2. Functions of the Muscular System
1. Body movement (Skeletal Muscle)
2. Maintenance of posture (Skeletal
Muscle)
3. Respiration (Skeletal Muscle)
4. Production of body heat (Skeletal
Muscle)
5. Communication (Skeletal Muscle)
6. Constriction of organs and vessels
(Smooth Muscle)
7. Heartbeat (Cardiac Muscle)
3. Functional Characteristics of Muscle
1. Contractility: the ability to shorten
forcibly
2. Excitability: the ability to receive and
respond to stimuli
3. Extensibility: the ability to be stretched
or extended
4. Elasticity: the ability to recoil and
resume the original resting length
4. Types of Muscle Tissue
• The three types of muscle tissue are
skeletal, smooth, and cardiac
• These types differ in
– Structure
– Location
– Function
– Means of activation
• Each muscle is a discrete organ
composed of muscle tissue, blood vessels,
nerve fibers, and connective tissue
5. Types of Muscle Tissue
• Skeletal muscles are responsible for most body
movements
– Maintain posture, stabilize joints, and generate heat
• Smooth muscle is found in the walls of hollow
organs and tubes, and moves substances through
them
– Helps maintain blood pressure
– Squeezes or propels substances (i.e., food, feces) through
organs
• Cardiac muscle is found in the heart and pumps
blood throughout the body
7. Skeletal Muscle Structure
• Skeletal muscle cells are elongated and are
often called skeletal muscle fibers
• Each skeletal muscle cell contains several nuclei
located around the periphery of the fiber near
the plasma membrane
• Fibers appear striated due to the actin and
myosin myofilaments
• A single fiber can extend from one end of a
muscle to the other
• Contracts rapidly but tires easily
• Is controlled voluntarily (i.e., by conscious
control)
8. Skeletal Muscle Structure
• Fascia is a general term for connective tissue sheets
• The three muscular fascia, which separate and
compartmentalize individual muscles or groups of
muscles are:
– Epimysium: an overcoat of dense collagenous
connective tissue that surrounds the entire muscle
– Perimysium: fibrous connective tissue that surrounds
groups of muscle fibers called fascicles (bundles)
– Endomysium: fine sheath of connective tissue
composed of reticular fibers surrounding each muscle
fiber
9. Skeletal Muscle Structure
• The connective tissue
of muscle provides a
pathway for blood
vessels and nerves to
reach muscle fibers
Fig. 8.1
10. Skeletal Muscle Structure
• The connective
tissue of muscle
blends with other
connective tissue
based structures,
such as tendons,
which connect
muscle to bone
Fig. 8.2
11. Skeletal Muscle Structure
• Muscle Fibers
– Terminology
• Sarcolemma: muscle cell plasma membrane
• Sarcoplasm: cytoplasm of a muscle cell
• Myo, mys, and sarco: prefixes used to refer to
muscle
– Muscle contraction depends on two kinds of
myofilaments: actin and myosin
• Myofibrils are densely packed, rod-like contractile
elements
• They make up most of the muscle volume
13. Skeletal Muscle Structure
• Actin (thin) myofilaments consist of two helical
polymer strands of F actin (composed of G actin),
tropomyosin, and troponin
• The G actin contains the active sites to which
myosin heads attach during contraction
• Tropomyosin and troponin are regulatory subunits
bound to actin
Fig. 8.2
14. Skeletal Muscle Structure
• Myosin (thick) myofilaments consist of myosin
molecules
• Each myosin molecule has
– A head with an ATPase, which breaks down ATP
– A hinge region, which enables the head to move
– A rod
• A cross-bridge is formed when a myosin head binds
to the active site on G actin
Fig. 8.2
15.
16. Skeletal Muscle Structure
• Sarcomeres
– The smallest contractile unit of a muscle
– Sarcomeres are bound by Z disks that hold actin
myofilaments
– Six actin myofilaments surround a myosin myofilament
– Myofibrils appear striated because of A bands and I
bands
Fig. 8.2
17. Skeletal Muscle Structure
• Thick filaments: extend the entire length of an A band
• Thin filaments: extend across the I band and partway
into the A band
• Z-disc: a coin-shaped sheet of proteins (connectins) that
anchors the thin filaments and connects myofibrils to one
another
• Thin filaments do not overlap thick filaments in the lighter
H zone
• M lines appear darker due to the presence of the protein
desmin
19. Sliding Filament Model
• Actin and myosin myofilaments do not change in length
during contraction
• Thin filaments slide past the thick ones so that the actin
and myosin filaments overlap to a greater degree
– Upon stimulation, myosin heads bind to actin and sliding begins
– Each myosin head binds and detaches several times during
contraction (acting like a ratchet to generate tension and propel
the thin filaments to the center of the sarcomere)
• In the relaxed state, thin and thick filaments overlap only
slightly
• As this event occurs throughout the sarcomeres, the
muscle shortens
• The I band and H zones become narrower during
contraction, and the A band remains constant in length
21. Sliding Filament Model
• Actin and myosin myofilaments in a relaxed
muscle (below) and a contracted muscle are the
same length. Myofilaments do not change
length during muscle contraction
Fig. 8.4
22. Sliding Filament Model
• During contraction, actin myofilaments at each
end of the sarcomere slide past the myosin
myofilaments toward each other. As a result,
the Z disks are brought closer together, and the
sarcomere shortens
Fig. 8.4
23. Sliding Filament Model
• As the actin myofilaments slide over the myosin
myofilaments, the H zones (yellow) and the I
bands (blue) narrow. The A bands, which are
equal to the length of the myosin myofilaments,
do not narrow because the length of the myosin
myofilaments does not change
Fig. 8.4
24. Sliding Filament Model
• In a fully contracted muscle, the ends of
the actin myofilaments overlap at the
center of the sarcomere and the H zone
disappears
Fig. 8.4
25.
26. Physiology of Skeletal Muscle Fibers
• Membrane Potentials
– The nervous system stimulates muscles to contract
through electric signals called action potentials
– Plasma membranes are polarized, which means there
is a charge difference (resting membrane potential)
across the plasma membrane
– The inside of the plasma membrane is negative as
compared to the outside in a resting cell
– An action potential is a reversal of the resting
membrane potential so that the inside of the plasma
membrane becomes positive
27. Physiology of Skeletal Muscle Fibers
• Ion Channels
– Assist with the production of action potentials
• Ligand-gated channels
• Voltage-gated channels
30. Physiology of Skeletal Muscle Fibers
• Action Potentials
– Depolarization results from an increase in the
permeability of the plasma membrane to Na+
– If depolarization reaches threshold, an action
potential is produced
– The depolarization phase of the action potential
results from the opening of many Na+ channels
Fig. 8.6
31. Physiology of Skeletal Muscle Fibers
• Action Potentials
– The repolarization phase of the action
potential occurs when the Na+ channels close
and K+ channels open briefly
Fig. 8.6
33. Physiology of Skeletal Muscle Fibers
• Action Potentials
– Occur in an all-or-none fashion
• A stimulus below threshold produces no action
potential
• A stimulus at threshold or stronger will produce an
action potential
– Propagate (travel) across plasma membranes
34.
35. Physiology of Skeletal Muscle Fibers
• Nerve Stimulus of Skeletal Muscle
– Skeletal muscles are stimulated by motor
neurons of the somatic nervous system
– Axons of these neurons travel in nerves to
muscle cells
– Axons of motor neurons branch profusely as
they enter muscles
– Each axonal branch forms a neuromuscular
junction with a single muscle fiber
36. Physiology of Skeletal Muscle Fibers
• The neuromuscular junction is formed from:
– Axonal endings
• Have small membranous sacs (synaptic vesicles)
• Contain the neurotransmitter acetylcholine (ACh)
– Motor end plate of a muscle
• Specific part of the sarcolemma
• Contains ACh receptors
• Though exceedingly close, axonal ends and
muscle fibers are always separated by a space
called the synaptic cleft
37. 1. An action potential (orange
arrow) arrives at the
presynaptic terminal and
causes voltage-gated Ca2+
channels in the
presynaptic membrane to
open
2. Calcium ions enter the
presynaptic terminal and
initiate the release of the
neurotransmitter
acetylcholine (ACh) from
synaptic vesicles
3. ACh is released into the
synaptic cleft by exocytosis
Fig. 8.8
Neuromuscular Junction Physiology
38. 1. An action potential (orange
arrow) arrives at the
presynaptic terminal and
causes voltage-gated Ca2+
channels in the
presynaptic membrane to
open
2. Calcium ions enter the
presynaptic terminal and
initiate the release of the
neurotransmitter
acetylcholine (ACh) from
synaptic vesicles
3. ACh is released into the
synaptic cleft by exocytosis
Fig. 8.8
Neuromuscular Junction Physiology
39. 1. An action potential (orange
arrow) arrives at the
presynaptic terminal and
causes voltage-gated Ca2+
channels in the
presynaptic membrane to
open
2. Calcium ions enter the
presynaptic terminal and
initiate the release of the
neurotransmitter
acetylcholine (ACh) from
synaptic vesicles
3. ACh is released into the
synaptic cleft by exocytosis
Fig. 8.8
Neuromuscular Junction Physiology
40. 4. ACh diffuses across the
synaptic cleft and binds to
ligand-gated Na+ channels on
the postsynaptic membrane
5. Ligand-gated Na+ channels
open and Na+ enters the
postsynaptic cell, causing the
postsynaptic membrane to
depolarize. If depolarization
passes threshold, an action
potential is generated along
the postsynaptic membrane
6. ACh is removed from the
ligand-gated Na+ channels,
which then close
Fig. 8.8
Neuromuscular Junction Physiology
41. 4. ACh diffuses across the
synaptic cleft and binds to
ligand-gated Na+ channels on
the postsynaptic membrane
5. Ligand-gated Na+ channels
open and Na+ enters the
postsynaptic cell, causing the
postsynaptic membrane to
depolarize. If depolarization
passes threshold, an action
potential is generated along
the postsynaptic membrane
6. ACh is removed from the
ligand-gated Na+ channels,
which then close
Fig. 8.8
Neuromuscular Junction Physiology
42. Neuromuscular Junction Physiology
4. ACh diffuses across the
synaptic cleft and binds to
ligand-gated Na+ channels on
the postsynaptic membrane
5. Ligand-gated Na+ channels
open and Na+ enters the
postsynaptic cell, causing the
postsynaptic membrane to
depolarize. If depolarization
passes threshold, an action
potential is generated along
the postsynaptic membrane
6. ACh is removed from the
ligand-gated Na+ channels,
which then close
Fig. 8.8
43. 7. The enzyme acetylcholinesterase,
which is attached to the postsynaptic
membrane, removes acetylcholine
from the synaptic cleft by breaking it
down into acetic acid and choline
8. Choline is symported with Na+ into
the presynaptic terminal, where it
can be recycled to make ACh.
Acetic acid diffuses away from the
synaptic cleft
9. ACh is reformed within the
presynaptic terminal using acetic
acid generated from metabolism and
choline recycled from the synaptic
cleft. ACh is then taken up by the
synaptic vesicles
Fig. 8.8
Neuromuscular Junction Physiology
44. 7. The enzyme acetylcholinesterase,
which is attached to the postsynaptic
membrane, removes acetylcholine
from the synaptic cleft by breaking it
down into acetic acid and choline
8. Choline is symported with Na+ into
the presynaptic terminal, where it
can be recycled to make ACh.
Acetic acid diffuses away from the
synaptic cleft
9. ACh is reformed within the
presynaptic terminal using acetic
acid generated from metabolism and
choline recycled from the synaptic
cleft. ACh is then taken up by the
synaptic vesicles
Fig. 8.8
Neuromuscular Junction Physiology
45. 7. The enzyme acetylcholinesterase,
which is attached to the postsynaptic
membrane, removes acetylcholine
from the synaptic cleft by breaking it
down into acetic acid and choline
8. Choline is symported with Na+ into
the presynaptic terminal, where it
can be recycled to make ACh.
Acetic acid diffuses away from the
synaptic cleft
9. ACh is reformed within the
presynaptic terminal using acetic
acid generated from metabolism and
choline recycled from the synaptic
cleft. ACh is then taken up by the
synaptic vesicles
Fig. 8.8
Neuromuscular Junction Physiology
47. Excitation-Contraction Coupling
• In order to contract, a skeletal muscle
must:
– Be stimulated by a nerve ending
– Propagate an electrical current, or action
potential, along its sarcolemma
– Have a rise in intracellular Ca2+ levels, the
final trigger for contraction
• Linking the electrical signal to the
contraction is excitation-contraction
coupling
48. Excitation-Contraction Coupling
• Invaginations of the sarcolemma form T tubules, which
wrap around the sarcomeres and penetrate into the cell’s
interior at each A band –I band junction
• Sarcoplasmic reticulum (SR) is
an elaborate, smooth
endoplasmic reticulum that
mostly runs longitudinal and
surrounds each myofibril
– Paired terminal cisternae form
perpendicular cross channels
– Functions in the regulation of
intracellular calcium levels
• A triad is a T tubule and two
terminal cisternae
Fig. 8.9
49.
50. Excitation-Contraction Coupling
1. An action potential produced at the
presynaptic terminal in the
neuromuscular junction is propagated
along the sarcolemma of the skeletal
muscle. The depolarization also
spreads along the membrane of the T
tubules
2. The depolarization of the T tubule
causes gated Ca2+ channels in the
SR to open, resulting in an increase
in the permeability of the SR to Ca2+,
especially in the terminal cisternae.
Calcium ions then diffuse from the
SR into the sarcoplasm
3. Calcium ions released from the SR
bind to troponin molecules. The
troponin molecules bound to G actin
molecules are released, causing
tropomyosin to move, exposing the
active sites on G actin
4. Once active sites on G actin
molecules are exposed, the heads of
the myosin myofilaments bind to
them to form cross-bridges
51. Excitation-Contraction Coupling
1. An action potential produced at the
presynaptic terminal in the
neuromuscular junction is propagated
along the sarcolemma of the skeletal
muscle. The depolarization also
spreads along the membrane of the T
tubules
2. The depolarization of the T tubule
causes gated Ca2+ channels in the
SR to open, resulting in an increase
in the permeability of the SR to Ca2+,
especially in the terminal cisternae.
Calcium ions then diffuse from the
SR into the sarcoplasm
3. Calcium ions released from the SR
bind to troponin molecules. The
troponin molecules bound to G actin
molecules are released, causing
tropomyosin to move, exposing the
active sites on G actin
4. Once active sites on G actin
molecules are exposed, the heads of
the myosin myofilaments bind to
them to form cross-bridges
52. Excitation-Contraction Coupling
1. An action potential produced at the
presynaptic terminal in the
neuromuscular junction is propagated
along the sarcolemma of the skeletal
muscle. The depolarization also
spreads along the membrane of the T
tubules
2. The depolarization of the T tubule
causes gated Ca2+ channels in the
SR to open, resulting in an increase
in the permeability of the SR to Ca2+,
especially in the terminal cisternae.
Calcium ions then diffuse from the
SR into the sarcoplasm
3. Calcium ions released from the SR
bind to troponin molecules. The
troponin molecules bound to G actin
molecules are released, causing
tropomyosin to move, exposing the
active sites on G actin
4. Once active sites on G actin
molecules are exposed, the heads of
the myosin myofilaments bind to
them to form cross-bridges
53. Excitation-Contraction Coupling
1. An action potential produced at the
presynaptic terminal in the
neuromuscular junction is propagated
along the sarcolemma of the skeletal
muscle. The depolarization also
spreads along the membrane of the T
tubules
2. The depolarization of the T tubule
causes gated Ca2+ channels in the
SR to open, resulting in an increase
in the permeability of the SR to Ca2+,
especially in the terminal cisternae.
Calcium ions then diffuse from the
SR into the sarcoplasm
3. Calcium ions released from the SR
bind to troponin molecules. The
troponin molecules bound to G actin
molecules are released, causing
tropomyosin to move, exposing the
active sites on G actin
4. Once active sites on G actin
molecules are exposed, the heads of
the myosin myofilaments bind to
them to form cross-bridges
54. Excitation-Contraction Coupling
1. An action potential produced at the
presynaptic terminal in the
neuromuscular junction is propagated
along the sarcolemma of the skeletal
muscle. The depolarization also
spreads along the membrane of the T
tubules
2. The depolarization of the T tubule
causes gated Ca2+ channels in the SR
to open, resulting in an increase in the
permeability of the SR to Ca2+,
especially in the terminal cisternae.
Calcium ions then diffuse from the SR
into the sarcoplasm
3. Calcium ions released from the SR
bind to troponin molecules. The
troponin molecules bound to G actin
molecules are released, causing
tropomyosin to move, exposing the
active sites on G actin
4. Once active sites on G actin
molecules are exposed, the heads of
the myosin myofilaments bind to them
to form cross-bridges
66. Muscle Relaxation
• Calcium ions are transported back into the
sarcoplasmic reticulum
• Calcium ions diffuse away from troponin
and tropomyosin moves, preventing
further cross-bridge formation
67. Muscle Twitch
• The contraction of a
muscle as a result of
one or more muscle
fibers contracting
• Has lag, contraction,
and relaxation
phases
Table 8.2
68.
69. Strength of Muscle Contraction
• For a given condition, a muscle fiber or motor
unit contracts with a consistent force in response
to each action potential
• For a whole muscle, stimuli of increasing
strength result in graded contractions of
increased force as more motor units are
recruited (multiple motor unit summation)
• Stimulus of increasing frequency increase the
force of contraction (multiple-wave summation)
71. Strength of Muscle Contraction
• Incomplete tetanus is partial relaxation between
contractions, and complete tetanus is no
relaxation between contractions
• The force of contraction of a whole muscle
increases with increased frequency of
stimulation because of an increasing
concentration of Ca2+ around the myofibrils
• Treppe is an increase in the force of contraction
during the first few contractions of a rested
muscle
76. Types of Muscle Contraction
• Isometric contractions cause a change in muscle
tension but no change in muscle length
• Isotonic contractions cause a change in muscle
length but no change in muscle tension
• Concentric contractions are isotonic contractions
that cause muscles to shorten
• Eccentric contractions are isotonic contractions
that enable muscles to shorten
• Muscle tone is the maintenance of a steady
tension for long periods
• Asynchronous contractions of motor units
produce smooth, steady muscle contractions
77.
78. Muscle Length and Tension
Fig. 8.17
• Muscle contracts
with less than
maximum force if
its initial length is
shorter or longer
than optimal
79.
80. Fatigue
• The decreased ability to do work
• Can be caused by
– The central nervous system (psychologic
fatigue)
– Depletion of ATP in muscles (muscular
fatigue)
• Physiologic contracture (the inability of
muscles to contract or relax) and rigor
mortis (stiff muscles after death) result
from inadequate amounts of ATP
81.
82. Energy Sources
• Creatine phosphate
– ATP is synthesized
when ADP reacts
with creatine
phosphate to form
creatine and ATP
– ATP from this
source provides
energy for a short
time
Fig. 8.18
83. Energy Sources
• Anaerobic respiration
– ATP synthesized provides
energy for a short time at
the beginning of exercise
and during intense
exercise
– Produces ATP less
efficiently but more rapidly
than aerobic respiration
– Lactic acid levels increase
because of anaerobic
respiration
Fig. 8.18
84. Energy Sources
• Aerobic respiration
– Requires oxygen
– Produces energy
for muscle
contractions under
resting conditions
or during
endurance exercise
Fig. 8.18
87. Speed of Contraction
• The three main types of skeletal muscle
fibers are
– Slow-twitch oxidative (SO) fibers
– Fast-twitch glycolytic (FG) fibers
– Fast-twitch oxidative glycolytic (FOG) fibers
• SO fibers contract more slowly than FG
and FOG fibers because they have slower
myosin ATPases than FG and FOG fibers
88. Fatigue Resistance
• SO fibers are fatigue-resistant and rely on
aerobic respiration
– Many mitochondria, a rich blood supply, and
myoglobin
• FG fibers are fatigable
– Rely on anaerobic respiration and have a high
concentration of glycogen
• FOG fibers have fatigue resistance
intermediate between SO and FG fibers
– Rely on aerobic and anaerobic respiration
89. Functions
• SO fibers maintain posture and are involved with
prolonged exercise
– Long-distance runners have a higher percentage of
SO fibers
• FG fibers produce powerful contractions of short
duration
– Sprinters have a higher percentage of FG fibers
• FOG fibers support moderate-intensity
endurance exercises
– Aerobic exercise can result in the conversion of FG
fibers to FOG fibers
91. Muscular Hypertrophy and Atrophy
• Hypertrophy is an increase in the size of
muscles
– Due to an increase in the size of muscle fibers
resulting from an increase in the number of myofibrils
in the muscle fibers
• Aerobic exercise
– Increases the vascularity of muscle
– Greater hypertrophy of slow-twitch fibers than fast-twitch fibers
• Intense anaerobic exercise
– Greater hypertrophy of fast-twitch fibers than slow-twitch
• Atrophy is a decrease in the size of muscle
– Due to a decrease in the size of muscle fibers or a
loss of muscle fibers
92. Effects of Aging on Skeletal Muscle
• By 80 years of age 50% of the muscle
mass is gone
– Due to a loss in muscle fibers
– Fast-twitch muscle fibers decrease in number
more rapidly than slow-twitch fibers
• Can be dramatically slowed if people
remain physically active
93. Types of Smooth Muscle
• Visceral smooth muscle fibers have many
gap junctions and contract as a single unit
• Multiunit smooth muscle fibers have few
gap junctions and function independently
– Found in the walls of hollow visceral organs,
such as the stomach, urinary bladder, and
respiratory passages
– Forces food and other substances through
internal body channels
– It is not striated and is involuntary
94. Regulation of Smooth Muscle
• Contraction is involuntary
– Multiunit smooth muscle contracts when
externally stimulated by nerves, hormones, or
other substances
– Visceral smooth muscle contracts
autorhythmically or when stimulated externally
• Hormones are important in regulating
smooth muscle
95. Structure of Smooth Muscle Cells
• Spindle-shaped with a single nucleus
• Have actin and myosin myofilaments
– Actin myofilaments are connected to dense bodies
and dense areas
• Not striated
• No T tubule
system and
most have less
SR than skeletal
muscle
• No troponin
96. Contraction and Relaxation of Smooth Muscle
• Calcium ions enter the cell to initiate
contraction
– Bind to calmodulin
– Activate myosin kinase, which transfers a
phosphate group from ATP to myosin
– When phosphate groups are attached to
myosin, cross-bridges form
• Relaxation results when myosin
phosphatase removes a phosphate group
from the myosin molecule
99. Functional Properties of Smooth Muscle
• Pacemaker cells are autorhythmic smooth muscle
cells that control the contraction of other smooth
muscle cells
• Smooth muscle cells contract more slowly than
skeletal muscle cells
• Smooth muscle tone is the ability of smooth muscle
to maintain a steady tension for long periods with
little expenditure of energy
• Smooth muscle in the walls of hollow organs
maintain a relatively constant pressure on the
contents of the organ despite changes in content
volume
• The force of smooth muscle contraction remains
nearly constant despite changes in muscle length
100. Cardiac Muscle Cells
• Occurs only in the heart
• Is striated like skeletal muscle but is not
voluntary
• Have a single nucleus
• Connected by intercalated disks that allowing
them to function as a single unit
• Capable of autorhythmicity
• Contracts at a fairly steady rate set by the
heart’s pacemaker
• Neural controls allow the heart to respond to
changes in bodily needs
We can identify the function of the muscles by its classification. Lets review the different types of muscle tissue.
Movement – all the muscles attached to the bone
Trapezius muscle – for maintaining posture
Respiration – intercostal muscles
Communication – because of the presence of neuromuscular junctions in muscle fibers
Muscular contraction and relaxation is controlled by the nervous system.
The basic unit comprising a muscle in known as the muscle fiber. 1 muscle fiber is composed of the SARCOLEMMA which covers the muscle fiber.
The actin is the thin myofilament while the mysosin is the thick myofilament.
During contraction, the myosin heads attach to the actin.
The arrangement of myofibrils within a fiber is so organized a perfectly aligned repeating series of dark A bands and light I bands is evident