Ch. 10 – Muscle Tissue and
Muscle Physiology
• A brief review from Ch. 4: there are 3 types of
muscle tissue…
– 1. Cardiac muscle is striated and involuntarily controlled
• It’s found in the walls of the heart
• It functions to pump blood
– 2. Smooth (visceral) muscle is nonstriated and
involuntarily controlled
• It’s found in the walls of hollow organs
• It functions to move eggs, sperm, urine, food, hairs, etc.
throughout the body
– 3. Skeletal muscle is striated and voluntarily controlled
• It’s attached to bone or fascia
• Skeletal muscle is the major focus of this chapter
• It has many functions (see the next slide)…
Skeletal muscles
• = organs that are made up mainly of skeletal muscle
tissue, but also CTs, nerves, and blood vessels
– Each skeletal muscle cell is called a muscle fiber
• Functions of skeletal muscles:
– 1. Produce skeletal movement
– 2. Maintain posture and body position
– 3. Support soft tissues
• E.g. the floor of pelvic cavity
– 4. Guard entrances and exits
• E.g. the upper part of the esophagus, the external anal sphincter,
and the external urethral sphincter
– 5. Produce heat to help maintain body temperature
– 6. Store nutrient (protein) reserves
1
Organization of
CTs in skeletal
muscles
Part 1
• Skeletal muscles
(as a whole):
– Are surrounded by
epimysium, which
is…
• Dense irregular CT
• Connected to deep
fascia
– Are subdivided into
many compartments
called fascicles
Fig. 10-1, p. 281
• Fascicles:
– Are
surrounded
by
perimysium,
which…
Organization of CTs
in skeletal muscles
Part 2
• Is dense
irregular CT
• Also
contains
blood
vessels and
nerves
– Contain
many
individual
muscle
fibers
Fig. 10-1, p. 281
2
• Muscle fibers:
– Are surrounded by
endomysium,
which…
• Is areolar CT
• Contains capillaries, nerve fibers
(axons), and…
– Myosatellite
cells = stem
cells that
function in
muscle
development,
repair, and
perhaps
growth (via
hyperplasia)
Organization of
CTs in skeletal
muscles
Part 3
– Contain long,
contractile
protein-filled
cylindrical
structures called
myofibrils
Fig. 10-1, p. 281
A summary of the CTs in skeletal muscles
•
All 3
“–mysiums”
fuse together
at the end of
the muscle to
form a
tendon,
which…
– Connects
muscle to
bone
– Is
continuous
with the
periosteum of
bone
– Is called
an aponeurosis if
it’s a
broad, flat
tendon
Fig. 10-1, p. 281
3
More about skeletal muscle fibers
•
They are…
–
–
–
–
A.k.a. muscle cells or myofibers
Formed by the fusion of embryonic myoblast cells
Extremely large – up to a foot long and 10X the diameter of a typical cell!
Multinucleate and striated
Fig. 10-2, p. 282
Skeletal muscle fiber structure
•
Sarcolemma = the cell
membrane of a muscle
fiber
– “Sarco” = “flesh”;
“lemma” = “husk”
– Transverse (T)
tubules = deep
invaginations of the
sarcolemma, which…
• Are continuous with
the sarcolemma
• Carry action
potentials
(electrical
impulses) deep
into the muscle
fiber
•
Sarcoplasm =
the
cytoplasm
of a muscle
fiber
Fig. 10-3, p. 283
4
Skeletal muscle fiber structure
• Sarcoplasmic reticulum (SR) = a membranous
network of tubules that surrounds each myofibril
– The SR is modified smooth ER
– Function: store and release Ca2+ ions
Fig. 10-3, p. 283
Calcium ions and muscle fibers
• Ca2+ is continuously pumped (via active transport) into the SR
from the sarcoplasm
– The SR is not very permeable (leaky) to Ca2+ in a resting muscle fiber
• SR contains a Ca2+-binding (the binding is reversible) protein
called calsequestrin
• As a result of the pumping of Ca2+ into the SR:
– The free (unbound) [Ca2+] in the SR is ~ 1,000X higher than in the
sarcoplasm
– The total [Ca2+] = free Ca2+ + Ca2+ bound to calsequestrin
– About 40X more Ca2+ is bound to calsequestrin than is in the form of
free Ca2+
– So, the total [Ca2+] in SR can be up to 40,000X higher than in the
sarcoplasm!
• During the contraction process, the SR membrane becomes
extremely permeable (leaky) to Ca2+, and Ca2+ rapidly
diffuses into the sarcoplasm
– Remember that flux = P x ΔC
5
Skeletal muscle fiber structure
• Myofibrils = long, parallel, cylindrical structures that are
surrounded and separated by SR
– They contain contractile protein filaments called myofilaments:
• Thin filaments are mostly made of the protein actin
• Thick filaments are mostly made of the protein myosin
• Sarcomeres = regular, repeating, functional sections/units of
myofilaments within myofibrils (see the next slide)
Fig. 10-3, p. 283
• Sarcomeres are the
smallest functional
units of muscle
contraction
Sarcomeres
– They are repeating
units along the entire
length of the myofibril
and thus the muscle
fiber
• Their regular arrangement causes skeletal
muscle tissue to have a
striated (banded) appearance microscopically
Fig. 10-2, p. 282
Fig. 10-4, p. 285
6
•
Sarcomere structure
A band = dark colored
– = the center of a sarcomere
– It does not shrink when
muscle contracts
– It contains:
• 1. The M line =
proteins that centrally
stabilize the thick
filaments
• 2. The H band (H zone) –
where there are thick
filaments only
– The H band does shrink
when muscle contracts
• 3. Two zones of overlap –
where both thin and thick
filaments are present
•
I band = light in color
– It shrinks when muscle contracts
– It contains thin filaments, titin
(an elastic protein), and the…
• Z line = the boundary
between adjacent sarcomeres
– It’s made of actinin proteins
that anchor the thin
filaments of adjacent
sarcomeres (see the next
slide)
– Titin attaches here, too
Fig. 10-4, p. 285
Cross-sections of
different
parts of a sarcomere
Fig. 10-5, p. 286
7
A closer look at the myofilaments
Fig. 10-7, p. 288
Thin filaments
• Contain 4 proteins:
– 1. F-actin (filamentous actin) = a twisted strand composed of 2 rows
of globular G-actin subunits; has active sites (= myosin-binding sites)
– 2. Nebulin – helps hold the G-actin subunits together in the F-actin
strand
– 3. Tropomyosin – covers the active sites on G-actin in resting muscle
– 4. Troponin – binds to G-actin and tropomyosin; it has a Ca2+-binding
site
Note: troponin and tropomyosin
combine to form the troponintropomyosin complex
Fig. 10-7ab, p. 288
8
Thick filaments
•
•
•
•
= bundles of myosin molecules
around a titin core
The myosin molecules have an
elongated tail, a globular head,
and a hinge region
The myosin heads have an
ATP-binding site
The myosin heads form crossbridges (connections/
interactions) with actin during
contraction
Fig. 10-7cd, p. 288
The sliding filament theory
of skeletal muscle contraction
• The sarcomere shortens as the thin and thick
filaments slide past one another
– The I bands and H band shrink; the A band does not
• The zones of overlap increase in length!
• Sarcomeres shorten → myofibrils shorten → muscle
fibers shorten → the whole muscle shortens!
Fig. 10-8, p. 288
9
the most macroscopic level
the most microscopic level
A summary of the
levels of
organization in a
skeletal muscle
Fig. 10-6, p. 287
An overview of
skeletal
muscle
contraction
Fig. 10-9, p. 289
10
The steps involved in muscle contraction
•
1. An electrical signal or impulse (= an action potential, or AP) travels
along the axon of a motor neuron to the neuromuscular junction (NMJ)
– NMJ = the synaptic terminal of a motor neuron and the
motor end plate of a muscle fiber, plus the synaptic cleft
in between
Note: my
numbered steps
differ slightly
from Martini’s, so
I’ve blanked out
the step numbers
on the figures in
these notes
Fig. 10-11, p. 292
The steps involved in muscle contraction
• 2. In response
to the
incoming
action
potential,
neurotransmitter
(acetylcholine,
or ACh) is
released via
exocytosis
into the
synaptic cleft
Fig. 10-11, pp. 292-293
11
The steps involved in
muscle contraction
• 3. ACh diffuses across the
synaptic cleft and binds to ACh
receptors on the surface of the
sarcolemma at the motor end
plate
• 4. The ACh receptors change
shape and allow Na+ to move
down its concentration gradient
into the sarcoplasm
Fig. 10-11, p. 293
The steps involved in muscle contraction
•
5. Excitation (of the muscle fiber) = another
AP is generated, and it spreads along the
sarcolemma and deep into the T tubules
– Meanwhile, the enzyme acetylcholinesterase
(AChE) breaks down the ACh, returning the
NMJ to its resting state
Fig. 10-11, pp. 292-293
12
Conditions in a resting
muscle fiber
• The [Ca2+] in the sarcoplasm is
relatively low
• The free [Ca2+] in the sarcoplasmic reticulum (SR) is
relatively high (~ 1,000X higher
than in the sarcoplasm)
• The myosin heads are already
“cocked” and storing potential
energy due to their prior
breakdown of ATP (see the next
slide)
• The active (myosin-binding) sites
on actin are blocked by the
troponin-tropomyosin complex
Fig. 10-10a, p. 291
The steps involved in muscle contraction
•
•
6. In response to the muscle fiber’s AP, the SR releases Ca 2+ into the sarcoplasm
(this is excitation-contraction coupling!)
7. The Ca2+ binds to the troponin, which then changes position, pulling the
tropomyosin to the side and uncovering the active (myosin-binding) sites on actin
Fig. 10-10b,
p. 291
Fig. 10-12, p. 294
13
The steps involved in
muscle contraction
• 8. The
“cocked”
(energized)
myosin heads
of the thick
filaments bind
to the actin of
the thin
filament,
forming crossbridges
Fig. 10-12, p. 295
Fig. 10-10c, p. 291
The steps involved in
muscle contraction
• 9. The myosin heads release
their stored energy as they pivot
(“uncock”), pulling the thin
filament toward the center
(M line) of the sarcomere
– This is the “power stroke” of
muscle contraction
Fig. 10-12, p. 295
14
The steps involved in
muscle contraction
• 10. The myosin heads
bind to new ATP,
breaking the crossbridges
Fig. 10-12, p. 295
The steps involved in
muscle contraction
• 11. The myosin heads break
down the newly bound ATP, and
“recock” to get ready for the next
power stroke
– Steps 8-11 are repeated (as long
as the [Ca2+] and [ATP] are high
enough), shortening the
sarcomeres and thus the entire
muscle, creating tension (which
is a pulling force)
– Cross-bridges are formed at
different times by different
individual myosin heads, causing
an overall smooth sliding of the
filaments
Fig. 10-12, p. 295
15
Ending contraction (= relaxation)
• The motor neuron quits firing (sending APs), so no additional
ACh is released at the NMJ
• AChE in the synaptic cleft continually breaks down previously
released ACh
• As a result:
– No new APs are generated along the sarcolemma of the muscle fiber
– The [Ca2+] in the sarcoplasm drops, because…
• No new Ca2+ is released from the SR
• Ca2+ is continuously pumped back into the SR
– The troponin-tropomyosin complex returns to its resting/original
position, covering up the active (myosin-binding) sites on the thin
filaments
– There is no interaction/cross-bridge formation between actin and
myosin
• The muscle returns (stretches) to its resting length passively
(due to other external forces, such as elasticity, gravity, or the
contraction of antagonist muscles)
A review of
skeletal muscle
contraction
Table 10-1, p. 297
16
→ due to a combination of elastic forces, opposing
(antagonistic) muscle contractions, and gravity
A review of
skeletal muscle
relaxation
Table 10-1, p. 297
Tension (force/strength) production
• By individual muscle fibers vs. by whole muscles
•
By individual muscle fibers:
•
By whole muscles:
•
The all-or-none principle = all sarcomeres
in an individual muscle fiber will contract
together maximally when the fiber is
stimulated; i.e., a muscle fiber is either “on”
(producing tension) or “off” (relaxed)
•
Main factors:
•
Ultimately, the amount of tension produced
by an individual muscle fiber depends on the
number of pivoting cross-bridges formed
•
Main factors:
– 1. Resting fiber length – affects the degree
to which thin and thick filaments overlap
– 2. Frequency of stimulation – affects the
duration of high [Ca2+]
– 3. The size (diameter) of the individual
muscle fiber – affects the amount of actin
and myosin available to interact with each
other
– 1. The amount of
tension produced
by individual
muscle fibers (see
the box to the left)
– 2. Recruitment –
affects the # of
motor units (and
thus fibers) that are
stimulated
– 3. The size of the
whole muscle –
which depends on
the # of muscle
fibers present (and
the diameter of
those fibers, as
discussed in the box
to the left)
17
•
•
The
resting
length of
a muscle
fiber
affects
the
amount
of
overlap
between
the thin
and thick
filaments
There is
an
optimal
resting
length for
a fiber at
which
force
generation is
maximal
Tension production by individual
muscle fibers: resting fiber length
Fig. 10-14, p. 298
Tension production by
individual muscle fibers:
frequency of stimulation
• 1. Single stimulus:
– Twitch
• 2. Multiple stimuli:
– Treppe
– Wave summation (a.k.a. summation of
twitches)
– Incomplete tetanus
– Complete tetanus
18
Single stimulus:
twitch
• A twitch = a single stimuluscontraction-relaxation
sequence in a muscle fiber
– Note: a single twitch is too brief
to be part of any useful muscular
activity by itself
Fig. 10-15, p. 299
• A twitch has 3 parts:
– 1. The latent period
• The AP is followed by Ca2+
release from the SR
– 2. The contraction phase
• Tension increases to a peak
– 3. The relaxation phase
• Tension decreases
• There’s no more stimulation, so
Ca2+ is pumped back into the SR
Multiple stimuli: treppe
• Treppe = the gradual
increase in tension (i.e.,
strength of contraction) that
is generated by a muscle
fiber when it is repeatedly
stimulated immediately after
each relaxation phase ends
• A relatively low maximum
tension is reached
• The main explanation for
treppe:
– There is increasing [Ca2+] in
the sarcoplasm
• There’s not enough time in
between stimuli to pump it all
back into the SR
Fig. 10-16a, p. 301
19
• Wave summation (a.k.a.
summation of twitches) = the
gradual increase in tension that
is generated by a muscle fiber
when it is repeatedly stimulated
before each relaxation phase
has been completed
Multiple stimuli:
wave summation
– One twitch is added to another,
so the contraction gets stronger
and stronger
• The stronger contractions are
probably due to:
– The prolonged presence of high
[Ca2+] in the sarcoplasm
– Action potential duration vs. twitch
duration
• An AP is short: 1-2 msec
• A muscle twitch is longer: up to
100 msec
• So another AP can stimulate a
muscle fiber before the relaxation
phase of the previous twitch has
ended
Fig. 10-1b6, p. 301
Multiple stimuli:
wave summation leading to tetanus
•
•
Incomplete tetanus = the muscle fiber never relaxes completely between
twitches
Complete tetanus = the stimulation rate is higher, so the relaxation phase
is eliminated entirely
– Almost all
normal
whole
muscle
contractions
involve
tetanic
contractions by
individual
muscle
fibers
Fig. 10-16bc, p. 301
20
Tension production by whole muscles: recruitment
•
Motor unit = one motor neuron and all of the muscle fibers that
it innervates
– The size of a motor unit is inversely related to the precision of its
control (e.g. eye muscles vs. leg muscles)
•
Recruitment = the stimulation of additional motor units
– The more motor units stimulated → the more actively contracting
muscle fibers → a stronger total
contraction by the whole muscle
Asynchronous motor
unit summation
Fig. 10-17, p. 302
Tension production by
whole muscles: muscle tone
• Muscle tone = the low level of resting tension that is
present in skeletal muscle at all times (it is NOT
enough tension to produce movement, however)
– Some motor units are active at any given point in time
– Which motor units are active varies constantly
• Functions of muscle tone:
– Stabilize bones and joints
– Maintain body position (posture)
– Allow more rapid activation of a whole muscle (i.e.,
accelerate recruitment)
– ↑ Energy usage when muscles are at rest (i.e., ↑ resting
metabolic rate)
– Lookin’ good!
21
Types of contractions: isotonic
• Isotonic contraction
(isotonic = “same
tension”)
– The muscle length changes,
so movement occurs (it’s a
“dynamic contraction”)
– There are 2 types of
isotonic contractions:
• 1. Concentric
contraction (shown
here) = the muscle
shortens if the tension
produced exceeds (even
if just barely) the load
• 2. Eccentric contraction =
the muscle lengthens in a
controlled manner (exerting
tension in opposition to an
external force such as gravity),
if the tension produced is slightly
less than the load
Fig. 10-18a, p. 303
Types of contractions: isometric
• Isometric contraction (isometric = “same length”)
• No movement occurs (it’s a “static contraction”)
– Tension is produced, but it isn’t strong enough to overcome the load
and cause shortening/movement, so the length of the muscle remains
the same
– E.g. maintaining posture against gravity
Fig. 10-18c, p. 303
22
Load and speed of contraction
• Contraction speed (= distance ÷ time) is inversely related to
load
– I.e., ↑ load (lifting a heavy weight) → ↓ contraction speed (slower)
• This should be intuitive and hopefully fairly obvious from
everyday life experiences!
Fig. 10-19, p. 304
Energy use and muscular activity
• Muscle contraction requires lots of ATP energy:
– There are 15 billion thick filaments per muscle fiber
– When a muscle fiber is actively contracting, each thick
filament breaks down 2,500 ATP molecules per second
– 15 billion X 2,500 = 37.5 X 1012 = 37,500,000,000,000
ATPs are needed per muscle fiber per second!
• There’s only enough ATP present in muscle fibers
for about 2 seconds of maximal (tetanic) contraction
• There are 3 main processes used to generate
additional ATP in skeletal muscle for contraction:
– 1. ATP and CP reserves
– 2. Glycolysis
– 3. Aerobic metabolism
• Which process muscles use depends upon both the
INTENSITY and DURATION of their activity
23
ATP and CP reserves
• This process is only found in muscle cells
• It involves creatine phosphate (CP) and ATP
• It is a fast, SHORT-TERM method of ATP
generation
– It involves only 1 enzyme (creatine kinase); i.e., it’s not a
long, time-consuming pathway
• CP “recharges” spent ADP into fresh ATP
– The reversible equation: CP + ADP ↔ creatine + ATP
• The total amount of CP stored in a muscle is enough
for a burst of MAXIMUM-intensity contraction for
ABOUT 15 SECONDS
– This allows time for other processes such as glycolysis to
“kick in”
Glycolysis
• Glucose (either absorbed from your last meal or released from
stored glycogen reserves) is broken down to form 2 pyruvate
(pyruvic acid) molecules (see Ch. 25 for much more detail)
• It does not require oxygen (i.e., it’s anaerobic)
• It occurs in the cytoplasm of cells
• It is relatively inefficient: a net of only 2 ATPs are generated
from each glucose molecule
• In anaerobic conditions, glycolysis is used after ATP/CP
reserves are depleted during a burst of maximum-intensity
contraction
– The problem: in anaerobic conditions, glycolysis ends up with the
pyruvate converted to lactate (lactic acid), leading to H+ buildup…
• Muscle fiber intracellular pH ↓
• Enzyme function is negatively affected
• So muscle fibers can only provide a burst of NEAR-MAXIMUM-intensity
contraction for ABOUT 2 MINUTES before fatigue kicks in
• Glycolysis also supplies 2 pyruvate molecules as organic
substrates for the initial step of aerobic metabolism (see the
next slide)
24
Aerobic metabolism
• Pyruvate (from glycolysis) or other organic substrates are
broken down in a multi-enzyme pathway (see Ch. 25 for
much more detail)
• It requires oxygen (i.e., it’s aerobic)
– So it depends on the ability of the respiratory and cardiovascular
systems to deliver enough oxygen to meet the demand for it
• It occurs in the mitochondria of cells
• It is very efficient: 17 ATPs are generated from each
pyruvate (so 34 ATPs are generated from each glucose)
• Resting skeletal muscle:
– Uses small quantities of mostly free fatty acids (from the bloodstream)
as substrates
• Moderately active skeletal muscle:
– Uses larger quantities of mostly pyruvate (from glycolysis) and free
fatty acids (from the bloodstream) as substrates
• It provides energy for LONG-TERM exercise (A FEW
MINUTES TO A FEW HOURS) of SUBMAXIMAL-intensity
muscular contractions
– E.g. a marathon run is almost all aerobic
• Resting = LOW
intensity
– There’s low ATP demand
– There’s lots of O2
available
• At rest, muscles use
small quantities of
mostly free fatty acids
(from the bloodstream)
as substrates for
aerobic metabolism in
mitochondria
• This restocks supplies
for maximum
intensity activity that
may be needed later:
ATP generation in
resting
skeletal muscle
– Surplus ATP → CP
– Surplus glucose →
glycogen
Fig. 10-20a, p. 307
25
• Moderate = SUBMAXIMAL intensity
– There’s increased
demand for ATP
– There’s increased
demand for O2, but
O2 delivery is still
matching demand
ATP generation in
moderately active
skeletal muscle
• So aerobic
metabolism is still
dominant
• Pyruvate (from
glycogen/glucose)
is the main
substrate
– But if you have low
glycogen reserves,
you can use fatty
acids (or even
amino acids) as
substrates
Fig. 10-20b, p. 307
• Peak = MAXIMUM
or NEAR-MAXIMUM
– O2 delivery cannot
meet O2 demand
• So aerobic/
mitochondrial ATP
production can
provide only about
1/3 of the ATP
needed
ATP generation in
skeletal muscle that is
in peak activity
• Most ATP is
produced from CP
(for the first 10-15
seconds) and via
anaerobic glycolysis
(for a few minutes)
– The downside:
lactate (lactic acid)
production and ↓
intracellular pH
limits exercise
duration
Fig. 10-20c, p. 307
26
Fatigue
• Muscle fatigue = skeletal muscle can no longer
perform at the desired level of activity
• Some factors that lead to muscle fatigue:
– ↓ Energy reserves, so there’s ↓ substrate availability
– ↓ pH effects:
• a) Changes in enzyme activity (usually for the worse)
• b) H+ displaces Ca2+ from troponin
• c) H+ interferes with hemoglobin reoxygenation
– Sarcolemma and SR damage, leading to slower Ca2+
uptake and release
• Consider also “central (mental/motivational)
fatigue”:
– ↓ pH has harmful effects on neurons
– Pain affects the brain (↑ weariness, ↓ desire)
Recovery from skeletal muscle activity
• Recovery = the return of conditions (pH, oxygen
consumption, temperature, etc.) in muscle fibers and
the entire body to normal, resting levels after exercise
• Recovery mechanisms include:
– Lactate removal and recycling
• Within a recovering muscle fiber, local lactate is converted back to
pyruvate, which can then be burned aerobically and/or used to
synthesize glucose and replenish glycogen reserves
• The Cori cycle – excess lactate that diffuses into the bloodstream
is transported to the liver, where it’s converted back to pyruvate,
which can then be burned aerobically and/or used to synthesize
glucose, which is then transported back to muscle fibers to
replenish their glycogen reserves
– Oxygen debt
• A.k.a. excess postexercise oxygen consumption (EPOC)
• = the amount of O2 required to restore normal resting conditions
– Heat loss
• E.g. via dermal vasodilation and/or sweating
27
Muscle performance
• Consider the tradeoffs of generating maximal
force/strength vs. having longer endurance
• Muscle performance is mainly dependent
upon:
– 1. Muscle fiber type
• Slow fibers (“dark meat”)
• Intermediate fibers
• Fast fibers (“white meat”)
– 2. Physical conditioning/training
Fast vs. slow fibers
Fig. 10-21, p. 310
28
A comparison of
skeletal muscle fiber types
Table 10-3, p. 309
Physical conditioning
• Anaerobic endurance – maximum or nearmaximum effort, shorter duration (up to 2 minutes)
– Improvements are due mainly to hypertrophy
– It’s limited by:
• ATP/CP availability
• Glycogen/glucose availability
• Tolerance for acidosis (due to lactate production)
• Aerobic endurance – sustained sub-maximal effort,
longer duration (from a few minutes to a few hours)
– Improvements are due mainly to muscle fiber type
alterations, ↑ cardiovascular and respiratory function, and
↑ capillary density
– It’s limited by:
• Oxygen delivery to mitochondria
• The number of mitochondria
• Aerobic substrate (glycogen/glucose, fatty acids, and/or amino
acids) availability
29
FYI
Cardiac muscle
tissue
• We will cover
this topic with
the rest of
Ch. 20
Fig. 10-22, p. 313
Smooth muscle tissue
• Is not striated (because there are no
sarcomeres/myofibrils)
• Has no T tubules, but it does have SR
• Myosin
– Is scattered within the sarcoplasm
– Has more heads than in skeletal
muscle
• Actin
– Is attached to dense bodies
• Some are anchored to the
sarcolemma
• Some are held in place by
intermediate filaments
• Some anchor one cell to another
• Dense bodies are analogous to
the Z lines in skeletal muscle
• Intermediate filaments
– Are made of a protein called desmin
– Form the “scaffolding” between dense
bodies
Fig. 10-23, p. 315
30
Smooth muscle contraction
• Smooth muscle contraction is slower and longerlasting than skeletal muscle contraction
• Stimulation of smooth muscle causes Ca2+ release
from the SR and Ca2+ entry from the ECF
– Ca2+ ions bind to the protein calmodulin
– The calmodulin-Ca2+ complex activates the enzyme
myosin light chain kinase
– Myosin light chain kinase activates myosin, allowing
cross-bridges to form
– Myosin pulls on actin, and the cell shortens (“bunches up”)
• Length-tension relationship
– If you stretch smooth muscle, it adapts to its new length,
and it can then contract again
– The range of lengths over which smooth muscle
contraction can occur is 4X that of skeletal muscle (this
property is called plasticity)
Control of smooth muscle contraction
• Remember, smooth muscle is involuntarily
(subconsciously/autonomically/automatically)
controlled
• There are 2 types of smooth muscle cells:
– 1. Multiunit smooth muscle cells
• Respond to stimuli from nerves that are arranged into motor units
• Are precisely controlled
• E.g. the iris, the walls of large arteries, and arrector pili
– 2. Visceral (single unit) smooth muscle cells
• May include pacesetter cells (similar to those in cardiac muscle)
• Respond to local stimuli (chemicals/hormones, stretching, etc.);
nervous stimulation is not required
• Have gap junctions, so the tissue contracts in a rhythmic wave
• E.g. the walls of the digestive tract and urinary bladder
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