting weights?
A.
B.
C.
D.
swimming laps
lifting weights
both A and B
neither A nor B
131
Which type of muscle fibers would you expect to
predominate in the large leg muscles of someone
who excels at endurance activities, such as cycling
or long-distance running?
A.
B.
C.
D.
slow fibers
fast fibers
nonvascular fibers
thick, glycogen-laden fibers
132
Cardiac Muscle Tissue
133
Cardiac Muscle Tissue
• Cardiac muscle is
striated, found only in
the heart
134
Figure 10–22
Cardiac Muscle Tissue
•
•
•
•
•
•
•
•
•
•
•
•
Forms the majority of heart tissue
Cells = cardiocytes
One or two nuclei
No cell division
Long branched cells
Myofibrils organized into sarcomeres (striated)
No triads (no terminal cisternae)
Transverse tubules encircle Z-lines
Aerobic Respiration Only
Mitochondria and myoglobin rich
Glycogen and lipid energy reserves
Intercalated discs at cell junctions (gap junctions and
desmosomes)
– allow transmission of action potentials
135
– link myofibrils from on cardiocyte (cell) to the next
Coordination of Cardiocytes
• Because intercalated discs link heart
cells mechanically, chemically, and
electrically, the heart functions like a
single, fused mass of cells
136
4 Functions of Cardiac Tissue
1. Automaticity:
–
–
contraction without neural stimulation
Automatically due to control by pacemaker cells
• These cells generate action potentials
spontaneously
2. Pace and amount of contraction tension:
–
Can be adjusted and controlled by the nervous system
3. Extended contraction time
-
Contraction is 10x longer than skeletal muscle
4. Only twitches, no complete tetanus
-
Prevention of wave summation and tetanic
contractions by cell membranes
137
Smooth Muscle Tissue
138
Structure of Smooth Muscle
• Nonstriated tissue
139
Figure 10–23
Smooth Muscle Tissue
•
Lines hollow organs
–
•
•
Regulates blood flow and movement of materials in
organs
Forms errector pili muscles
Usually organized into two layer
1. Circular
2. Longitudinal
•
•
•
•
•
•
Spindle shaped cells
Single central nucleus
Cells capable of division
No myofibrils, sarcomeres, or T tubules
SER/ER throughout cytoplasm
No tendons
140
Smooth Muscle Tissue
• Thick filaments (myosin fibers) scattered
– Myosin fibers have more heads per thick
filament
• Thin filaments are attached to dense
bodies on desmin cytoskeleton (web)
• Adjacent cells attach at dense bodies
with gap junctions (firm linkage and
communication)
– Dense bodies transmit contractions from cell
to cell
• Contraction compresses the whole cell
141
Smooth Muscle in Body Systems
• Forms around other tissues
• In blood vessels:
– regulates blood pressure and flow
• In reproductive and glandular systems:
– produces movements
• In digestive and urinary systems:
– forms sphincters
– produces contractions
• In integumentary system:
– arrector pili muscles cause goose bumps
142
Smooth Excitation-Contraction
• Different than striated muscle:
–
no troponin so active sites on actin are always
exposed
• Events:
1. Stimulation causes Ca2+ release from SR
2. Ca2+ binds calmondulin in the sarcoplasm
- Calmondulin = CALcium MODULated proteIN
3. Calmondulin activates myosin light chain kinase,
this complex phosphorylates myosin
4. MLC Kinase converts ATP ADP to cock myosin
head
5. Cross bridge form  contraction, cells pull
toward center
143
Smooth Excitation-Contraction
Stimulation is by involuntary control from
- Autonomic Nervous System
- Hormones
- Other Chemical Factors
Skeletal Muscle = Motor Neurons
Cardiac Muscle = Automatically
144
Characteristics of Skeletal,
Cardiac, and Smooth Muscle
145
Table 10–4
Why are cardiac and smooth muscle
contractions more affected by changes in
extracellular Ca2+ than are skeletal muscle
contractions?
A. Extracellular Ca2+ inhibits actin.
B. Crossbridges are formed
extracellularly.
C. Most calcium for contractions
comes from SR stores.
D. Most calcium for contractions
comes from extracellular fluid.
146
Smooth muscle can contract over a wider
range of resting lengths than skeletal
muscle can. Why?
A. Smooth muscle sarcomeres are
longer.
B. Myofilament arrangement is less
organized in smooth muscle.
C. Smooth muscle cells are shorter.
D. Smooth muscle actin is longer.
147
Effects of Aging
• Skeletal Muscle fibers become thinner
– Decrease myofibrils, Decrease reserves =
Decrease in strength and endurance and
Increase in fatigue
- Decrease cardiac and smooth muscle function =
Decrease cardiovascular performance
- Increase fibrosis (CT):
- Skeletal muscle less elastic
- Decrease ability to repair
- Decrease satellite cells
- Increase scar formation
148
SUMMARY
• 3 types of muscle tissue:
– skeletal
– cardiac
– smooth
• Functions of skeletal muscles
• Structure of skeletal muscle cells:
– endomysium
– perimysium
– epimysium
• Functional anatomy of skeletal muscle fiber:
– actin and myosin
149
SUMMARY
• Nervous control of skeletal muscle fibers:
– neuromuscular junctions
– action potentials
• Tension production in skeletal muscle fibers:
– twitch, treppe, tetanus
• Tension production by skeletal muscles:
– motor units and contractions
• Skeletal muscle activity and energy:
– ATP and CP
– aerobic and anaerobic energy
150
SUMMARY
• Skeletal muscle fatigue and recovery
• 3 types of skeletal muscle fibers:
– fast, slow, and intermediate
• Skeletal muscle performance:
– white and red muscles
– physical conditioning
• Structures and functions of:
– cardiac muscle tissue
– smooth muscle tissue
151