MUSCLE TISSUE

INTRODUCTION TO MUSCLE TISSUE

Muscle tissue
 A primary tissue, consisting of three types
O Skeletal muscle
O Cardiac muscle
O Smooth muscle
FUNCTIONS OF MUSCLE TISSUE
 Cells are specialized for contraction
 Skeletal muscles move the body by pulling on bones
 Cardiac and smooth muscles control movements inside
 the body
 Common properties include
O Excitability (responsiveness)
O Contractility (ability of cells to shorten)
O Extensibility (stretching)  Skeletal muscles
O Elasticity (recoil)  Have extensive vascular networks that
FUNCTIONS OF SKELETAL MUSCLE o Deliver oxygen and nutrients
o Remove metabolic wastes
 Producing movement
 Contract only when stimulated by central nervous
 Maintaining posture and body position system
 Supporting soft tissues o Often called voluntary muscles
 Guarding body entrances and exits o The diaphragm usually works
 Maintaining body temperature subconsciously
 Storing nutrients  Skeletal muscle fibers
Skeletal muscles contain o Are enormous compared to other cells
o Contain hundreds of nuclei (multinucleate)
 Skeletal muscle tissue (primarily)
o Develop by fusion of embryonic cells (myoblasts)
 Connective tissues
o Also known as striated muscle cells due to
 Blood vessels
striations
 Nerves
THE FORMATION OF A MULTINUCLEATE
Skeletal muscles have three layers of connective tissue
SKELETAL MUSCLE FIBER
 Epimysium
 Perimysium
 Endomysium
EPIMYSIUM
 Layer of collagen fibers that surrounds the muscle
 Connected to deep fascia
 Separates muscle from surrounding tissues
PERIMYSIUM
 Surrounds muscle fiber bundles (fascicles)
 Contains
o Collagen fibers
o Elastic fibers
o Blood vessels Figure A
o Nerves
ENDOMYSIUM
 Surrounds individual muscle cells (muscle fibers)
 Contains
o Capillary networks
o Myosatellite cells (stem cells) that repair damage
o Nerve fibers

 Collagen fibers of epimysium, perimysium, and endomysium

come together
o At ends of muscles to form
 A tendon (bundle)
 Or aponeurosis (sheet)
o To attach skeletal muscles to bones Figure B

SKELETAL MUSCLE FIBERS

 MUSCLE TISSUE
 Sarcolemma
o Plasma membrane of a muscle fiber
o Surrounds the sarcoplasm (cytoplasm of a
muscle fiber)
o A sudden change in membrane potential initiates
a contraction
 Transverse tubules (T tubules)
o Tubes that extend from surface of muscle fiber
deep into sarcoplasm Figure C
o Transmit action potentials from sarcolemma into  Sarcomeres
cell interior o Smallest functional units of a muscle fiber
- Action potentials trigger contraction o Interactions between filaments produce
 Sarcoplasmic reticulum (SR) contraction
o A tubular network surrounding each myofibril o Arrangement of filaments accounts for striated
o Similar to smooth endoplasmic reticulum pattern of myofibrils
o Forms chambers (terminal cisternae) that attach - Dark bands (A bands)
to T tubules - Light bands (I bands)
- Two terminal cisternae plus a T tubule  The A band
forms a triad o M line
o Specialized for storage and release of calcium - In center of A band
ions - Proteins stabilize positions of thick
- Ions are actively transported from filaments
cytosol into terminal cisternae o H band
 Myofibrils - On either side of M line
o Lengthwise subdivisions within a muscle fiber - Has thick filaments but no thin
o Responsible for muscle contraction filaments
o Made of bundles of protein filaments o Zone of overlap
(myofilaments) - Dark region
o Two types of myofilaments - Where thick and thin filaments overlap
 Thin filaments  The I band
- Composed primarily of actin o Contains thin filaments but no thick filaments
 Thick filaments o Z lines
- Composed primarily of - Bisect I bands
myosin - Mark boundaries between adjacent
THE STRUCTURE AND INTERNAL ORGANIZATION sarcomeres
OF A SKELETAL MUSCLE FIBER o Titin
- Elastic protein
- Extends from tips of thick filaments to
the Z line
- Keeps filaments in proper alignment
- Aids in restoring resting sarcomere
length
SARCOMERE STRUCTURE: LONGITUDINAL VIEWS

Figure A

I bands have only thin filaments. A bands have both thin and thick
filaments. H bands have thick filaments and bisect A bands. M lines
Figure B
are the middle of H bands. Z lines bisect the I bands.

A corresponding longitudinal section of a sarcomere in a myofibril from

Figure C a muscle fiber in the gastrocnemius (calf) muscle of the leg
SARCOMERE STRUCTURE, SUPERFICIAL
 MUSCLE TISSUE
AND CROSS-SECTIONAL VIEWS

Figure E
 Thin filaments
o Contain F-actin, nebulin, tropomyosin, and
troponin proteins
o Filamentous actin (F-actin)
- Twisted strand composed of two rows
of globular G-actin molecules
- Active sites on G-actin bind to myosin
o Nebulin
- Holds F-actin strand together
o Tropomyosin
- Covers active sites on G-actin
- Prevents actin–myosin interaction
o Troponin
LEVELS OF FUNCTIONAL ORGANIZATION - A globular protein
IN A SKELETAL MUSCLE - Binds tropomyosin, G-actin, and Ca2+
 Thick filaments
o Each contains about 300 myosin molecules
o Each myosin molecule consists of
- Tail
 Binds to other myosin
molecules
- Head
 Made of two globular protein
subunits
 Projects toward nearest thin
filament
o Core of titin recoils after stretching
Figure A
THIN AND THICK FILAMENTS

Figure B

Figure C  Sliding-filament theory

o During a contraction,
1. H bands and I bands narrow
2. Zones of overlap widen
3. Z lines move closer together
4. Width of A band remains constant
o Thus, thin filaments must slide towards the center
of sarcomere

Figure D CHANGES IN THE APPEARANCE OF A SARCOMERE DURING

THE CONTRACTION OF A SKELETAL MUSCLE FIBER
 MUSCLE TISSUE
neurotransmitter, a chemical released by a neuron to change the
permeability or other properties of another cell’s plasma membrane.
The synaptic cleft and the motor end plate contain molecules of the
enzyme acetylcholinesterase (AChE), which breaks down ACh.

A relaxed sarcomere showing location of the A band,Z lines, and I

band.

2. The stimulus for ACh release is the arrival of an electrical impulse,

or action potential, at the axon terminal. An action potential is a
sudden change in the membrane potential that travels along the length
of the axon.

During a contraction, the A band stays the same width, but the Z lines
move closer together and the I band gets smaller. When the ends of a
myofibril are free to move, the sarcomeres shorten simultaneously and
the ends of the myofibril are pulled toward its center.
SHORTENING DURING A CONTRACTION

3. When the action potential reaches the neuron’s axon terminal,

permeability changes in its membrane trigger the exocytosis of ACh
into the synaptic cleft. Exocytosis occurs as vesicles fuse with the
When both ends are free to move, the ends of a contracting muscle neuron’s plasma membrane.
fiber move toward the center of the muscle fiber.

When one end of a myofibril is fixed in position, the free end is pulled
toward the fixed end.
THE NEUROMUSCULAR JUNCTION
 Excitable membranes
o Are found in skeletal muscle fibers and neurons 4. ACh molecules diffuse across the synaptic cleft and bind to ACh
o Depolarization and repolarization events produce receptor membrane channels. ACh binding opens the membrane
action potentials (electrical impulses) channel on the surface of the motor end plate. Because the
 Skeletal muscle fibers contract due to stimulation by motor extracellular fluid contains a high concentration of sodium ions, and
neurons sodium ion concentration inside the cell is very low, sodium ions rush
 Neuromuscular junction (NMJ) into the cytosol.
o Synapse between a neuron and a skeletal
muscle fiber
o Axon terminal of the motor neuron releases a
neurotransmitter into the synaptic cleft
- The neurotransmitter is acetylcholine
(ACh)
o ACh binds to and opens a chemically gated Na+
channel on the muscle fiber
- Na+ enters cell and depolarizes motor
end plate
- An action potential is generated

SHORTENING DURING A CONTRACTION 5. The sudden inrush of sodium ions results in the generation of an
action potential in the sarcolemma. ACh is removed from the synaptic
1. The cytoplasm of the axon terminal contains vesicles filled with cleft in two ways. ACh either diffuses away from the synapse, or it is
molecules of acetylcholine, or ACh. Acetylcholine is a broken down by AChE into acetic acid and choline. This removal
 MUSCLE TISSUE
closes the ACh receptor membrane channels. The muscle fiber
pictured above indicates the propagation of the action potential along  Contraction cycle
the sarcolemma.
1. Contraction cycle begins
2. Active-site exposure
3. Cross-bridge formation (myosin binds to actin)
4. Myosin head pivoting (power stroke)
5. Cross-bridge detachment
6. Myosin reactivation
THE CONTRACTION CYCLE AND CROSS-BRIDGE FORMATION
1. Contraction Cycle Begins
The contraction cycle involves a series of interrelated steps. It
begins with the arrival of calcium ions (Ca2+) within the zone
 Excitation–contraction coupling of overlap in sarcomere.
o Action potential travels down T tubules to triads
- Ca2+ is released from terminal
cisternae of SR
o Ca2+ binds to troponin and changes its shape
o Troponin–tropomyosin complex changes position
- Exposes active sites on thin filaments
o Contraction cycle is initiated
EXCITATION–CONTRACTION COUPLING
1. Neural Control
2. Active-Site Exposure
A skeletal muscle fiber contracts when stimulated by a
motor neuron at a neuromuscular junction. The Calcium ions bind to troponin, weakening the bond between
stimulus arrives in the form of an action potential at the actin and the troponin–tropomyosin complex. The troponin
axon terminal. molecule then changes position, rolling the tropomyosin
molecule away from the active sites on actin and allowing
interaction with the energized myosin heads.
2. Excitation
The action potential causes the release of ACh into the
synaptic cleft, which leads to excitation—the
production of an action potential in the sarcolemma.

3. Release of Calcium Ions

This action potential travels along the sarcolemma and
down T tubules to the triads. This triggers the release
of calcium ions (Ca2+) from the terminal cisternae of 3. Cross-Bridge Formation
the sarcoplasmic reticulum. Once the active sites are exposed, the energized myosin
heads bind to them, forming cross-bridges.

4. Contraction Cycle Begins

The contraction cycle begins when the calcium ions
(Ca2+) bind to troponin, resulting in the exposure of
the active sites on the thin filaments. This allows cross-
bridge formation and will continue as long as ATP is
available. (See Spotlight Figure 10-11 for the details of
the contraction cycle.).
4. Myosin Head Pivoting
After cross-bridge formation, the energy that was stored in the
resting state is released as the myosin head pivots toward the
5. Sarcomere Shortening M line. This action is called the power stroke; when it occurs,
the bound ADP and phosphate group are released.
As the thick and thin filaments interact, the sarcomeres
shorten, pulling the ends of the muscle fiber closer
together.
6. Generation of Muscle Tension
During the contraction, the entire skeletal muscle
shortens and produces a pull, or tension, on the
tendons at either end.
 MUSCLE TISSUE
-68 pull Ca2+ from the cytosol and store it within the
ion pumps
 69-143
terminal cisternae. Troponin molecules then shift position,
swinging the tropomyosin strands over the active sites and
preventing further cross-bridge formation.
 Generation of muscle tension
o When muscle cells contract, they produce tension
(pull)
o To produce movement, tension must overcome the
load (resistance)
o The entire muscle shortens at the same rate
5. Cross-Bridge Detachment o Because all sarcomeres contract together
When another ATP binds to the myosin head, the link o Speed of shortening depends on cycling rate
between the myosin head and the active site on the actin (number of power strokes per second)
molecule is broken. The active site is now exposed and able  Duration of a contraction depends on
to form another cross-bridge. o Duration of neural stimulus
o Presence of free calcium ions in cytosol
o Availability of ATP
 As Ca2+ is pumped back into SR and Ca2+ concentration in
cytosol falls
o Ca2+ detaches from troponin
o Troponin returns to original position
o Active sites are re-covered by tropomyosin and the
contraction ends
 Rigor mortis
o Fixed muscular contraction after death
6. Myosin Reactivation o Results when
Myosin reactivation occurs when the free myosin head splits  ATP runs out and ion pumps cease to function
 Calcium ions build up in cytosol
ATP into ADP and P. The energy released is used to recock
the myosin head.

7. Resting Sarcomere
In the resting sarcomere, each myosin head is already
“energized”—charged with the energy that will be used to TENSION PRODUCTION
power a contraction. Each myosin head points away from the  The number of contracting sarcomeres in a muscle fiber is fixed
M line. In this position, the myosin head is “cocked” like the o So, a muscle fiber is either producing tension or relaxed
spring in a mousetrap. Cocking the myosin head requires  The amount of tension produced depends on the
energy, which is obtained by breaking down ATP; in doing so, o Number of power strokes performed
the myosin head functions as ATPase, an enzyme that breaks o Fiber’s resting length at time of stimulation
down ATP. At the start of the contraction cycle, the breakdown o Frequency of stimulation
products, ADP and phosphate (represented as P), remain  Length–tension relationship
bound to the myosin head. o Tension produced by a muscle fiber relates to the length of
the sarcomeres
o Amount of tension produced depends on the
o Number of power strokes performed by cross-bridges
o Amount of overlap between thick and thin filaments
o Maximum tension is produced when the maximum number
of cross-bridges is formed
o Occurs when zone of overlap is large

8. Contracted Sarcomere
The entire cycle is repeated several times each second, as
long as Ca2+ concentrations remain elevated and ATP
reserves are sufficient. Calcium ion levels will remain elevated
only as long as action potentials continue to pass along the T
tubules and stimulate the terminal cisternae. Once that
stimulus is removed, the calcium channels in the SR close
 MUSCLE TISSUE
1. A myogram showing differences in tension over time for a twitch
in the fibers from different skeletal muscles.
 Treppe
o A stair-step increase in tension
o Caused by repeated stimulations immediately after
relaxation phase
 Stimulus frequency <50/second
 Produces a series of contractions with increasing
tension
o Typically seen in cardiac muscle and not skeletal muscles
 Wave summation
o Increasing tension due to summation of twitches
o Caused by repeated stimulations before the end of
2. The details of tension over time for a single twitch in a fiber of
relaxation phase
the gastrocnemius muscle. Notice the presence of a latent period.
 Stimulus frequency >50/second
It corresponds to the time needed for the propagation of an action
potential and the subsequent release of calcium ions by the EFFECTS OF REPEATED STIMULATIONS
sarcoplasmic reticulum. Treppe
o Treppe is an increase in peak tension with each
successive stimulus delivered shortly after the
completion of the relaxation phase of the preceding
twitch.
o The fiber’s maximum potential tension is not reached
until tetanus (part d).

Wave summation
o Wave summation occurs when successive stimuli arrive
before the relaxation phase has been completed.

 Frequency of stimulation
o A single neural stimulation produces a single contraction, or
twitch  Tetanus is maximum tension
 Lasts 7–100 msec o Incomplete tetanus
o Sustained muscular contractions  Muscle produces near-maximum tension
 Require many repeated stimuli  Caused by rapid cycles of contraction and relaxation
o A myogram is a graph showing tension development in o Complete tetanus
muscle fibers  Higher stimulation frequency eliminates relaxation
 A single twitch has three phases phase
1. Latent period  Muscle is in continuous contraction
o Action potential moves across sarcolemma  All potential cross-bridges form
o SR releases Ca2+
EFFECTS OF REPEATED STIMULATIONS
2. Contraction phase
o Calcium ions bind to troponin and cross-bridges form Incomplete tetanus
o Tension builds to a peak o Incomplete tetanus
3. Relaxation phase occurs if the stimulus
o Ca2+ levels in cytosol fall frequency increases
o Cross-bridges detach and tension decreases further. Tension
production rises to a
THE DEVELOMENT OF TENSION IN A TWITCH peak, and the periods
 MUSCLE TISSUE
of relaxation are very brief. 1. Muscle fibers of different motor units are intermingled, so the
forces applied to the tendon remain balanced regardless of which
motor units are stimulated.

Complete tetanus
o During complete tetanus, the stimulus frequency is so
high that the relaxation phase is eliminated. Tension
plateaus at a maximum
level.

2. The tension applied to the tendon remains fairly constant, even

though individual motor units cycle between contraction and
relaxation.

MUSCLE CONTRACTIONS
 Tension production by skeletal muscles
o Depends on the number of stimulated muscle fibers
 A motor unit is a motor neuron and all of the muscle fibers it
controls
o May contain a few muscle fibers or thousands
o All fibers in a motor unit contract at the same time
 Fasciculation
o Involuntary “muscle twitch”
o Unlike a true twitch, it involves more than one muscle fiber
 Recruitment
o Increase in the number of active motor units
o Produces smooth, steady increase in tension
o Maximum tension is achieved when all motor units reach
complete tetanus  Muscle tone
 Can be sustained for a very short time o The normal tension and firmness of a muscle at rest
o Sustained contractions o Without causing movement, motor units actively
 Produce less than maximum tension  Stabilize positions of bones and joints
 Motor units are allowed to rest in rotation  Maintain balance and posture
o Elevated muscle tone increases resting energy consumption
THE ARRANGEMENT AND ACTIVITY OF MOTOR UNITS IN A
SKELETAL MUSCLE TYPES OF MUSCLE CONTRACTIONS
 Contractions are classified based on their pattern of tension
production
o Isotonic or isometric
1. Isotonic contractions
o Skeletal muscle changes length
 Resulting in motion
a. Isotonic concentric contraction
o Muscle tension >load (resistance)
o Muscle shortens
b. Isotonic eccentric contraction
o Muscle tension < load
o Muscle elongates
c. Isometric contractions
o Skeletal muscle develops tension that never exceeds the
load
o Muscle does not change length
CONCENTRIC, ECCENTRIC, AND ISOMETRIC CONTRACTIONS
a. Isotonic concentric contraction. A muscle is attached to a weight
(2 kg) that is ½ its maximum potential tension (4 kg). When
stimulated, it develops enough tension to lift the weight. The
tension remains constant, but the muscle shortens.
 MUSCLE TISSUE
o More ATP must be generated to sustain a contraction
 At rest, skeletal muscle fibers produce more ATP than needed
o ATP transfers energy to creatine
o Creating creatine phosphate (CP)
 Used to store energy and convert ADP back to ATP
 The enzyme creatine kinase (CK)
o Catalyzes the conversion of ADP to ATP using the energy
stored in CP
b. Isotonic eccentric contraction. The tension remains constant, but  When CP is used up, other mechanisms are used to generate
the muscle lengthens. ATP
 ATP is generated by
o Direct phosphorylation of ADP by creatine phosphate (CP)
o Anaerobic metabolism (glycolysis)
o Aerobic metabolism (citric acid cycle and electron transport
chain)
 Glycolysis
o Anaerobic process
o Important energy source for peak muscular activity
o Breaks down glucose from glycogen stored in skeletal
muscles
c. Isometric contraction.
o Produces two ATP per molecule of glucose
When stimulated, the tension rises, but the muscle length stays the
same.  Aerobic metabolism
o Primary energy source of resting muscles
o Breaks down fatty acids
 Muscle metabolism
o Skeletal muscles at rest metabolize fatty acids and store
glycogen and CP
o During moderate activity, muscles generate ATP through
aerobic breakdown of glucose, primarily
o At peak activity, pyruvate produced via glycolysis is
converted to lactate

 Recovery period
o The time required after exertion for muscles to return to
  Load and speed of contraction
normal
o Are inversely related
o The heavier the load, the longer it takes for movement to
begin
o Tension must exceed the load before shortening can
occur

 Muscle relaxation and the return to resting length

o Elastic forces
 Tendons recoil after a contraction
 Helps return muscle fibers to resting length
 Lactate removal and recycling (Cori cycle)
o Opposing muscle contractions
o Lactate is transferred from muscles to the liver
 Opposing muscles return a muscle to resting length
o Liver converts lactate to pyruvate
quickly
o Gravity o Most pyruvate molecules are converted to glucose
 Assists opposing muscles o Glucose is used to rebuild glycogen reserves in muscle
ENERGY TO POWER CONTRACTIONS cells
 ATP (adenosine triphosphate) is the only energy source used  Oxygen debt
directly for muscle contraction o Also called excess postexercise oxygen consumption
o Contracting muscles use a lot of ATP (EPOC)
o Muscles store enough ATP to start a contraction o After exercise or other exertion
 MUSCLE TISSUE
 Body needs more oxygen than usual to normalize o Reduction of muscle size, tone, and power due to lack of
metabolic activities activity
 Breathing rate and depth are increased  Changes in muscle tissue as we age
 Heat production and loss o Skeletal muscle fibers become smaller in diameter
o Active skeletal muscles produce heat o Skeletal muscles become less elastic
 Release up to 85 percent of the heat needed to  Fibrosis—Increase in fibrous connective tissue
maintain normal body temperature o Tolerance for exercise decreases
 Hormones and muscle metabolism o Ability to recover from muscular injuries decreases
o Several hormones increase metabolic activities in skeletal  Muscle fatigue
muscles o When muscles can no longer perform at a required level,
 Growth hormone they are fatigued
 Testosterone o Correlated with
 Thyroid hormones  Depletion of metabolic reserves
 Epinephrine  Damage to sarcolemma and sarcoplasmic reticulum
MUSCLE PERFORMANCE  Decline in pH, which affects calcium ion binding and
 Force alters enzyme activities
o The maximum amount of tension produced  Weariness due to low blood pH and pain
 Endurance  Physical conditioning improves power and endurance
o The amount of time an activity can be sustained o Anaerobic endurance (e.g., 50-meter dash, weight lifting)
 Force and endurance depend on  Uses fast fibers and stimulates hypertrophy
o The types of muscle fibers  Improved by frequent, brief, intensive workouts
o Physical conditioning o Aerobic endurance (prolonged activities)
THREE TYPES OF SKELETAL MUSCLE FIBERS  Supported by mitochondria
 Fast fibers  Does not stimulate muscle hypertrophy
o Majority of skeletal muscle fibers  Training involves sustained, low levels of activity
o Contract very quickly  Effects of training
o Large diameter o Improvements in aerobic endurance result from
o Large glycogen reserves o Alterations in the characteristics of muscle fibers
o Few mitochondria o Improvements in cardiovascular performance
o Produce strong contractions, but fatigue quickly CARDIAC MUSCLE TISSUE
 Slow fibers  Cardiac muscle tissue
o Slow to contract and slow to fatigue o Cardiac muscle cells
o Small diameter  Found only in the heart
o Numerous mitochondria  Have excitable membranes
o High oxygen supply from extensive capillary network  Striated like skeletal muscle cells
o Contain myoglobin (red pigment that binds oxygen)  Structural characteristics of cardiac muscle tissue
o Unlike skeletal muscle cells, cardiac muscle cells
 Intermediate fibers
o Are mid-sized
o Are small
o Little myoglobin
o Are typically branched with a single nucleus
o Slower to fatigue than fast fibers
o Have short, wide T tubules
 No triads
o Have SR with no terminal cisternae
o Are almost totally dependent on aerobic metabolism
 Contain lots of myoglobin, many mitochondria
o Contact each other via intercalated discs
 Intercalated discs
o Specialized connections
o Join sarcolemmas of adjacent cardiac muscle cells by gap
junctions and desmosomes
 Muscle performance and the distribution of muscle fibers o Functions include
o White muscles  Stabilizing positions of adjacent cells
 Mostly fast fibers  Maintaining three-dimensional structure of tissue
 Pale (e.g., chicken breast)  Allowing ions to move from one cell to another
o Red muscles - So cardiac muscle cells beat in rhythm
 Mostly slow fibers
 Dark (e.g., chicken legs) a. A light
o Most human muscles
 Contain a mixture of fiber types and are pink
 Muscle hypertrophy
o Muscle growth from heavy training that causes increases in
 Diameter of muscle fibers
 Number of myofibrils
 Number of mitochondria
 Glycogen reserves
 Muscle atrophy
 MUSCLE TISSUE
micrograph of cardiac muscle tissue.
b. A diagram of cardiac muscle tissue. Note the striations and a. Many visceral organs contain several layers of smooth muscle
intercalated discs. tissue oriented in different directions. Here, a single sectional view
shows smooth muscle cells in both longitudinal (L) and transverse
(T) sections.

c. Cardiac muscle tissue has short, broad T tubules and an SR that

lacks terminal cisternae.
b. A single relaxed smooth muscle cell is spindle shaped and has
no striations. Note the changes in cell shape as contraction occurs.

 Functional characteristics of cardiac muscle

o Automaticity
 Contraction without neural stimulation
 Controlled by pacemaker cells  Functional characteristics of smooth muscle tissue
o Nervous system can alter pace and tension of contractions o Smooth muscle differs from other muscle tissue in
o Contractions last 10 times longer than those in skeletal  Excitation–contraction coupling
o muscle, and refractory periods are longer  Length–tension relationships
o Wave summation and tetanic contractions are prevented  Control of contractions
due to special properties of sarcolemma  Smooth muscle tone
 Smooth muscle tissue  Excitation–contraction coupling
o Integumentary system o Free Ca2+ in cytoplasm triggers contraction
 Arrector pili muscles erect hairs o Ca2+ binds with calmodulin
o Cardiovascular and respiratory systems  Activates myosin light chain kinase
 Regulates blood pressure and airflow  Allows myosin heads to attach to actin
o Digestive and urinary systems  Length–tension relationships
 Forms sphincters o Due to the lack of sarcomeres,
 Moves materials along and out of the body  Tension and resting length are not directly related
o Reproductive system o Even a stretched smooth muscle can contract
 Transports gametes and expels fetus  Plasticity—the ability to function over a wide range of
 Structural characteristics of smooth muscle lengths
o Long, slender, spindle-shaped cells  Control of contractions
o Single, central nucleus o Multiunit smooth muscle cells
o No T tubules, myofibrils, or sarcomeres  Innervated in motor units
 Non striated muscle  Each cell may be connected to more than one motor
o Scattered thick filaments with many myosin heads neuron
o Thin filaments attached to dense bodies o Visceral smooth muscle cells
 Dense bodies connect adjacent cells, transmitting  Not connected to motor neurons
contractions  Arranged in sheets or layers
o No tendons or aponeuroses
 MUSCLE TISSUE
 Rhythmic cycles of activity are controlled by pacesetter
cells
 Smooth muscle tone
o Normal background level of activity
o Can be decreased by neural, hormonal, or chemical factors