Anatomy and Physiology An Integrative Approach 2nd Edition Mckinley Solutions Manual Full Chapter PDF

Anatomy and Physiology An Integrative
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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 there 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
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 a 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.
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.
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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 be 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 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.
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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
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, 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 the 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 than 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.
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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 has been reset into its resting 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.
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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 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.
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 to 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 that the process of covering binding sites after a contraction is the basis of 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 of 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.
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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 to
lysosomal release of enzymes which break down 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.
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 re -form 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 (Kreb’s 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 can 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 convert
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 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.
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 muscle
fibers it innervates.
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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 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 stimulus.
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 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.
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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 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 cross-bridge cycling; elevated inorganic
phosphate levels (Pi) in the sarcoplasm due to excessive ATP breakdown can interfere with Pi
release from the myosin head; also, low amounts of calcium ions in the sarcoplasmic reticulum
can cause 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; 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 glycogen 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.
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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 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 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.
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.
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k. Explain that the myofilaments of smooth muscle differ in some ways from 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.
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.
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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.
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. (p. 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 waking 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. 333–341)
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.
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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 aponeuroses.
7. A sheet of dense irregular connective tissue external to the epimysium that separates
individual muscles is called deep fascia or visceral fascia.
8. Fascia composed of areolar connective tissue and adipose tissue separating muscle from skin
is called superficial fascia.
9. Skeletal muscle composed of a network of blood vessels delivering both oxygen and a
nutrient to muscle fibers while eliminating waste products is termed vascularized.
10. Skeletal muscle is innervated or connected to and controlled by motor neurons.
11. Extending from the brain and spinal cord to muscle fibers are motor neurons, each having a
long branched extension at its terminal end called an axon, or nerve fiber.
12. Skeletal muscle contains neuromuscular junctions which exist between axons and muscle
fibers and is considered voluntary muscle, as it is consciously controlled by the nervous
system.
B. Microscopic Anatomy of Skeletal Muscle (pp. 334–338)
1. Cytoplasm of muscle fibers containing typical cellular structures is called the sarcoplasm.
2. Skeletal muscle fibers are approximately 10–500 micrometers in length, multinucleated, and
contain myoblasts, or groups of embryonic cells.
3. Satellite cells do not fuse with muscle fibers during development, but instead remain in the
tissue until triggered to differentiate due to muscular injury.
4. The skeletal muscle fiber, plasma membrane, is called the sarcolemma.
5. T-tubules, or transverse tubules, are a network of membranous tubules or deep invaginations
of the sarcolemma.
6. Sodium/potassium pumps are located along the length of the sarcolemma and establish the
resting membrane potential based on the unequal distribution of sodium and potassium ions,
since sodium concentration is greater outside and potassium is greater inside.
7. Resting membrane potential accounts for the excitability of muscle fibers.
8. Voltage-gated sodium channels and voltage-gated potassium channels are located along the
sarcolemma and establish the conductivity or electrical charge of that fiber.
9. The sarcoplasmic reticulum is an internal membrane complex which encases groups of
myofibrils, or contractile proteins.
10. Blind sacs located at each end of individual segments of the sarcoplasmic reticulum are called
terminal cisternae.
11. Terminal cisternae lie adjacent to each T-tubule and serve as calcium ion reservoirs.
12. A triad, the combination of two terminal cisternae and a central T-tubule, participates in
muscle contraction.
13. Two types of transport proteins, calmodulin and calsequestrin are located in the
sarcoplasmic reticulum and control the release of calcium ions, and thus muscle contraction.
14. 80% of muscle fiber volume is made up of myofibrils, long cylindrical structures,
approximately one to two micrometers in diameter that extend the length of each fiber.
15. Each myofibril contains bundles of protein filaments called myofilaments.
16. Two types of myofilaments exist, thick and thin.
17. Thick filaments are comprised of bundles of 200 to 500 myosin protein molecules and are
approximately 11 nanometers in diameter.
18. Myosin consists of two strands, with each strand having a head and a tail.
19. Myosin heads serve as binding sites for actin or thin filaments and sites where ATP attaches
and splits into ADP and phosphate by ATPase to generate the energy for contraction.
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20. Thin filaments are composed of two strands of actin protein and are approximately five to
six nanometers in diameter.
21. F-actin, filamentous actin, resembles two beaded necklaces intertwined, while G-actin,
globular actin, resembles individual beads and contains a feature called a myosin binding
site, where the myosin head attaches during muscle contraction.
22. Troponin and tropomyosin are regulatory proteins and make up the troponin-tropomyosin
complex.
23. Tropomyosin is a short, thin twisted filament that covers actin strands and myosin binding
sites of non-contracting muscle.
24. Troponin is a globular protein and binding site for Ca2+.
25. Sarcomeres are myofilaments within myofibrils, arranged in repeating cylindrical units
approximately two micrometers in length and composed of overlapping thick and thin
filaments.
26. Each end of a sarcomere is delineated by Z discs, or Z lines, positioned perpendicular to
myofilaments and anchor thin filaments.
27. I bands are bisected by the Z disc, contain only thin filaments, and are pulled past thick
filaments during maximal muscle contraction, at which point they disappear.
28. A bands, the central region of the sarcomere, contains the entire thick filament; thin
filaments only partially overlap the thick filaments.
29. H zones, or H bands, the most central portion of the A band in a resting sarcomere, consists
of only thick filaments and lack any thin filament overlap.
30. M lines are thin transverse protein networks in the center of the H zone, where thick and
thin filaments attach and are kept aligned during contraction and relaxation.
31. Overlapping myofilaments form light and dark regions, thus appearing striated due to size
and density differences of the thin and thick filaments.
32. Connectin, also called titin, is a combination of cablelike and springlike proteins that extend
from Z discs to M lines and functions to either stabilize and align thick filaments, or
compress during contraction to produce passive tension which will be released during
relaxation.
33. Nebulin is the actin-binding protein part of the I band that is proportional in length to thin
filaments and thus is responsible for thin filament length during sarcomere construction.
34. Dystrophin anchors myofibrils adjacent to the sarcolemma to proteins in the sarcolemma,
as well as internal myofilament proteins to external proteins.
35. Skeletal muscles have approximately 300 mitochondria performing aerobic cellular
respiration, myoglobin serving as an oxygen-binding molecule that also aids mitochondria in
the production of ATP and phosphate, which supplies ATP anaerobically.
C. Innervation of Skeletal Muscle Fibers (pp. 338–339)
1. Motor units are composed of a single motor neuron and the muscle fibers it controls.
2. Motor unit size has an inverse relationship with degree of control, such that the smaller the
motor neurons the greater the degree of control, as seen in eye muscles.
3. Motor unit muscle fibers are dispersed throughout the muscle rather than clustered and
produce a strong contraction in a localized area and weak contraction over a wide area.
4. Each muscle fiber has one neuromuscular junction, or specific location, in the mid-region of a
fiber where it is innervated by a motor neuron.
5. The expanded tip of an axon is called the synaptic knob, which enlarges and flattens,
covering a large area of sarcolemma as well as housing synaptic vesicles containing the
neurotransmitter acetylcholine within its cytosol.
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6. The synaptic knob contains calcium ion pumps that establish a concentration gradient,
maintaining more calcium ions outside the neuron than inside, and voltage-gated calcium
ion channels that allow calcium ions to flow down its concentration gradient.
7. The synaptic knob, due to its negative charge based on the presence of phosphate groups,
repels negatively charged vesicles.
8. A specialized region of the sarcolemma, containing numerous indentations and junction
folds which increase the membrane surface area covered by the synaptic knob, is called the
motor end plate.
9. The motor end plate has multiple Ach receptors, or plasma membrane protein channels, that
provide for the binding of Ach and thus the opening of these channels, allowing the entry of
sodium and exit of potassium.
10. A narrow, fluid-filled space separating the synaptic knob and motor end plate is called the
synaptic cleft.
11. The synaptic cleft houses the enzyme acetylcholinesterase, which breaks down Ach
molecules released into the synaptic cleft.
D. Skeletal Muscle Fibers at Rest (pp. 339–341)
1. At rest, the skeletal muscle cell’s membrane voltage is −90mV; this is the skeletal muscle
cell’s resting membrane potential.
2. Since no acetylcholine is being delivered to the muscle, the voltage-gated Na+ channels and
voltage-gated K+ channels in the sarcolemma and T-tubules are closed.
3. Calcium ion is stored within the terminal cisternae of the sarcoplasmic reticulum.
4. The contractile proteins (myofilaments) within the sarcomeres are in their relaxed position.
10.3 Physiology of Skeletal Muscle Contraction: A contracting muscle decreases in length as
thick and thin protein filaments within sarcomeres interact to cause sarcomeres to shorten.
(pp. 341–350)
1. During muscle contraction, muscle fiber decreases in length as thick and thin filaments cause
sarcomeres to shorten.
2. Tension exerted on the skeleton where muscle is attached generates movement of the body.
A. Neuromuscular Junction: Excitation of a Skeletal Muscle Fiber (p. 343)
1. Two events occur at the neuromuscular junction: Acetylcholine from a synaptic vesicle is
released and Ach binds to Ach receptors, which causes muscle fiber contraction.
2. Excitation-contraction coupling involves propagation of an action potential triggered by the
binding of Ach along the sarcolemma and T-tubules to the sarcoplasmic reticulum,
stimulating the release of calcium ions.
3. Crossbridge cycling involves calcium ion binding to troponin, which triggers the sliding of thin
filaments past thick and thus the shortening of sarcomeres and muscle contraction.
4. A nerve signal is passed down a motor axon, triggering the entry of calcium ions into the
synaptic knob, calcium ions then bind to proteins in the synaptic membrane, and this
binding of calcium ions with synaptic vesicles triggers the release of Ach into the synaptic
cleft.
5. Once Ach is released from the synaptic knob, Ach diffuses across the synaptic cleft in the
motor end plate and is available to bind with Ach receptors.
6. Clinical View: Myasthenia Gravis (p. 341)
a. Myasthenia Gravis is an autoimmune disease that occurs in about 1 in 10,000 people,
primarily women between 20 and 40 years of age.
b. Antibodies attach acetylcholine receptors on the muscle, causing them to cluster
together, which results in them being carried into the muscle cell by endocytosis; this
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loss of receptors leads to muscle weakness due to insufficient stimulation by

acetylcholine.
c. Some patients die quickly due to overall loss of physical stamina and some have a
normal life span.
B. Sarcolemma, T-tubules, and Sarcoplasmic Reticulum: Excitation-Contraction Coupling (pp. 343–
345)
1. Binding of Ach to Ach receptors in the motor end plate triggers the opening of channels that
allow for the rapid diffusion of sodium into the muscle fiber and slow diffusion of potassium
out.
2. End-plate potential is a reversal in polarity, whereby there is a reversal in electrical charge
difference at the motor end plate.
3. Action potential involves two events: depolarization, where an influx of sodium causes the
sarcolemma to become more positive, and repolarization, where the flow of potassium of
the sarcolemma returns the sarcolemma back to its original negative resting membrane
potential of −95 millivolts.
4. Repolarization allows the muscle fiber to generate a new action potential time and time
again when stimulated by a motor neuron.
5. The period of time between depolarization and repolarization when a muscle cannot be
restimulated is called the refractory period.
C. Sarcomere: Crossbridge Cycling (pp. 345−346)
1. When calcium is released from the sarcoplasmic reticulum and binds to globular troponin,
troponin changes shape, and the troponin-tropomyosin complex moves, exposing the
myosin binding sites of actin and thus crossbridge cycling is initiated.
2. Crossbridge cycling occurs in four steps: crossbridge formation, power stroke, release of
myosin heads, and reset of myosin heads.
3. Step one in crossbridge cycling, the process of myosin heads attaching to myosin binding
sites and forming a crossbridge between thick and thin filaments, is called crossbridge
formation.
4. Step two in crossbridge cycling, the process of myosin heads swiveling and pulling thin
filaments past thick filaments toward the center of the sarcomere, is called a power stroke.
5. During the power stroke process ADP and phosphate are released and the ATP binding site
once again is available.
6. Step three in crossbridge cycling involves the binding of ATP to the ATP binding site of a
myosin head, resulting in the release of the myosin head from the actin binding site.
7. Step four in crossbridge cycling involves the enzyme ATPase splitting ATP into ADP and
phosphate, resulting in a release of energy which will serve to reset the myosin head in a
cocked position.
8. Changes that occur in contracted muscle are: H zone disappearance, I band narrowing, and Z
discs in one sarcomere moving closer to one another.
9. The repetitive sliding movement of thin filaments past thick is called the sliding filament
theory.
D. Skeletal Muscle Relaxation (pp. 347–350)
1. Relaxation involves the returning of all muscle fibers to resting state when stimulation
ceases.
2. Muscle relaxation starts with nerve signal termination, therefore preventing further release
of Ach, while acetylcholinesterase continually hydrolyzes Ach in the synaptic cleft, thus
dissociating it from its receptor and terminating stimulation.
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3. The closing of Ach receptors at the end plate, motor end plate, action potential along the
sarcolemma and T-tubules causes cessation.
4. Following cessation; remaining calcium ions in the sarcoplasm are transported back into the
sarcoplasmic reticulum’s storage, troponin reverts back to its original shape following the
removal of calcium ions, and tropomyosin moves over the myosin binding sites on actin.
5. Clinical View: Muscular Paralysis and Neurotoxins (p. 345)
a. Muscular paralysis may occur due to either dysfunction at the neuromuscular
junction or a problem with excitation-contraction coupling.
b. There are two types of paralysis, a spastic paralysis or a flaccid paralysis; a spastic
paralysis is a paralysis where the muscles become excessively tight and motionless,
whereas a flaccid paralysis is where the muscles are motionless due to no muscle
tension.
c. Tetanus is a condition caused by a toxin produced by the bacterium Clostridium
tetani; the toxin inhibits the release of the inhibitory neurotransmitter glycine from
neurons in the spinal cord, thus leading to a spastic paralysis due to overstimulation
of the muscle.
d. Botulism is a condition caused by a toxin produced by the bacterium Clostridium
botulinum; the toxin inhibits the release of acetylcholine from the synaptic knobs,
thus leading to a flaccid paralysis due to inadequate stimulation of the skeletal
muscle.
6. Clinical View: Rigor Mortis (p. 350)
a. Rigor mortis is a condition that occurs at death when skeletal muscles become
excessively tight and hard due to a sustained contraction.
b. The condition is caused by nonproduction of ATP that occurs at death.
c. Without ATP, calcium ions cannot be pumped back into the sarcoplasmic reticulum,
thus they stay attached to troponin C, which prevents tropomyosin from covering
the myosin binding sites on actin.
d. Without ATP, the actin binding site on myosin also remains open, thus the actin and
myosin can lock together.
e. Though the actin and myosin are locked together there can be no contraction,
because there is no ATP to energize the contraction.
f. Rigor mortis only lasts for a certain amount of time because lysosomal enzymes in
the muscle open and cause destruction of the muscle.
g. Forensic pathologists can use the timing of rigor mortis and its resolution to
estimate the time of death of an individual.
10.4 Skeletal Muscle Metabolism: The energy for skeletal muscle contraction is provided by
ATP; the supply of ATP can be classified into an immediate supply, short-term supply, and
long-term supply. (pp. 350–352)
A. Supplying Energy for Skeletal Muscle Contraction (pp. 350–352)
1. The phosphagen system is an anaerobic system which generates ATP by use of high-energy
phosphate molecules.
2. ATPase hydrolyzes ATP into ADP and phosphate, providing the muscle fiber with
approximately five to six seconds of energy at maximum exertion.
3. Myokinase causes a yielding of ATP and AMP by transferring a phosphate from one ADP to
another.
4. Additional energy, ATP and creatine, are generated by creatine kinase transfer of phosphate
from creatine phosphate.
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5. The oxygen deficient metabolic process of generating two ATP molecules from the enzymatic
break down of glucose into two pyruvate molecules is called anaerobic cellular respiration,
or glycolysis.
6. Insufficient oxygen during aerobic cellular respiration causes buildup of pyruvate and thus a
buildup of lactic acid which will either be used by the heart as fuel to generate ATP or by the
liver to produce glucose by gluconeogenesis.
7. Aerobic cellular respiration occurs within the mitochondria, requires oxygen, and is fueled by
the pyruvate generated from anaerobic cellular respiration.
8. Aerobic cellular respiration involves the oxidation of pyruvate into carbon dioxide through
metabolic pathways and the citric acid cycle.
9. Pyruvate oxidation causes energy transfer to NADH and FADH2 as well as the generation of
ATP in the electron transport system, a process called oxidative phosphorylation.
10. Aerobic cellular respiration also generates ATP from fatty acids, its preferred fuel molecule;
the longer the fatty acid chain, the more ATP is generated.
11. Immediate ATP supply comes from the phosphagen system while short-term ATP supply
comes from anaerobic cellular respiration, and long-term ATP supply comes from aerobic
cellular respiration.
12. Exercise intensity and duration dictate which ATP supply will accessed.
13. Clinical View: Creatinine Kinase (p. 351)
a. Creatine phosphokinase is the enzyme that helps transfer a phosphate between
creatine and ATP.
b. Two different forms of this enzyme are found in cardiac muscle and skeletal muscle.
c. If a person suffers a heart attack (myocardial infarction), they will release an
increased amount of the cardiac form of the enzyme into the bloodstream, thus
assisting the diagnosis of a myocardial infarction.
d. If a person suffers significant damage to skeletal muscle or a degenerative muscle
disease, the skeletal muscle form of this enzyme will be released into the
bloodstream, thus assisting in the diagnosis of the disorder.
B. Oxygen Debt (p. 352)
1. Oxygen debt occurs when oxygen demand exceeds oxygen availability.
2. Oxygen debt requires that additional oxygen be inhaled post-exercise to restore pre-exercise
oxygen.
10.5 Skeletal Muscle Fiber Types: Skeletal muscle fiber types are organized into three primary
categories. (pp. 353–354)
A. Criteria for Classification of Muscle Fiber Types (p. 353)
1. Skeletal muscle fibers that compose a muscle are differentiated into three categories based
upon two criteria: (1) the type of contraction generated, and (2) the primary means used to
for supplying ATP.
2. Skeletal muscle fibers differ in power, speed, and duration of the muscle contraction.
3. Muscle contraction power relates to fiber diameter in that the larger the fiber, the more
powerful.
4. Muscle contraction speed depends on the number of fast-twitch and slow-twitch fibers the
muscle has.
5. Higher numbers of fast-twitch fibers result in increased muscle contraction speed.
6. Fast-twitch fibers contain fast a genetic variant of myosin ATPase, produce a powerful
contraction, initiate contraction quicker, and produce shorter contraction duration.
7. Oxidative fibers use aerobic cellular respiration and contain an extensive capillary network,
abundant mitochondria, and myoglobin.
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8. The ability of fibers to continue contracting for long periods of time without wearing out is
called fatigue-resistance.
9. Glycolytic fibers use anaerobic cellular respiration; they have a limited capillary network, few
mitochondria, and minimal myoglobin.
B. Classification of Muscle Fiber Types (pp. 353–354)
1. Slow oxidative fibers contain slow ATPase and large amounts of myoglobin, producing
slower, less powerful contractions.
2. Fast oxidative fibers contain fast ATPase and produce fast, powerful contractions.
3. Fast glycolytic fibers contain fast ATPase and produce both powerful and speedy
contractions, but can only contract for short bursts.
C. Distribution of Muscle Fiber Types (p. 354)
1. While muscles contain all three fiber types, muscle function determines what percentage of
each type the muscle will exhibit.
10.6 Measurement of Skeletal Muscle Tension: Muscle tension is the force generated when a
skeletal muscle is stimulated to contract. (pp. 354–356)
A. Muscle Twitch (pp. 354–355)
1. A single, brief muscle contraction and relaxation period in response to a single stimulus is
called a twitch.
2. Threshold is the minimum voltage required to cause a muscle twitch.
3. The delay period in a twitch after the stimulation, but before muscle contraction when there
is no fiber length change, is called the latent period.
4. The period where consecutive power strokes pull thin filaments past thick filaments and
sarcomeres are shortened is called the contraction period.
5. The passive process depending on the elasticity of connectin, in which crossbridges are
released and muscle tension decreases, is called the relaxation period.
B. Changes in Stimulus Intensity: Motor Unit Recruitment (p. 355)
1. Voltage increases cause a greater number of motor units to contract due to their variance in
sensitivity.
2. Recruitment, or multiple motor unit summation, involves the increase in muscle tension
occurring with an increase in stimulus intensity until maximum contraction is reached.
3. The all-or-none law states that, if and only if a stimulus is sufficient, will a muscle contract,
otherwise no contraction will take place.
C. Changes in Stimulus Frequency: Treppe, Wave Summation, Incomplete Tetany, and Tetany (pp.
355–356)
1. An increase in stimulus frequency causes greater muscle tension due to an insufficient time
for removal of all calcium ions from the sarcoplasm.
2. Increased stimulus frequency results in the formation of more crossbridges, stronger
contractions, and heat elevation, and thus more efficient molecular interactions such as the
activity of ATPase.
3. Treppe, or the ‘warming-up’ effect, is a stepwise increase in contraction strength.
4. Wave summation, or temporal summation, occurs when stimulation occurs so rapidly that
relaxation cannot take place before the next stimulation and, therefore, contraction waves
are added together.
5. Incomplete tetany occurs when tension increases and distance between waves decreases,
resulting in less time for relaxation between contractions.
6. Tetany occurs when muscle fibers ‘fuse’ and contractions become continuous without any
relaxation period.
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7. Muscle fatigue occurs when repetitive stimulation eventually causes a decrease in muscle
tension.
10.7 Factors Affecting Skeletal Muscle Tension Within the Body: There are several factors that
influence the actions of muscles with the human body, including resting tension in the
muscle, the relationship between muscle tension and resistance, how contraction force
generated is dependent upon myofilament overlap, and the factors that influence muscle
fatigue. (pp. 357–359)
A. Muscle Tone (p. 357)
1. Muscle resting tension generated by involuntary nervous muscle stimulation is called muscle
tone.
2. Resting muscle tone is the random contraction of small numbers of motor units that do not
produce enough tension for movement.
B. Isometric Contractions and Isotonic Contractions (pp. 357–358)
1. Isometric contraction occurs when muscle tension cannot overcome resistance, therefore,
muscles do not shorten and movement cannot take place.
2. Isotonic contraction occurs when muscle tension overcomes resistance, allowing for either
the shortening of muscles, called concentric contraction, or the lengthening of muscles,
called eccentric contraction, and thus movement.
3. Clinical View: Isometric Contraction and Increase in Blood Pressure (p. 357)
a. Sustained isometric contractions can lead to an increase in blood pressure.
b. Individuals with hypertension should be very careful when excessively performing
isometric exercises.
C. Length-Tension Relationship (p. 358)
1. The length-tension relationship is the degree of overlap between thick and thin filaments at
the start of contraction.
2. The length-tension curve is a graphical representation of the muscle tension related to its
pre-contraction resting length.
D. Muscle Fatigue (pp. 358–359)
1. Reduced ability or inability of a muscle to produce tension due to excessive or sustained
exercise and decreased glycogen stores is called muscle fatigue.
2. Insufficient calcium ions at the neuromuscular junction and decreased synaptic vesicle
numbers available for release of neurotransmitters cause a decrease in the ability of motor
neuron stimulation.
3. Fatigue may occur by excitation-contraction coupling when there is a change in ion
concentration, thus prohibiting fibers from conducting action potentials along the
sarcolemma.
4. Crossbridge cycling causes fatigue as increased phosphate concentration of the sarcoplasm
interferes with the release of phosphate from the myosin head.
5. Clinical View: Muscle Pain Associated with Exercise (p. 359)
a. The buildup of lactic acid in muscle has generally been accepted with the cause for
muscle pain after sustained exercise; this concept is changing.
b. Studies show that muscle pain after exercise is, in part, due to minor muscle tearing
and inflammation.
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10.8 Effects of Exercise and Aging on Skeletal Muscle: Exercise and aging both have effects on
skeletal muscles. (pp. 359–360)
A. Effects of Exercise (p. 358)
1. Exercise involving repetitive stimulation causes muscle hypertrophy, or an increase in muscle
size, mitochondria numbers, glycogen reserves, and myofibrils, and thus ATP production.
2. An increase in the number of muscle fibers is termed hyperplasia.
3. Atrophy is a decrease in muscle size due to a lack of exercise.
4. Fibrosis occurs when muscle mass is replaced by dense regular connective tissue, decreasing
flexibility and increasing collagen fibers.
5. Clinical View: Anabolic Steroids as Performance-Enhancing Compounds (p. 360)
a. Anabolic steroids are synthetic substances that mimic the actions of testosterone.
b. Over 100 different anabolic steroid preparations have been developed, but they all
require a prescription for legal use in the United States.
c. Anabolic steroids only have a few accepted medical uses—among them, the
treatment of delayed puberty, certain types of impotence, and the wasting condition
associated with HIV infection and other diseases.
d. Because anabolic steroids stimulate the manufacture of muscle proteins, these
compounds have become popular with some athletes as performance enhancers;
this form of usage is detrimental to an individual’s health for numerous reasons.
10.9 Cardiac Muscle Tissue: Cardiac muscle is located in the heart; a more extensive
description of the anatomy and physiology of cardiac muscle will be presented in the heart
chapter. (p. 360)
1. Cardiac muscle cells: are striated, longer than skeletal muscle cells, contain sarcomeres and
multiple mitochondria, are used for aerobic respiration, and are arranged in thick bundles
within the heart walls.
2. Intercalated discs are comprised of desmosomes, gap junctions, and one or two nuclei.
3. Cardiac muscle is controlled by the autonomic nervous system and stimulated by an auto
rhythmic pacemaker responsible for repetitious and rhythmic heartbeat.
10.10 Smooth Muscle Tissue: Smooth muscle is located throughout the body, typically
composing 2% of the body weight of an adult. (pp. 361–365)
A. Location of Smooth Muscle (p. 361)
1. Smooth muscle is located in the: vessels of the cardiovascular system, bronchioles of the
respiratory system, stomach, small intestines, large intestines of the digestive system,
ureters of the urinary system, and uterus of the female reproductive system.
2. Smooth muscle is capable of hypertrophy, increase in muscle size; and hyperplasia, increase
in number via mitosis.
B. Microscopic Anatomy of Smooth Muscle (pp. 361–362)
1. Smooth muscle cells are small with a diameter of approximately five to ten micrometers and
length of 50–200 micrometers, and are surrounded by an endomysium.
2. Smooth muscle sarcolemma contains multiple types of calcium ion voltage-gated channels
and chemically gated channels.
3. Intermediate filaments extend across the cell along with dense bodies, and anchor to the
plasma membrane.
4. The latchbridge mechanism allows myosin heads to ‘latch on’ to actin of thin filaments and
remain attached without additional ATP usage.
5. Two additional proteins are necessary for smooth muscle contraction, Ca2+-calmodulin
complex, and myosin light-chain kinase.
167
6. Calmodulin protein binds Ca2+, forming Ca2+-calmodulin complex, and MLCK enzyme is
activated by Ca2+-calmodulin complex to phosphorylate the myosin head of smooth muscle.
C. Smooth Muscle Contraction (pp. 362–364)
1. Smooth muscle contraction is initiated by Ca2+, requires ATP, and involves thin filaments
sliding past thick filaments.
2. Smooth muscle contraction has a maximum tension of approximately 500 milliseconds post
stimulation.
3. Smooth muscle must maintain a contracted state for extended periods of time to maintain
continuous tone in visceral walls such as the GI tract and blood vessels.
4. Smooth muscle is more fatigue-resistant than skeletal muscle in that it has low energy
requirements, and employs the use of the latchbridge mechanism, thus maintaining
contraction without the need for additional ATP usage.
5. Smooth muscle has a broader length-tension curve due to the fact that it is not limited by Z
discs preventing additional shortening, nor by a lack of myosin heads within its thick
filaments.
D. Controlling Smooth Muscle (p. 364)
1. Smooth muscle contraction and relaxation is not controlled voluntarily, but rather is
controlled by the autonomic nervous system in response to the release of a specific
neurotransmitter.
2. The stress-relaxation response occurs when smooth muscle is ‘stressed’ by being stretched
for extended periods of time, eventually inducing relaxation.
E. Functional Categories (pp. 364—365)
1. Multiunit smooth muscle contracts individually, whereas single-unit smooth muscle
contracts in unison, or syncytium.
2. Multiunit smooth muscle contraction is controlled by the number of motor units activated,
thus the more motor units stimulated, the more tension generated.
3. Single-unit smooth muscle, or visceral smooth muscle, is typically comprised of two to three
sheets, found in the walls of viscera, linked by gap junctions.
4. Single-unit smooth muscle stimulation by the autonomic nervous system occurs through
swellings, or varicosities, of the ANS neurons that pass close in proximity to smooth muscle
cells.
5. Diffuse junctions of single-unit smooth muscle are scattered and loosely arranged receptors.
DISCUSSIONS, IN CLASS VISUALS, AND DEMONSTRATIONS

1. Show models of the three types of muscle tissue.
2. Show a model of the sarcomere and the sarcoplasmic reticulum.
3. Using the SMART Board, show skeletal muscle excitability, muscle conductivity, muscle
contractility, muscle elasticity, and extensibility.
4. Discuss the importance (purposes) for the three noncontractile connective tissue coverings
around skeletal muscle tissue: epimysium, perimysium, and endomysium.
5. Using BIOPAC or other computerized systems, demonstrate and explain the actions of a muscle
twitch; using a computerized program, demonstrate the differences between an isotonic and
isometric contraction.
6. Chart the role of each anatomic structure associated with skeletal muscle contraction.
7. Use myography to discuss and demonstrate the three phases of muscle contraction; use the
gastrocnemius muscle of the frog if that capability is present in the lab.
8. Discuss skeletal muscle metabolism and rigor mortis.
168
9. Using the SMART Board, list the three types of muscle fibers based on their primary means to
supply ATP.
10. Discuss the frequency of stimulation to a skeletal muscle, as it relates to fused and unfused
tetany and treppe.
11. Using weights, demonstrate that the best lift is when the muscle is at its optimal sarcomere
length.
12. Discuss the importance of ‘warming-up’ the muscle before exercising.
13. Discuss the importance of stretching prior to some exercises.
14. Using PowerPoint slides, show and discuss the effects of skeletal muscle aging.
15. Using weights, demonstrate the time to muscle fatigue of slow-oxidative muscles versus fast
glycolytic muscles.
Related Media
Integral Anatomy Series: Volume 2 Deep Fascia and Muscle. DVD, Gil Hedleg, Ph.D.
Anatomy: The Muscular System. DVD, Classroom Productions.
Anatomy Muscles: Volume 2. DVD, Standard Deviants.
Muscle Tissue and Physiology. DVD, Minnay Institute of Health Sciences.
3D Anatomy: Resistance Training. Jeffrey M. Willardson.
Anatomy for Exercise. Primal Pictures.
Muscles; Films for the Humanities and Sciences. NIMCO.
Muscles and joints: Muscle power; Films for the Humanities and Sciences.
Anatomy and Physiology Revealed 3. McGraw-Hill.
Interactive Functional Anatomy. Denoyer-Geppert.
Muscle: Chemistry of Contraction. Insight Media.
169
Another random document with
no related content on Scribd:
Nu was de beurt aan den vroedsman Starkenbolte, een
Groningerlander, een rijk man en een fijn man; fijn in de kerk, en fijn
in de wereld. Toen diens beurt was om te spreken, zeide hij in zijne
eigene Groningerlandsche spreektaal: „Ik wijt nijt, ik leuf
Burgemeister! dat onze Meister Douwe nog geliik had het, dat et
nomentlik ’n Bosiliscus of ’n ploagbeest is, doar de Heere ons met
besuiken wil veur onze sonden en [25]ongerechtigheid, en al dat
goddelooze vlouken, dat in Dokkom doan wordt. Doarom hol ik mi
oan Meister Douwe.”
„Meister Douwe,” viel vroedsman Grada daarop in, „die het wel
eerder de planke mis weest. Ferleden jaar song er foor it bordtsje in
’e kerk: „Aller oogen wachten”, op ’n Karsmorgen.”
Bij dezen uitval begon de geheele raad van Dokkum te lachen, maar
de burgemeester niet. Die moest zijne deftigheid ophouden, en hij
sprak weêr:
„Als er dan niemand fan de Heeren is, die mij eenige inlichting in de
saak geven kan, soo laat dan eens de beide stadsboden boven
komen, of die ons in dit gefal ook nog souden kunnen dienen.”
De boden kwamen boven, en zagen een voor een in den korf. De

een was een stakker; hij durfde het beest niet bezien, en geloofde
ook steevast aan Meester Douwe. „Ik sil der miin oogen niet na
draaye, Heeren!” zei die man. „Want as it gien Basiliscus is, dan is it
’n plaaigbeest, die nachts omloope en pest en kwalen ferkondige, en
ik suud er foor weze om it heele beest met korf en al te ferbrannen.”
Maar de tweede stadsbode zei ronduit, dat het een kleermaker was,
omdat hij twee flinke scharen vooruit stak.
Toen werd er ook nog een kleermaker, een oude Duitscher, ten
raadhuize geroepen. Maar toen die man den kreeft in de mand zag
liggen, toen werd hij nog bleeker om zijne smalle kaken als tien
bleeke kleermakers met elkanderen, en hij riep het uit: „Gott beware,
Her Pirgemeister! soll mich die sweernoot straffen, wenn ich solchen
Peest langer in de Stadt von Dokkom tolden sollte. Et is de Teufel,
prave Herren! de lebendige Teufel. On wann ikke Pirgemeister war,
ik that den Hundsfot in de Graft gooyen on versupen him.”
„Heb ik it nijt seid,” zei vroedsman Starkenbolte, „dat we ’t hijr met de

kwoade te doun hebben? Dat komt nou van ’t vervlouken en ’t
koartspeulen, dat de noatie hyr dout; nou loat de Heere hem los, en
geeft hem an de kwoade over.”
„Ja,” zei vroedsman Inia, „as it de kwaaide is, dan is fersupen de

baais, want dan helpt gien ferbrannen, want die is fuurfast.”
En de heele Raad van Dokkum riep: „Fersupe mar, fersupe!” [26]De

turfdrager smeet den kreeft in de gracht, en de heele stad van
Dokkum was blijde. Maar de kreeft nog blijder.
Ettelijke jaren daarna, toen de kreeft al lang vergeten was, toen

vischten de Heeren van Dokkum de stadsgrachten met een’ zegen
af, en toen vingen ze onzen maat den kreeft weêr in hunne netten.
„Soo’n groote garnaait is der nog nooit in Europa fonnen, as dizze
hier in dit kleine Dokkum,” zei een hopman van de burgerwacht. „Die
sal ik bewaaire, soo lang tot Syn Hoochheit de Prins hier komt!” Hij
legde de kreeft (anders gezegd de groote garnaat van Dokkum), om
hem in ’t leven te houden, met een zilveren kettinkje vast in ’t water
onder eene brug.—
Nog heden ten dage pleegt men er de Dokkumers veelvuldig mede

te plagen, dat hun „groote garnaat” te Dokkum onder de „Syl” ligt,
dat is onder de breede, gewelfde steenen brug over het vaarwater
dat midden door de stad stroomt, en welke „Syl”, als een plein vlak
voor het Raadhuis gelegen, als ’t ware het middenpunt van de stad
uitmaakt. De Dokkumers zijn zeer gevoelig op dit punt; zij worden
wrevelig, als men er hen, met geveinsde belangstelling en ernst,
naar vraagt of hun „groote garnaat” nog wel veilig aan de ketting ligt.
Juist dien tengevolge worden ze daar nog altijd mede voor den gek
gehouden.
Buitendien, onder de Friesche steden lijdt Dokkum altijd veel

aanstoot. Het overoude, gansch niet onaardige, vroeger ook
bloeiende stadje, met herinneringen, in overblijfselen en in
overleveringen, aan Bonifacius, den Apostel der Friezen, moet in
Friesland de zelfde ongelukkige rol vervullen, die in de andere
Nederlandsche gewesten aan Kampen eigen is, evenals aan Büsum
in Noord-Friesland, aan Schilda en Krähwinkel in Duitschland, aan
de Pintschgau in Duitsch-Oostenrijk, aan Iglau in Bohemen, aan
Beaune in Frankrijk, enz. Van de Dokkumers vertelt men in Friesland
honderd en meer domme stukjes, zotternijen, uien, grappen en
grollen, de zelfde honderd en meer, die men elders van Kampen,
van Büsum, van Schilda vertelt, en nog honderd anderen bovendien.
Deze kluchten strekken nog steeds tot vermaak voor andere
Friezen, en worden nog steeds in vroolijke gezelschappen verteld,
vooral als er een Dokkumer bij is, en vooral als deze zich daarover
gekrenkt toont te zijn—zooals in den regel het geval [27]is. Wij willen
hier het leed der Dokkumers niet vermeerderen, en laten de domme
stukjes die men hen nahoudt, hier verder onvermeld, al zijn velen
daarvan ook nog zoo vermakelijk, en geschikt om geestig verteld en
lachende aangehoord te worden.
De Dokkumers zijn onder de Nederlanders de eenigen niet wier

bijnaam aan de garnaal is ontleend. Ook de ingezetenen van het
zeedorp Blankenberge in Vlaanderen, deelen in deze zaak hun lot.
Immers ook dezen dragen bij de andere Vlamingen den spotnaam
Geernaarts.
K l o k k e d i e v e n , dat is de bijnaam van de burgers van Franeker,
en zij dragen dezen leelijken naam om de onnoozele reden dat het
wapenschild hunner stad een gouden klok vertoont op een blauw
veld. Onschuldiger is wel niemand ooit aan eenen leelijken bijnaam
gekomen dan die van Franeker aan den hunnen. Zij dragen hem
echter niet alleen. Ook de ingezetenen van Oudewater, van Delfzijl,
van Schermerhorn en van Carolinensyl (Oost-Friesland) deelen hun
lot. Maar bij dezen moet eene andere oorzaak als te Franeker in het
spel zijn; immers op hunne wapenschilden prijkt er geen klok.
Ook andere Friezen, die van ’t eiland Ameland, moeten zich zulk
eenen oneerlijken spotnaam laten welgevallen, naar aanleiding van
het wapenschild hunner woonplaats. Het wapenschild van het
Ameland vertoont op de eene helft drie balken, op de andere eene
halve maan. Dies noemen de andere Friezen de Amelanders
B a l k e t s j e a v e n , B a l k e d i e v e n , en zingen hen ook dit
spotrijmke toe:
De Amelander schalken,
Die stalen eens drie balken,
’s Avonds in den maneschijn,
Daarom zal ’t hun wapen zijn.
Een schalk en een guit, dat is vrijwel het zelfde, volgens de

hedendaagsche beteekenis van deze woorden. En zoo heeten de
Amelanders niet enkel S c h a l k e n , ze heeten ook G u i t e n . Te
Holwerd, het Friesche dorp aan den vasten wal waar het hoofdveer
is op het Ameland, waar dus de Amelanders in den regel eerst voet
aan wal zetten, zingt de straatjeugd dien eilanders toe—in het
Friesch natuurlijk: [28]
De Amelanner Guten,
Dy komme hjir mei skuten:
Hja geane foar de finsters stean
En kypje troch de ruten.
Voor eenen Amelander is Holwerd, wat voor eenen Holwerder

Leeuwarden is, voor eenen Leeuwarder Amsterdam, voor eenen
Amsterdammer Londen. Als een Amelander jongmensch voor het
eerst aan den vasten wal komt, ziet hij daar zoo veel, dat zijne
nieuwsgierigheid grootelijks opwekt. Hij kan zich niet bedwingen, en,
gewend als hij is aan het vertrouwelijke, ongedwongene,
gemeenzame verkeer van de menschen onderling op zijn eiland,
gaat hij ook te Holwerd al te vrij voor de ramen der ingezetenen
staan om naar binnen in de kamer te turen.
Die van Workum heeten B r ĳ b e k k e n . De uitlegging van den

oorsprong van dezen spotnaam is tweeërlei. Sommigen meenen, dat
er van ouds onder de Workumers steeds velen geweest zijn, die de
letter r niet wel konden uitspreken, die dus behept waren met het
spraakgebrek dat men in Friesland brijen, en in Holland brouwen
noemt; en dat men deswegen den Workumers den spotnaam van
B r ĳ b e k k e n gegeven heeft. Anderen denken eenvoudig aan eene
bijzondere liefhebberij der Workumers voor het eten van brij. Welke
van deze twee meeningen nu de ware is, moet ik in het midden
laten. De eene reden is zoo waarschijnlijk of zoo mogelijk, als de
andere. Onder de Friezen, vooral onder de Friesche stedelingen, zijn
er steeds velen voor wie de goede uitspraak der letter r een
struikelblok is—meer in aantal dan elders in de Nederlanden het
geval is. Wijl dit spraakgebrek veelal erfelijk is, van ouder op kind
overgaat, zoo kan het zeer wel zijn dat er een tijd geweest is, waarin
een groot deel der Workumers brijde. En aan den anderen kant, brij,
de bekende melk- en meelspijze, is steeds eene zeer algemeen en
dagelijks gebruikte spijze bij het Friesche volk geweest; en is dit nog.
De Workumers deelen hunnen spotnaam met de Zwollenaars.
Immers de inwoners van Zwolle, ofschoon meest als
B l a u w v i n g e r s bekend, moeten zich toch ook den spotnaam van
B r ĳ b e k k e n laten welgevallen. En bij de Zwollenaars behoeft men
niet te twijfelen of hun spotnaam B r ĳ b e k k e n van het [29]brijen of
gebrekkig spreken herkomstig zij, dan wel van de bekende
volksspijze. De Zwollenaren brijen schier allen. Te Zwolle zijn
duizenden menschen, die de r niet goed uitspreken; ’t zij dan dat
deze gebrekkige uitspraak veroorzaakt wordt door eenig aangeboren
gebrek aan de spraakwerktuigen—’t zij dat bij dit brijen eenvoudig
nabootsing van anderen, of eenvoudig gewoonte in het spel is. In
der daad zijn er duizenden Zwollenaars die, als ze in Holland zijn, of
met Hollanders spreken, of anderszins bij andere gelegenheden
eens niet hunne aangeborene stadstaal willen spreken, maar
Hollandsch,—alsdan volstrekt niet brijen. Maar die anders, als ze in
hunne eigene stad zijn, of elders met stadgenooten spreken en dus
hunne eigenlijke, aangeborene, hunne ware moedertaal spreken,
terstond weer in die zonderlinge uitspraak vervallen. Zulk een echte
Zwollenaar zal in het eerste geval heel duidelijk b.v. Overijssel
zeggen, en in ’t andere geval zoo ongeveer Ovechiissel (Ovech-
iissel).
Hindeloopen en Staveren zijn twee hoogst merkwaardige stedekens.

Hindeloopen, wegens talrijke bijzonderheden en eigenaardigheden
in de taal, de kleeding, de zeden en gebruiken der ingezetenen,
waardoor ze zich van andere Friezen onderscheiden. En Staveren,
omdat het in de middeleeuwen eene welvarende, wijd vermaarde
handelstad was, als ’t ware de poorte des lands—ja meer! omdat
het, volgens de overlevering, de woonplaats is geweest der Oud-
Friesche koningen, omdat het de oudste hoofdstad is geweest van
het Land tusschen Flie en Lauwers. Het is wel opmerkelijk dat de
eigenaardigheden van het bijzondere Hindeloopen en van het Oud-
Friesche Staveren als ’t ware eenen weêrklank gevonden hebben in
de spotnamen, waarmede andere Friezen de ingezetenen dezer
steden noemen. Immers is (of was althans voor een 50-tal jaren nog)
de spreektaal der Hindeloopers, ofschoon oorspronkelijk goed Oud-
Friesch, toch voor andere Friezen ten deele onverstaanbaar, althans
moeielijk verstaanbaar,—hunne spotnamen (want ze hebben er wel
drie) zijn dit ook. Ik vind als spotnamen der Hindeloopers
aangegeven, volgens Halbertsma T h j e u n k e n of T j e e u n k e n
(Waling Dykstra spelt T j e u n k e n en zelfs T h é - u n k e n ) en
T h j o a t e n of Ts j o a t e n . Deze namen zijn bij het tegenwoordige
geslacht niet [30]meer in gebruik. Ik weet niet wat ze beteekenen,
noch ook wat hun oorsprong is, en niemand heeft mij dit ook kunnen
verkondigen, al hoe dikwijls ik er naar gevraagd, of er anderszins
onderzoek naar gedaan heb. Ook W. P. de Vries, in zijnen Lapekoer
trochskodde (Deventer, 1895), schrijft er van: „Ik haw in bulte war
dien om to witten to kommen hwat dizze wirden bitsjutte, mar it wier
om ’e nocht.”
De spot naam van de Hindeloopers, heden ten dage meest in

gebruik, is U i l e n (ûlen in het Friesch, ulen in den tongval der
stedelingen); sommigen echter zeggen hûlen, of huwlen volgens
Halbertsma’s spelling. Deze tweeërlei uitspraak is bij de nog
Friesch sprekende Friezen zeer vreemd, en komt anders nooit voor,
tenzij dan bij de Schellingers. Immers de letter h pleegt in den mond
der Friezen wel goed vast te staan, en geenszins te wankelen,
zooals bij Vlamingen en Zeeuwen, bij Flielanders en Zwollenaren en
sommige andere Nederlanders. En waarom de Hindeloopers dan
ûlen moeten heeten, of anders hûlen, heb ik ook niet kunnen
uitvorschen. Inderdaad, het schijnt wel of de Hindeloopers altijd en in
alles iets bijzonders moeten hebben, of iets vreemds. Het gaat niet
anders!
De lieden van Staveren, die oude Friezen, heeten
R i b b e k l i u w e r s —en dit is een naam, dien ik niet met een enkel
woord verdietschen kan. Bij hunne wedstrijden in het schaatsrijden,
rijden de Friesche hirdriders in voorover gebogene houding (mei de
noas op ’t iis, zooals de term luidt), al roeiende met de armen, alsof
dit molenwieken waren, met korte, krachtige, krassende streken,
geenszins met lange, sierlijke zwaaien, maar schier rennende,
scharrelende voort; en deze voor ’t oog zoo leelijke, maar snel
vorderende wijze van schaatsrijden heet in het Friesch kliuwe,
volgens den tongval der stedelingen klouwe. Oudtijds, in overoude
tijden, toen de hedendaagsche, maar ook reeds zeer oude ijzeren, in
hout gevatte schaatsen nog niet bekend en in gebruik waren, reed
men op het ijs, op beenderen, op pijpbeenderen uit de pooten, of
ook op de ribben van het rund. Zulke runderbeenderen, die den
ouden Friezen als schaatsen hebben gediend, glad afgeslepen op
hunnen vlakken kant door het schuren over ’t ijs, en met gaten
doorboord, waar men de riemen door stak, die dienden om ze aan
[31]den voet te bevestigen, vindt men nog wel in Friesland in den
bodem. Bij het slatten van vaarten en stroomen, bij het afgraven van
terpen, komen ze nog wel aan den dag. Natuurlijk was er, bij het
gebruiken dezer beenderen-schaatsen geen sprake van
schaatsrijden in den hedendaagschen zin met bevallige draaien, met
zwierige zwenkingen en zwaaien. Het kan niet anders dan een
onbevallig en onbeholpen kliuwen geweest zijn. Al is het nu eeuwen
en eeuwen geleden, dat de oude Friezen zich met zulke runder-
pijpbeenderen en runderribben op het ijs behielpen, de heugenis aan
deze zaak is nog steeds bij het Friesche volk in leven gebleven, zoo
als blijkt uit eene spreekwijze, nog heden in zwang. Een
overmoedige Friesche schaatsrijder daagt nog wel, al spottende en
snoevende, eenen anderen uit, in wedstrijd tegen hem te rijden om
het hardst of snelst, daarbij aanbiedende dat de tegenpartij op
gewone ijzeren schaatsen mag rijden, hij zelf daarentegen het wel
op koeribben zal doen. Zoo daagt ook, in het overschoone gedicht
van Dr. E. H. Halbertsma, „De Winter yn it Wetterlân”, een
overmoedige Friesche jongeling, Worp met name, de
Groningerlanders uit, tegen hem te rijden:
„Sa geide do d’útlitt’ne Woarp:

’k Wol ride om liif en libben,
’k Wol tsjin de bêste út jimm’ doarp,
Den ik op koueribben.” 6
En ook uit den spotnaam der inwoners van Staveren,

R i b b e k l i u w e r s , blijkt het gebruik dat de oude Friezen van zulke
beender-, van zulke ribbeschaatsen hebben gemaakt. Onder de
Friezen die in de vijfde eeuw, met Sassen en Angelen, in Brittanje
hunne volkplantingen stichtten, was dit rijden of kliuwen op
beenderschaatsen natuurlijk ook in gebruik; en zelfs heeft het, onder
hunne nakomelingen, de Engelschen, nog stand gehouden tot in het
laatst der vorige eeuw. Immers Dr. J. H. Halbertsma deelt ons
mede: „Het schijnt dat men in Friesland eertijds ook gebruik maakte
van koeribben; althans de zwetsers op het ijs, om hunne minachting
voor het rijden van eenen mededinger [32]uit te drukken, nemen aan
op koeribben tegen hem op ijzeren schaatsen om snelst te rijden. En
deze gissing is mij tot zekerheid geworden, toen de bedaagde pedel
van het antiquarisch kabinet te Newcastle mij verhaalde, dat hij in
zijne kindschheid op koeribben gereden had.” 7
Slooten is de laatste en de kleinste der Friesche steden, en de

inwoners van dit stadje hebben geenen bijzonderen spotnaam. Toch
blijven ze van spot niet vrij. Integendeel! De gebruikelijke
hoeveelheid hoon en smaad wordt hun door de andere Friezen
rijkelijk toegediend in een vierregelig rijmke.
Men verhaalt dat een gezelschap vroolijke en overmoedige
jongelingen (en espel biisfeinten), met elkanderen, des avonds laat,
den koster van de kerk te Slooten een bezoek bracht, en den man
zoo onthaalde op meêgebrachten sterken drank, dat hij daar
dronken van werd, ja zich aanstelde alsof hij stapel gek was. Dit
werkte aanstekelijk op het jonge volkje. Zij ontnamen den man den
sleutel van den kerktoren, klommen in den toren naar boven, en
verstelden het uurwerk, zoo dat het te middernacht zes ure zoude
wijzen en slaan. Toen weer naar beneden gaande, vonden ze
beneden in den toren, in het vertrekje dat den nachtwachter van het
stedeke tot verblijfplaats diende als hij zijne ronde had gedaan, dien
man slapende. Zij namen zijnen ratel, waarmede hij op zijne ronde
het uur verkondigde, al zingende: tsien ûre hat de klok! en verstaken
dien, waar de man hem niet zoude kunnen vinden. Ook, van kwaad
tot erger vervallende, namen zij zijnen toethoorn, waarmede hij den
dageraad verkondigde, en de burgerij wekte (des winters te zes ure),
en deden daarin iets wat er volstrekt niet in behoorde. Toen maakten
ze door eenig gedruisch den man wakker. Hij hoorde daarop de
torenklok zes ure slaan, en geheel verbijsterd denkende dat hij den
geheelen nacht doorgeslapen had, wilde hij zijnen ratel nemen, en
vond dien niet; nam zijnen hoorn, en wierp dien vol afschuw weer
weg; ging naar den koster, en vond dien gek van dronkenschap. In
vertwijfeling holde hij de straat op, roepende: [33]
Boargers fen Sleat, stean op! it is dei;

De hoarn is fol skyt, en de rottel is wei,
De koster is gek, en de toer is mal,
Ik wyt net hwet ik roppe sal!
Met dit rijmke worden nu nog steeds de ingezetenen van Slooten

geplaagd, alsof zij het kunnen helpen dat het oudtijds eens zóó is
toegegaan in hun stadje.
Hebben we hiermede de spotnamen van de elf steden van Friesland
(en nog van een Friesch eiland op den koop toe) afgehandeld, thans
zijn die van de Friesche dorpen en vlekken aan de beurt. Het aantal
dorpen in Friesland is zeer groot; maar onder die dorpen zijn er dan
ook velen die zeer klein zijn. Volgens de volksmeening zijn er 365
dorpen in Friesland: „sa folle doarpen as der dagen yn ’t jier binne”,
zegt men. En het getal spotnamen is weinig kleiner dan het aantal
dorpen is; immers schier ieder dorp in Friesland heeft zijnen
spotnaam. In der daad zijn er in geen ander Nederlandsch gewest
zoo vele spotnamen bekend en in gebruik als juist in Friesland. Dr.
J. H. Halbertsma zegt van deze zaak: „Dit sit yn ’t Frysce laech om
eltsjoar to narjen mei bynammen, dorp tsjin dorp, ind stæd tsjin
stæd. De Anglen ind Angelsaxen hienen dat eak hiem, ind de
scrandre Kemble het yn Sept. 1845 ien geleard stik foarlæzen yn it
Archaeological Institute of Great Britain to London, oer de by- ind
sceldnammen, dy de Angelsaxen eltsjoar joegen.” De Friezen zijn
dus met hunne spotnamen in oud en goed gezelschap.
Maar al zijn die spotnamen ook al oud en volkseigen, ze strekken

juist niet ter beschavinge des volks, noch ook ter bevordering van
vrede en eendracht, van goede verstandhouding en vriendschap.
Waling Dykstra schrijft hiervan: „Overal waren” (oudtijds in
Friesland) „befaamde vechtersbazen, die snoefden op hunne kracht
en dapperheid, en door velen werden gevreesd. De feesten waar ’t
jonge volk samenkomt om pret te hebben, bezochten zij met het
bepaalde doel om te vechten. Maar dan moest er eerst twist gezocht
worden, en hiervoor was gewoonlijk niets anders noodig dan het
noemen van den schimpnaam waarmeê de inwoners van een dorp
gebrandmerkt waren. Een [34]gezelschap jonge lieden van
Menaldum b.v. bezocht de kermis te Berlikum, en begon daar in de
herberg, ten aanhoore van de aanwezigen, te zinspelen op het
konsumeeren van honden. De Belkumers verstonden dat, en
kwamen spoedig tot het besluit dat die Menamer Beren voor hun
geschimp eens duchtig dienden afgerost te worden. Zoo ontstond
niet zelden een allerbloedigst gevecht, dat voor de belhamels
correctioneele gevangenisstraf ten gevolge had.”
In bonte rij wil ik die dorps-spotnamen hier opnoemen (voor zooverre

ze mij bekend zijn—immers daar zijn er zekerlijk nog veel meer).
Zoo heeten de ingezetenen van Berlikum H o u n e f r e t t e r s
(Hondevreters), bij verkorting H o u n e n (Honden). Ook die van
Peasens moeten den hondennaam dragen, maar dan in
verkleinvorm; men noemt ze Peasumer H o u n t s j e s (Hondtjes), in
tegenstelling met hunne buren, die van Wierum, die men K a t s j e s
(Katjes) noemt. Honden en katten behooren bij elkanderen, even
goed of even kwaad, als Peasumers en Wierumers, beide
visscherliên op de Noordzee, dus vrienden of vijanden al naar het
valt, medestanders tegenover de boeren van Ternaard en Anjum en
Metslawier, maar onderling tegenstanders. De Wierumer K a t s j e s
hebben hunne naamgenooten in de bewoners van het dorp
Winaldum, en in die van Baard, die beide K a t t e n heeten. Bij de
katten noemt men zoowel de ratten, als in ’t bovenstaande geval de
honden. Dies heeten dan de ingezetenen van Midlum, het dorp dat
het naaste bij Winaldum ligt, R o t t e n . Men heeft van deze
Winaldumer Katten en Midlumer Rotten zelfs een volksgezegde, dat
eigenlijk een raadsel is, maar waarvan ik de oplossing niet weet:
De Winamer Katten
Jeye de Mullumer Rotten
Troch de Harnser kloksgatten.
Verder heeten de ingezetenen van Warga B r ê g e b i d l e r s

(Bruggebedelaars), even als die van Heeg, omdat in deze plaatsen
op de bruggen tol placht geheven te worden. Die van Oldeboorn
heeten To e r m j i t t e r s (Torenmeters) en die van Tzum
L y n t s j e s n i d e r s (Lijntjesnijders); deze twee namen staan met
elkanderen in verband, zoo als verder in dit opstel zal worden
aangetoond. Die van Ureterp heeten O a n b r e i d e [35]H o a s e n
(Aangebreide Kousen), en die van Eernewoude L u z e k n i p p e r s .
Dit is een leelijke naam, die de Eernewoudsters als onzindelijke en
vuile menschen voorstelt, ’t welk bij de Friezen, die zindelijkheid en
reinheid zoo hoog in eere houden, eene groote blaam is. De
Eernewoudsters nemen het dan ook driedubbel kwalijk, als ze met
hunnen bijnaam genoemd worden, en juist daarom is hun
schimpnaam meer bekend en wordt meer genoemd dan met die van
de bewoners der naburige plaatsen het geval is. Volgens het
volksverhaal zoude ’t geheele dorp Eernewoude zoo dik in ’t
ongedierte zitten, dat dit er zelfs den toren bedekt. Als het dan
kermis wezen zal te Eernewoude, en de Eernewoudsters zich
zelven, hunne kleeding en hunne huizen wat opknappen tegen dien
tijd, wordt het ongedierte dan ook vooraf met bezemen van den
toren geveegd. En zoo hijschen dan de overmoedige jongelieden uit
Leeuwarden en Grouw, die des zomers, al spelevarende, met hunne
jachten en boeiers op de breede stroomen langs Eernewoude zeilen,
wel eenen bezem in den mast van hun vaartuig, tot eene
stilzwijgende beschimping; even als ze des winters te Bolsward op
de gracht wel met oliekoeken op de schaatsen rijden (zie bladzijde
19 hiervoren). En even als de Bolswarders door die oliekoeken, zoo
worden de Eernewoudsters dan door dien bezem in den mast, in
helle woede ontstoken en tot wraak geprikkeld, die dan in vervolging
en beschimping van de beleedigers, en zelfs in vechtpartijen, soms
te water, als in een zeeslag, voldoening eischt en vindt.
De inwoners van Arum heeten M o u d e k r û p e r s (Kruipers in het

stof van den weg), en die van de naburige dorpen Pingjum en
Kimswerd noemt men ook wel zoo. Deze bijnaam, die nog al
raadselachtig is, schijnt dus aan den geheelen noordwestelijken
hoek van Wonseradeel eigen te zijn. De ingezetenen van Blija noemt
men B e l l e f l e u r e n , die van Holwerd R o e k e f r e t t e r s
(Roekevreters), die van Marrum G i b b e n (Wilde duiven,
Veldduiven), van Hallum K o e k e f r e t t e r s (Koekvreters), van
Stiens R o t t e n (Ratten), als die van Midlum; van Hijum
S k i e p e b i n g e l s (Schapebengels), van Britsum
K e a l l e k o p p e n (Kalfskoppen), van Rinsumageest
H o u n e w i p p e r s (Hondewippers), [36]van Kollum
K a t t e f r e t t e r s (Kattevreters), van Ternaard B a r g e s t r û p e r s
(Varkenvilders), van Hantum M a r g e - i t e r s (Merg-eters), van
Birdaard S k i e p e k o p p e n (Schaapskoppen), van Grouw
Ts j i i s f o r d o u n s e r s (Kaasverdansers), van Irnsum
K a t t e k n e p p e l d e r s (Katteknuppelaars), van Akkrum
S k y t s t o e l e n (men zie de verklaring van dezen naam verder in
dit opstel), van Makkum S t r â n j u t t e n en M i i g e n (ook deze
namen worden verder in dit opstel nader verklaard), van Wirdum
To e r k e f r e t t e r s (Torentjevreters), van Menaldum Beren, van
Finkum F l i n t e r s (Vlinders), van Sint-Jacobi-Parochie
R a m m e v r e t e r s , van Sint-Anna-Parochie R a a p k o p p e n , van
Onze-Lieve-Vrouwen-Parochie W o r t e l k o p p e n , van Oude
Bildtzijl V l a s h a l e n (Vlasstengels)—deze vier laatstgenoemde
namen worden niet in het Friesch gesproken, noch door mij
geschreven, maar in het Nederlandsch, omdat op het Bildt, de
grietenij waarin deze vier plaatsen gelegen zijn, niet het Friesch de
volksspreektaal is, maar een Oud-Hollandsch, met Friesch
vermengd dialect.
Verder heeten de ingezetenen van Lekkum M i e u w e n (Meeuwen),

van Tietjerk B i i z e s n i d e r s , van Garijp K l i t s e f r e t t e r s , van
Suameer S a m a r i t a n e n , van Bergum K o u s t i r t e n
(Koestaarten), van Oostermeer B r o e k o p h â l d e r s
(Broekophouders), van Eestrum O k s e n (Ossen), van Veenwouden
G l e a u n k o p p e n (Gloedkoppen, Heethoofden), van de Valom,
een gehucht in Dantumadeel, G n o b ; van Buitenpost B r i m s t e r s ,
van Kollumerzwaag H y n g s t e f i l d e r s of H y n g s t e s t r û p e r s ,
(Paardevilders), van de Rottevalle G l ê s d r a g e r s , van Drachten
K e a l l e s t i r t e n (Kalverstaarten) en B ô l l e n (Wittebrooden), van
Boksum K n e p p e l d e r s (Knuppelaars), van Beetgum
S k i e r r o e k e n (Bonte Kraaien), een naam dien ze gemeen
hebben met die van Balk; van Dronrijp S l e e p s l o f f e n , van
Minnertsga K e a l l e b o u t e n (Kalfsbouten), van Lollum
S t i p p e r s , van Pingjum B e a n n e h û l e n (Boonehullen), van
Spannum E a r t e p û l e n (Erwtepeulen), van Winsum
S p i n s e k k e n (Spinzakken), van Baayum E a r t e p o t t e n
(Erwtepotten), van Ooster-Littens R o p e i n e n (Roepeenden), van
Jorwerd D w e i l s t i k k e n , van Weidum W y n h o u n e n
(Windhonden), van Hilaard P r o m m e n (Pruimen), van Molkwerum
Ts j o e n s t e r s (Heksen of Toovenaars), [37]van Warns
S k i e p e l o a r t e n (Schapekeutels), van Woudsend
D r i u w p ô l l e n (Drijvende eilandjes—zooals er in de meren en
stroomen rondom Woudsend wel voorkomen), van Koudum
B e a n t s j e s (men spreekt uit: Bjentsjes) of ook S i i k e
i e r d a p p e l s (Boontjes of zieke aardappelen); van Achlum
F j û r s k i t e r s , (Vuurschijters), van Idsegahuizen
B e a n n e f r e t t e r s (Boonevreters), van Gaast O t t e r f r e t t e r s ,
van de Gaastmeer B l ĳ e n , van de Joure K l i e n r o g g e n (kleine,
zoete broodjes van rogge gebakken; aan de Joure bijzonder eigen),
van Langweer D y k w o a r t e l s , (Dijkwortels, een groot en grof
soort van wortels of peeën). Eindelijk de inwoners van het vlek
Heerenveen noemt men P o e h o ä n n e n , dat een bijnaam is voor
hoogmoedige en opgeblazene, veel drukte en beweging makende
menschen.
Elke naam, die onder menschen gegeven en gedragen wordt, heeft
eenen oorsprong, eene reden van bestaan, eene beteekenis. Dit is
zonder twijfel ook met alle deze spotnamen het geval, maar—die
oorsprong, die beteekenis is geenszins meer bij alle namen bekend.
Integendeel, het grootste gedeelte dezer namen is duister van
oorsprong en beduidenis. Wie weet er onder de hedendaagsche
Friezen waarom bijvoorbeeld de ingezetenen van Langweer
D y k w o a r t e l s heeten, die van Bergum K o u e s t i r t e n , die van
Britsum K e a l l e k o p p e n ? Waarom de Lekkumers M i e u w e n ,
de Marrumers G i b b e n , de Balksters en de Beetgumers
S k i e r r o e k e n heeten? En die van Arum M o u d e k r û p e r s , van
Hijum S k i e p e b i n g e l s , van Pingjum B e a n n e h û l e n ?
De huislieden te Warns houden, of hielden, veelal een melkschaap

op het erf hunner woning (’t welk trouwens in Friesland in ’t
algemeen gebruikelijk is bij de geringe burgerij ten platten lande);
des avonds en des morgens verzamelen ze de schapekeutels, ten
deele om het erf zindelijk te houden, ten deele om die keutels als
mest te gebruiken op de hooge, zandige akkers van hun dorp.
Daarom hoont men die van Warns met den naam van
S k i e p e l o a r t e n , (Schapekeutels).
De oude vrouwen te Winsum sponnen oudtijds, en nog in het begin

dezer eeuw, veelvuldig het garen voor de wevers te Franeker; zij
brachten dan het gesponnen garen in groote zakken naar [38]die
naburige stad. Dies noemt men de Winsumers S p i n s e k k e n . Hoe
eenvoudig, hoe huiselijk was toen nog de nijverheid! De wevers
betaalden het spinloon aan die oude vrouwen niet altijd in geld. Zij
betaalden haar wel met levensbehoeften, met allerlei
benoodigdheden des dagelijkschen levens, vooral met het spek van
hunne eigengeslachte varkens. Vandaar dat het Friesche volk zulk
ruilverkeer, met een aardig, zeker overoud stafrijm noemt: spek om
spinnen. Hoe eenvoudig, hoe huiselijk was toen nog de handel!
De kermis te Hilaard valt in den tijd dat eerst de pruimen rijp zijn en
ter markt komen. Zoo is die smakelijke, bij de Friezen zeer beminde
vrucht alsdan veelvuldig te Hilaard te koop, en zoo moeten
dientengevolge de Hilaarders het geheele jaar door P r o m i t e r s
(Pruimeneters) of enkel P r o m m e n (Pruimen) heeten. Ook de
kermis van Irnsum valt in dien zelfden tijd van het jaar. De
Grouwsters trekken dan naar het naburige dorp Irnsum om kermis te
houden, en pruimen te koopen; zij noemen de Irnsumer kermis dan
ook steeds Jinsumer Prommerk (Irnsumer Pruimenmarkt—merke of
merk is het Friesche woord zoowel voor kermis als voor markt.)
Maar de eigenlijke spotnaam van de Irnsumers is

K a t t e k n e p p e l d e r s (Kattenknuppelaars), en ook deze naam
hangt met de Irnsumer kermis samen. Oudtijds, en nog in het begin
dezer eeuw, bestond eene der zoogenoemde vermakelijkheden, die
bijzonderlijk de Irnsumer kermis den volke bracht, in het
katteknuppelen—een barbaarsch spel van afschuwelijke
dierkwellerij, dat met het hondewippen, het aaltrekken en het
ganzesabelen thans (ofschoon dan ook nog maar sedert korten tijd),
gelukkig volkomen tot het verledene behoort, en nergens meer wordt
uitgeoefend. Midden aan een touw, tusschen twee boomen of
tusschen de topgevels van twee tegenover elkanderen staande
huizen dwars over den weg gespannen, werd een biertonnetje
bevestigd, waarin men eene kat besloten had. Door het spongat
kreeg de kat lucht, en uit het spongat klonken weldra hare
angstkreten omhoog. De jongelingen en jonge mannen, om hunne
vaardigheid in het mikken te toonen, smeten dan met knuppels naar
het hangende tonnetje. Wien het gelukte met zijnen knuppel eenen
van de niet al te vast bevestigde bodems van het tonnetje uit te
smijten, of anders te verbrijzelen, had het spel en den
[39]uitgeloofden prijs gewonnen. Als de bodem uitgesmeten was,
sprong de arme, verbijsterde kat uit het tonnetje, en kwam, naar
kattenaard, veelal ongedeerd, ofschoon in doodsangst, op hare vier
pooten, op den weg terecht, onder het gejuich der knuppelaars en
der toeschouwers, die haar nog menigen knuppel op hare vlucht
nasmeten. Men begrijpt, de oude moedertjes te Irnsum hielden
tegen den tijd dat de kermis kwam, wijsselijk hare poesjes in huis
opgesloten.
Naar eene soortgelijke, als vermakelijkheid geldende

dierenmishandeling dragen ook de ingezetenen van het dorp
Rinsumageest hunnen spotnaam, die in deze gevallen wel een
schandenaam heeten mag. Als het kermis was te Rinsumageest—
eene van ouds vermaarde kermis, waar de lui uit de
Dokkumerwouden en uit Dokkum in groote scharen heentrokken—
had men op den voormiddag van den dag, voor de feestelijke (?)
hondewipperij bestemd, alle honden die men machtig kon worden, in
eene schuur bij elkanderen verzameld. Dan gingen twee jongelingen
tegenover elkanderen aan weêrszijden van den dorpsweg staan,
midden in het dorp, voor de herberg. Zij hielden een zeel of reep
(platgevlochten touw) strak gespannen laag over den weg. Langs
beide zijden van den weg tusschen de schuur en de herberg, stond
het volk in gesloten gelid geschaard. Dan werden de honden uit de
schuur losgelaten, een voor een, en tusschen de dubbele
menschenhaag door over het gespannen zeel gejaagd, waarbij de
arme dieren door het gegil der wreede menschen geheel verbijsterd
werden. Op het oogenblik dat de hond over het zeel liep of sprong,
werd dit plotseling met eenen forschen ruk omhoog getrokken,
zoodat de hond met kracht omhoog geslingerd, gewipt werd, soms
zeer hoog, hoe hooger hoe mooier—om daarna, al jankende, met
een smak weêr op den weg neêr te vallen, en soms, anders als de
katten te Irnsum, pooten, ribben of nek te breken. Waling Dykstra
vermeldt dat er bij dit feest eene vlag, waar de hondewipperij op
afgebeeld stond, uit de herberg hing, en dat, naar hij meende, die
vlag nog in 1882 te Rinsumageest bewaard werd. Naar dit wreede
spel, dat nog omstreeks de helft dezer eeuw alle jaren met veel
omhaal en drukte op de kermis te Rinsumageest vertoond werd,
dragen de ingezetenen [40]van dat dorp nog heden hunnen bijnaam
Hounewippers.
De kerktoren van het dorp Tzum is zeer hoog; volgens de

volksmeening is hij de hoogste toren van Friesland. De hooge toren
van de oude Sint-Martens-kerke in het naburige Franeker is eene
Deventerkoeks-lengte lager, zegt het volk. In de 17de eeuw zoude te
Oldeboorn een nieuwe kerktoren gebouwd worden. In dat groote en
schoone, van ouds reeds aanzienlijke dorp wilde men nu ook eenen
bijzonder fraaien toren bij de kerk hebben; en niet alleen de fraaiste
—het moest ook de hoogste toren van Friesland worden, hooger nog
dan de Tzummer toren. De Boornsters vaardigden dus twee man uit
hun midden af naar Tzum, om den Tzummer toren te meten, ten
einde daarnaar het bestek van hunnen eigenen nieuwen toren te
kunnen maken. Die Boornster mannen maten dan ook den Tzummer
toren, en berekenden zijne hoogte, en, toen ze daarmede klaar
waren, gingen ze in de herberg te Tzum wat rusten en zich
verkwikken met spijs en drank, eer ze weêr op de t’huisreis gingen
naar Oldeboorn. Maar de Tzummers, die de eere van hun dorp niet
wilden prijsgeven, de eere van den hoogsten toren des lands te
hebben, sneden onderwijl in de herberg listiglijk een paar ellen af
van het touw (it lyntsje, lijntje), dat de Boornsters als torenmaat
mede naar huis nemen wilden. De Boornsters bemerkten niet, hoe
de Tzummers hun, in den letterlijken zin des woords, te kort gedaan
hadden; zij kwamen met de maat van den Tzummer toren t’huis (met
de goede maat, zoo ze meenden), en bouwden in hun dorp eenen
nieuwen toren, die nog eene el hooger was, als hunne maat aangaf.
En een fraaie toren met opengewerkte spits was het, ook een hooge
toren—en zoo staat hij nog heden ten dage, een sieraad van het
dorp Oldeboorn. Ja, maar in stede van de hoogste toren van
Friesland te zijn, hooger dan de Tzummer toren, was hij integendeel
nog eene el lager. In het begin hielden de Tzummers zich stil. Maar
toen de Boornster toren kant en klaar was, brachten ze, vol vermaak
in het leed van anderen, zelve hun schelmstuk uit.
Sedert heeten die van Oldeboorn To e r m j i t t e r s (Torenmeters),

en die van Tzum L y n t s j e s n i d e r s .
De ingezetenen van het dorp Grouw hebben den naam van een
vroolijk en levenslustig volkje te zijn, en gaarne, als het, [41]pas of
ook geen pas geeft, eens een deuntje te dansen. Oudtijds was daar
eens een gezelschap jongvolk bijeen, en, wijl er juist dien dag een
reizende speelman in het dorp gekomen was, die daar ook
overnachten zoude, zoo brachten de jongelui dien man in de
herberg, en weldra kwamen de beenen van den vloer, en draaiden
en zwaaiden ze lustig rond. De speelman moest betaald worden, en
dat deden de Grouwsters ook. Maar zij hadden nog van dansen niet
genoeg; al weêr en al weêr moest de speelman vedelen, tot laat in
den avond, tot middernacht. Eindelijk had niemand van het
gezelschap nog geld in den zak, om den vedelaar te betalen. Maar
een van de jongelingen, de zoon van eenen kaaskoopman, wist wel
raad. Hij haalde uit zijns vaders pakhuis eene groote nagelkaas, om
die den speelman als loon te geven. Deze nam daarmede gaarne
genoegen—maar of de vader, des anderen daags, toen het geval
uitkwam, dit ook deed, meen ik te moeten betwijfelen.
En sedert heeten de Grouwsters Ts j i i s f o r d o u n s e r s ,

Kaasverdansers.
In der daad is men te Grouw, spoediger dan wel elders in Friesland,

klaar met een dansje. In de jaren 1864 en ’65, toen ik als
levenslustig jongeling veel te Grouw verkeerde, en onder de
Grouster fammen eene trouwe verloofde, eene lieve bruid had, werd
daar veel gedanst bij ’t gezellig samenzijn van het jongvolk, en het
devies Efternei dounsje, in Friesland zoo bekend, werd daar toen
strijk en zet toegepast bij elke feestelijke volksbijeenkomst, van

Anatomy and Physiology An Integrative Approach 2nd Edition Mckinley Solutions Manual Full Chapter PDF

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Anatomy and Physiology An Integrative Approach 2nd Edition Mckinley Solutions Manual Full Chapter PDF

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Anatomy and Physiology An Integrative

Approach 2nd Edition McKinley

CHAPTER 10: Muscle Tissue

KEY POINTS TO EMPHASIZE WHEN TEACHING THE BIOLOGY OF

1. List and explain the functions of skeletal muscle.

c. Explain and describe skeletal muscle contractility.

u. Explain and discuss myoglobin.

ADDITIONAL TOPICS FOR DISCUSSION

3. Further discuss dystrophin in terms of muscular dystrophy.

SUGGESTED CHAPTER OUTLINE

loss of receptors leads to muscle weakness due to insufficient stimulation by

DISCUSSIONS, IN CLASS VISUALS, AND DEMONSTRATIONS

De boden kwamen boven, en zagen een voor een in den korf. De

„Heb ik it nijt seid,” zei vroedsman Starkenbolte, „dat we ’t hijr met de

„Ja,” zei vroedsman Inia, „as it de kwaaide is, dan is fersupen de

En de heele Raad van Dokkum riep: „Fersupe mar, fersupe!” [26]De

Ettelijke jaren daarna, toen de kreeft al lang vergeten was, toen

Nog heden ten dage pleegt men er de Dokkumers veelvuldig mede

Buitendien, onder de Friesche steden lijdt Dokkum altijd veel

De Dokkumers zijn onder de Nederlanders de eenigen niet wier

Een schalk en een guit, dat is vrijwel het zelfde, volgens de

Voor eenen Amelander is Holwerd, wat voor eenen Holwerder

Die van Workum heeten B r ĳ b e k k e n . De uitlegging van den

Hindeloopen en Staveren zijn twee hoogst merkwaardige stedekens.

De spot naam van de Hindeloopers, heden ten dage meest in

„Sa geide do d’útlitt’ne Woarp:

En ook uit den spotnaam der inwoners van Staveren,

Slooten is de laatste en de kleinste der Friesche steden, en de

Boargers fen Sleat, stean op! it is dei;

Met dit rijmke worden nu nog steeds de ingezetenen van Slooten

Maar al zijn die spotnamen ook al oud en volkseigen, ze strekken

In bonte rij wil ik die dorps-spotnamen hier opnoemen (voor zooverre

Verder heeten de ingezetenen van Warga B r ê g e b i d l e r s

De inwoners van Arum heeten M o u d e k r û p e r s (Kruipers in het

Verder heeten de ingezetenen van Lekkum M i e u w e n (Meeuwen),

De huislieden te Warns houden, of hielden, veelal een melkschaap

De oude vrouwen te Winsum sponnen oudtijds, en nog in het begin

Maar de eigenlijke spotnaam van de Irnsumers is

Naar eene soortgelijke, als vermakelijkheid geldende

De kerktoren van het dorp Tzum is zeer hoog; volgens de

Sedert heeten die van Oldeboorn To e r m j i t t e r s (Torenmeters),

En sedert heeten de Grouwsters Ts j i i s f o r d o u n s e r s ,

In der daad is men te Grouw, spoediger dan wel elders in Friesland,

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