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isotonic contractionmotor unitmyoﬁbrilmyoﬁlamentneuromuscular junctionsarcolemmasarcomere sarcoplasmsarcoplasmic reticulumT tubulestetanusthreshold… [619458]

Byadmin ianuarie 1, 2024

CHAPTER 11
PHYSIOLOGY
OF THEMUS CULAR
SYSTEM
KEY TERMS
isometric contraction
isotonic contractionmotor unitmyoﬁbrilmyoﬁlamentneuromuscular junctionsarcolemmasarcomere
sarcoplasmsarcoplasmic reticulumT tubulestetanusthreshold stimulusIn Chapter 10, we explored the anatomy of skeletal muscle
organs and how they work together to accomplish speciﬁcbody movements. In this chapter, we continue our study of
the muscular system by examining the basic characteristics ofskeletal muscle tissue. We uncover the mechanisms that permitskeletal muscle tissue to move the body’s framework, as well asperform other functions vital to maintaining a constant inter-nal environment. We also brieﬂy examine smooth and cardiacmuscle tissues, contrasting them with skeletal muscle tissue.
GENERAL FUNCTIONS
Ifyou have any doubts about the importance of muscle
function to normal life, think about what it would be likewithout it. It is hard to imagine life with this matchless
power lost. However, as cardinal as it is, movement is not theonly contribution muscles make to healthy survival. Theyalso perform two other essential functions: production of alarge portion of body heat and maintenance of posture.
1.Move ment. Skeletal muscle contractions produce move-
ments of the body as a whole (locomotion) or of its parts.
2.Heat production. Muscle cells, like all cells, produce heat
by the process known as catabolism (discussed in Chap-
ters 4 and 27). But because skeletal muscle cells are both
highly active and numerous, they produce a major shareof total body heat. Skeletal muscle contractions thereforeconstitute one of the most important parts of the mech-
anism for maintaining homeostasis of temperature.
3.Posture. The continued partial contraction of many
skeletal muscles makes possible standing, sitting, andmaintaining a relatively stable position of the body whilewalking, running, or performing other movements.
FUNCTION OF SKELETAL
MUSCLE TISSUE
Skeletal muscle cells have several characteristics that permitthem to function as they do. One such characteristic is theability to be stimulated, often called excitability or irritabil-
ity.Because skeletal muscle cells are excitable, they can re-CHAPTER OUTLINE
General Functions, 312
Function of Skeletal Muscle Tissue, 312
Overview of the Muscle Cell, 313Myoﬁlaments, 315
The Mechanism of Contraction, 316
Excitation of the sarcolemma, 316Contraction, 317Relaxation, 318
Energy Sources for Muscle Contraction, 318
ATP, 318
Glucose and oxygen, 319Aerobic respiration, 319Anaerobic respiration, 319Heat production, 319
Function of Skeletal Muscle Organs, 322
Motor Unit, 322Myography, 322
The Twitch Contraction, 322Treppe: the Staircase Phenomenon, 323
Tetanus, 324
Muscle Tone, 324The Graded Strength Principle, 324Isotonic and Isometric Contractions, 325
Function of Cardiac and Smooth Muscle Tissue, 328
Cardiac Muscle, 328Smooth Muscle, 330
The Big Picture, 331Mechanisms of Disease, 332Case Study, 334Career Choices, 339
312

spond to regulatory mechanisms such as nerve signals. Con-
tractility of muscle cells, the ability to contract or shorten,
allows muscle tissue to pull on bones and thus produce bodymovement. Extensibility ,the ability to extend or stretch, al-
lows muscles to return to their resting length after havingcontracted. These characteristics are related to the micro-
scopic structure of skeletal muscle cells. In the following pas-sages, we ﬁrst discuss the basic structure of a muscle cell. Wethen explain how a muscle cell’s structural components al-low it to perform its specialized functions.
OVERVIEW OF TH E MUSCLE CELL
Look at Figure 11-1. As you can see, a skeletal muscle is com-
posed of bundles of skeletal muscle ﬁbers that generally extend the entire length of the muscle. They are called
ﬁbers ,instead of cells,because of their threadlike shape (1 to
40 mm long but with a diameter of only 10 to 100 m). Skele-tal muscle ﬁbers have many of the same structural parts as
other cells. Several of them, however, bear different names inmuscle ﬁbers. For example, sarcolemma is the plasma mem-
brane of a muscle ﬁber. Sarcoplasm is its cytoplasm. Muscle
cells contain a network of tubules and sacs known as the sar-
coplasmic reticulum (SR) —a structure analogous, but not
identical, to the endoplasmic reticulum of other cells. Mus-cle ﬁbers contain many mitochondria, and, unlike mostother cells, they have several nuclei.
Certain structures not found in other cells are present in
skeletal muscle ﬁbers. For instance, bundles of very ﬁneﬁbers— myoﬁ brils —extend lengthwise along skeletal muscle
ﬁbers and almost ﬁll their sarcoplasm. Myoﬁbrils, in turn, aremade up of still ﬁner ﬁbers, called thick and thin myoﬁlaments
(Figure 11-1, D). Find the label sarcomere in this drawing.
Note that a sarcomere is a segment of the myoﬁbril between
two successive
Zlines (Box 11-1). Each myoﬁbril consists ofPhysiology of the Muscular System Chapter 11 313
Box 11-1
A More Detailed Look at the Sarcomere
The sarcomere is the basic contractile unit of the muscle
cell. As you read the explanation of the sarcomere’s struc-
ture and function, you might wonder what the Z line, M line,and other components really are—and what they do for themuscle cell.
First of all, it is important that you appreciate the three-
dimensional nature of the sarcomere. You can then realizethat the Z line is actually a dense plate or disk to which thethin ﬁlaments directly anchor. As a matter of fact, the Z lineis often called the Z disk . Besides being an anchor for
myoﬁbrils, the Z line is useful as a landmark separating onesarcomere from the next.
Detailed analysis of the sarcomere also shows that the
thick (myosin) ﬁlaments are held together and stabilized byprotein molecules that form the M line . Note that the regions
of the sarcomere are identiﬁed by speciﬁc zones or bands:
•A band —the segment that runs the entire length of the
thick ﬁlaments•I band —the segment that includes the Z line and the
ends of the thin ﬁlaments where they do not overlap the thick ﬁlaments
•H zone —the middle region of the thick ﬁlaments where
they do not overlap the thin ﬁlaments
•Later, as you review the process of contraction, note howthese regions change during each step of the process.
In addition to thin and thick ﬁlaments, each sarcomere
has numerous elastic ﬁlaments . Elastic ﬁlaments, composed
of a protein called titin (connectin), anchor the ends of the
thick ﬁlaments to the Z line, as the ﬁgure shows. The elasticﬁlaments are believed to give myoﬁbrils, and thus muscleﬁbers, their characteristic elasticity. Dystrophin , not shown
here, is a protein that holds the actin ﬁlaments to the sar-colemma. Dystrophin and a complex of connected moleculesanchors the muscle ﬁber to surrounding matrix so that themuscle doesn’t break during a contraction. Dystrophin andits role in muscular dystrophy is discussed further on p. 332.

a lineup of many sarcomeres, each of which functions as a con-
tractile unit. The A bands of the sarcomeres appear as relatively
wide, dark stripes (cross striae) under the microscope, and they
alternate with narrower, lighter colored stripes formed by the Ibands (see Figure 11-1, D). Because of its cross striae, skeletal
muscle is also called striated muscle .Electron microscopy of
skeletal muscle (Figure 11-2) has revealed details that have rev-olutionized our concept of its structure and its function.
Another structure unique to muscle cells is a system of
transverse tubules, or
Ttubules .This name derives from
the fact that these tubules extend transversely across thesarcoplasm, at a right angle to the long axis of the cell. AsFigures 11-1, B,and 11-3 show, the
Ttubules are formed by
inward extensions of the sarcolemma. The chief function of
Ttubules is to allow electrical signals, or impulses ,traveling
along the sarcolemma to move deeper into the cell.
The SR is also a system of membranous tubules in a muscle
ﬁber. It is separate from the Ttubule system, forming extensive
networks of connected canals and sacs. The membrane ofthe SR continually pumps calcium ions (Ca
/H11001/H11001)from the
sarcoplasm and stores them within its sacs. Notice in Fig-ures 11-1, B,and 11-3 that a tubular sac of the SR butts up
against each side of every
Ttubule in a muscle ﬁber. This triplet
of tubules (a Ttubule sandwiched between sacs of the SR) is
called a triad .The triad is an important feature of the muscle
cell because it allows an electrical impulse traveling along a
Ttubule to stimulate the membranes of adjacent sacs of the SR.314 Unit 2 Support and Movement
CA
DB
Figure 11-1 Structure of skeletal muscle. A , Skeletal muscle organ,
composed of bundles of contractile muscle ﬁbers held together byconnective tissue. B,Greater magniﬁcation of single ﬁber showing
smaller ﬁbers—myoﬁbrils—in the sarcoplasm. Note sarcoplasmic reticulum and T tubules forming a three-part structure called a triad.
C,Myoﬁbril magniﬁed further to show sarcomere between successive
Z lines. Cross striae are visible. D,Molecular structure of myoﬁbril
showing thick myoﬁlaments and thin myoﬁlaments.
M line
Muscle
ﬁberMyoﬁbril
Myoﬁbril
Mitochondria Nucleus Z line Z line SarcomereCross striationsI band A band I bandAB
Figure 11-2 Electron micrographs of striated muscle. B shows detail of Aat greater magniﬁcation. Note
that the myoﬁlaments of each myoﬁbril form a pattern that, when viewed together, produces the striatedpattern typical of skeletal muscle. 1.What are the three major functions of the skeletal
muscles?
2.Name some features of the muscle cell that are not
found in other types of cells.
3.What causes the striations observed in skeletal muscle ﬁbers?
4.Why is the triad relationship between Ttubules and SR
important?

MYOFILAMENTS
Each muscle ﬁber contains a thousand or more parallel sub-
units, called myoﬁ brils ,that are only about 1 m thick. Lying
side by side in each myoﬁbril are thousands of thick and thin
myoﬁlaments .Over the years, a clear picture of the molecu-
lar structure of myoﬁlaments has emerged. This picture re-veals the mechanism of how muscle ﬁbers contract and do
so powerfully. It is wise, therefore, to take a moment to studythe molecular structure of myoﬁlaments before discussingthe detailed mechanism of muscle contraction.
First of all, four different kinds of protein molecules make
up myoﬁlaments: myosin, actin, tropomyosin ,and troponin .T h e
thin ﬁlaments are made of a combination of three proteins:actin, tropomyosin, and troponin. Figure 11-4, A,shows thatglobular actin molecules are strung together like beads to form
two ﬁbrous strands that twist around each other to form thebulk of each thin ﬁlament. Actin and myosin molecules have achemical attraction for one another, but, at rest, the active sites
on the actin molecules are covered by long tropomyosin mol-ecules. The tropomyosin molecules seem to be held in thisblocking position by troponin molecules spaced at intervalsalong the thin ﬁlament (see Figure 11-4, A).
As Figure 11-4, B,shows, the thick ﬁlaments are made al-
most entirely of myosin molecules. Notice that the myosinmolecules are shaped like golf clubs, with their long shaftsbundled together to form a thick ﬁlament and their “heads”sticking out from the bundle. The myosin heads are chemi-cally attracted to the actin molecules of the nearby thin ﬁla-Physiology of the Muscular System Chapter 11 315
MitochondriaSarcolemma
T tubule Sarcoplasmic
reticulumTriadMyoﬁbril Sarcomere
A
C
B
Actin
MyosinTroponin Tropomyosin
Myosin headThin myoﬁlament
Myosin
head
Thick myoﬁlament
Figure 11-4 Structure of myoﬁlaments. A, Thin myoﬁlament. B,Thick myoﬁlament. C, Cross section of
several thick and thin myoﬁlaments, showing the relative positions of myoﬁlaments and the myosin heads thatwill form cross bridges between them.Figure 11-3 Unique features of the skeletal muscle cell. Notice especially the T tubules, which are exten-
sions of the plasma membrane, or sarcolemma, and the sarcoplasmic reticulum (SR), which forms networks oftubular canals and sacs. A triad is a triplet of adjacent tubules: a terminal (end) sac of the SR, a T tubule, andanother terminal sac of the SR.

ments, so they angle toward the thin ﬁlaments. When they
bridge the gap between adjacent myoﬁlaments, the myosinheads are usually called cross bridges .
Within a myoﬁbril the thick and thin ﬁlaments alternate,
as shown in Figure 11-1, D.This arrangement is crucial for
contraction. Another fact important for contraction is that
the thin ﬁlaments attach to both
Zlines of a sarcomere and
that they extend in from the Zlines partway toward the cen-
ter of the sarcomere. When the muscle ﬁber is relaxed, the
thin ﬁlaments terminate at the outer edges of the H zones. Incontrast, the thick myosin ﬁlaments do not attach directly to
the
Zlines, and they extend only the length of the A bands of
the sarcomeres.
THE MECHAN ISM OF CONTRACTION
To accomplish the powerful shortening, or contraction, of a
muscle ﬁber, several processes must be coordinated in a step-
wise fashion. These steps are summarized in the following
and in Box 11-2.
Excitation of the Sarcolemma
Under normal circumstances, a skeletal muscle ﬁber remains
“at rest” until it is stimulated by a signal from a special type
of nerve cell called a motor neuron .As Figure 11-5 shows,
motor neurons connect to the sarcolemma of a muscle ﬁberat a folded motor endplate to form a junction called a neu-
romuscular junction. A neuromuscular junction is a type of
connection called a synapse ,characterized by a narrow gap,
or synaptic cleft, across which neurotransmitter molecules
transmit signals. When nerve impulses reach the end of a
motor neuron ﬁber, small vesicles release a neurotransmit-ter,acetylcholine ,into the synaptic cleft. Diffusing swiftly
across this microscopic gap, acetylcholine molecules contactthe sarcolemma of the adjacent muscle ﬁber. There theystimulate acetylcholine receptors and thereby initiate an316 Unit 2 Support and Movement
Box 11-2
Major Events of Muscle Contraction
and Relaxation
Excitation and Contraction
1.A nerve impulse reaches the end of a motor neuron, trig-
gering the release of the neurotransmitter acetylcholine.
2. Acetylcholine diffuses rapidly across the gap of the neu-
romuscular junction and binds to acetylcholine recep-tors on the motor endplate of the muscle ﬁber.
3. Stimulation of acetylcholine receptors initiates an im-
pulses that travels along the sarcolemma, through the T tubules, to the sacs of the SR.
4. Ca
/H11001/H11001is released from the SR into the sarcoplasm, where
it binds to troponin molecules in the thin myoﬁlaments.
5. Tropomyosin molecules in the thin myoﬁlaments shift,
exposing actin’s active sites.
6. Energized myosin cross bridges of the thick myoﬁla-
ments bind to actin and use their energy to pull the thinmyoﬁlaments toward the center of each sarcomere. Thiscycle repeats itself many times per second, as long as
adenosine triphosphate (ATP) is available.
7.As the ﬁlaments slide past the thick myoﬁlaments, the
entire muscle ﬁber shortens.
Relaxation
1.After the impulse is over, the SR begins actively pump-
ing Ca
/H11001/H11001back into its sacs.
2. As Ca/H11001/H11001is stripped from troponin molecules in the think
myoﬁlaments, tropomyosin returns to its position,blocking actin’s active sites.
3. Myosin cross bridges are prevented from binding to
actin and thus can no longer sustain the contraction.
4. Because the thick and thin myoﬁlaments are no longer
connected, the muscle ﬁber may return to its longer,resting length.
Box 11-3 FYI
Rigor Mortis
The term rigor mortis is a Latin phrase that means “stiff-
ness of death.” In a medical context the term rigor mor-
tisrefers to the stiffness of skeletal muscles sometimes ob-
served shortly after death. What causes rigor mortis? At thetime of death, stimulation of muscle cells ceases. However,muscle ﬁbers of postural muscles may have been in mid-contraction at the time of death—when the myosin-actincross bridges are still intact. Also, the SR releases much ofthe Ca
/H11001/H11001it had been storing, causing even more cross
bridges to form. ATP is required to release the crossbridges and “energize” the myosin heads for their next at-tachment. Because the last of a cell’s ATP supply is used upat the time it dies, many cross bridges may be left “stuck” inthe contracted position. Thus muscles in a dead body maybe stiff because individual muscle ﬁbers ran out of the ATPrequired to “turn off” a muscle contraction.
Motor neuron
ﬁber
Acetylcholine
receptor sites
Synaptic
cleftMotor endplateSarcolemmaSynaptic
vesiclesSchwann cellSarcoplasmMyelin
sheath
Figure 11-5 Neuromuscular junction. This ﬁgure shows how the
distal end of a motor neuron ﬁber forms a synapse, or “chemicaljunction,” with an adjacent muscle ﬁber. Neurotransmitters (speciﬁ-cally, acetylcholine) are released from the neuron’s synaptic vesiclesand diffuse across the synaptic cleft. There they stimulate receptors inthe motor endplate region of the sarcolemma.

electrical impulse in the sarcolemma. The process of synap-
tic transmission and induction of an impulse—a process of-ten called excitation —is discussed in detail in Chapter 12.
Contraction
The impulse, a temporary electrical imbalance, is conducted
over the muscle ﬁber’s sarcolemma and inward along the
Ttubules (Figure 11-6). The impulse in the Ttubules triggersthe release of a ﬂood of calcium ions from the adjacent sacs of
the SR. In the sarcoplasm, the calcium ions combine with tro-ponin molecules in the thin ﬁlaments of the myoﬁbrils. Recallthat troponin normally holds tropomyosin strands in a posi-tion that blocks the chemically active sites of actin. When cal-cium binds to troponin, however, the tropomyosin shifts toexpose active sites on the actin molecules (Figure 11-7). Once
the active sites are exposed, energized myosin heads of thePhysiology of the Muscular System Chapter 11 317
E
ATPADP
+
Pi iP+ADPCa++B AC D
Figure 11-7 The molecular basis of muscle contraction.
A,Each myosin head in the thick filament moves into a resting
position after an ATP binds and transfers its energy. B, Calcium
ions released from the SR bind to troponin in the thin filament, allowing tropomyosin to shift from its position blocking the activesites of actin molecules. C,Each myosin head then binds to an
active site on a thin filament, displacing the remnants of ATP hy-drolysis—adenosine diphosphate (ADP) and inorganic phosphate(Pi). D,The release of stored energy from step A provides the force
needed for each head to move back to its original position, pullingactin along with it. Each head will remain bound to actin untilanother ATP binds to it and pulls it back into its resting position(A). E, This scanning electron micrograph of a thin filament shows
the myosin-binding active sites on actin covered by tropomyosin(TM) when calcium is absent. In the presence of calcium, bottom,the tropomyosin has changed position, revealing the active sites on actin.Figure 11-6 Effects of excitation on a muscle ﬁber. Excitation of the sarcolemma by a nerve impulse initi-
ates an impulse in the sarcolemma. The impulse travels across the sarcolemma and through the T tubules,where it triggers adjacent sacs of the SR to release a ﬂood of calcium ions (Ca
/H11001/H11001) into the sarcoplasm. The Ca/H11001/H11001
are then free to bind to troponin molecules in the thin ﬁlaments. This binding, in turn, initiates the chemical re-actions that produce a contraction.

thick ﬁlaments bind to actin molecules in the nearby thin ﬁl-
aments. The myosin heads bend with great force, literallypulling the thin ﬁlaments past them. Each head then releasesitself, binds to the next active site, and pulls again. Figure 11-8shows how the sliding of the thin ﬁlaments toward the centerof each sarcomere quickly shortens the entire myoﬁbril—andthus the entire muscle ﬁber. This model of muscle contractionhas been called the sliding ﬁlament theory .
Relaxation
Almost immediately after the SR releases its ﬂood of calcium
ions into the sarcoplasm, it begins actively pumping themback into its sacs once again. Within a few milliseconds,much of the calcium is recovered. Because the active trans-
port carriers of the SR have a greater afﬁnity to calcium thantroponin molecules, the calcium ions are stripped off the
troponin molecules and returned to the sacs of the SR. As
you might suspect, this shuts down the entire process of con-
traction. Troponin without its bound calcium allows the
tropomyosin to once again block actin’s active sites. Myosin
heads reaching for the next active site on actin are blocked,and thus the thin ﬁlaments are no longer being held—orpulled—by the thick ﬁlaments. The muscle ﬁber may remainat its contracted length, but forces outside the muscle ﬁberare likely to pull it back to its longer resting length. In short,the contraction process in a skeletal muscle ﬁber automati-cally shuts itself off within a small fraction of a second afterthe initial stimulation.ENERGY SOURCES FOR
MUSCLE CO NTRACTION
ATP
The energy required for muscular contraction is obtained by
hydrolysis of a nucleotide called adenosine triphosphate, or
ATP.Recall from Chapter 2 (Figure 2-26, p. 62) that this
molecule has an adenine and ribose group (together calledadenosine ) attached to three phosphate groups. Two of the
three phosphate groups in ATP are attached to the moleculeby high-energy bonds .Breaking of these high-energy bonds
provides the energy necessary to pull the thin myoﬁlamentsduring muscle contraction. As Figure 11-7, A,shows, before
contraction occurs, each myosin cross head moves into a
resting position when an ATP molecule binds to it. The ATP
molecule breaks its outermost high-energy bond, releasingthe inorganic phosphate (Pi) and transferring the energy tothe myosin head. In a way, this is like pulling back the elasticband of a sling-shot—the apparatus is “at rest” but ready tospring. When myosin binds to actin, the stored energy is re-leased, and the myosin head does indeed spring back to itsoriginal position. Thus the energy transferred from ATP isused to do the work of pulling the thin ﬁlaments during con-traction. Another ATP molecule then binds to the myosin
head which then releases actin and moves into its resting position again—all set for the next “pull.” This cycle repeats,as long as ATP is available and actin’s active sites are unblocked.
Muscle fibers must continually resynthesize ATP be-
cause they can store only small amounts of it. Immediatelyafter ATP breaks down, energy for its resynthesis can besupplied by the breakdown of another high-energy com-pound, creatine phosphate (CP), which is also present insmall amounts in muscle fibers (Figure 11-9). Ultimately,energy for both ATP and CP synthesis comes from the ca-tabolism of foods.318 Unit 2 Support and Movement
A
B
Figure 11-8 Sliding ﬁlament theory. A , During contraction, myosin cross bridges pull the thin ﬁlaments
toward the center of each sarcomere, thus shortening the myoﬁbril and the entire muscle ﬁber. B, Scanning
electron micrograph showing the myosin cross bridges that connect the thick ﬁlaments to the thin ﬁlaments,pulling on the thin ﬁlaments and causing them to slide.
1.Describe the structure of thin myoﬁlaments and thick
myoﬁlaments, naming the kinds of proteins that com-prise them.
2.What is a neuromuscular junction? How does it work?
3.What is the role of calcium ions (Ca/H11001/H11001) in muscle contraction?

Glucose and Oxygen
Note that continued, efﬁcient nutrient catabolism by muscle
ﬁbers requires two essential ingredients: glucose and oxygen.Glucose is a nutrient molecule that contains many chemicalbonds. The potential energy stored in these chemical bonds isreleased during catabolic reactions in the sarcoplasm and mi-
tochondria and transferred to ATP or CP molecules. Some
muscle ﬁbers ensure an uninterrupted supply of glucose by
storing it in the form of glycogen .O x y g e n ,w hich is needed for
a catabolic process known as aerobic respiration ,can also be
stored by cells. During rest, excess oxygen molecules in thesarcoplasm are bound to a large protein molecule called myo-
globin .Myoglobin is a reddish pigment similar to the pig-
ment hemoglobin that gives blood its red color. Like hemo-
globin, myoglobin contains iron (Fe) groups that attract
oxygen molecules and hold them temporarily. When the oxy-
gen concentration inside a muscle ﬁber decreases rapidly—asit does during exercise—it can be quickly resupplied from themyoglobin. Muscle ﬁbers that contain large amounts of myo-
globin take on a deep red appearance and are often called red
ﬁbers .Muscle ﬁbers with little myoglobin in them are light
pink and are often called white ﬁbers .Most muscle tissues
contain a mixture of red and white ﬁbers (Box 11-4).
Aerobic Respiration
Aerobic (oxygen-requiring) respiration is a catabolic process
that produces the maximum amount of energy availablefrom each glucose molecule. When oxygen concentration is
low, however, muscle ﬁbers can shift toward an increased useof another catabolic process: anaerobic respiration. As its
name implies, anaerobic respiration does not require the im-mediate use of oxygen. Besides its ability to produce ATPwithout oxygen, anaerobic respiration has the added advan-
tage of being very rapid. Muscle ﬁbers having difﬁculty get-ting oxygen—or ﬁbers that generate a great deal of force veryquickly—may rely on anaerobic respiration to resynthesizetheir ATP molecules.
Anaerobic Respiration
Anaerobic respiration may allow the body to avoid the use of
oxygen in the short term, but not in the long term. Anaero-
bic respiration results in the formation of an incompletelycatabolized molecule called lactic acid .Lactic acid may ac-
cumulate in muscle tissue during exercise and cause a burn-ing sensation. Some of the lactic acid eventually diffuses intothe blood and is delivered to the liver, where an oxygen-consuming process later converts it back into glucose. This is
one of the reasons that after heavy exercise, when the lack ofoxygen in some tissues caused the production of lactic acid,
a person may still continue to breathe heavily. The body isrepaying the so-called oxygen debt by using the extra oxygen
gained by heavy breathing to process the lactic acid that wasproduced during exercise.
Heat Production
Because the catabolic processes of cells are never 100% efﬁ-cient, some of the energy released is lost as heat. Becauseskeletal muscle tissues produce such a massive amount ofheat—even when they are doing hardly any work—theyhave a great effect on body temperature. Recall from Chap-ter 6 that various heat-loss mechanisms of the skin can be
employed to cool the body when it becomes overheated (seeFigure 6-7, p. 174). Skeletal muscle tissues can likewise beemployed when the body’s temperature falls below the setpoint value determined by the “thermostat” in the hypothal-amus of the brain. As Figure 11-10 shows, a low externaltemperature can reduce body temperature below the set
point. T emperature sensors in the skin and other parts of thebody feed this information back to the hypothalamus, whichcompares the actual value to the set point value (usually
about 37° C). The hypothalamus responds to a decrease inbody temperature by signaling skeletal muscles to contract.The shivering contractions that result produce enough wasteheat to warm the body back to the set point temperature—and homeostatic balance is maintained.
The subject of energy metabolism is discussed more thor-
oughly in Chapter 27.Physiology of the Muscular System Chapter 11 319
P P P
PP P
P P Pi
C P C PiC P
+
+EnergyEnergy EnergyAdenosine Phosphate groups Creatine Phosphate
High-energy bonds
ATP
ADP
To cellular
processes
From storage in
CP molecules
Phosphate CreatineCreatine-
phosphateFrom nutrient
catabolismATP
High-energy bondA
A
A
Figure 11-9 Energy sources for muscle contraction. A, The basic
structure of two high-energy molecules in the sarcoplasm: adenosinetriphosphate (ATP) and creatine phosphate (CP). B,This diagram
shows how energy released during the catabolism of nutrients can betransferred to the high-energy bonds of ATP directly, or insteadstored temporarily in the high-energy bond of the CP. During con-traction, ATP is hydrolyzed and the energy of the broken bond trans-ferred to a myosin head.
1.Where does the energy stored in ATP come from?
2.Contrast aerobic respiration and anaerobic respiration
in muscle ﬁbers.
3.What is the role of myoglobin in muscle ﬁbers?

320 Unit 2 Support and Movement
Box 11-4
Types of Muscle Fibers
Skeletal muscle ﬁbers can be classiﬁed into three types ac-
cording to their structural and functional characteristics:
(1) slow (red) ﬁbers , (2) fast(white) ﬁbers , and (3) intermediate
ﬁbers . Each type is best suited to a particular type or style of
muscular contraction. Although each muscle organ containsa mix of all three ﬁber types, different organs have these ﬁbersin different proportions, depending on the types of contrac-tion that they most often perform.
Slow ﬁbers are also called red ﬁbers because they contain
a high concentration of myoglobin, the reddish pigmentused by muscle cells to store oxygen. They are called slow
ﬁbers because their thick myoﬁlaments are made of a type of
myosin (Type I) that reacts at a slow rate. Because they con-tract so slowly, slow ﬁbers are usually able to produce ATPquickly enough to keep pace with the energy needs of themyosin and thus avoid fatigue. This effect is enhanced by alarger number of mitochondria than other ﬁber types andthe rich oxygen store provided by the myoglobin. The slow,nonfatiguing characteristics of slow ﬁbers make them espe-cially well suited to the sustained contractions exhibited bypostural muscles. Postural muscles containing a high pro-portion of slow ﬁbers can hold the skeleton upright for longperiods without fatigue.
Fast ﬁbers are also called white ﬁbers because they con-
tain very little myoglobin. Fast ﬁbers can contract much morerapidly than slow ﬁbers because they have a faster type ofmyosin (Type IIx) and because their system of T tubules andSR is more efﬁcient at quickly delivering Ca
/H11001/H11001to the sar-
coplasm. The price of a rapid contraction mechanism is therapid depletion of ATP. Despite the fact that fast ﬁbers typi-cally contain a high concentration of glycogen, they have fewmitochondria and so must rely primarily on anaerobic respi-ration to regenerate ATP. Because anaerobic respiration pro-duces relatively small amounts of ATP, fast ﬁbers cannot pro-duce enough ATP to sustain a contraction for very long.Because they can generate great force very quickly but notfor a long duration, fast ﬁbers are best suited for musclesthat move the ﬁngers and eyes in darting motions.
Intermediate ﬁbers have characteristics somewhere in
between the two extremes of fast and slow ﬁbers. They aremore fatigue resistant than fast ﬁbers and can generate moreforce more quickly than slow ﬁbers. This type of muscle ﬁberpredominates in muscles that both provide postural supportand are occasionally required to generate rapid, powerfulcontractions. One example is the soleus , or calf muscle, that
helps to support the leg but is also used in walking, running,and jumping.
The graph shows that the relative proportions of muscle
ﬁber types, body wide, varies with the type of work a persondoes with his or her muscles. A person with a spinal cord in-jury eventually loses nearly all of the postural slow ﬁbers whileretaining mostly intermediate and fast ﬁbers. An extreme en-durance athlete, on the other hand, develops the slow ﬁbers somuch as to greatly dominate the faster ﬁber types.

Physiology of the Muscular System Chapter 11 321
Figure 11-10 The role of skeletal muscle tissues in maintaining a constant body temperature. This
diagram shows that a drop in body temperature caused by cold weather can be corrected by a negative feed-back mechanism that triggers shivering (muscle contraction), which in turn produces enough heat to warm thebody.
Temperature decrease
Detected by
Temperature
receptors
Sensor
Artery
VeinSkin
Sensory nerve ﬁbers
Set point
valueActual
value
Feeds information via
nerve ﬁbers back to
IntegratorTemperature increase
Shivering
Effector Muscles
Motor nerve ﬁbers
Hypothalamus
Correction signals
via nerve ﬁbers

FUNCTION OF SKELETAL
MUSCLE ORGANS
Although each skeletal muscle ﬁber is distinct from all other
ﬁbers, it operates as part of the large group of ﬁbers thatform a skeletal muscle organ. Skeletal muscle organs, oftensimply called muscles ,a r e c o m p osed of bundle upon bundle
of muscle ﬁbers held together by ﬁbrous connective tissues(see Figure 11-1, A). The details of muscle organ anatomy
are discussed in Chapter 10. For now, we turn attention tothe matter of how skeletal muscle organs function as a singleunit.
MOTOR UNIT
Recall that each muscle ﬁber receives its stimulus from a mo-
tor neuron. This neuron, often called a somatic motor neu-
ron,is one of several nerve cells that enter a muscle organ to-
gether in a bundle called a motor nerve .One of these motor
neurons, plus the muscle ﬁbers to which it attaches, consti-tutes a functional unit called a motor unit (Figure 11-11).
The single ﬁber of a somatic motor neuron divides into avariable number of branches on entering the skeletal muscle.The neuron branches of some motor units terminate in onlya few muscle ﬁbers, whereas others terminate in numerousﬁbers. Consequently, impulse conduction by one motor unitmay stimulate only a half dozen or so muscle ﬁbers to con-tract at one time, whereas conduction by another motor unit
may activate a hundred or more ﬁbers simultaneously. Thisfact bears a relationship to the function of the muscle as awhole. As a rule, the fewer the number of ﬁbers supplied bya skeletal muscle’s individual motor units, the more precisethe movements that muscle can produce. For example, incertain small muscles of the hand, each motor unit includes
only a few muscle ﬁbers, and these muscles produce preciseﬁnger movements. In contrast, motor units in large abdom-
inal muscles that do not produce precise movements are re-ported to include more than a hundred muscle ﬁbers each.
MYOGRAPHY
Many experimental methods have been used to study the
contractions of skeletal muscle organs. They vary from rela-
tively simple procedures, such as observing or palpatingmuscles in action, to the more complicated method of elec-
tromyo graphy (recording electrical impulses from muscles as
they contract). One method of studying muscle contractionparticularly useful for the purposes of our discussion iscalled, simply, myography .Myogr aphy ,a term that means
“muscle graphing,” is a procedure in which the force or ten-
sion from the contraction of an isolated muscle is recordedas a line that rises and falls as the muscle contracts and re-laxes. T o get the muscle to contract, an electrical stimulus ofsufﬁcient intensity (the threshold stimulus ) is applied to the
muscle. A single, brief threshold stimulus produces a quick
jerk of the muscle, called a twitch contraction .
THE TWITCH CONTRACTION
The quick, jerky twitch contraction seen in a myogram
serves as the fundamental model for how muscles operate.The myogram of a twitch contraction shown in Figure 11-12shows that the muscle does not begin to contract at the in-stant of stimulation but rather a fraction of a second later.The muscle then increases its tension (or shortens) until apeak is reached, after which it gradually returns to its restingstate. These three phases of the twitch contraction are called,respectively, the latent period ,the contraction phase ,and the
relaxation phase .The entire twitch usually lasts less than one
tenth of a second.322 Unit 2 Support and Movement
Schwann
cellMyelinsheath
Motorneuron
Neuromuscular
junction
Nucleus
Muscle ﬁbers
Myoﬁbrils
Figure 11-11 Motor unit. A motor unit consists of one somatic motor neuron and the muscle ﬁbers sup-
plied by its branches.

During the latent period, the impulse initiated by the
stimulation travels through the sarcolemma and Ttubules to
the SR, where it triggers the release of calcium ions into thesarcoplasm. It is not until the calcium binds to troponin andthe sliding of the myoﬁlaments begins that contraction isobserved. After a few milliseconds, the forceful sliding of themyoﬁlaments ceases and relaxation begins. By the end of
the relaxation phase, all of the myosin-actin reactions in allthe ﬁbers have ceased.
Twitch contractions of muscle organs rarely happen in
the body. Even if we tried to make our muscles twitch vol-untarily, they won’t. Instead, our nervous system subcon-sciously “smoothes out” the movements to prevent injuryand to make our movements more useful to us. In otherwords, motor units are each controlled by separate somatic
motor neurons that normally do not all “ﬁre” at the sametime. Only when an electrical stimulus is applied, or whenoveractivity of the nervous system stimulates most of the
motor neurons in a muscle, do such contractions occur.However,knowledge of the twitch contraction gives us im-
portant insights about the mechanisms of more typical typesof muscle organ contractions.
TREPPE: THE STAIRCASE PHENOMENON
One interesting effect that can be seen in myographic studies
of the twitch contraction is called treppe ,or the staircase phe-
nomenon .Treppe is a gradual, steplike increase in the strength
of contraction that can be observed in a series of twitch con-tractions that occur about 1 second apart (Figure 11-13, B).
In other words, a muscle contracts more forcefully after it
has contracted a few times than when it ﬁrst contracts—aprinciple used by athletes when they warm up. There are sev-eral factors that contribute to this phenomenon. For exam-ple, in warm muscle ﬁbers calcium ions diffuse through thesarcoplasm more efﬁciently and more actin-myosin reac-tions occur. Also, calcium ions accumulate in the sarcoplasmof muscles that have not had time to relax and pump muchof the calcium back into their SR. Thus up to a point, a warm
ﬁber contracts more strongly than a cool ﬁber. Thus, afterthe ﬁrst few stimuli muscle responds to successive stimuliwith maximal contractions. Eventually, it will respond with
less and less strong contractions. The relaxation phase be-comes shorter and ﬁnally disappears entirely. In other words,
the muscle stays partially contracted—an abnormal state ofprolonged contraction called contracture .
Repeated stimulation of muscle in time lessens its ex-
citability and contractility and may result in muscle fatigue ,
a condition in which the muscle does not respond to thestrongest stimuli. Complete muscle fatigue can be readily in-duced in an isolated muscle but very seldom occurs in thebody. (See Box 11-5.)Physiology of the Muscular System Chapter 11 323
0.1sec
Relaxation
phaseContraction
phaseLatent
period
TimeStimulus
appliedTension
Tension
TimeKey:
Latent period
ContractionRelaxation
Stimulus
Single twitch
Tension
TimeTreppeSeries of twitches
Tension
TimeWave summation
Incomplete tetanus
Tension
TimeWave summation
Complete tetanusA
B
C
D
Figure 11-12 The twitch contraction. Three distinct phases are ap-
parent: (1) the latent period, (2) the contraction phase, and (3) the re-laxation phase.Figure 11-13 Myograms of various types of muscle contrac-
tions. A, A single twitch contraction. B,The treppe phenomenon, or
“staircase effect,” is a steplike increase in the force of contraction over
the ﬁrst few in a series of twitches. C,Incomplete tetanus occurs
when a rapid succession of stimuli produces “twitches” that seem toadd together (wave summation) to produce a rather sustained con-traction. D,Complete tetanus is a smoother sustained contraction,
produced by the summation of “twitches” that occur so close togetherthat the muscle cannot relax at all.

TETANUS
The concept of the simple twitch can help us understand the
smooth, sustained types of contraction that are commonlyobserved in the body. Such smooth, sustained contractions arecalled tetanic contractions ,or,simply, tetanus. Figure 11-13, C,
shows that if a series of stimuli come in a rapid enough suc-cession, the muscle does not have time to relax completely be-
fore the next contraction phase begins. Muscle physiologistsdescribe this effect as multiple wave summation —so named
because it seems as if multiple twitch waves have been addedtogether to sustain muscle tension for a longer time. The type
of tetanus produced when very short periods of relaxation oc-cur between peaks of tension is called incomplete tetanus .I t is
“incomplete” because the tension is not sustained at a com-pletely constant level. Figure 11-13, D,shows that when the
frequency of stimuli increases, the distance between peaks oftension decrease to a point at which they seem to fuse into a
single, sustained peak. This produces a very smooth type oftetanic contraction, called complete tetanus .
In a normal body, tetanus results from the coordinated
contractions of different motor units within the muscle or-
gan. These motor units ﬁre in an overlapping time sequenceto produce a “relay team” effect that results in a sustained
contraction. T etanus is the kind of contraction exhibited by
normal skeletal muscle organs most of the time.MUSCLE TONE
A tonic contraction (tonus ,“tone”) is a continual, partial
contraction in a muscle organ. At any one moment a small
number of the total ﬁbers in a muscle contract, producing a
tautness of the muscle rather than a recognizable contrac-tion and movement. Different groups of ﬁbers scatteredthroughout the muscle contract in relays. T onic contraction,or muscle tone ,is the low level of continuous contraction
characteristic of the muscles of normal individuals when
they are awake. It is particularly important for maintainingposture. A striking illustration of this fact is the following:when a person loses consciousness, muscles lose their tone,and the person collapses in a heap, unable to maintain a sit-ting or standing posture. Muscles with less tone than normalare described as ﬂaccid ,and those with more than normal
tone are called spastic .
Muscle tone is maintained by negative feedback mecha-
nisms centered in the nervous system, speciﬁcally in thespinal cord. Stretch sensors in the muscles and tendons de-tect the degree of stretch in a muscle organ and feed this in-
formation back to an integrator mechanism in the spinalcord.When the actual stretch (detected by the stretch recep-
tors) deviates from the set point stretch, signals sent via the
somatic motor neurons adjust the strength of tonic contrac-tion. This type of subconscious mechanism is often called aspinal reﬂex (discussed further in Chapters 12 to 15).
THE GRADED STRENGTH PRINCIPLE
Skeletal muscles contract with varying degrees of strength at
different times—a fact called the graded strength principle .
Because muscle organs can generate different grades ofstrength, we can match the force of a movement to the de-mands of a speciﬁc task (Box 11-6).
Various factors contribute to the phenomenon of graded
strength. We have already discussed some of these factors.For example, we stated that the metabolic condition of indi-
vidual ﬁbers inﬂuences their capacity to generate force. Thus
if many ﬁbers of a muscle organ are unable to maintain ahigh level of ATP and become fatigued, the entire muscle or-gan suffers some loss in its ability to generate maximumforce of contraction. On the other hand, the improved meta-bolic conditions that produce the Treppe effect allow a mus-cle organ to increase its contraction strength.
Another factor that inﬂuences the grade of strength ex-
hibited by a muscle organ is the number of ﬁbers contract-ing simultaneously. Obviously, the more muscle ﬁbers con-tracting at the same time, the stronger the contraction of the
entire muscle organ. How large this number is depends onhow many motor units are activated or recruited .R e c r u i t –
ment of motor units, in turn, depends on the intensity andfrequency of stimulation. In general, the more intense andthe more frequent a stimulus, the more motor units are re-cruited and the stronger the contraction. Figure 11-14 showsthat increasing the strength of the stimulus beyond thethreshold level of the most sensitive motor units causes anincrease in strength of contraction. As the threshold level of324 Unit 2 Support and Movement
Box 11-5 SPORTS AND FITNESS
Muscle Fatigue
Broadly deﬁned, muscle fatigue is simply a state of ex-
haustion (a loss of strength or endurance) produced by
strenuous muscular activity. Physiological muscle fatigue is
caused by a relative lack of ATP, rendering the myosinheads incapable of producing the force required for furthermuscle contractions. The low levels of ATP that producefatigue may result from a depletion of oxygen or glucosein muscle ﬁbers or from the inability to regenerate ATPquickly enough. The most frequent cause of physiologicalfatigue is depletion of glycogen in the muscle. High levelsof lactic acid or other metabolic waste products also con-tribute to physiological fatigue. Under ordinary circum-stances, however, complete physiological fatigue seldomoccurs. It is usually psychological fatigue that produces the
exhausted feeling that stops us from continuing a muscu-lar activity. Thus in physiological muscle fatigue, we cannot
contract our muscles, but in psychological muscle fatigue,we simply will not contract our muscles because we feel
tired.
1.What are the three phases of a twitch contraction? What
molecular events occur during each of these phases?
2.What is the difference between a twitch contraction and
a tetanic contraction?
3.How does the treppe effect relate to the warm-up exercises of
athletes?

each additional motor unit is crossed, the strength of con-
traction increases. This continues as the strength of stimula-
tion increases until the maximal level of contraction isreached. At this point, the limits of the muscle organ to re-
cruit new motor units have been reached. Even if stimula-tion increases above the maximal level, the muscle cannotcontract any more strongly. As long as the supply of ATP
holds out, the muscle organ can sustain a tetanic contractionat the maximal level when motor units contract and relax inoverlapping “relays” (see Figure 11-13, D).
The maximal strength that a muscle can develop is di-
rectly related to the initial length of its ﬁbers—this is the
length-tension relationship (Figure 11-15). A muscle that be-
gins a contraction from a short initial length cannot develop
much tension because its sarcomeres are already com-
pressed. Conversely, a muscle that begins a contraction froman overstretched initial length cannot develop much tensionbecause the thick myoﬁlaments are too far away from thethin myoﬁlaments to effectively pull them and thus com-press the sarcomeres. The strongest maximal contraction ispossible only when the muscle organ has been stretched toan optimal initial length. T o illustrate this point, extend your
elbow fully and try to contract the biceps brachii muscle on
the ventral side of your upper arm. Now ﬂex the elbow justa little and contract the biceps again. Try it a third time withthe elbow completely ﬂexed. The greatest tension—seen asthe largest “bulge” of the biceps—occurs when the elbow ispartly ﬂexed and the biceps only moderately stretched.
Another factor that inﬂuences the strength of a skeletal
muscle contraction is the amount of load imposed on the
muscle. Within certain limits, the heavier the load, the
stronger the contraction. Lift your hand with palm up infront of you and then put this book in your palm. Y ou canfeel your arm muscles contract more strongly as the book isplaced in your hand. This occurs because of a stretch reﬂex ,a
response in which the body tries to maintain a constancy of
muscle length (Figure 11-16). An increased load threatens to
stretch the muscle beyond the set point length that you aretrying to maintain. Y our body exhibits a negative feedback
response when it detects the increased stretch caused by an
increased load, feeds the information back to an integratorin the nervous system, and increases its stimulation of themuscle to counteract the stretch. This reﬂex maintains a rel-
atively constant muscle length as load is increased up to amaximum sustainable level. When the load becomes tooheavy and thus threatens to cause injury to the muscle orskeleton, the body abandons this reﬂex and forces you to re-lax and drop the load.
The major factors involved in the graded strength princi-
ple are summarized in Figure 11-17.
ISOTONIC AND ISOMETRIC CONTRACTIONS
The term isotonic literally means “same tension” ( iso-,“ e qual”; –
tonic ,“tension”). An isotonic contraction is a contraction in
which the tone or tension within a muscle remains the same asPhysiology of the Muscular System Chapter 11 325
Box 11-6
Effects of Exercise on Skeletal Muscles
Most of us believe that exercise is good for us, even if
we have no idea what or how many speciﬁc beneﬁts
can come from it. Some of the good consequences of reg-ular, properly practiced exercise are greatly improved mus-cle tone, better posture, more efﬁcient heart and lung func-tion, less fatigue, and looking and feeling better.
Skeletal muscles undergo changes that correspond to
the amount of work that they normally do. During pro-longed inactivity, muscles usually shrink in mass, a condi-tion called disuse atrophy . Exercise, on the other hand,
may cause an increase in muscle size called hypertrophy.
Muscle hypertrophy can be enhanced by strength
training , which involves contracting muscles against heavy
resistance. Isometric exercises and weight lifting are com-mon strength-training activities. This type of training re-sults in increased numbers of myoﬁlaments in each mus-cle ﬁber. Although the number of muscle ﬁbers stays thesame, the increased number of myoﬁlaments greatly in-creases the mass of the muscle.
Endurance training , often called aerobic training ,
does not usually result in muscle hypertrophy. Instead, thistype of exercise program increases a muscle’s ability tosustain moderate exercise over a long period. Aerobic ac-tivities such as running, bicycling, or other primarily iso-tonic movements increase the number of blood vessels ina muscle without signiﬁcantly increasing its size. The in-creased blood ﬂow allows a more efﬁcient delivery of oxy-gen and glucose to muscle ﬁbers during exercise. Aerobictraining also causes an increase in the number of mito-chondria in muscle ﬁbers. This allows production of moreATP as a rapid energy source.
Strength of
contraction
Strength of
stimulus
Subthreshold Submaximal Supramaximal
Threshold MaximalTension Tension
Figure 11-14 The strength of muscle contraction compared with
the strength of the stimulus. After the threshold stimulus is reached,
a continued increase in stimulus strength produces a proportional in-crease in muscle strength until the maximal level of contractionstrength is reached.

the length of the muscle changes (Figure 11-18, A). Because the
muscle is moving against its resistance (load) in an isotonic
contraction, the energy of contraction is used to pull on the
thin myoﬁlaments and thus change the length of a ﬁber’s sar-comeres. Put another way, in isotonic contractions the myosincross bridges “win” the tug-of-war against a light load and are
thus able to pull the thin myoﬁlaments. Because the muscle ismoving in an isotonic contraction, it is also called dynamic
tension.
There are two basic varieties of isotonic contractions
(Figure 11-18, A).Concentr ic contractions are those in
which the movement results in shortening of the muscle, aswhen you pick up this book. Eccentric contractions are
those in which the movement results in lengthening of themuscle being contracted. For example, when you slowly
lower the book you have just picked up, you are contractingthe same muscle you just used to lift it—but this time youare lengthening the muscle, not shortening it.
An isometric contraction, in contrast to the isotonic con-
traction, is a contraction in which muscle length remains the
same while the muscle tension increases (Figure 11-18, B).
The term isometric literally means “same length.” Y ou can
observe isometric contraction by lifting up on a stationaryhandrail and feeling the tension increase in your arm mus-cles. Isometric contractions can do work by “tightening” toresist a force, but they do not produce movements. In iso-
metric contractions, the tension produced by the “powerstroke” of the myosin cross bridges cannot overcome theload placed on the muscle. Using the tug-of-war analogy, wecan say that in isometric contractions the myosin cross326 Unit 2 Support and Movement
Muscle
length
Muscle
length
Muscle lengthTension
Muscle
lengthSarcomere
position
Sarcomere Sarcomere
Figure 11-15 The length-tension relationship. As this graph of muscle tension shows, the maximum strength
that a muscle can develop is directly related to the initial length of its ﬁbers. At a short initial length the sarcom-eres are already compressed and thus the muscle cannot develop much tension (position A). Conversely, thethick and thin myoﬁlaments are too far apart in an overstretched muscle to generate much tension (position B).Maximum tension can be generated only when the muscle has been stretched to a moderate, optimal length(position C).
Box 11-7 HEALTH MATTERS
Abnormal Muscle Contractions
Cramps are painful muscle spasms (involuntary twitches).
Cramps often occur when a muscle organ is mildly in-
ﬂamed, but they can be a symptom of any irritation or ionand water imbalance.
Convulsions are abnormal, uncoordinated tetanic con-
tractions of varying groups of muscles. Convulsions mayresult from a disturbance in the brain or seizure in whichthe output along motor nerves increases and becomes disorganized.
Fibrillation is an abnormal type of contraction in which
individual ﬁbers contract asynchronously rather than at thesame time. This produces a ﬂutter of the muscle but no ef-fective movement. Fibrillation can also occur in cardiacmuscle, where it reduces the heart’s ability to pump blood.

Physiology of the Muscular System Chapter 11 327
Load
Increases
DecreasesMuscle
length
Detected by
Muscle spindle
Actual
length
Set point
lengthSkeletal muscle organ
Muscle spindle
(stretch detector)
Sensory
nerve
ﬁber
Spinalcord
SensoryMotorSensor-integratorCorrection signal viamotor nerve ﬁbersSkeletal
muscle ContractsEffector
Figure 11-16 The stretch reﬂex. The strength of a muscle organ can be matched to the load imposed on it
by a negative feedback response centered in the spinal cord. Increased stretch (caused by increased load) is de-tected by a sensory nerve ﬁber attached to a muscle cell (called a muscle spindle) specialized for this purpose.The information is integrated in the spinal cord and a correction signal is relayed through motor neurons backto the same muscle, which increased tension to return to the set point muscle length.
Amount of load
(stretch reﬂex)Metabolic condition
(fatigue, treppe)
Strength of
muscle
contraction
Initial length of
muscle ﬁbers
(length-tension
relationship)Recruitment
of motor units
(number of
ﬁbers activated)Figure 11-17 Factors that inﬂuence the strength of muscle contraction.

bridges reach a “draw”—they hold their own against the
load placed on the muscle but do not make any progress in sliding the thin myoﬁlaments. Because muscles remainstable during isotonic contraction, it is also called static
tension.FUNCTION OF CARDIAC AND
SMOOTH MUSCL E TISSUE
Cardiac and smooth muscle tissues operate by mechanisms
similar to those in skeletal muscle tissues. The detailed studyof cardiac and smooth muscle function will be set aside un-til we discuss speciﬁc smooth and cardiac muscle organs inlater chapters. However, it may be helpful to preview some ofthe basic principles of cardiac and smooth muscle physiol-ogy so that we can compare them with those that operate inskeletal muscle tissue. Table 11-1 summarizes the character-istics of the three major types of muscle.
CARDIAC MUSCLE
Cardiac muscle, also known as striated involuntary muscle ,i s
found in only one organ of the body: the heart. Forming the328 Unit 2 Support and Movement
1.What is meant by the term muscle tone ?
2.Name four factors that inﬂuence the strength of a skele-
tal muscle contraction.
3.What is meant by the phrase “recruitment of motor units”?
4.What is the difference between isotonic and isometric contrac-
tions? Concentric and eccentric?
Figure 11-18 Isotonic and isometric contraction. A, In isotonic contraction the muscle shortens, producing
movement. Concentric contractions occur when the muscle shortens during the movement. Eccentric contrac-tions occur when the contracting muscle lengthens. B,In isometric contraction the muscle pulls forcefully
against a load but does not shorten.

bulk of the wall of each heart chamber, cardiac muscle con-
tracts rhythmically and continuously to provide the pumping
action necessary to maintain a relative constancy of bloodﬂow through the internal environment. As you shall see, itsphysiological mechanisms are well adapted to this function.The functional anatomy of cardiac muscle tissue resem-
bles that of skeletal muscle to a degree but exhibits special-ized features related to its role in continuously pumpingblood. As Figure 11-19 shows, each cardiac muscle ﬁber con-tains parallel myoﬁbrils. Each myoﬁbril comprises sarcom-Physiology of the Muscular System Chapter 11 329
Table 11-1 Characteristics of Muscle Tissues
Skeletal Cardiac Smooth
Principal location
Principal functions
Type of control
Structural features
StriationsNucl eus
Ttubules
Sarcoplasmic
reticulum
Cell junctions
Contra ction styleSkeletal muscle organs
Movement of bones, heat produc-
tion, posture
Voluntary
Present
Many near sarcolemma
Narrow;form triads with SR
Extensive; stores and releases Ca/H11001/H11001
No g ap junctions
Rapid twitch contractions of motor
units usually summate to producesustained titanic contractions;must be stimulated by a neuronWall of heart
Pumping of blood
Involuntary
Present
Single
Large diameter; form diads with
SR, regulate Ca
/H11001/H11001entry into
sarcoplasm
Less extensive than in skeletal muscle
Intercalated disks
Syncytium of ﬁbers compress heart
chambers in slow, separate contrac-
tions (does not exhibit tetanus orfatigue); exhibits autorhythmicityWalls of many hollow organs
Moveme nt in walls of hollow
organs (peristalsis, mixing)
Involuntary
Absent
Single; near center of cell
Absent
Ver y poor ly de velop ed
Visceral: many gap junctions
Multiunit: few gap junctions
Visceral: electrically coupled
sheets of contract autorhyth-mically, producing peristalsisor mixing movements
Multiunit: individual ﬁbers
contract when stimulated
by neuron
Nucleus
DiadT tubule
Mitochondrion
MyoﬁbrilSarcolemmaSarcomereIntercalated disksSarcoplasmic
reticulum
Figure 11-19 Cardiac muscle ﬁber. Unlike other types of muscle ﬁbers, the cardiac muscle ﬁber is typically
branched and forms junctions, called intercalated disks , with adjacent cardiac muscle ﬁbers. Like skeletal muscle
ﬁbers, cardiac muscle ﬁbers contain sarcoplasmic reticula and T tubules—although these structures are not ashighly organized as in skeletal muscle ﬁbers.

eres that give the whole ﬁber a striated appearance. However,
the cardiac muscle ﬁber does not taper like a skeletal muscleﬁber but, instead, forms strong, electrically coupled junc-tions (intercalated disks) with other ﬁbers. This feature,along with the branching exhibited by individual cells, al-lows cardiac ﬁbers to form a continuous, electrically coupledmass, called a syncytium (meaning “unit of combined cells”).
Cardiac muscles thus form a continuous, contractile bandaround the heart chambers that conducts a single impulseacross a virtually continuous sarcolemma—features neces-sary for an efﬁcient, coordinated pumping action.
Unlike skeletal muscle, in which a nervous impulse ex-
cites the sarcolemma to produce its own impulse, cardiacmuscle is self-exciting. Cardiac muscle cells thus exhibit a
continuing rhythm of excitation and contraction on their
own, although the rate of self-induced impulses can be al-
tered by nervous or hormonal input. Figure 11-20 shows
that impulses triggering cardiac muscle contractions aremuch more prolonged than the nerve impulses that trigger
skeletal. Because the sarcolemma of the cardiac muscle sus-tains each impulse longer than in skeletal muscle, Ca
/H11001/H11001re-
mains in the sarcoplasm longer. This means that eventhough many adjacent cardiac muscle cells contract simulta-neously, they exhibit a prolonged contraction rather than arapid twitch. It also means that impulses cannot come
rapidly enough to produce tetanus. Because it cannot sustain
long tetanic contractions, cardiac muscle does not normallyrun low on ATP and thus does not experience fatigue. Obvi-
ously, this characteristic of cardiac muscle is vital to keepingthe heart continuously pumping.
Although the cardiac muscle ﬁber has
Ttubules and SR,
they are arranged a little differently than in skeletal muscleﬁbers. The
Ttubules are larger, and they form diads (double
structures) rather than triads (triple structures), with arather sparse SR. Much of the calcium (Ca
/H11001/H11001) that enters the
sarcoplasm during contraction enters from the outside ofthe cells through the
Ttubules, rather than from storage in
the SR.
The structure and function of the heart are discussed fur-
ther in Chapters 18 and 19.
SMOOTH MUSCLE
As we mentioned in Chapter 5, smooth muscle is composed
of small, tapered cells with single nuclei. Smooth musclecells do not have
Ttubules and have only loosely organized
sarcoplasmic reticula. The calcium required for contractioncomes from outside the cell and binds to a protein called
calmodulin ,rather than to troponin, to trigger a contraction
event.
The lack of striations in smooth muscle ﬁbers results
from the fact that the thick and thin myoﬁlaments arearranged quite differently than in skeletal or cardiac muscleﬁbers. As Figure 11-21 shows, thin arrangements of myoﬁla-ments crisscross the cell and attach at their ends to the cell’splasma membrane. When cross bridges pull the thin ﬁla-ments together, the muscle “balls up” and thus contracts thecell. Because the myoﬁlaments are not organized into sar-
comeres, they have more freedom of movement and thus
can contract a smooth muscle ﬁber to shorter lengths thanin skeletal and cardiac muscle.
There are two types of smooth muscle tissue: visceral and
multiunit .I n visceral ,o r single-unit ,muscle, gap junctions
join individual smooth muscle ﬁbers into large, continuoussheets—much like the syncytium of ﬁbers observed in car-diac muscle. This is the most common type of smooth mus-cle, forming a muscular layer in the walls of many hollowstructures such as the digestive, urinary, and reproductivetracts. Like cardiac muscle, this type of smooth muscle com-
monly exhibits a rhythmic self-excitation or autorhythmicity
(meaning “self-rhythm”) that spreads across the entire tis-sue. When these rhythmic, spreading waves of contractionbecome strong enough, they can push the contents of a hol-low organ progressively along its lumen. This phenomenon,called peristalsis ,moves food along the digestive tract, assists
the ﬂow of urine to the bladder, and pushes a baby out of thewomb during labor. Such contractions can also be coordi-
nated to produce mixing movements in the stomach andother organs.
Multiunit smooth muscle tissue does not act as a single
unit (as in visceral muscle) but instead is composed of manyindependent single-cell units. Each independent ﬁber doesnot usually generate its own impulse but rather respondsonly to nervous input. Although this type of smooth musclecan form thin sheets, as in the walls of large blood vessels, it330 Unit 2 Support and Movement
Figure 11-20 Cardiac and skeletal muscle contractions compared.
A brief nerve impulse triggers a brief twitch contraction in skeletalmuscle (blue) but a prolonged impulse in the heart tissue produces arather slow, drawn out contraction in cardiac muscle (red).

is more often found in bundles (for example, the arrector pili
muscles of the skin) or as single ﬁbers (such as those sur-
rounding small blood vessels).
The structure and function of smooth muscle organs are
discussed in later chapters.Physiology of the Muscular System Chapter 11 331
Relaxed
ContractedPlasma
membrane
Thin myoﬁlament
Thick myoﬁlamentA
BA
B
Figure 11-21 Smooth muscle ﬁber. A, Thin bundles of myoﬁlaments span the diameter of a relaxed ﬁber.
The scanning electron micrograph (right) shows that the surface of the cell is rather ﬂat when the ﬁber is
relaxed. B,During contraction, sliding of the myoﬁlaments causes the ﬁber to shorten by “balling up.” The mi-
crograph shows that the ﬁber becomes shorter and thicker, exhibiting “dimples” where the myoﬁlament bundlesare pulling on the plasma membrane.
1.How do slow, separate, autorhythmic contractions of
cardiac muscle make it well suited to its role in pumpingblood?
2.What produces the striations in cardiac muscle?
3.How are myoﬁlaments arranged in a smooth muscle ﬁber?
The function of all three major types of muscle (skeletal,
smooth, and cardiac) is integral to the function of the en-
tire body. What does the function of muscle tissue contributeto the homeostasis of the whole body? First, all three types ofmuscle tissue provide the movement necessary for survival.Skeletal muscle moves the skeleton so that we can seek shel-ter, gather food, and defend ourselves. All three muscle typesproduce movements that power vital homeostatic mecha-nisms such as breathing, blood ﬂow, digestion, and urine ﬂow.
The relative constancy of the body’s internal temperature
could not be maintained in a cool external environment if not for the “waste” heat generated by muscle tissue—especially the large mass of skeletal muscle found throughoutthe body. Maintenance of a relatively stable body position—posture—is also a primary function of the skeletal muscularsystem. Posture, speciﬁc body movements, and other contri-butions of the skeletal muscular system to the homeostasisof the whole body was discussed in Chapter 10. The homeo-static roles of smooth muscle organs and the cardiac muscleorgan (the heart) are examined in later chapters.Like all tissues of the body, muscle tissue gives and takes.
A number of systems support the function of muscle tissues.Without these systems, muscle would cease to operate. Forexample, the nervous system directly controls the contrac-tion of skeletal muscle and multiunit smooth muscle. It alsoinﬂuences the rate of rhythmic contractions in cardiac mus-cle and visceral smooth muscle. The endocrine system pro-duces hormones that assist the nervous system in regulationof muscle contraction throughout the body. The blood deliv-ers nutrients and carries away waste products. Nutrients forthe muscle are ultimately procured by the respiratory system(oxygen) and digestive system (glucose and other foods). Therespiratory system also helps get rid of the waste of musclemetabolism, as does the urinary system. The liver processeslactic acid produced by muscles and converts it back to glu-cose. The immune system helps defend muscle tissue againstinfection and cancer—as it does for all body tissues. Theﬁbers that comprise muscle tissues, then, are truly membersof the large, interactive “society of cells” that forms the hu-man body.
THE BIG PICTURE
Muscle Tissue and the Whole Body

332 Unit 2 Support and Movement
Major Muscular Disorders
As you might expect, muscle disorders, or myopathies ,g e n –
erally disrupt the normal movement of the body. In mildcases, these disorders vary from inconvenient to slightlytroublesome. Severe muscle disorders, however, can impair
the muscles used in breathing—a life-threatening situation.
Muscle Injury
Injuries to skeletal muscles resulting from overexertion or
trauma usually result in a muscle strain .Figure 11-22 shows
an unusually severe muscle strain that resulted in a massivetear to the entire muscle organ. Muscle strains are character-
ized by muscle pain, or myalgia (my-AL-jee-ah), and involve
overstretching or tearing of muscle ﬁbers. If an injury occurs
in the area of a joint and a ligament is damaged, the injurymay be called a sprain .Any muscle inﬂammation, including
that caused by a muscle strain, is termed myositis (my-o-
SYE-tis). If tendon inﬂammation occurs with myositis, as ina charley horse, the condition is termed ﬁbromyositi s (ﬁ-
bro-my-o-SYE-tis). Although inﬂammation may subside ina few hours or days, it usually takes weeks for damaged mus-cle ﬁbers to repair. Some damaged muscle cells may be re-placed by ﬁbrous tissue, forming scars. Occasionally, hardcalcium is deposited in the scar tissue.
Cramps are painful muscle spasms (involuntary twitches).
Cramps often result from mild myositis or ﬁbromyositis, but
they can be a symptom of any irritation or of an ion and wa-ter imbalance.
Minor trauma to the body, especially a limb, may cause a
muscle bruise, or contusion .Muscle contusions involve local
internal bleeding and inﬂammation. Severe trauma to askeletal muscle may cause a crush injury .Crush injuries
greatly damage the affected muscle tissue, and the release of
muscle ﬁber contents into the bloodstream can be lifethreatening. For example, the reddish muscle pigment myo-
globin can accumulate in the blood and cause kidney failure.
Stress-induced muscle tension can result in myalgia and
stiffness in the neck and back and is thought to be one causeof “stress headaches.” Headache and back-pain clinics usevarious strategies to treat stress-induced muscle tension.These treatments include massage, biofeedback, and relax-ation training.
Muscle Infections
Several bacteria, viruses, and parasites may infect muscle tissue—often producing local or widespread myositis. Forexample, in trichinosis, widespread myositis is common. The
muscle pain and stiffness that sometimes accompany in-
ﬂuenza is another example.
Once a tragically common disease, poliomyelitis is a viral
infection of the nerves that control skeletal muscle move-ment. Although the disease can be asymptomatic, it oftencauses paralysis that may progress to death. Virtually elimi-nated in the United States as a result of a comprehensive vac-cination program, it still affects millions in other parts of theworld.
Muscular Dystrophy
Muscular dystrophy (DIS-tro-fee) is not a single disorder
but a group of genetic diseases characterized by atrophy(wasting) of skeletal muscle tissues. Some, but not all, formsof muscular dystrophy can be fatal.
The common form of muscular dystrophy is Duchenne
(doo-SHEN) muscular dystrophy (DMD) .This form of the
disease is also called pseudohypertrophy (meaning “false
muscle growth”) because the atrophy of muscle is masked by
excessive replacement of muscle by fat and ﬁbrous tissue.
DMD is characterized by mild leg muscle weakness that pro-gresses rapidly to include the shoulder muscles. The ﬁrst
signs of DMD are apparent at about 3 years of age, and thestricken child is usually severely affected within 5 to 10 years.Death from respiratory or cardiac muscle weakness often oc-curs by the time the individual is 21 years old.
We now know that DMD is caused by a mutation in X
chromosome, although other factors may be involved. DMD
occurs primarily in boys. Because girls have two X chromo-somes and boys only one, genetic diseases involving X chro-mosome abnormalities are more likely to occur in boys. Thisis true because girls with one damaged X chromosome maynot exhibit an “X-linked” disease if their other X chromo-some is normal (see Chapter 34). The gene involved in DMDnormally codes for the protein dystrophin (DIS-trof-in),
which forms strands in each skeletal muscle ﬁber and helpsto hold the cytoskeleton to the sarcolemma. Dystrophin thus
helps to keep the muscle ﬁber from breaking during con-tractions. Normal dystrophin is missing in DMD because a
deletion or mutation of part of the dystrophin gene (thelargest human gene ever discovered) causes the resulting
MECHANISMS OF DISEASE
S
A P
I
Figure 11-22 Muscle strain. Severe strain of the biceps brachii
muscle. In a severe muscle strain, a muscle may break in two pieces,causing a visible gap in muscle tissue under the skin. Notice how thebroken ends of the muscle reﬂexively contract (spasm) to form a knotof tissue.

Physiology of the Muscular System Chapter 11 333
protein to be nonfunctional (it has the wrong shape to do the
job). Thus in DMD muscle ﬁbers break apart more easily—causing the symptoms of progressive muscle weakness.
Myasthenia Gravis
Myasthenia gravis (my-es-THEE-nee-ah GRA-vis) is a
chronic disease characterized by muscle weakness, especially
in the face and throat. Most forms of this disease begin withmild weakness and chronic muscle fatigue in the face, thenprogress to wider muscle involvement. When severe muscleweakness causes immobility in all four limbs, a myasthenic
crisisis said to have occurred. A person in myasthenic crisis
is in danger of dying from respiratory failure because ofweakness in the respiratory muscles.
Myasthenia gravis is an autoimmune disease in which the
immune system attacks muscle cells at the neuromuscularjunction. Nerve impulses from motor neurons are then un-able to fully stimulate the affected muscle.Hernias
Weakness of abdominal muscles can lead to a hernia ,o r pro-
trusion, of an abdominal organ (commonly the small intes-
tine) through an opening in the abdominal wall. There areseveral types of hernias. The most common one, inguinal
hernia (Figure 11-23), occurs when the hernia extends down
the inguinal canal, often into the scrotum or labia. Males ex-perience this most often, and it can occur at any age. Womenmay experience a femoral hernia below the groin because of
changes during pregnancy.
Hernia is referred to as “reducible” when the protruding
organ is manipulated back into the abdominal cavity, eithernaturally by lying down or by manual reduction through asurgical opening in the abdomen. A “strangulated” herniaoccurs when the mass is not reducible and blood ﬂow to theaffected organ (i.e., intestine) is stopped. Obstruction andgangrene can occur. Pain and vomiting are usually experi-enced and emergency surgical intervention is required.
Inguinal hernia.
S
IL R
NormalPeritoneum
Normal Congenital inguinal
herniaIntestine
protruding
into scrotum
S
P A
I
Figure 11-23 Inguinal hernia in infant male.

C.A ﬂood of calcium ions combines with troponin
molecules in the thin ﬁlament myoﬁbrils.
D.Nerve impulses from motor neuromuscular junc-
tions are unable to fully stimulate the affectedmuscle.
2.Based on the action of edrophonium chloride, as stated
above, how will this drug work in Ms. Pulaski’s case?Edrophonium chloride:
A.Increases the availability of acetylcholine at the
postsynaptic receptor sites
B.Decreases the availability of acetylcholine at the
postsynaptic receptor sites
C.Increases the attachment of thick myosin ﬁlaments
to the sarcomere
D.Decreases electrical impulses in the sarcolemma
3.Based on the action of edrophonium chloride, as stated
above, which one of the following physical effects willmost likely be noted by Ms. Pulaski?
A.Relaxation of muscle
B.Decreased muscle excitation and contraction
C.Increased muscle excitation and contraction
D.Increased ﬂaccidity of muscle
4.Based on the information presented in the case study,
which one of the following disorders does Ms. Pulaskihave?
A.Muscular dystrophy
B.Poliomyelitis
C.Fibromyositis
D.Myasthenia gravisCecelia Pulaski, age 27, noticed changes in her energy
level accompanied with muscle weakness. Particularly
when she swallowed, she would sometimes feel that foodwas stuck in her throat. She had difﬁculty combing herhair, and she noticed that her voice was very weak. Theweakness would usually improve when she rested. She was
admitted to the hospital for myalgia, paresthesia, and im-mobility of all extremities. At the time of admission, shewas having difﬁculty breathing. She recently experiencedan extremely stressful divorce.
On physical examination, Ms. Pulaski is unable to close
her eyes completely. Her pupils respond normally to lightand show normal accommodation. She has lost 15 poundsin the last month. Her tongue has several ﬁssures. Her lab-oratory data are essentially normal except for a positive an-tibody test, which is indicative of an autoimmune disorderattacking muscle cells at the neuromuscular junction. Elec-trical testing of the neuromuscular junction shows some
blocking of discharges. A pharmacological test using edro-phonium chloride is positive. Edrophonium chloride in-hibits the breakdown of acetylcholine at the postsynapticmembrane.
1.Based on what is known about myasthenia gravis, which
of the following explanations for Cecelia’s symptomswould be physiologically correct?
A.Adenosine triphosphate pulls the thin myoﬁla-
ments during muscle contraction.
B.Active sites on the actin molecules are exposed.CASE STUDY334 Unit 2 Support and Movement

Physiology of the Muscular System Chapter 11 335
INTRODUCTION
A.Muscular system is responsible for moving the frame-
work of the body
B.In addition to movement, muscle tissue performs
various other functions
GENERAL FUNCTIONS
A.Movement of the body as a whole or of its parts
B.Heat production
C.Posture
FUNCTION OF SKELETAL MUSCLE TISSUE
A.Characteristics of skeletal muscle cells
1.Excitability (irritability)—ability to be stimulated
2.Contractility—ability to contract, or shorten, and
produce body movement
3.Extensibility—ability to extend, or stretch, allowing
muscles to return to their resting length
B.Overview of the muscle cell (Figures 11-1 through 11-3)
1.Muscle cells are called ﬁbers because of their thread-
like shape
2.Sarcolemma—plasma membrane of muscle ﬁbers
3.Sarcoplasmic reticulum
a.Network of tubules and sacs found within muscle
ﬁbers
b.Membrane of the sarcoplasmic reticulum contin-
ually pumps calcium ions from the sarcoplasmand stores the ions within its sacs
4.Muscle ﬁbers contain many mitochondria and several
nuclei
5.Myoﬁbrils—numerous ﬁne ﬁbers packed close to-
gether in sarcoplasm
6.Sarcomere
a.Segment of myoﬁbril between two successive
Zlines
b.Each myoﬁbril consists of many sarcomeres
c.Contractile unit of muscle ﬁbers
7.Striated muscle
a.Dark stripes called A bands ;light H zone runs
across midsection of each dark A band
b.Light stripes called I bands ;dark Zline extends
across center of each light I band
8.Ttubules
a.Transverse tubules extend across the sarcoplasm
at right angles to the long axis of the muscle ﬁber
b.Formed by inward extensions of the sarcolemma
c.Membrane has ion pumps that continually trans-
port Ca/H11001/H11001ions inward from the sarcoplasm
d.Allow electrical impulses traveling along the sar-
colemma to move deeper into the cell
9.Triad
a.Triplet of tubules; a Ttubule sandwiched between
two sacs of sarcoplasmic reticulum. Allows anelectrical impulse traveling along a Ttubule to
stimulate the membranes of adjacent sacs of thesarcoplasmic reticulum
C.Myoﬁlaments (Figure 11-4)
1.Each myoﬁbril contains thousands of thick and thin
myoﬁlaments
2.Four different kinds of protein molecules make up
myoﬁlaments
a.Myosin
(1)Makes up almost all the thick ﬁlament
(2)Myosin “heads” are chemically attracted to
actin molecules
(3)Myosin “heads” are known as cross bridges
when attached to actin
b.Actin—globular protein that forms two ﬁbrous
strands twisted around each other to form thebulk of the thin ﬁlament
c.Tropomyosin—protein that blocks the active sites
on the actin molecules
d.Troponin—protein that holds tropomyosin mole-
cules in place
3.Thin ﬁlaments attach to both
Zlines of a sarcomere
and extend part way toward the center
4.Thick myosin ﬁlaments do not attach to the Zlines
D.The mechanism of contraction
1.Excitation and contraction (Figures 11-5 through 11-7;
Table 11-1)
a.A skeletal muscle ﬁber remains at rest until stimu-
lated by a motor neuron
b.Neuromuscular junction—motor neurons con-
nect to the sarcolemma at the motor endplate(Figure 11-5)
c.Neuromuscular junction is a synapse where neu-
rotransmitter molecules transmit signals
d.Acetylcholine—the neurotransmitter released into
the synaptic cleft that diffuses across the gap,stimulates the receptors, and initiates an impulsein the sarcolemma
e.Nerve impulse travels over the sarcolemma and
inward along the
Ttubules, which triggers the re-
lease of calcium ions
f.Calcium binds to troponin, causing the
tropomyosin to shift and expose active sites on
the actin
g.Sliding ﬁlament theory (Figure 11-8)
(1)When active sites on the actin are exposed,
myosin heads bind to them
(2)Myosin heads bend, pulling the thin ﬁlaments
past them
(3)Each head releases, binds to the next active
site, and pulls again
(4)The entire myoﬁbril shortens
CHAPTER SUMMARY

2.Relaxation
a.Immediately after the Ca/H11001/H11001ions are released, the
sarcoplasmic reticulum begins actively pumpingthem back into the sacs
b.Ca
/H11001/H11001ions are removed from the troponin mole-
cules, shutting down the contraction
3.Energy sources for muscle contraction (Figure 11-9)
a.Hydrolysis of ATP yields the energy required for
muscular contraction
b.Adenosine triphosphate (ATP) binds to the
myosin head and then transfers its energy to the
myosin head to perform the work of pulling the
thin ﬁlament during contraction
c.Muscle ﬁbers continually resynthesize ATP from
the breakdown of creatine phosphate
d.Catabolism by muscle ﬁbers requires glucose and
oxygen
e.At rest, excess O 2in the sarcoplasm is bound to
myoglobin(1)Red ﬁbers—muscle ﬁbers with high levels
of myoglobin
(2)White ﬁbers—muscle ﬁbers with little
myoglobin
f.Aerobic respiration occurs when adequate O
2is
available
g.Anaerobic respiration occurs when low levels of
O2are available and results in the formation of
lactic acid
h.Skeletal muscle contraction produces waste heat
that can be used to help maintain the set pointbody temperature (Figure 11-10)
FUNCTION OF SKELETAL MUSCLE ORGANS
A.Muscles are composed of bundles of muscle ﬁbers that
are held together by ﬁbrous connective tissue
B.Motor unit (Figure 11-11)
1.Motor unit—motor neuron plus the muscle ﬁbers to
which it attaches
2.Some motor units consist of only a few muscle ﬁbers,
whereas others consist of numerous ﬁbers
3.Generally, the smaller the number of ﬁbers in a mo-
tor unit, the more precise the movements available;
the larger the number of ﬁbers in a motor unit, themore powerful a contraction is available
C.Myography
D.Twitch contraction (Figure 11-12)
1.A quick jerk of a muscle that is produced as a result
of a single, brief threshold stimulus (generally occursonly in experimental situations)
2.The twitch contraction has three phases
a.Latent phase—nerve impulse travels to the
sarcoplasmic reticulum to trigger release of Ca
/H11001/H11001
b.Contraction phase—Ca/H11001/H11001binds to troponin and
sliding of ﬁlaments occurs
c.Relaxation phase—sliding of ﬁlaments ceasesE.Treppe—the staircase phenomenon (Figure 11-13, B)
1.Gradual, steplike increase in the strength of contrac-
tion that is seen in a series of twitch contractions thatoccur 1 second apart
2.Eventually, the muscle responds with less forceful
contractions, and relaxation phase becomes shorter
3.Ifrelaxation phase disappears completely, a contrac-
ture occurs
F.Tetanus—smooth, sustained contractions
1.Multiple wave summation—multiple twitch waves are
added together to sustain muscle tension for a longertime
2.Incomplete tetanus—very short periods of relaxation
occur between peaks of tension (Figure 11-13, C)
3.Complete tetanus—the stimulation is such that
twitch waves fuse into a single, sustained peak (Figure 11-13, D)
G.Muscle tone
1.Tonic contraction—continual, partial contraction of a
muscle
2.At any one time, a small number of muscle ﬁbers
within a muscle contract, producing a tightness or
muscle tone
3.Muscles with less tone than normal are ﬂaccid
4.Muscles with more tone than normal are spastic
5.Muscle tone is maintained by negative feedback
mechanisms
H.Graded strength principle
1.Graded strength principle—skeletal muscles contract
with varying degrees of strength at different times
2.Factors that contribute to the phenomenon of graded
strength (Figure 11-17)
a.Metabolic condition of individual ﬁbers
b.Number of muscle ﬁbers contracting simultane-
ously; the greater the number of ﬁbers contract-ing, the stronger the contraction
c.Number of motor units recruited
d.Intensity and frequency of stimulation
(Figure 11-14)
3.Length-tension relationship (Figure 11-15)
a.Maximal strength that a muscle can develop bears
a direct relationship to the initial length of its ﬁbers
b.A shortened muscle’s sarcomeres are compressed,
therefore the muscle cannot develop much tension
c.An overstretched muscle cannot develop much
tension because the thick myoﬁlaments are too
far from the thin myoﬁlaments
d.Strongest maximal contraction is possible only
when the skeletal muscle has been stretched to itsoptimal length
4.Stretch reﬂex (Figure 11-16)
a.The load imposed on a muscle inﬂuences the
strength of a skeletal contraction
b.Stretch reﬂex—the body tries to maintain a con-
stancy of muscle length in response to increasedload336 Unit 2 Support and Movement

c.Maintains a relatively constant length as load is
increased up to a maximum sustainable level
I.Isotonic and isometric contractions (Figure 11-18)
1.Isotonic contraction
a.Contraction in which the tone or tension within a
muscle remains the same as the length of the
muscle changes
(1)Concentr ic—muscle shortens as it contracts
(2)Eccentric—muscle lengthens while
contra cting
b.Isotonic—literally means “same tension”
c.All of the energy of contraction is used to pull on
thin myoﬁlaments and thereby change the lengthof a ﬁber’s sarcomeres
2.Isometr ic contraction
a.Contraction in which muscle length remains the
same while the muscle tension increases
b.Isometric—literally means “same length”
3.Most body movements occur as a result of both types
of contractions
FUNCTION OF CARDIAC AND SMOOTH
MUSCLE TISSUE
A.Cardiac muscle (Figure 11-19)
1.Found only in the heart, forming the bulk of the wall
of each chamber
2.Also known as striated involuntary muscle
3.Contracts rhythmically and continuously to provide
the pumping action needed to maintain a constantblood ﬂow
4.Cardiac muscle resembles skeletal muscle but has spe-
cialized features related to its role in continuouslypumping blood
a.Each cardiac muscle contains parallel myoﬁbrils
(Figure 11-19)
b.Cardiac muscle ﬁbers form strong, electrically
coupled junctions (intercalated disks) with other
ﬁbers; individual cells also exhibit branching
c.Syncytium—continuous, electrically coupled mass
d.Cardiac muscle ﬁbers form a continuous, contrac-
tile band around the heart chambers that con-ducts a single impulse across a virtually continu-ous sarcolemma
e.T tubules are larger and form diads with a rather
sparse sarcoplasmic reticulumf.Cardiac muscle sustains each impulse longer
than in skeletal muscle, therefore impulses cannot come rapidly enough to produce tetanus(Figure 11-20)
g.Cardiac muscle does not run low on ATP and
does not experience fatigue
h.Cardiac muscle is self-stimulating
B.Smooth muscle
1.Smooth muscle is composed of small, tapered cells
with single nuclei (Figure 11-21)
2.No
Ttubules are present, and only a loosely orga-
nized sarcoplasmic reticulum is present
3.Ca/H11001/H11001comes from outside the cell and binds
to calmodulin instead of troponin to trigger a
contra ction
4.No striations, because thick and thin myoﬁlaments
are arranged differently than in skeletal or cardiacmuscle ﬁbers; myoﬁlaments are not organized into
sarcomeres
5.Two types of smooth muscle tissue
a.Visceral muscle (single unit)
(1)Gap junctions join smooth muscle ﬁbers into
large, continuous sheets
(2)Most common type; forms a muscular layer
in the walls of hollow structures such as thedigestive, urinary, and reproductive tracts
(3)Exhibits autorhythmicity, producing
peristalsis
b.Multiunit
(1)Does not act as a single unit but is composed
of many independent cell units
(2)Each ﬁber responds only to nervous input
THE BIG PICTURE: MUSCLE TISSUE
AND THE WHOLE BODY
A.Function of all three major types of muscle is integral
to the function of the entire body
B.All three types of muscle tissue provide the movement
necessary for survival
C.Relative constancy of the body’s internal temperature is
maintained by “waste” heat generated by muscle tissue
D.Maintains the body in a relatively stable positionPhysiology of the Muscular System Chapter 11 337

338 Unit 2 Support and Movement
1.Deﬁne the terms sarcolemma, sarcoplasm ,and sar-
coplasmic reticulum .
2.Describe the function of the sarcoplasmic reticulum.
3.How are acetylcholine, Ca/H11001/H11001,and adenosine triphos-
phate (ATP) involved in the excitation and contractionof skeletal muscle?
4.Describe the general structure of ATP and tell how it
relates to its function.
5.How do es ATP provide energy for a muscle contraction?
6.Describe the anatomical arrangement of a motor unit.
7.List and describe the different types of skeletal muscle
contra ctions.
8.Deﬁne the term recruited .
9.Describe rigor mortis.
10.What are the effects of exercise on skeletal muscles?
REVIEW QUESTIONS
1.Explain how skeletal muscles provide movement, heat,
and posture. Are all of these functions unique tomuscles? Explain your answer.
2.The characteristic of excitability is shared by what
other system? Relate contractility and extensibility tothe concept of agonist and antagonist discussed inChapter 10.
3.What structures are unique to skeletal muscle ﬁbers?
Which of the structures are involved primarily in con-
tractility and which are involved in excitability?
4.Explain how the structure of myoﬁlaments is related to
their function.
5.Explain how the sliding ﬁlament theory allows for the
shortening of a muscle ﬁber.
6.Compare and contrast the role of Ca
/H11001/H11001in excitation,
contraction, and relaxation of skeletal muscle.
7.People who exercise seriously are sometimes told to
work a muscle until they “feel the burn.” In terms of
how the muscle is able to release energy, explain whatis going on in the muscle early in the exercise andwhen the muscle is “burning.”
8.Using ﬁber types, design a muscle for a marathon
runner and a different muscle for a 100-yard–dash
sprinter. Explain your choice.
9.Explain the meaning of a “unit of combined cells” as it
relates to cardiac muscle. How does this structural
arrangement affect its function?
10.Which of the two smooth muscle types would be most
affected by damage to the nerves that stimulate them?
CRITICAL THINKI NG QUESTIONS

Physiology of the Muscular System Chapter 11 339
CAREER CHOICES
Massage Therapist
Massage therapy improves
circulation and helps to
correct imbalances in the soft tis-
sue areas of the body, as in musclesand fascia. As a massage therapist,I am self-employed. My clienteleconsist of hospital-referred pa-
tients for lymph drainage therapyand people who seek traditionalmassage for various reasons. Themajority of my work consists of
home visits; however, I also work part-time at Endless Cre-ations Spa and at private massage parties.
I have been massaging people since I was 5 years old. I
massaged my other classmates whenever they had prob-lems or hurt themselves. It has always been natural and en-joyable to work on others with my hands.
My certiﬁ cations are as follows:
CMT—Certiﬁed Massage Therapist (Swedish Massage)
MLDT—Manual Lymph Drainage Massage TherapistCDT—Combined Decongestive Therapist
Monteo Myers,
CMT, MLDT, CDT,OBT, NCTMB OBT—Oriental Bodywork Therapist (Shiatsu)
NCTMB—Nationally Certiﬁed Therapist of Massage and
Bodywork
I am also certiﬁed in La Stone Therapy, Reki 2, Reﬂex-
ology, and Myofacial Release. I have completed additionalstudy in Zero Balancing, NeuroMuscular Therapy, SportsMassage, and CrainoSacral Therapy.
Some of the current trends in the massage profession
are La Stone Therapy, treatment of cancer patients (with adoctor’s approval), and stress and pain relief.
My job is extremely rewarding. I rarely encounter a cli-
ent in a bad mood before a massage, and never after com-pletion! It is very rewarding to see a client or patient’sproblem improve, or simply see a look of contentment ontheir face. There is a personal, respectful bond between thetherapist and the client. In addition this profession can beﬁnancially rewarding.
Knowledge of anatomy and physiology is deﬁnitely
needed to effectively treat muscular/skeletal problems be-cause isolation of the involved muscle is necessary. I still re-view anatomy and physiology of the muscular, skeletal, and
lymphatic areas all the time. My advice is to study anatomyand physiology in a quiet room, do not study an entire chap-ter in one sitting, spread the chapter out, and take notes!Physiology of the Muscular System Chapter 11 339

340 Unit 2 Support and Movement

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