Saladin 5e Extended Outline
Chapter 11
Muscular Tissue
I. Types and Characteristics of Muscular Tissue (pp. 404–405)
A. In animals, muscle cells have evolved that are specialized for movement. (p. 404)
B. Skeletal muscle is the type of muscle that holds the body erect against the pull of gravity and
produces its outwardly visible movement. (p. 404)
C. Muscle cells have five universal characteristics. (p. 404)
1. Responsiveness (excitability). Responsiveness is a property of all living cells, but
muscle and nerve cells have developed this property to the highest degree.
2. Conductivity. Stimulation of a muscle fiber produces a wave of excitation that travels
along the fiber and initiates muscle contraction.
3. Contractility. Muscle fibers are unique in their ability to shorten when stimulated,
allowing them to pull on bones and other tissues.
4. Extensibility. In order to contract, a muscle cell must be able to stretch again between
contractions; skeletal muscle fibers can stretch to as much as three times their contracted
length.
5. Elasticity. When a muscle cell is stretched and then the tension released, it recoils to its
original resting length.
C. Skeletal muscle may be defined as voluntary striated muscle that is usually attached to one or
more bones. (pp. 404–405)
1. Skeletal muscle has light and dark transverse bands called striations. (Fig. 11.1)
2. Skeletal muscle is called voluntary because it is usually subject to conscious control;
other types of muscle are involuntary, and they are never attached to bones.
3. A typical skeletal muscle cell is about 100 μm in diameter and 3 cm long; some are a
thick as 500 μm and 30 cm long.
4. Because of their length, skeletal muscle cells are usually called muscle fibers of
myofibers.
5. A skeletal muscle is composed of not only muscle cells but also fibrous connective
tissue.
a. The endomysium surrounds each muscle fiber.
b. The perimysium bundles muscle fibers together into fascicles.
c. The epimysium encloses the entire muscle.
d. These connective tissues are continuous with collagen fibers of the matrix,
which in turn are continuous with the collagen of the bone matrix.
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6. The collagen of muscles is neither excitable nor contractile, but it is somewhat
extensible and elastic.
a. The collagen resists excessive stretching when a muscle lengthens and
protects the muscle from injury.
b. Some believe that the recoil of tendons contribute to power output and
efficiency of a muscle; others feel that the elasticity in humans is negligible.
II. Microscopic Anatomy of Skeletal Muscle (pp. 405–410)
A. The muscle fiber has a complex, tightly organized internal structure that is closely tied to its
contractile function (pp. 405–406)
1. The plasma membrane is called the sarcolemma, and its cytoplasm is the sarcoplasm.
a. The sarcoplasm is occupied mainly by long protein bundles called myofibrils
about 1 μm in diameter. (Fig. 11.2)
b. It also contains glycogen, a starchlike carbohydrate, which stores energy, and
the red pigment myoglobin, which stores oxygen.
2. Muscle fibers have multiple flattened or sausage-shaped nuclei pressed against the
inside of the sarcolemma.
a. During embryonic development, several stem cells called myoblasts fuse to
produce each muscle fiber, each contributing a nucleus.
b. Some myoblasts remain as unspecialized satellite cells between the muscle
fiber and endomysium; these can multiply and produce new muscle fibers to
some degree.
3. Most other organelles are packed into the spaces between the myofibrils.
a. The smooth endoplasmic reticulum, called the sarcoplasmic reticulum (SR),
forms a network around each myofibril; it periodically has dilated end-sacs
called terminal cisternae.
b. Osteocytes function to resorb or deposit bone matrix, contributing to the
homeostatisis of bone density and blood concentrations of calcium and
phosphate ions
c. The sarcolemma has tubular infolding called transverse (T) tubules that
penetrate through the cell and open onto the other side.
i. Each tubule is closely associated with two terminal cisternae.
ii. A T tubule and its associated two terminal cisternae constitute a
triad.
d. The sarcoplasmic reticulum is a reservoir of calcium ions; it has gated
channels in its membranes that allow a flood of calcium ion into the cytosol
where it activates muscle contraction.
e. The T tubule signals that SR when to release these calcium bursts.
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B. Each myofibril is a bundle of parallel protein microfilaments called myofilaments; there are
three kinds of myofilaments. (pp. 406–407)
1. The thick filaments are about 15 nm in diameter is each is made of several hundred
myosin molecules. (Fig. 11.3a, b, d)
a. A myosin molecule is shaped like a golf club, with two chains intertwined to
form a shaftlike tail and a double globular head projecting from the tail at an
angle.
b. A thick filament may be likened to a bundle of 200 to 500 such “golf clubs,”
with their heads directed outward around the bundle.
c. Half of the heads angle to the left and half to the right, with a bare zone in the
middle.
2. The thin filaments, 7 nm in diameter, are composed of two intertwined strands of
fibrous (F) actin. (Fig. 11.3c, d)
a. Each F actin strand is string of subunits called globular (G) actin.
b. Each G actin has an active site that can bind to the head of a myosin
molecule.
c. A thin filament also has 40 to 60 molecules of the protein tropomyosin, which
blocks active sites of some G actins when a muscle fiber is relaxed.
d. A calcium-binding protein, troponin, is bound to every tropomyosin molecule.
3. Elastic filaments, 1 nm in diameter, are made of a large protein called titin (connectin).
(Fig. 11.5b)
a. Elastic filaments flank each thick filament and anchor it to a structure called
the Z disc, helping to stabilize the thick filament.
4. Myosin and actin are called contractile proteins because they accomplish the
shortening of the muscle fiber.
5. Tropomyosin and troponin are called regulatory proteins because they act like a switch
to determine when the fiber can contract or not contract.
a. The action of these regulatory proteins depends on the availability of calcium
ions, which bind to troponin.
6. At least seven other accessory proteins occur in the thick and thin filaments or are
associated with them; the most clinically important is dystrophin.
a. Dystrophin is an enormous protein located between the sarcolemma and the
outermost myofilaments; it links actin filaments to a peripheral protein on the
inner face of the sarcolemma. (Fig. 11.4)
b. The peripheral protein in turn is linked to transmembrane proteins that
connect with proteins external to the fiber that ultimately link with the basal
lamina and to the endomysium.
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c. Dystrophin is therefore a key element in transferring the forces of
myofilament movement to the connective tissue of the muscle as a whole.
d. Genetic defects in dystrophin are responsible for muscular dystrophe.
C. Striations are a precise array of the abundant myosin and actin found in skeletal and cardiac
muscle. (pp. 407–410) (Fig. 11.5)
1. Striated muscle has dark A (anisotropic) bands and lighter I (isotropic) bands, referring
to their effect on polarized light.
a. Each A band consists of thick filaments lying side by side.
i. Part of the A band is especially dark, hwere each thick filament is
surrounded by thin filaments.
ii. In the middle of the A band is a light region called the H band, into
which thin filaments do not reach.
iii. The thick filaments originate at a dark M line in the middle of the H
band.
b. Each light I band is bisected by a dark narrow Z disc (Z line), which provides
anchorage for the thin filaments and elastic filaments.
c. Each segment of a myofibril from one Z disc to the next is called a sarcomere;
it is the functional contractile unit of the muscle fiber.
i. A muscle shortens because its individual sarcomeres shorten and pull
the Z discs closer together.
ii. Dystrophin and the linking proteins pull on the extracellular proteins
of the muscle.
iii. The Z discs pull on the sarcolemma to achieve overall shortening of
the cell.
d. The terminology of muscle fiber structure is shown in Table 11.1.
III. The Nerve–Muscle Relationship (pp. 410–413)
A. The relationship between nerve and muscle cells is important to understanding muscle
contraction because skeletal muscle never contracts unless it is stimulated by a nerve (or
artificially with electrodes). (p. 410)
B. Nerve cells called somatic motor neurons, with cell bodies in the brainstem and spinal cord,
stimulate muscle fibers via their axons, called somatic motor fibers; a single motor fiber and all
the muscle fibers it innervates are collectively called a motor unit. (pp. 410–411) (Fig. 11.6)
1. The muscle fibers of a single motor unit are not clustered together but are dispersed
throughout a muscle, so that their stimulation causes a weak contraction over a wide area.
2. On average, about 200 muscle fibers are innervated by each motor neuron, but wide
variation exists for different purposes.
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a. Small motor units are present where fine control is needed, such as in the
muscles of eye movement (3 to 6 muscle fibers per neuron).
b. Large motor units are present where strength is more important than fine
control, such as in the gastrocnemius (1,000 muscle fibers per neuron).
3. Multiple motor units also have the advantage of allowing “shifts” in muscle
contraction, so that when some units become fatigued, others can take over.
C. The point where a nerve fiber meets its target cell is a synapse, and when the target cell is a
muscle fiber, the synapse is called a neuromuscular junction (NMJ) or motor end plate. (pp. 411–
413) (Fig. 11.7) (Table 11.2)
1. One nerve fiber stimulates the muscle fiber at several points within the NMJ; each
terminal branch of the nerve fiber has its own synapse point to the muscle fiber.
2. At each synapse, the nerve fiber ends in a bulbous swelling called a synaptic knob,
which is separated from the muscle fiber by a narrow space 60–100 nm wide called the
synaptic cleft.
a. A third cell, a Schwann cell, envelopes the entire junction.
b. A synaptic knob contains spheroidal organelles called synaptic vesicles,
which are filled with acetylcholine (ACh).
c. ACh is released into the synaptic cleft when the nerve impulse reaches the
nerve endings.
d. The muscle fiber has about 50 million ACh receptors incorporated into its
sarcolemma, which contains numerous infoldings at the junction called
junctional folds that increase surface area for receptors.
e. A deficiency of ACh receptors leads to the muscle paralysis of myasthenia
gravis.
3. The muscle fiber and the Schwann cell of the NMJ are surrounded by a basal lamina
that separates them from the surrounding connective tissue.
a. The basal lamina bases through the synaptic cleft and fills it.
b. Both the sarcolemma and the basal lamina within the cleft contain the enzyme
acetylcholinesterase (AChE), which breaks down ACh.
Insight 11.1 Neuromuscular Toxins and Paralysis
D. Muscle fibers and neurons are considered electrically excitable cells because their plasma
membranes exhibit voltage changes in response to stimulation. (p. 412–413)
1. The study of the electrical activity of cells is called electrophysiology.
2. In an unstimulated (resting) cell, more anions (negative ions) are found on the inside of
the plasma membrane than on the outside; the membrane is therefore polarized, or
charged.
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a. In a resting muscle cell, Na+ is in excess in the extracellular fluid (ECF) and
K+ is in excess in the intracellular fluid (ICF).
b. Anions such a proteins, nucleic acids, and phosphates are also inside the ICF
and cannot cross the membrane.
3. A difference in electrical charge between two points is called an electrical potential, or
voltage.
a. The voltage across the sarcolemma of a muscle cell is only about –90 mV and
is called the resting membrane potential (RMP).
b. The negative sign indicates that the negative charge is greater on the inside of
the membrane.
c. The resting membrane potential is maintained by the sodium–potassium
pump.
4. When a nerve or muscle cell is stimulated, ion gates open in the plasma membrane and
Na+ diffuses down its concentration gradient into the cell.
a. These cations override the negative charges in the ICF, and the inside of the
membrane briefly becomes positive, a change termed depolarization.
5. The Na+ gates then close and the K+ gates open; K+ rushes out of the cell turning the
inside of the membrane negative again.
a. This change is termed repolarization.
6. The voltage shift of depolarization followed by repolarization is called an action
potential.
7. Action potentials perpetuate themselves along a membrane; a wave of action potentials
moving along a nerve fiber is called a nerve impulse or nerve signal.
IV. Behavior of Skeletal Muscle Fibers (pp. 414–420)
A. The process of muscle contraction and relaxation has four major phases: excitation; excitation–
contraction coupling; contraction; and relaxation. (p. 414) (Figs. 11.8, 11.9, 11.10, 11.11)
B. Excitation is the process in which action potentials in the nerve fiber lead to action potentials in
the muscle fiber; it can be divided into five steps. (p. 414) (Fig. 11.8)
1. A nerve signal arrives at a synaptic knob and stimulates voltage-regulated Ca2+ gates to
open; calcium ions enter the synaptic knob.
2. Ca2+ stimulates exocytosis of synaptic vesicles, which release ACh into the synaptic
cleft.
3. ACh diffuses across the synaptic cleft and binds to receptor proteins on the
sarcolemma.
4. The receptors are ligand-regulated ion gates that bind two ACh molecules to open.
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a. When the gates are opened, Na+ diffuses into the cell and K+ diffuses out; the
sarcolemma reverses polarity from –90 mV to +75 mV, then falls back again as
K+ diffuses out.
b. This rapid fluctuation in membrane voltage at the motor end plate is called
end-plate potential (EPP).
5. Areas adjacent to the NMJ have ion-specific voltage-regulated gates that open in
response to the EPP, allowing flow of Na+ in and K+ out, generating an action potential;
the muscle fiber is now excited.
C. Excitation–contraction coupling refers to the events that link the action potentials on the
sarcolemma to activation of the myofilaments; this process has four steps that follow from
excitation. (p. 414) (Fig. 11.9)
1. (6) A wave of action potentials spreads from the end plate in all directions, and enters
the T tubules, continuing down them into the sarcoplasm.
2. (7) Action potentials open voltage-regulated ion gates in the T tubules.
a. These gates are linked to calcium channels in the terminal cisternae of the
sarcoplasmic reticulum (SR).
a. When the channels in the SR open, Ca2+ diffuses out of the SR and into the
cytosol down its concentration gradient.
3. (8) Calcium binds to the troponin of the thin filaments.
4. (9) The troponin–tropomyosin complex changes shape, exposing active sites on the
actin filaments that can bind to myosin heads.
C. Contraction is the step in which the muscle fiber develops tension and may shorten; the
mechanism of contraction was proposed in 1954 by Hanson and Huxley as the sliding filament
theory. The process can be divided into four steps that follow excitation–contraction coupling. (pp.
414–418) (Fig. 11.10)
1. (10) Myosin ATPase hydrolyzes ATP that is bound to the myosin head; the energy
released activates the head by changing its shape into a “cocked” position.
2. (11) With ADP and phosphate still bound, the activated myosin head binds to an
exposed active site on the thin filament, forming a cross bridge.
3. (12) Myosin releases the ADP and phosphate and flexes into a bent, low energy shape,
tugging the thin filament along with it; this is called the power stroke.
4. (13) Upon binding to another ATP, myosin releases the actin; it is now prepared to
repeat the process by hydrolyzing the ATP and recocking (the recovery stroke). It will
then attach to a new active site farther down.
a. When one myosin releases an actin, many other heads on the same thick
filament are still bound to actin on the thin filament so it does not slide back.
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b. Even though the muscle fiber contracts, the myofilaments do not become
shorter; instead, the thin filaments slide over the thick ones.
c. The cycle of power and recovery is repeated many times by each myosin
head, at a rate of about five strokes per second.
D. When stimulation ceases, a muscle fiber relaxes and returns to it resting length; the process can
be divided into five steps that follow the contraction phase. (p. 419) (Fig. 11.11)
1. (14) Nerve signals stop arriving at the NMJ, so the synaptic knob stops releasing ACh.
2. (15) As ACh dissociates from the receptor, AChE breaks it down; the synaptic knob
reabsorbs the fragments as usual, but now no new ACh replaces that which is broken
down.
3. (16) Active transport pumps in the SR pump Ca2+ from the cytosol back into the
cisternae.
a. The Ca2+ in the cisternae binds to a protein called calsequestrin and is stored
until stimulation occurs again.
b. Active transport requires ATP; therefore ATP is needed for both muscle
contraction and muscle relaxation.
4. (17) As Ca2+ dissociates from troponin, it is pumped into the SR and not replaced.
5. (18) Tropomyosin moves back into position, blocking the active sites of the actin
filament and preventing myosin binding.
6. A muscle returns to its resting length with the aid of two forces.
a. Its intracellular and perhaps extracellular elastic components stretch it, like a
recoiling rubber band.
b. The contraction of an antagonist muscle lengthens it; for example, contraction
of the triceps brachii stretches the biceps brachii.
Insight 11.2 Rigor Mortis
E. The amount of tension a muscle generates depends on how stretched or contracted it was before
it was stimulated; this principle is termed the length–tension relationship. (p. 420) (Figure 11.12)
1. If a muscle fiber is overly contracted at rest, then upon stimulation the thick filaments
can contract no farther than the Z discs and the contraction is weak.
2. If a muscle fiber is too stretched, then upon stimulation there is little overlap between
thick and thin filaments, and the myosin heads cannot get a good grip on the actin and the
contraction is weak.
3. Muscle has an optimum resting length at which it can respond with greatest force; the
central nervous system continually adjusts the length of resting muscles in a state of
partial contraction called muscle tone.
V. Behavior of Whole Muscles (pp. 420–425)
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A. A nerve–muscle preparation, such as the gastrocnemius and sciatic nerve from a frog attached
to stimulating electrodes, can be used to record a chart of stimulation and muscle contraction
called a myogram. (p. 421)
1. A weak (subthreshold) electrical stimulus causes no contraction; as voltage is
increased the threshold is reached—the minimum voltage necessary to generate an action
potential and cause contraction.
a. The action potential triggers the release of Ca 2+ into the cytosol and activates
the sliding filament mechanism.
b. At threshold or higher, a stimulus causes a quick cycle of contraction and
relaxation called a twitch. (Fig. 11.13)
2. A delay, or latent period, of about 2 milliseconds occurs between the onset of the
stimulus and the onset of the twitch.
a. During this time excitation, excitation–contraction coupling, and tensing of
elastic components occurs.
b. The force generated is called internal tension, and it does not show up on the
myogram because the muscle does not yet shorten.
3. Once elastic components are taut, the muscle begins to produce external tension; this is
called the contraction phase of the twitch.
a. The resisting load in a preparation is the sensor of the recording apparatus, so
the movement is recorded on the myogram.
b. In the body, the resisting load is usually a bone.
4. The contraction phase is short-lived because the SR reabsorbs Ca2+ before the muscle
develops maximum force; as the Ca2+ level falls, muscle tension declines during the
relaxation phase.
a. The muscle is quicker to contract than it is to relax.
b. The entire twitch lasts from 7 to 100 msec.
Insight 11.3 Galvani, Volta, and Animal Electricity
B. Although electrical excitation of a muscle fiber obeys an all-or-none law, muscle fibers do not
exhibit all-or-none twitches in response to excitation. (pp. 421–423)
1. Twitches vary in strength for a number of reasons:
a. Twitch strength varies with stimulation frequency: stimuli arriving close
together produce stronger twitches than those arriving far apart.
b. Twitches vary with the concentration of Ca2+ in the sarcoplasm, which can
vary with stimulation frequency.
c. Twitch strength depends on how stretched the muscle was just before
stimulation (length–tension relationship).
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d. Twitches vary with the temperature of the muscle; warmer muscle contracts
more strongly.
e. Twitches are weaker when the pH of the sarcoplasm falls below normal,
producing fatigue.
f. Twitches vary with the state of hydration of the muscle, which affect overlap
between filaments and ability of myosin to form cross-bridges with actin.
2. Muscles must be able to contract with variable strength for different tasks, so it is not
surprising that twitches vary in strength.
3. Stimulus intensity and stimulus frequency have contrasting effects. (Fig. 11.14)
a. At threshold, a weak twitch occurs, and if voltage is increased, twitches are
stronger.
i. Higher voltages excite more and more nerve fibers in the motor nerve
and thus stimulate more motor units.
ii. This effect is called recruitment or multiple motor unit (MMU)
summation.
b. Even at constant voltage, a higher frequency of stimulation produces stronger
twitches than does a lower frequency.
c. Up to 10 stimuli per second, a muscle produces an identical twitch for each
stimulus and recovers fully between twitches. (Fig. 11.15a)
d. Between 10 and 20 stimuli per second, the muscle recovers fully between
twitches, but each twitch develops more tension than the one before it; this
pattern is called treppe or the staircase phenomenon. (Fig. 11.15b)
i. One cause of treppe is that the SR does not have time to completely
reabsorb all the Ca+2 released.
ii. Another factor is that the heat of each twitch causes muscle enzymes
to work more efficiently
e. At higher stimulus frequency (20–40 stimuli per second) each new stimulus
arrives before the previous twitch is over; each new twitch “piggybacks” on the
previous one and generates higher tension. (Fig. 11.15c)
i. This phenomenon is called temporal summation or wave summation.
ii. It produces a state of sustained fluttering contraction called
incomplete tetanus.
f. At still higher frequency (40–50 stimuli per second) the muscle has no time to
relax at all and the twitches fuse into a smooth, prolonged contraction called
complete tetanus. (Fig. 11.15d)
i. This state should not be confused with the disease tetanus caused by
the tetanus toxin.
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ii. Complete tetanus rarely if ever occurs in the body.
C. Contraction does not always mean the shortening of a muscle; it may mean only that the muscle
is producing internal tension. (pp. 423–425)
1. Physiologists speak of isotonic versus isometric contraction, and concentric versus
eccentric contraction.
2. Isometric contraction is contraction without a change in length. (Fig. 11.16a)
a. Isometric contraction of antagonistic muscles at a joint maintains joint
stability.
b. Isometric contraction of postural muscles keeps the body erect.
3. Isotonic contraction is contraction with a change in length but no change in tension.
(Fig. 11.16b)
a. Isotonic contraction moves a load as the muscle shortens.
4. Isometric and Isotonic contraction are both phases of normal muscular action. (Fig.
11.17)
5. Isotonic contraction has two forms: concentric and eccentric.
a. In concentric contraction, a muscle shortens as it maintains tension, such as
when the biceps brachii contracts and flexes the elbow to lift a weight.
b. In eccentric contraction, a muscle lengthens as it maintains tension, such as
when the biceps brachii lengthens as a weight is lowered.
VI. Muscle Metabolism (pp. 425–430)
A. All muscle contraction depends on ATP, and the supply of ATP depends on the availability of
oxygen and organic energy sources such as glucose and fatty acids. (pp. 425–426)
1. The two main sources of ATP synthesis are anaerobic fermentation and aerobic
respiration; during the course of exercise, different mechanisms produce ATP depending
on duration. (Fig. 11.18)
a. Anaerobic fermentation allows the cell to produce ATP in the absence of
oxygen, but yield is limited and lactic acid, a toxic end product, is a major factor
in muscle fatigue.
b. Aerobic respiration produces more ATP and less toxic end products, but
requires a continual supply of oxygen.
c. In a resting muscle, most ATP is generated by the aerobic respiration of fatty
acids.
2. Immediate energy such as that needed for a 100 m dash relies on oxygen stored in
myoglobin.
a. The muscle borrows phosphate groups from other molecules and transfers
them to ADP to form ATP; two enzymes systems control these transfers. (Fig.
11.19)
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i. Myokinase transfers phosphate from one ADP to another to form
ATP.
ii. Creatine kinase obtains phosphate from creatine phosphate (CP) and
donates it to ADP to make ATP.
b. ATP and CP, collectively called the phosphagen system, provide nearly all
the energy used for short bursts of intense activity, such as sprinting for 6
seconds.
3. As the phosphagen system is exhausted, the muscles shift into anaerobic fermentation
for short-term energy until cardiopulmonary function can catch up with the oxygen
demand
a. During this period, muscles obtain glucose from the blood and from their own
stored glycogen.
b. The pathway from glycogen to lactic acid, called the glycogen–lactic acid
system, produces enough ATP for 30 to 40 seconds of maximum activity.
4. After 40 seconds or so, the respiratory and cardiovascular system deliver oxygen to the
muscles fast enough for aerobic respiration to meet most of the ATP demand.
a. Aerobic respiration produces much more ATP and is a very efficient means of
meeting the ATP demands of prolonged exercise.
b. Oxygen consumption rises for 3 to 4 minutes and then levels off at a steady
state in which ATP production keeps pace with demand.
c. Little lactic acid accumulates under steady state, but the depletion of glycogen
and blood glucose, together with loss of fluid and electrolytes, set limits to
endurance and performance even when lactic acid does not.
B. Muscle fatigue is the progressive weakness and loss of contractility that results from prolonged
use of the muscles. (pp. 426–427)
1. Fatigue has multiple causes.
a. ATP synthesis declines as glycogen is consumed.
b. An ATP shortage slows down the sodium–potassium pumps, which affects
the resting membrane potential and muscle excitability.
c. Lactic acid lowers the pH of the sarcoplasm, inhibiting enzymes.
d. The accumulation of K+ in the ECF lowers the membrane potential.
e. Motor nerve fibers use up their ACh (junctional fatigue).
f. The CNS fatigues by processes not yet understood, so that less signal output to
the muscles occurs.
2. The maximum oxygen uptake (Vo2max) is the point at which the rate of oxygen
consumption reaches a plateau and does not increase further; it determines a person’s
ability to maintain high-intensity exercise for more than 4 to 5 minutes.
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a. Vo2max is proportional to body size, peaks at around age 20, and is usually
greater in males than in females.
b. It can be twice as great in a trained endurance athlete as in an untrained
person.
i. A typical sedentary adult weighing 160 pounds has a Vo 2max of
about 35 mL/min/kg.
ii. An elite endurance athlete of the same weight can have a Vo 2max of
about 70 mL/min/kg.
iii. Lance Armstrong’s Vo2max was measured at 83.8 mL/min/kg.
Insight 11.4 Beating Fatigue—Some Athletic Strategies and Their Hazards
C. Oxygen debt is the difference between the resting rate of oxygen consumption and the elevated
rater after exercise; it is also known as excess postexercise oxygen consumption (EPOC). (pp.
427–428)
1. Typically about 11 L of extra oxygen is consumed after strenuous exercise and is used
for the following purposes:
a. Replacing the body’s depleted oxygen reserves, such as oxygen in myoglobin
and hemoglobin, dissolved in the blood plasma, and in the air in lungs.
b. Replenishing the phosphagen system by synthesizing ATP and transferring
phosphates to creatine to restore ATP and CP levels.
c. Oxidizing lactic acid to pyruvic acid in the kidneys, cardiac muscle, and
especially the liver, where pyruvic acid is then converted into glucose.
d. Serving the elevated metabolic rate resulting from body heating.
D. Muscle fibers can be classed according to their physiological characteristics. (pp. 428–429)
(Table 11.3)
1. Slow oxidative (SO), slow-twitch, red, or type I fibers have relatively abundant
mitochondria, myoglobin, and blood capillaries and a deep red color.
a. SO fibers do not fatigue easily and exhibit a relatively long twitch (~100
msec) in response to a single stimulus
b. Examples are the soleus muscle of the calf and the postural muscles.
2. Fast glycolytic (FG), fast-twitch, white, or type II fibers are adapted for quick
responses but not for fatigue resistance.
a. They are rich in enzymes of the phosphagen and glycogen–lactic acid
systems.
b. Their SR releases and reabsorbs Ca2+ quickly.
c. FG fibers are poorer in mitochondria, myoglobin, and blood capillaries than
SO fibers, so they are relatively pale.
e. They produce twitches as short as 7.5 msec.
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f. Examples are the gastrocnemius of the calf, brachii of the arm, and muscles of
eye movement.
3. Some authorities recognize two subtypes of FG fibers called types IIA and IIB.
a. Type IIB is the common type just described, whereas IIA, or intermediate
fibers, combine fast twitch with fatigue resistance.
i. Type IIA is rare except in some endurance-trained athletes.
b. The fiber types can be distinguished histologically with stains for
mitochondrial enzymes. (Fig. 11.20)
4. All muscle fibers of a single motor unit are of the same physiological type.
5. Nearly all muscles are composed of both SO and FG fibers, but the proportions differ.
a. Muscles composed mainly of SO fibers are called red muscles and those
composed mainly of FG fibers are called white muscles.
b. The proportions differ even in a single muscle in people with different types
and levels of physical activity. (Table 11.4)
c. Heredity may play a role in whether a person is a “born sprinter” or “born
marathoner.”
d. Sometimes when two or more muscles appear to have the same function, they
may have different proportions of SO to FG fibers and so actually allow a wider
range of function.
E. Humans have far more muscular strength than is normally used, and muscles can generate more
tension than the bones and tendons can withstand. (pp. 429–430)
1. Muscular strength depends on anatomical and physiological factors:
a. Muscle strength is primarily determined by muscle size.
b. Fascicle arrangement contributes to strength; pinnate muscles such as the
quadriceps femoris are stronger than parallel muscles such as the sartorius,
which in turn are stronger than circular muscles such as the orbicularis oculi.
c. Large motor units produce stronger contractions than small ones.
d. Recruitment, or multiple motor unit (MMU) summation produces a stronger
muscle contraction.
e. Temporal summation of action potentials causes stronger contraction.
f. The length–tension relationship contributes in that a muscle resting at
optimum length can contract more forcefully.
g. Fatigue contributes in that fatigued muscles contract more weakly.
2. Resistance exercise, such as weight lifting, can stimulate muscle growth even if only
done a few minutes at a time a few times a week.
a. Growth results primarily form cellular enlargement, not cell division.
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b. Myofibrils grow thicker and split longitudinally when they reach a certain
size.
c. Muscle fibers are incapable of mitosis, but some evidence indicates that they
may also split longitudinally as they enlarge.
3. Endurance (aerobic) exercise, such as jogging and swimming, improves the fatigue
resistance of the muscles.
a. Slow-twitch fibers produce more mitochondria and glycogen and acquire a
greater density of blood capillaries with endurance exercise.
b. This form of exercise also improves skeletal strength, increases red blood cell
count and oxygen transport capacity, and enhances cardiovascular, respiratory,
and nervous system function.
4. Cross-training incorporates elements of both resistance training and endurance training
for optimal performance.
VII. Cardiac and Smooth Muscle (pp. 430–434)
A. Any of the three types of muscle cells can be called myocytes, a term preferable to muscle
fibers for smooth and cardiac muscle cells because they are relatively short and have only one
nucleus. (p. 430)
B. Cardiac and smooth muscle are termed involuntary muscles because they are usually not
subject to conscious control. (p. 430)
C. Cardiac muscle cells are also called cardiocytes; cardiac muscle is limited to the heart, where its
function is to pump blood. (p. 430)
1. To fulfill its function, cardiac muscle must have five properties: (Table 11.5)
a. It must contract with a regular rhythm.
b. The cells of a given heart chamber must contract in unison.
c. Each contraction must last long enough to expel blood from the chamber.
d. The muscle must function in sleep and wakefulness.
e. It must be highly resistant to fatigue.
2. Cardiac muscle is striated like skeletal muscle but has shorter and thicker cells with
uneven, notched ends. (Fig. 19.11)
3. Each myocyte is joined to several others at its ends through linkages called intercalated
discs.
a. These discs appear as thick dark lines in stained tissue sections.
b. An intercalated disc has electrical gap junctions that allow each myocyte to
stimulate neighbors and mechanical junctions to hold the myocytes together.
4. The sarcoplasmic reticulum of cardiocytes is less developed than in skeletal muscle but
has larger T tubules.
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5. Damaged cardiac muscle is repaired by fibrosis; although mitosis has been detected in
cardiac myocytes following heart attacks, it does not produce significant regenerated
muscle.
6. Cardiac muscle contains a built-in pacemaker that rhythmically sets off a wave of
electrical excitation.
a. Cardiac muscle is said to be autorhythmic because of this ability.
b. The heart does receive fibers from the autonomic nervous system that can
increase or decrease heart rate and contraction strength.
c. Cardiac muscle does not exhibit quick twitches but maintains tension for 200–
250 msec.
7. Cardiac muscle uses aerobic respiration almost exclusively.
a. It is rich in myoglobin and glycogen and has large mitochondria that fill 25%
of the cell.
b. It is adaptable with respect to fuel, but vulnerable to lack of oxygen.
c. Because little anaerobic fermentation takes place, cardiac muscle is highly
resistant to fatigue.
D. Smooth muscle is composed of myocytes with a fusiform shape, about 30–200 μm long, 5–10
μm wide at the middle, and tapering to a point at each end; there is only one nucleus. (pp. 431–
434)
1. Thick and thin filaments are both present, but they are not aligned and produce no
visible striations.
2. Z discs are absent and in their place are protein plaques on the inner plasma membrane
and protein masses called dense bodies in arrays in the cytoplasm.
3. Their cytoplasm contains an extensive cytoskeleton of intermediate fibers, which are
also attached to the plasma membrane. (Fig. 11.24)
4. The sarcoplasmic reticulum is scanty, and there are no T tubules.
a. Ca2+ for contraction comes mainly from the ECF by way of channels in the
sarcolemma.
b. During relaxation, Ca2+ is pumped back out of the cell.
5. Some smooth muscle has not nerve supply, but when nerve fibers are present, they are
autonomic, not somatic.
6. Smooth muscle is capable of mitosis and hyperplasia.
7. There are two functional types of smooth muscle: multiunit and single-unit. (Fig.
11.21)
a. Multiunit smooth muscle occurs in some large arteries and pulmonary air
passages, in piloerector muscles, and in the iris.
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i. Its autonomic nerve innervation is similar to the motor nerve
innervation of skeletal muscle, with motor units that contract
independently.
b. Single-unit smooth muscle is more widespread, occurring in most blood
vessels and in the digestive, respiratory, urinary, and reproductive tracts.
i. It is also called visceral muscle.
ii. In hollow organs, it forms two or more layers, and inner circular
layer and an outer longitudinal layer. (Fig. 11.22)
iii. Its name refers to the fact that myocytes are electrically coupled to
each other by gap junctions, so that cells directly stimulate each other
and can contract as a unit.
8. Smooth muscle contraction is involuntary and does not require nerve stimulation.
a. Some smooth muscle contracts in response to chemical stimuli and in
response to stretch.
b. Some single-unit smooth muscle, especially in the stomach and intestines, has
pacemaker cells that set off waves of contraction; thus it is autorhythmic.
c. Most smooth muscle is innervated by autonomic nerve fibers that can trigger
or modify its contraction.
i. These nerve fibers stimulate smooth muscle with either acetylcholine
or norepinephrine.
ii. The nerves have contrasting effects in different locations, such as
relaxing smooth muscle in the arteries while contracting smooth muscle
in the bronchioles.
d. In single-unit smooth muscle, each autonomic nerve fiber has up to 20,000
beadlike swellings called varicosities along its length consisting of synaptic
vesicles and a few mitochondria. (Figs. 11.21, 11.23)
e. Instead of approaching any one myocyte, the nerve fiber passes among several
myocytes and stimulates all of them when it releases neurotransmitter.
i. The muscle cells do not have motor end plates, but instead have
receptor sites on their surface.
f. These nerve–muscle relationships are called diffuse junctions because there is
no one-to-one relationship between nerve fiber and myocyte.
9. Contraction in smooth muscle is triggered by Ca2+, energized by ATP, and involves
sliding of thin filaments over thick filaments, but the mechanism of excitation–
contraction coupling is very different.
a. Most Ca2+ comes from the extracellular fluid, not from the sarcoplasmic
reticulum.
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b. Calcium channels in the sarcolemma admit the Ca2+, but they are of different
types, including voltage regulated, ligand-regulated, and mechanically regulated
(respond to stretch).
c. Smooth muscle has no troponin; instead, calcium binds to a protein called
calmodulin, associated with thick filaments.
i. Calmodulin activates the enzyme myosin light-chain kinase, which
adds a phosphate to a protein on the myosin head.
ii. This phosphate addition activates myosin ATPase, so that myosin
can bind to actin and hydrolyze ATP.
d. Thick filaments pull on thin filaments, which in turn pull on the dense bodies
and membrane plaques, transferring force to the plasma membrane and
shortening the entire cell.
e. When a smooth muscle cell contracts, it puckers and twists somewhat like
wringing out a wet towel. (Fig. 11.24)
f. Compared to skeletal muscle, smooth muscle is very slow to contract and
relax.
i. The latent period between stimulation and contraction in smooth
muscle is 50–100 msec, compared with 2 msec in skeletal muscle.
ii. Tension in smooth muscle peaks about 0.5 sec after stimulus and
then declines over a period of 1 to 2 sec.
iii. Smooth muscle’s myosin ATPase is a slow enzyme, and the pumps
that remove Ca2+ from the cell are also slow.
g. As Ca2+ falls, myosin’s ability to hydrolyze ATP drops, but it does not detach
from actin immediately; its latch bridge mechanism enables it to remain attached
to actin for a prolonged time without consuming ATP.
h. Smooth muscle often exhibits tetanus and is highly resistant to fatigue.
i. It makes ATP aerobically, but its ATP requirement is small.
ii. It requires 10 to 300 times less ATP as does skeletal muscle to
maintain the same amount of tension.
i. Smooth muscle’s fatigue resistance and latch-bridge mechanism allow
maintenance of smooth muscle tone (tonic contraction) that keeps arteries in a
state of partial constriction called vasomotor tone.
i. A loss of vasomotor tone can cause a dangerous drop in blood
pressure.
j. Smooth muscle tone also keep the intestines partially contracted.
10. Stretch alone sometimes causes smooth muscle to contract.
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a. Distension of the esophagus with food or the colon with feces causes a wave
of contraction called peristalsis.
b. Smooth muscle exhibits a reaction called the stress-relaxation response or
receptive relaxation response. When stretched, it briefly contracts and resists,
but then relaxes.
i. This response allows hollow organs such as the urinary bladder to
fill, without the smooth muscle in the walls expelling the contents
immediately.
ii. Smooth muscle is also not subject to the limitations of the length–
tension relationships as is skeletal muscle, so that even when stretched,
smooth muscle can contract forcefully, such as when emptying a full
urinary bladder.
c. Three features contribute to smooth muscle’s ability to stretch extensively and
then contract powerfully:
i. It has no Z discs, so thick filaments do not butt up against them and
stop contracting.
ii. The thick and thin filaments are not arranged in orderly sarcomeres,
so having too little overlap for cross-bridging does not occur.
iii. The thick filaments have myosin heads along their entire length,
with no bare zone, so cross bridges can form anywhere.
d. Smooth muscle also exhibits plasticity—the ability to adjust its tension to the
degree of stretch; an organ such as the bladder can be greatly stretched yet not
become flabby when empty.
E. The muscular system suffers few diseases but does have some common dysfunctions. (Table
11.6)
Insight 11.5 Muscular Dystrophy and Myasthenia Gravis(Fig. 11.25)
Cross References
Additional information on topics mentioned in Chapter 11 can be found in the chapters listed below.
Chapter 2: Anaerobic and aerobic ATP synthesis
Chapter 3: The sodium–potassium pump
Chapter 5: The three types of muscular tissue
Chapter 10: Composition of a skeletal muscle
Chapter 12: Neurotransmitters
Chapter 12: Electrophysiology
Chapter 12: Action potentials
Chapter 12: All-or-none law
Saladin Outline Ch.11
Chapter 19: Cardiac muscle
Chapter 29: Effects of aging on the muscular system
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