Solution Manual for Anatomy and Physiology

1st Edition McKinley 0077927044

9780077927042
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CHAPTER 10: Muscle Tissue

CHAPTER OVERVIEW
This chapter is designed to help students understand the anatomical and physiological
concepts involving muscle tissue. Muscle tissue, like all tissues, is composed of cells.
Muscle cells can contract and they can propagate a charge along their surfaces; charge
propagation will be fully explained in the nervous tissue chapter. There are three types
of muscle cells: skeletal muscle cells, cardiac muscle cells, and smooth muscle cells. As a
result of their being three types of muscle tissue cells, there are three types of muscle:
skeletal muscle, cardiac muscle, and smooth muscle.

Detailed anatomical descriptions of all three types of muscle are presented in this
chapter. Detailed descriptions of the connective tissue coverings surrounding muscle
tissue will be presented. The physiology of muscle contraction is explained. How muscle
obtains its energy is described along with what happens when muscle does not have
quite enough energy for all of its muscle contractions. Types of skeletal muscle fibers
are presented and explained. The events occurring in one isolated muscle contraction,
muscle twitch, are detailed; summation of individual muscle twitches is explained.
Isometric and isotonic contractions are discussed. The effects of exercise on skeletal
muscle and the changes in skeletal muscle as a result of aging are delineated. Cardiac
muscle is described. A detailed discussion of smooth muscle anatomy and physiology is
presented.

KEY POINTS TO EMPHASIZE WHEN TEACHING THE BIOLOGY

OF MUSCLE TISSUE
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 An instructional understanding: It is very important for students taking human
anatomy and physiology to understand the anatomical and physiological intricacies
of muscle. It is important to explain the functions and characteristics of skeletal
muscle, then relate these to the anatomical construct and/or physiological actions
of muscle. A major physiological concept that must be presented is the coupling of
action potential propagation along the muscle cell with the muscle cell contraction;
a concept oftentimes referred to as excitation-contraction coupling. The crucial role
of calcium in muscle contraction should be explained. It should be reiterated that
bone does need calcium, but calcium is more vitally needed in muscle contractions,
nerve conduction, and whole myriad of other needs; bone serves as a bank for
calcium so that these vital needs can be satisfied along with its own need for bone
strength. Other topics students need to understand are muscle fatigue and rigor
mortis. Since the majority of students taking a human anatomy and physiology
course are seeking healthcare fields, integration of pathological conditions is
important.

1. List and explain the functions of skeletal muscle.

a. Explain skeletal muscle’s role in body movement.
b. Explain skeletal muscle’s role in the maintenance of body posture.

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 c. Explain skeletal muscle’s role in protection and support.
d. Explain skeletal muscle’s role in the storage and movement of materials.
e. Explain skeletal muscle’s role in the production of heat.
2. Describe the characteristics of skeletal muscle.
a. Explain and describe skeletal muscle excitability.
b. Explain and describe skeletal muscle conductivity.
c. Explain and describe skeletal muscle contractility.
d. Explain and describe skeletal muscle elasticity.
e. Explain and describe skeletal muscle extensibility.
3. Show and explain the gross anatomical construct of skeletal muscle tissue.
a. Define and show a muscle fascicle.
b. Show, explain and discuss the three connective tissue coverings involved in
skeletal muscle tissue: epimysium, perimysium, and endomysium.
c. Define, show, and explain the construct and role of a tendon.
d. Show, explain and discuss the deep fascia and superficial fascia; discuss these
two fascias in relation to skeletal muscle.
e. Show, explain and discuss nerve innervation to skeletal muscle along with
skeletal muscle vascularization.
f. Explain that skeletal muscle action is considered to voluntary, whereas cardiac
muscle and smooth muscle actions are considered to be involuntary.
4. Show, explain and discuss the cytological construct of skeletal muscle cells.
a. Inform students that the skeletal muscle cell can be termed a muscle fiber or
myofiber.
b. Inform students that the skeletal muscle cells have many of the same
organelles as any other cell.
c. Inform students that the cytoplasm of the skeletal muscle cell is called the
sarcoplasm.
d. Discuss the muscle stem cell known as the myoblast.
e. Describe and explain skeletal muscle cell length and skeletal muscle cell
multinucleation.
f. Show, explain, and discuss the structure of the sarcolemma, another name for
the skeletal muscle cell membrane along with the structure and function of the
t-tubules.
g. Explain the concept of the resting membrane potential (RMP) along the cell
membrane of the skeletal muscle cell; explain that the RMP was discussed to
some extent in the cell chapter and will be better discussed in the nervous
tissue chapter.
h. Provide a cursory explanation of the action potentials involved in skeletal
muscles, but inform students that a better explanation will be given in the
nervous tissue chapter.
i. Show, explain, and discuss the structure and functions of the sarcoplasmic
reticulum.
j. Explain and discuss the functions of calmodulin and calsequestrin; explain the
calcium voltage-gated channels.
k. Explain and differentiate three terms: myofiber, myofibril, and myofilament.
l. Show and explain the myofibril arrangement of myofilaments; explain that the
myofibril arrangement is found in both skeletal muscle cells and cardiac muscle

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 cells, thus giving these two muscle cell types a striated (striped) appearance
when viewed using the light microscope.
m. Show, explain, and discuss the two major myofilaments that comprise the
myofibril: actin and myosin.
n. Explain that actin is also termed the thin filament and myosin is termed the
thick filament.
o. Discuss the construct and function of three molecular components attached to
and residing on the thin filament: the myosin binding site, tropomyosin, and
troponin.
p. Discuss the construct and function of two molecular components attached to
and residing on the thick filament: ATP and ATPase.
q. Show, explain, and discuss the construct of the various bands, lines, and discs
found in a sarcomere: I-band, A-band, H-band, M-line, and Z-disc.
r. Explain and discuss some of the other molecular components found in a
sarcomere: connectin, nebulin, and dystrophin.
s. Explain and discuss skeletal muscle energy production.
t. Explain mitochondrial action in muscle cell energy production.
u. Explain and discuss myoglobin.
5. Show, explain, and discuss nerve innervation to skeletal muscle.
a. Show, explain and discuss the construct and function of a motor unit; explain
the rationale for differences in sizes of motor units in various skeletal muscles
in the human body.
b. Show, explain, and discuss the anatomical structures and chemical components
involved at the neuromuscular junction.
c. Show and discuss the anatomical components of the neuromuscular junction:
somatic motor neuron, synaptic end knob, synaptic vesicles, synaptic cleft,
and motor end plate.
d. Discuss the chemicals involved at the neuromuscular junction: acetylcholine
and acetylcholinesterase.
e. Explain the physiological actions occurring at the neuromuscular junction;
inform students that chemical synaptic transmission will be further explained
in the nervous tissue chapter.
6. Show, explain, and discuss the physiology of skeletal muscle contraction; explain the
sliding filament model of skeletal muscle contraction.
7. List and explain the role of each anatomic structure associated with skeletal muscle
contraction: neuromuscular junction, sarcolemma, T-tubules, sarcoplasmic
reticulum, and sarcomere.
8. Explain skeletal muscle contraction in three phases: excitation phase, contraction
phase, and the relaxation phase.
9. Explain and discuss the excitation phase.
a. Make it clear to students that though action potentials are discussed to some
extent in this chapter, a further explanation will be presented in the nervous
tissue chapter.
b. Show, explain, and discuss that a wave of excitation (action potentials) passes
down the membrane of the somatic motor neuron; somatic motor action
potentials will be discussed in the nervous tissue chapter.
c. Show, explain, and discuss that once the wave of excitation reaches and crosses
over the membrane of the synaptic knob, voltage dependent calcium gates,

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 located along the membrane of the synaptic end knob, open allowing calcium
ions to enter into the synaptic end knob.
d. Explain that the calcium ions attach to synaptotagmin proteins located in the
membrane of synaptic vesicles, causing approximately 300 synaptic vesicles to
move to interior side of synaptic end knob membrane; the synaptic vesicles
contain a neurotransmitter chemical known as acetylcholine.
e. Explain that upon the synaptic vesicles fusing with the interior of the synaptic
end knob membrane, exocytosis occurs which causes a release of acetylcholine
into the synaptic cleft.
f. Explain that the acetylcholine molecules diffuse across the synaptic cleft and
attach to acetylcholine receptors located at the motor end plate of the skeletal
muscle cell.
g. Explain that the acetylcholine causes the opening of chemical-gated cation ion
channels found along the membrane of the motor end plate.
h. Explain that once the cation ion channels open, sodium ions rush into the
skeletal muscle cell and potassium ions rush out of the cell; the directions of
both ion movements are in accordance with their respective electrochemical
gradients.
i. Explain that as a result of the electrochemical gradient of sodium compared to
that of potassium, more sodium ions rush in that potassium ions rush out; this
rush of ions creates a motor end plate potential.
j. Explain that the overwhelming movement of sodium ions into the cell through
the chemical-gated channels may cause the cell membrane (sarcolemma) to
reach a voltage value known as threshold voltage, which results in the opening
of voltage-gated sodium channels, also located on the sarcolemma.
k. Explain that when threshold voltage is reached, the voltage-gated sodium
channels open, and sodium ions rush into the cell in accordance with their
electrochemical gradient.
l. Explain that the entrance of sodium cations into the muscle cell causes the cell
membrane to lose its resting membrane potential, an action known as
depolarization of the cell membrane.
m. Explain that the opening of the voltage-gated sodium channels is the first event
that occurs in an action potential.
n. Explain that an action potential is an all-or-none event comprised of three
membrane potential changes: depolarization, repolarization, hyperpolarization,
and subsequent reestablishment of the resting membrane potential.
o. Explain that depolarization results from an influx of sodium ions into the cell
interior; repolarization occurs after depolarization as a result of the later
opening of voltage-gated potassium ion channels.
p. Explain that potassium ions rush out of the cell in accordance with their
electrochemical gradient.
q. Explain that the slowness of closure of the potassium channels lead to the
hyperpolarization.
r. Explain that the membrane returns to its resting membrane potential as a result
of several factors inclusive of the actions of the sodium-potassium pump.
s. Explain that a muscle cell membrane cannot perform another action potential
until the voltage-gated sodium channel have been reset into its resting

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 condition; the time that it takes to reset the voltage-gated sodium channel is
known as the absolute refractory period.
t. Explain that the initial action potential occurred in one specific spot on the
muscle cell membrane.
u. Explain that initial action potential is able to produce a wave of action potentials
that propagate along the entire sarcolemma and into the T-tubules; the voltage
created by the initial action potential causes adjacent areas of the sarcolemma
to reach threshold, thus causing a propagation of actions potentials along the
sarcolemma surface.
v. Explain that once the action potentials propagate into the T-tubules, excitation-
contraction coupling begins.
10. Explain and discuss the contraction phase.
a. Explain that when the wave of action potentials transverse along the
sarcolemma in the T-tubule this causes the opening of voltage-gated calcium ion
channels located along the membrane of the terminal cisternae.
b. Explain that stored calcium ions rush out from the terminal cisternae and enter
the sarcoplasm.
c. Describe the actin structure along with its attached molecules: the troponin
complex and tropomyosin.
d. Explain that the calcium is then attracted to troponin C, a member of the
troponin complex.
e. Explain that calcium ions bind to troponin C, resulting in the shift in the entire
troponin complex in such a way that the bonded tropomyosin shifts and
uncovers the myosin binding site on actin.
f. Describe the myosin molecule and explain that the head of the molecule has
three components: an ATP binding site, ATPase, and an actin binding site.
g. Explain how the same action potentials that caused calcium release from the
terminal cisternae also result in the activation of ATPase causing the splitting of
ATP to ADP, thus liberating energy that causes the head of myosin to cock into a
triggering position.
h. Explain that this ATP splitting process is involved in the opening of the actin
binding site on myosin.
i. Explain that when both the actin binding site and myosin binding sites are open,
actin can bind to myosin, a process known as cross-bridging.
j. Explain that once cross-bridging has occurred, the myosin head is released from
its cocked position, a process known as the power-stroke.
k. Explain that the power-stroke process results in actin sliding over myosin, thus
the H-band possibly disappears and the I-band gets narrower; refamiliarize the
student with the H and I bands.
11. Explain and discuss the relaxation phase of muscle contraction.
a. Explain that if the somatic motor neuron sends down no more action potentials,
the skeletal muscle will relax.
b. Explain that no further acetylcholine will be released from the synaptic knob
and that existing acetylcholine in the synaptic cleft will be undergo catabolic
breakdown as a result of the action of acetylcholinesterase.
c. Explain that if adequate ATP is available in the sarcoplasm it attaches to
available ATP-binding sites on the head of the myosin molecule.

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 d. Explain that once ATP is placed back on the myosin head, the actin binding site
on myosin is covered.
e. Explain that active transport pumps in the sarcoplasmic reticulum membrane
constantly pull calcium ions from the sarcoplasm into the cisternae of the
sarcoplasmic reticulum; calsequestrin and calmodulin molecules stored in the
interior of the terminal cisternae pull calcium ions to the interior of the terminal
cisternae for storage.
f. Explain that once calcium is removed from troponin-C the troponin complex
shifts in such a manner as to cause tropomyosin cover the myosin binding sites
on actin.
g. Explain that once the actin binding site on myosin and myosin binding site on
actin is covered, actin cannot bind to myosin; without the binding there can be
no contraction.
h. Explain the process of covering binding sites after a contraction is the basis or
skeletal muscle relaxation.
12. Explain and discuss some pathological conditions associated with excitation and
contraction of skeletal muscles.
a. Explain and discuss myasthenia gravis which is an autoimmune disease
affecting the acetylcholine receptors; acetylcholine receptors are attacked by
antibodies.
b. Explain and discuss the muscular paralysis caused by neurotoxins produced by
two microorganisms: Clostridium tetani and Clostridium botulinum.
c. Explain that Clostridium tetani produces a neurotoxin that causes a spastic
paralysis as a result of inhibiting the release the inhibitory neurotransmitter
glycine from neurons in the spinal cord.
d. Explain that Clostridium botulinum produces a neurotoxin that inhibits the
release of acetylcholine at the synaptic end knobs leading to a flaccid paralysis.
e. Explain and discuss the condition of rigor mortis; a condition that begins within
3 –8 hours after death.
f. Explain that rigor mortis is a condition that occurs at death due to a failure to
further produce ATP; all of the energy requiring processes in skeletal muscles
must cease as a result of ATP loss.
g. Explain that calcium cannot be actively transported back into the sarcoplasmic
reticulum, thus the myosin binding site on actin stays open.
h. Explain that ATP cannot be placed back on the myosin molecule head, thus the
actin binding site on myosin stays open.
i. Explain that as a result of both binding sites staying open, cross-bridging
continues with no release of actin from myosin.
j. Explain that no power stroke can occur because there is no energy to cock back
the myosin head.
k. Explain that the skeletal muscles lock but have no motion; this is termed rigor
mortis.
l. Explain that after 8–24 hours post-mortem, the rigor mortis begins to decrease
due lysosomal release of enzymes that breakdown myofibrils.
13. Explain and discuss skeletal muscle metabolism.
a. Explain that there are three major methods whereby skeletal muscles generate
ATP: the phosphagen system, anaerobic cellular respiration, and aerobic cellular
respiration.

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 b. Remind students that anaerobic cellular respiration and aerobic cellular
respiration was presented in chapter three of this text.
c. Explain that the phosphagen system provides immediate energy for muscle
contractions; it includes readily available ATP in the cell along with creatine
phosphate.
d. Explain that the exergonic hydrolysis of ATP yields enough energy for a little
greater than 6 seconds of muscle contraction.
e. Explain that muscle has creatine phosphate which when enzymatically catalyzed
by creatine kinase can transfer a Pi to ADP, so as to reform ATP; creatine
phosphate provides an approximate 10 to 15 seconds of additional energy for
muscle contractions.
f. Explain that anaerobic cellular respiration (glycolysis) provides short-term
energy for muscle contractions; it can yield enough ATP for additional seconds
of muscle contraction; how many additional seconds depends on how much
glucose and glycogen are available to form ATP.
g. Explain that aerobic cellular respiration (Krebs cycle) provides a long-term
supply of energy for muscle contractions.
h. Remind students that deficiency of oxygen for cellular respiration was
discussed; if inadequate oxygen is available pyruvic acid will be converted to
lactic acid.
i. Explain that the use of immediate, short-term, or long-term sources for
supplying ATP is dependent upon both the intensity and duration of an activity;
very short-term activities that are 6 seconds or less in duration, such as a 50-
meter sprint require only the immediate source of energy.
j. Explain that the 400-meter run which is longer in duration requires the
immediate source of energy and energy supplied by anaerobic cellular
respiration; the 26-mile marathon requires all the sources of energy.
14. Explain and discuss the oxygen debt.
a. Explain that when an individual participates in an activity that exceeds the
amount of oxygen that be delivered to the skeletal muscle tissue, an oxygen
debt is incurred.
b. Explain that the oxygen debt is the amount of oxygen that must be inhaled
following exercise to restore pre-exercise conditions.
c. Explain that the additional oxygen after exercise is used to adequately resupply
hemoglobin with oxygen, replenish glycogen stores, replenish ATP and creatine
phosphate, and covert lactic acid back into glucose.
15. Show, explain, and discuss the three different types of skeletal muscle fibers: slow
oxidative fibers, fast oxidative fibers, and fast glycolytic fibers.
a. Explain that skeletal muscle fibers are categorized based on two criteria: type of
contraction generated and primary means to supply ATP.
b. Explain that the type of contraction generated depends on the muscle cells
speed of contraction and power of contraction; speed of contraction is
dependent on the fast and slow variants of myosin ATPase, while power
depends on the diameter of the muscle fiber.
c. Explain that skeletal muscle fibers with the fast variant ATPase are termed fast-
twitch fibers and those with the slow variant ATPase are termed slow-twitch
fibers; fast-twitch fibers initiate a faster contraction than the slow-twitch fibers
but the duration of contraction is shorter.

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 d. Explain that there are types of skeletal muscle fibers based on the two primary
means to supply ATP: oxidative fibers and glycolytic fibers.
e. Explain that compared to glycolytic fibers, oxidative fibers are redder in color
due to increased amounts of myoglobin, have a more extensive surrounding
blood vessels, and have more mitochondria; oxidative fibers are called red fibers
and provide extensive endurance, thus are fatigue-resistant.
f. Explain that glycolytic fibers primarily use glycolytic cellular respiration and have
less myoglobin, less vasculature, and fewer mitochondria; the lack of much
hemoglobin makes the fibers appear white, thus they are sometimes called
white fibers.
g. Explain that white fibers fatigue faster than red fibers.
16. List, explain, and discuss the three types of muscle fibers based on the two criteria
presented.
a. Explain that slow oxidative fibers, termed type I fibers, typically have half the
diameter of other skeletal muscle fibers and contain slow ATPase; these cells
produce contractions that are slower and less powerful, but longer in
endurance.
b. Explain that fast oxidative fibers, termed type IIa fibers or intermediate fibers,
are intermediate in diameter and contain a fast ATPase; these cells produce fast
powerful contractions.
a. Explain that fast glycolytic fibers, termed type IIb fibers or fast anaerobic fibers,
typically have the largest diameter and contain a fast ATPase; these fibers are
the most abundant in the body and produce fast powerful contractions, but
endurance is poor.
b. Explain that almost all skeletal muscles have a mixture of the three types of
fibers, but the relative proportions of fibers differ depending on the muscle.
c. Explain that extraocular muscles have mainly fast glycolytic fibers, while
postural muscles, like the trunk and calf muscles, contain mainly slow oxidative
fibers; thigh muscles contain primarily fast oxidative fibers.
17. Explain and discuss skeletal muscle tension.
a. Explain that muscle tension is the force generated when a skeletal muscle is
stimulated to contract.
b. Show a demonstration, explain, and discuss various methods to measure muscle
tension.
c. Explain and discuss the loss of hardness and compression strength as a result of
aging.
d. Explain and discuss a muscle twitch which is a single brief contraction and
relaxation as a result of one isolated stimulus to the muscle.
e. Explain that in order to initiate a muscle twitch a threshold voltage must be
delivered to the muscle; a voltage less that threshold is termed a subthreshold
stimulus.
f. Show a graph, list, and explain the three periods of a muscle twitch: latent
phase, contraction phase, and the relaxation phase.
g. Explain that the latent period is the period after the threshold stimulus is
applied and before the muscle begins to contract; this is the time necessary for
all of the events prior to the first actual contraction which include action
potential propagation, calcium ion release, crossbridge formation, and
generation of the first power strokes.

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 h. Explain that the contraction period is the power stroke pulls leading to
generation of muscle tension.
i. Explain that the relaxation period is time it takes for crossbridge release and
calcium removal from the sarcoplasm back into the sarcoplasmic reticulum.
18. Show, explain, and discuss the anatomy of a motor unit and the physiology of motor
unit recruitment
a. Remind students that a motor unit is one somatic motor neuron and all the
skeletal muscles fibers it innervates.
b. Explain to students that motor units vary in size in that some motor neurons
innervate as much as several thousand skeletal muscle fibers and some
innervate only as few as five; there is an inverse relationship between the size
of the motor unit and the degree of precise of control of muscle movements.
c. Explain that motor units in the extraocular muscles of the eye are small because
there is more finite precision required for eye movements, whereas motor units
in the lower limb muscles are large in that only powerful gross movements are
needed with little requirement for precision.
d. Explain the all-or-none rule of muscle contraction; if a skeletal muscle fiber is
stimulated to point of reaching threshold it will contract to its fullest extent,
however if it does not get a threshold stimulus it will not contract at all.
e. Explain that motor units also work in an all-or-none manner; when a somatic
motor neuron activates a motor unit, all the fibers in the motor unit contract in
an all-or-none manner.
f. Since a muscle is comprised of multiple motor units and each motor unit
operates as one individual all-or-none unit, full power-generation of an entire
muscle, like the biceps, requires activation of all of the motor units in that
muscle; addition or summation of motor units in termed recruitment.
g. Explain that the degree of motor unit recruitment is in accordance with the
need for power-generation in the muscle so as to perform the particular
activity.
19. Discuss the frequency of stimulation to a skeletal muscle.
a. Explain that the frequency of stimulation of a skeletal muscle will determine its
pattern of contraction; if the frequency of stimulation to the muscle is too slow
(less than 10 stimuli per second), isolated muscle twitches will be observed, in
that the fiber will contract and fully relax between each stimuli.
b. Explain that if the stimuli to the muscle cell are very fast, each twitch will be
summated and no relaxation will be observed between each stimulus.
c. Explain using a graph that each muscle twitch produces a wave and that when
the twitches are combined, it is termed wave summation.
d. Explain using a graph that if each tetanic wave gives some relaxation, it is
termed incomplete or unfused tetany; if there is no relaxation between waves it
is termed complete or fused tetany.
e. Explain that the summation of muscle twitches is termed wave summation; it is
also termed temporal summation since the summation occurs as a result of
increasing frequency of stimulation over time.
f. Explain using a graph that when a muscle fiber is initially simulated with
sufficient frequency, each successive contraction will generate increased

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 tension up to a point; the progressive increase in tension is termed treppe, the
staircase effect.
g. Explain that treppe is due to the muscle having increased amounts of calcium
ions in its sarcoplasm leading to more cross-bridge formation and decreased
viscosity of sarcoplasmic fluid due to heat generation; thus the skeletal muscle
fiber has warmed-up.
20. List and discuss the factors that influence muscle tension in the body.
a. Explain and discuss muscle tone which is termed resting muscle tension;
explain that involuntary nervous stimulation to the muscle is responsible for
the resting muscle tension.
b. Explain the differences between an isometric contraction and an isotonic
contraction; isometric contractions maintain the same fiber length but muscle
tension changes during the contraction, whereas isotonic contractions maintain
a constant fiber length, but change muscle tension during the contraction.
c. Give examples of isotonic contractions and isometric contractions; explain the
advantages and disadvantages of each type of contraction, especially discussing
blood pressure changes that occur as a result of isometric contractions.
21. Explain and discuss the length-tension relationship in skeletal muscle.
a. Show and explain the length-tension curve for skeletal muscle.
b. Show and explain why force of contraction can be affected by the length of the
sarcomere at the time of contraction.
22. Explain and discuss skeletal muscle fatigue.
a. Explain that muscle fatigue is the reduced ability or inability of the muscle to
produce muscle tension; there are many reasons for muscle fatigue.
b. Explain that one cause of muscle fatigue is due to depletion of glycogen stores
after an extensive exercise.
c. Explain that another cause of fatigue is due to insufficient calcium ions in the
synaptic cleft to cause release of acetylcholine from the synaptic knob; an
insufficient blood calcium ion level is one reason for this type of fatigue.
d. Explain that insufficient electrolyte levels (Na+ and/or K+) can cause skeletal
muscle fatigue.
e. Explain that muscle fatigue can result from inadequate crossbridge cycling;
elevated inorganic phosphate levels (Pi) in the sarcoplasm due to excessive ATP
breakdown can interfered with Pi release from the myosin head, also low
amounts of calcium ions in the sarcoplasmic reticulum can casus muscle fatigue.
f. Explain that new findings show that muscle pain associated with exercise may
not be due to lactic acid formation but rather to minor tearing of muscle during
exercise.
g. Explain that muscle fatigue is different from mental fatigue; mental fatigue
occurs when high levels of tryptophan are released from cells into the
bloodstream for the purpose of converting tryptophan into glucose
(gluconeogenesis) so as to be used for energy.
h. Explain that some tryptophan crosses the blood-brain barrier and is converted
into serotonin, a neurotransmitter in the brain that produces sleepiness.
23. Explain and discuss the effects of exercise on skeletal muscles.
a. Explain that when skeletal muscles are sufficiently exercised, particularly in
strength building exercises, the muscle cells enlarge, known as hypertrophy;

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 hypertrophy results in more myofibrils and myofilaments, more mitochondria,
an increase in glycogen reserves, and an increased ability to produce ATP.
b. Explain that some recent evidence suggests that there may be an increase in
the number of skeletal muscle cells, a process known as hyperplasia; the ability
of skeletal muscle cells to undergo hyperplasia is a disputed issue.
c. Explain that the opposite may occur when skeletal muscles are not exercised;
non-exercise can lead to muscle atrophy, which is a decrease in muscle fiber
size.
d. Inform students of the adage “the hypertrophy of use and the atrophy of
disuse.”
24. Discuss the effects of skeletal muscle aging.
a. Inform students that skeletal muscle mass generally begins to decline in the
mid-30s; the size and power of skeletal muscles also begin to decrease during
that age.
b. Explain to students that reductions in cell size and number are due to loss of
some myofilaments and myofibrils, a decrease in mitochondria, a decrease in
glycogens reserves, and other decreases.
c. Explain that as a result of skeletal muscle aging, there is a decreased endurance
capacity, decreased strength, and decreased capacity to heal.
d. Explain that muscle mass is replaced by adipose tissue or dense regular
connective tissue; the replacement by dense regular connective tissue is the
basis of scar formation, also termed fibrosis.
25. Discuss the effects of taking anabolic steroids.
a. Explain that anabolic steroids are synthetic substances that mimic testosterone.
b. Inform students that there are over 300 developed anabolic steroid compounds;
all anabolic steroids require a prescription for legal use.
c. Explain to students that the accepted medical uses for anabolic steroids are
treatment of delayed puberty, certain types of impotence, and the wasting
condition associated with HIV.
d. Inform students that because anabolic steroids do enhance skeletal muscle
strength and endurance, these drugs have illegally been used to by athletes to
enhance their athletic abilities.
e. Explain to students that in order for anabolic steroids to significantly enhance
strength and endurance, large doses must be taken; large doses of anabolic
steroids cause many side effects.
f. List and explain the side effects associated with anabolic steroids.
26. Show, explain, and discuss cardiac muscle tissue.
a. Explain that cardiac muscle is found in the heart and is an involuntary muscle.
b. Show, explain, and discuss that cardiac muscle cells are striated like skeletal
muscle cells but are shorter and thicker than skeletal muscle cells and only have
one or two nuclei.
c. Show that cardiac muscle cells are joined together by a light microscope
structure known as intercalated discs; an intercalated disc when viewed under
the electron microscope is composed of gap junctions and desmosomes.
d. Explain that cardiac muscle cells have more mitochondria, and use aerobic
respiration exclusively to produce ATP; cardiac muscle cells need considerable
endurance.

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 e. Explain that the heart muscle is stimulated by a special autorhythmic
pacemaker.
f. Inform students that cardiac muscle will be further discussed in chapter 19.
27. Show, explain, and discuss smooth muscle tissue.
a. Show and explain that smooth muscle is termed smooth because the cell
appears smooth and not striped under the light microscope.
b. Explain that smooth muscle is involuntary and found in the wall of many internal
organs; list and explain the role of smooth muscle in various organs.
c. Explain that smooth muscle can increase in size due to both hypertrophy and
hyperplasia; smooth muscle can perform mitosis unlike skeletal muscle and
cardiac muscle.
d. Show and explain that smooth muscle compared to the other two types of
muscle has a fusiform shape, single centrally placed nucleus, and much smaller
size.
e. Show and explain that each smooth muscle cell is wrapped by an endomysium
and the small tapered ends allow smooth muscle cells to pack closer.
f. Explain and discuss that smooth muscle is quite dependent on extracellular
calcium ions for its contraction, unlike that of skeletal muscle; smooth muscle
has no T-tubules, and no troponin, thus calcium action in smooth muscle is
different than that in skeletal muscle.
g. Explain that caveolae replace the function of T-tubules and the molecule
calmodulin replaces the function of troponin C.
h. Show, explain and discuss the structure and role of intermediate filaments,
dense bodies and dense plaques found in smooth muscle.
i. Show and explain that smooth muscle does not have sarcomeres like skeletal
muscle and cardiac muscle because the myofilaments (actin and myosin) are not
arranged in the myofibril pattern, thus the cell appears smooth under the
microscope.
j. Show and explain that the myofilaments of smooth muscle are arranged in an
oblique angle rather than a longitudinal angle as in skeletal muscle and cardiac
muscle, thus when smooth muscle contracts it forms a corkscrew appearance.
k. Show, list, and explain that the myofilaments of smooth muscle differ in some
ways than those of skeletal muscle and cardiac muscle.
l. Explain the mechanics and advantages of the latchbridge mechanism of smooth
muscle versus the crossbridge mechanism found in skeletal muscle and cardiac
muscle contractions.
m. Explain the actions of calmodulin and myosin light-chain kinase; discuss how
calmodulin and myosin light-chain kinase replace the actions of troponin C
found in skeletal muscle and cardiac muscle.
n. Show, explain, and discuss the mechanism of smooth muscle contraction;
explain the slight differences between smooth muscle contraction and skeletal
muscle contraction.
o. Carefully explain that relaxation of smooth muscle requires additional steps of
action than that of skeletal muscle; the dephosphorylation of the myosin head
by myosin light-chain phosphorylase must occur, otherwise smooth muscle will
stay locked in a contraction due to the latchbridge mechanism.

166
p. Explain and discuss three special characteristics required of smooth muscle:
considerable endurance, provision of more sustained contractions, and a wider
working range (length-tension range)
q. Explain and discuss that the rationale behind these required needs of smooth
muscle is that certain body organs, like the intestines and urinary bladder, need
to maintain a proper constant wall tension no matter how much they are
stretched as a result of their increasing content amounts of food, feces, and
urine.
r. Explain and discuss the mechanism behind smooth muscle contractions
generally being slow to develop tension but long in duration.
s. Explain the mechanism behind why smooth muscle is more fatigue resistant;
discuss its aerobic respiration and latchbridge action.
t. Using the length-tension curve, show and explain why smooth muscle has a
wider working range of effective contractions.
u. Explain the concept of stress-relaxation of smooth muscle and the rationale for
this action.
v. Explain that unlike skeletal muscle which can only be stimulated to contract by
the somatic nervous system, smooth muscle can be stimulated by the
autonomic nervous system, hormones, changes in pH, low oxygen
concentration, increased carbon dioxide levels, certain drugs, certain pacemaker
cells, and some cytokines.
w. Show, explain, and discuss that smooth muscle is classified into two broad
functional groups based on whether the smooth muscle fibers are either
stimulated to contract independently or as one unit; the two functional groups
are single-unit and multiple-unit.
x. Explain that the multiunit type is found in muscles such as the eye, large airway
passages, and the larger arteries; the multiunit arrangement is similar to the
skeletal muscle motor unit construct with its neuromuscular junction.
y. Explain that the single unit construct is in sheets of smooth muscle cells, found
in the digestive, urinary, and reproductive tracts; these sheets of cells are
connected by gap junctions forming a syncytium which contracts as one unit.
z. Show and explain that autonomic neurons that innervate smooth muscle have
varicosities rather than synaptic end knobs.

ADDITIONAL TOPICS FOR DISCUSSION

1. Explain and discuss how cells can become multinucleated.
2. Discuss an additional molecule found associated with the sarcomere, which is
myomesin, also known as m-line protein.
3. Further discuss dystrophin in terms of muscular dystrophy.
4. Further discuss the formation and use of creatine phosphate; discuss creatine
nutritional supplements.
5. Discuss and differentiate temporal summation versus spatial summation in
skeletal muscle innervation.
6. Show, explain, and discuss the working range concept in muscle.
7. Discuss the role of acetylcholinesterase inhibitors in the treatment of
myasthenia gravis.

167
 8. Explain and discuss the use of blood isoenzyme levels in the diagnosis of certain
disorders.

SUGGESTED CHAPTER OUTLINE

10.1 Introduction to Skeletal Muscle: Skeletal muscle typically composes 40-50% of
the weight of an adult. (pp. 332)
1. Skeletal muscles make up approximately 40–50% of an adult’s weight.
A. Functions of Skeletal Muscle (p. 332)
1. One function of skeletal muscle is body movement that occurs from
contraction of muscles attached to skeletal bones.
2. A second function of skeletal muscle is maintenance of posture: which occurs
by skeletal muscle contracting and thus stabilizing joints, holding the head
and trunk erect and contracting continuously during wake periods to prevent
bodily collapse.
3. A third function of skeletal muscle is protection and support of internal
organs within the abdominopelvic cavity by muscle layering along walls of
the abdominal and pelvic cavities.
4. A fourth function of skeletal muscle is storage and movement of materials via
the contraction and relaxation of circular muscle bands, or sphincters which
allow the passage of materials through openings, or orifices.
5. A fifth function of skeletal muscle is heat production which occurs when
muscles use energy to contract, noted in the second law of thermodynamics.
B. Characteristics of Skeletal Muscle Tissue (p. 332)
1. Excitability is the process of muscles responding to nervous system
stimulation where neurotransmitters released by neurons bind to muscle
receptors.
2. Conductivity is the process whereby an electrical change travels along the
plasma membrane due to neurotransmitter molecule binding.
3. Contractility occurs when contractile proteins slide past one another causing
muscle shortening and tension pulls on skeletal bones causing movement.
4. Elasticity occurs when muscles contract like coils until tension is released
causing them to return back to original length.
5. Extensibility is muscle lengthening upon contraction, such as elbow flexion.
10.2 Anatomy of Skeletal Muscle: A single muscle is composed of thousands of muscle
cells, also termed muscle fibers. (pp. 333–340)
A. Gross Anatomy of Skeletal Muscle (pp. 333–334)
1. Bundles of muscle fibers are called fascicles.
2. Dense irregular connective tissue surrounding the entire skeletal muscle is
called the epimysium.
3. Dense irregular connective tissue containing an extensive network of blood
vessels and nerves surrounding the fascicles is called the perimysium.
4. The innermost areolar connective tissue layer that insulates each muscle
fiber is called the endomysium.
5. Cordlike structures composed of three layers of dense regular connective
tissue which attach muscle to bone, skin or another muscle are called
tendons.
6. Thin, flattened sheets of dense irregular tissue are called aponeurosis.

168
Another random document with
no related content on Scribd:
Falle der Stimmengleichheit entscheidet die Stimme des
Vorsitzenden, bei Wahlen das Los.
Abstimmungen des Gesamt-Vorstandes und des
geschäftsführenden Vorstandes können auch auf schriftlichem Weg
erfolgen.

§ 17.
Änderungen dieser allgemeinen Satzung, sowie des
Vereinszweckes kann die Hauptversammlung mit einer Mehrheit von
drei Viertel der Anwesenden beschließen.

VII. Auflösung des Vereins

§ 18.
Zur Auflösung des Vereins bedarf es des übereinstimmenden und
jedesmal von wenigstens vier Fünftel der erschienenen Mitglieder
gefaßten Beschlusses zweier mindestens vier Wochen
auseinanderliegender Hauptversammlungen. Der Antrag auf
Auflösung muß wenigstens drei Monate vor der Versammlung beim
Gesamt-Vorstande schriftlich angebracht und öffentlich durch die
»Sächsische Staatszeitung« bekannt gemacht werden.

§ 19.
Im Falle der Auflösung wird das Vereinsvermögen dem
Gesamtministerium zur freien Verfügung überwiesen.

§ 20.
Die am 14. Juli 1908 errichtete Satzung ist am 15. Mai 1909, 15.
Mai 1911, 8. Mai 1912 und am 1. September 1919 abgeändert und
am 1. September 1923 in vorliegender Fassung neu errichtet
worden.
Dresden, am 1. September 1923.

Lehmannsche Buchdruckerei, Dresden-N.

 Weitere Anmerkungen zur Transkription
Offensichtliche Fehler wurden stillschweigend korrigiert. Unterschiedliche
Schreibweisen von Ortsnamen wurden beibehalten. Die Darstellung der Ellipsen
wurde vereinheitlicht.
 *** END OF THE PROJECT GUTENBERG EBOOK
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