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Chapter 12- Muscles (Part 1)
Use this summary in addition to your EOC assignments and your LRG questions. Where indicated, you will need to fill in
some blanks and draw in representative diagrams found in your textbook. Please come by if you need help.
Types of Muscle Tissue
Skeletal Muscle Tissue - Attached to bones. Striated and voluntary.
Cardiac M.T. - Wall of heart. Striated and involuntary.
Smooth (Visceral) M.T. - In viscera, blood vessels, & arrector pili muscles. Non-striated (smooth) and involuntary.
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Functions of Muscle Tissue
Motion
 Move the body by pulling on bones of the skeleton.
 Heart pushes blood thru the circulatory system.
 Smooth muscle pushes food and solids through the digestive tract. It also regulates the diameter of small arteries and
causes piloerection (goose bumps).
Posture and body support
 Gives the body form and support around flexible joints.
 Certain muscles are active postural muscles whose primary function is to work in opposition to gravity. (Ever
experienced a “rubber neck-head bob”, while nodding off in class?)
Heat production
 Only 30-40 % of energy used from Glucose to make ATP; 60-70% lost as heat
 As you exercise strenuously, the rate of heat production increases immensely. (Ever jumped up and down to
keep warm?)
Characteristics of Muscle Tissue
EXCITABILITY (irritability) - ability to respond to certain stimuli by producing electrical signals called action potentials (impulses).
CONTRACTILITY - ability to shorten & thicken (contract), generating force to do work.
ELASTICITY - ability to be extended (stretched) w/o damage.
EXTENSIBILITY - ability to return to original shape after contraction or extension.
Motor Unit
= A single motor neuron may
innervate 10-2000 muscle
fibers (ave. 150)
Skeletal Muscle
Functions of Skeletal Muscle
 Highly specialized for contraction.
 Produces skeletal movement, range of motion, and generates force.
 Skeletal muscle contractions pull on tendons and move the bones of the skeleton.
 Effects range from simple motions (extending the arm) to highly coordinated movements (skiing, swimming, typing,
running).
 Stabilizing body positions.
 Tension in muscles also maintains body posture – holding the head in position when reading your physiology book
or balancing the weight of the body above your feet while walking from building to building on ASU’s campus.
 Without constant muscular activity you would not be able to sit upright at the Rambell’s basketball games without
collapsing into a heap or stand in line for a soda at the Ram’s football games without topping over.
 Support soft tissues.
 The abdominal wall and the floor of the pelvic cavity consist of layers of skeletal muscle.
 These muscles:
 Support the weight of visceral organs
 Shield internal tissues from injury
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Guard entrances and exits.
 Openings of the digestive & urinary tracts are encircled by skeletal muscle.
 These muscles provide voluntary control over swallowing, defecation, & urination.
Generation of heat & maintenance of body temperature.
 Muscle contractions require energy.
 Whenever energy is used in the body some of it is converted to heat.
 Heat released by working muscles keeps body temperature in the range required for normal homeostasis.
Somatic Motor Neurons
 A motor neuron transmits nerve impulse (ap’s) to skeletal muscles.
 Acetylcholine (ACh) release by motor neuron triggers a muscle action potential
Anatomy Review: Be sure to be familiar with the structure of skeletal muscle and the sarcomere: see figures 12-3 & 12-5 in your
text and draw the pictures below.
Sarcomere Organization
 Myofibrils are bundles of actin and myosin filaments.
o The actin is found in the thin filaments
o The myosine is found in the THICK filaments.
 Myofilaments are organized in repeating functional units called sarcomeres.
 A-band = the length of a typical THICK filament.
o Divided into several subdivisions:
o M line = THICK filaments linked with accessory proteins
o H zone = THICK filaments only
o Zone of overlap = Outer edge of A band, where THICK & thin filaments overlap
 I-band = extends from A-band of one sarcomere to A-band of adjacent sarcomere
o Thin filaments only
o Center contains Z-disk
 Z-disk = boundary line between adjacent sarcomeres (1 sarcomere extends from z-disk to z-disk)
o Attachment site for thin filaments
Thin Filaments (~5-6 nm diam.) = ACTIN
 Contains 3 different proteins, F-actin, tropomyosin, & troponin:
o F-actin = double twisted strand of 300-400 globular molecules of G-actin.
o G-actin contains active sites that are covered by strands of tropomyosin to prevent actin-myosin interaction during
muscle relaxation
o Tropomyosin is bound to one molecule of troponin midway along its length.
o A contraction cannot occur unless there is a change in the position of the troponin-tropomysin complex that exposes
the active site.
THICK Filaments = MYOSIN
 Contains a pair of myosin subunits twisted around one another
o Long attached tail bound to other myosin molecules
o Free globular head projecting outward toward the nearest thin filament.
 Head is hinged at its connection with the tail
 Also called a cross-bridge due to the connection formed with the thin filaments during contraction
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Titian & Nebulin
 Titian provides elasticity (returns stretched muscle to resting length) and stabilized the myosin by spanning the distance from
one Z disk to the next M line.
 Nebulin helps align actin.
Skeletal Muscle Physiology
 The force created by the contracting muscle is called the muscle tension.
 The load is a weight or force that opposes contraction of a muscle.
 For example, in order to pick up a book your muscle must generate enough muscle tension (force) to overcome load it is
trying to lift (the weight of the book)
 Also, you are unable to push over the wall of this building because the muscle tension (force) you are generating is not large
enough to overcome the load (weight of the wall) you are trying to push.
Neuromuscular Junction/Myoneural Junction
 Skeletal muscle fibers contract only under the control of the nervous system.
 Communication between the nervous system and skeletal muscle fibers occurs at NMJ’s.
Overview of Contraction-Relaxation
o The link between the generation of an action potential in the sarcolemma and the start of a muscle contraction is
called excitation-contraction coupling.
Steps
Events at the neuromuscular junction:
1. Action potential in somatic motor neuron arrives at axon terminal.
2. Voltage-gated calcium channels open. Calcium triggers exocytsosis
3. Causing synaptic vesicles to release ACh (acetylcholine)
4. ACh diffuses across the synaptic cleft at the NMJ and binds to nicotinic receptors on the sarcolemma
5. Sarcolemma depolarizes and causes a muscle action potential in the sarcolemma
Excitation-contraction coupling:
6. The impulse travels over the surface of the muscle cell where it is diverted into the interior of the cell through the Ttubules to the sarcoplasmic reticulum.
5. Calcium released from the SR into the sarcoplasm.
7. Ca++ ions combine w/ troponin causing it to pull on the tropomyosin and change its orientation, thus exposing the myosinbinding sites on actin.
Sliding Filament Theory:
8. Once the binding sites on actin are exposed upon the influx of calcium, the following events occur in rapid succession:
 Cross bridge attachment: The activated myosin heads are strongly attracted to the exposed binding sites on actin
and cross bridge binding occurs.
9. Power Stroke:
As a myosin head binds, it changes from its high-energy conformation (shape) to its bent, low-energy shape, which
causes the head to pull on the thin filament, sliding it toward the center of the sarcomere.
At the same time, ADP and inorganic phosphate (Pi) generated during the prior contraction cycle are released
from the myosin head.
10. Cross-bridge Attachment: As a new ATP molecule binds to the myosin head, the myosin cross-bridge is released from
actin.
11. “Cocking” of the Myosin Head. Hydrolysis of ATP to ADP and Pi by ATPase provides the energy needed to return the
myosin head to its high-energy, or “cocked,” position, which gives it the potential energy needed for the next
attachment-power stroke sequence. Now we are back where we started, the cycle is repeated, and the myofibrils
shorten.
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12. A single power stroke of all the cross bridges in a muscle results in a shortening of only about 1%. Since contracting
muscles routinely shorten 35% to 50% of their total resting length, it is obvious that each myosin crossbridge attaches and
detaches many time during the course of a single contraction.
It has been estimated that only half of the myosin heads of a thick filament are actively exerting a pulling force at
the same instant: the remaining are randomly seeking their next binding site.
Sliding of thin filaments continues as long as the calcium signal is present.
Removal of calcium ion from the sarcoplasm, by the sarcoplasmic reticulum, restores the tropomyosin inhibition,
contraction ends, and the muscle fiber relaxes.
13. Relaxation occurs when ACh is broken down by the enzyme acetylcholinesterase (AChE) and Ca++ is moved back into the
sarcoplasmic reticulum by active calcium transport pumps and a calcium binding protein called calsequestrin
14. Linkages between actin and myosin are disengaged.
15. Troponin and tropomyosin inhibt interaction between actin and myosin
16. Actin and myosin slide apart and muscle returns to resting length/relaxes aided by titian (at the moleclular level) and
connective tissue components.
Draw a summary diagram of these processes here (Use Fig. 12-9, 12-10, & 12-11 to assist you):
Rigor Mortis = state of muscular rigidity following death. Results from a lack of ATP to split myosin-actin cross bridges; therefore,
the muscles remain “locked” in a contracted state. (Ca++ leaks out to initiate troponin) (last about 24 hours).
Remember…it takes ATP for muscles to relax.
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Muscle Metabolism
On demand, skeletal muscle fibers can step up ATP production
Energy utilization:
 The primary function of ATP is the transfer of energy from one location to another, rather than the long-term storage of
energy.
 At rest skeletal muscles fibers produce more ATP than they need, and under these conditions ATP transfers energy to another
high-energy compound, creatine phosphate.
o This reaction can be summarized as:
 At rest ……….ATP from metabolism + creatine  ADP + creatine phosphate
 During a contraction each myosin cross-bridge breaks down ATP, producing ADP and a phosphate group.
 The energy stored in creatine phosphate is then used to “recharge” ADP, converting it back to ATP thru the reverse reaction.
o This reaction can be summarized as:
 During work/contraction….ADP + creatine phosphate -------creatine phosphokinase------> ATP & creatine
 See Fig. 12-13
(creatine kinase)
 When muscle cells sustain serious damaged, CPK leaks across the cell membrane and into the circulation. What
would a high blood concentration of CPK indicate?
 Aerobic metabolism (w/O2)  glucose  glycolysis  Krebs cycle  ETC…..lots of ATP.
 Anaerobic metabolism (w/o O2 )  glucose  lactic acid cycle….not at much ATP, but quicker.
Use the following 4 terms and filling the correct blanks below.
1) ATP --very little stored
2) CP --- creatine phosphate
3) aerobic respiration
4) anaerobic respiration
5) oxygen debt
1. __________________ - (aka phosphocreatine) can transfer its high-energy phosphate group to ADP to make ATP.
Can power maximal contractions for up to 15 sec.
2. ____________________ - generates ATP from the partial catabolism (break-down) of glucose anaerobically.
Provides power for ~30-40 sec
Hhmmmm? Why does this pathway occur, if aerobic system is so much more energetically efficient?
Hint--what happens to blood vessels when the muscle is contracting powerfully?
3. _________________________ . Muscular activity lasting more than 30 seconds requires oxygen. The aerobic system will provide
enough ATP for prolonged activity as long as O2 & nutrients are available.
4. Elevated O2 use after exercise is called _________________________ . In such a situation the muscles can continue to break
down glucose to liberate energy for a short time using anaerobic respiration. This partial breakdown produces lactic acid, which results
in a sensation of fatigue when it reaches certain levels in the muscles and the blood. This explains why it is possible to run faster in a
sprint than over longer distances. During the sprint, the muscles can respire anaerobically. Once the vigorous muscle movements cease,
the body breaks down the accumulated lactic acid on top of the ‘normal’ breakdown of glucose in aerobic respiration, using up extra
oxygen to do so. Panting after exercise is an automatic mechanism to ‘pay off’ the oxygen debt.
Muscle Fatigue (this is different than muscle pain)
 Inability of a muscle to maintain its strength of contraction or tension
 Causes Peripheral Fatigue:
o depletion of glycogen stores, ATP, PCr
o buildup of lactic acid, hydrogen ions, inorganic phosphate
o K+ efflux (decreasing Ca+2 release)
o depletion of ATP
o interference w/availability of Ca+2 (usually due to interference of Ach events @ myoneural jxn) thus decreaseing
calcium-troponin interaction
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 Central Fatigue
o Subjective feelings of tiredness and loss of desire to exercise--usually precedes physiological fatigue
o cause???????? maybe Serotonin (a brain neurotransmitter related)?
 See Fig. 12-11 (if you can explain this….you know PF and CF)
Muscle Tone:
 Results from a sustained partial contraction
 Maintains posture
 Hypotonia (aka atrophy)- decreased or lost muscle tone (flaccid muscles)
o Skeletal muscle is not stimulated by a motor neuron on a regular basis (i.e. not stimulation, no contraction)  results
in loss of muscle tone and mass.
o The muscle may reduce in size, tone, and power (not able to contract forcefully  loss of muscle tension)
o Spinal cord injuries or other damage to the NS will gradually lead to loss in muscle tone and size in the affected area
o Temporary reduction in muscle use can lead to hypotonia. Have you ever worn a cast on your arm or leg for a
period of time? What was the muscle like before the cast? What was it like after? Did you have to go to physical
therapy?
o Physical therapy after an immobilizing injury is extremely important for restoring muscle tone and mass
o Remember…If you don’t use it, you LOSE it!!!
 Hypertonia (aka hypertrophy)- increased muscle tone -- expressed as spasticity or rigidity.
o Condition marked by an abnormal increase in muscle tension and a reduced ability of a muscle to stretch.
o Caused by injury to motor pathways that carry information from the CNS to the muscles for control of posture,
muscle tone, and reflexes.
o Can be so severe that joint movement is not possible.
o Untreated, it can lead to loss of function and deformity.
o May result from injury, disease, or conditions such as spasticity, dystonia (prolonged muscle contractions that cause
twisting and repetitive movements or abnormal posture), rigidity, or a combination of factors.
 Spastic hypertonia involves uncontrollable muscle spasms, stiffening or straightening out of muscles,
shock-like contractions of all or part of a group of muscles, and abnormal muscle tone.
 It is seen in disorders such as cerebral palsy, stroke, and spinal cord injury.
o Dystonic hypertonia refers to muscle resistance to passive stretching and a tendency of a limb to return to a fixed
involuntary (and sometimes abnormal) posture following movement.
o Rigidity is an involuntary stiffening or straightening out of muscles, accompanied by abnormally increased muscle
tone and the reduced ability of a muscle to stretch.
Muscles & Exercise
Although the # of skeletal muscle fibers does not change* (evidence now indicates that #’s can increase due to satellite cell activity and
also cell splitting), but there is no real mitosis. The characteristics of those muscle cells present can change w/ exercise & the type of
exercise. Exercise usually results in increased mitochondria, increased myofilaments, increased myofibrils within the individual cells,
thus cells get “bigger”…and therefore the whole muscle appears “bigger.” Remember muscle cells are also called muscle fibers or
myofibers.
Hypertrophy
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Result of repeated, exhaustive stimulation.
Muscle fibers develop a larger number of mitochondria, a higher concentration of glycolytic enzymes, and larger
glycogen reserves.
Muscle fibers (aka muscle cells) have more MYOFIBRILS (NOT myofibers/muscle cells)
 You cannot increase the number of muscle fibers/cells!!!!
 The muscle as a whole enlarges because each muscle fiber increases in DIAMETER.
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Physical Conditioning
(Anyone thinking of coaching or just getting into shape? Listen up to this part.)
 Anaerobic endurance
o It is the length of time muscular contraction can continue, supported by glycolysis and the existing energy reserves of
ATP and CP.
o Anaerobic endurance is limited by:
 1. the amt. of ATP and CP already at hand
 2. the amt. of glycogen available for breakdown
 3. the ability of the muscle to tolerate the lactic acid generated during the anaerobic period
o Activites requiring anaerobic endurance include:
 Short sprints
 Short swims
 Pole vault
 Power lifting
o Athletes training to develop anaerobic endurance should perform frequent, brief, intensive workouts that stimulate
muscle hypertrophy. How will this help the limits above?
 Aerobic endurance
o It is the length of time that a muscle can continue to contract while supported by mitochondrial activities.
o Determined primarily by the availability of substrates for aerobic respiration, which the muscle fiber can obtain by
breaking down carbs., lipids, & amino acids
o Many of the nutrients catabolized by muscle cells are obtained from reserves within the muscle cells themselves;
however, prolonged aerobic activity must be supported by nutrients provided by the circulating blood.
 During exercise, blood vessels in skeletal muscle dilate, and the increased blood flow brings oxygen and
nutrients to the active muscle tissue
 Long distance runners often load up on carbohydrates for 2-3 days before an event.
o Training to improve aerobic endurance involves:
 Jogging
 Distance swimming
 Other exercises that do not require peak tension production (low weight, high repetitions)
 Exercises that do not promote hypertrophy
 Improvements in aerobic endurance result from altering the characteristics of the muscle fibers and
improving the performance of the cardiovascular system.
 Aerobic endurance
o It is the length of time that a muscle can continue to contract while supported by mitochondrial activities.
o Determined primarily by the availability of substrates for aerobic respiration, which the muscle fiber can obtain by
breaking down carbs., lipids, & amino acids
o Many of the nutrients catabolized by muscle cells are obtained from reserves within the muscle cells themselves;
however, prolonged aerobic activity must be supported by nutrients provided by the circulating blood.
 During exercise, blood vessels in skeletal muscle dilate, and the increased blood flow brings oxygen and
nutrients to the active muscle tissue
 Long distance runner , often load up on carbohydrates for 2-3 days before an event.
o Training to improve aerobic endurance involves:
 Jogging
 Distance swimming
 Other exercises that do not require peak tension production (low weight, high repetitions)
 Exercises that do not promote hypertrophy
 Improvements in aerobic endurance result from altering the characteristics of the muscle fibers and
improving the performance of the cardiovascular system.
 A trained, highly conditioned athlete should not experience muscle fatigue for several hours.
o This can be accomplished by training, using a combination of aerobic and anaerobic exercise
 Goal is to enlarge muscles (strength) and improve both anaerobic and aerobic endurance (conditioning)
 Can be accomplished by interval training:
o Alternating aerobic activities (swimming, slow long runs, distance cycling) with anaerobic
activities (sprinting, weight lifting)
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Delayed Onset Muscle Soreness:
 Delayed onset muscle soreness (DOMS), after a workout is quite common, if you are just beginning an exercise program or
changing activities.
 You wake up one day and go a three mile walk, followed by push-ups and sit-ups, there is bound to be some muscle pain and
soreness the next day or two.
o This is a normal response to unusual exertion and is part of an adaptation process that leads to greater stamina and
strength as the muscles recover and build.
o The soreness is generally at its worst within the first 2 days following the activity and subsides over the next few
days.
 Occurs hours after the exercise is over.
 This is much different than the acute pain of a pulled or strained muscle.
o A muscle tear, is felt as an abrupt, sudden, acute pain that occurs during activity, which is often accompanied by
swelling or bruises.
 DOMS is thought to be a result of microscopic tearing of the muscle fibers.
o The amount of tearing (and soreness) depends on how hard and how long you exercise and what type of exercise
you do.
 Activities that require muscles to forcefully contract while they are lengthening, (eccentric contractions), seem to cause the
most soreness.
o You use eccentric contractions when you descend stairs, run downhill, lower a weight, or perform the downward
motion of squats and push-ups.
 In addition to muscle tearing, swelling can occur in and around a muscle, which can also cause soreness hours later.
Types of Skeletal Muscle Fibers (See TABLE 12-2 for a comparison summary)
 all skeletal muscle fibers are not identical in structure or function
 color varies w/ myoglobin content, an O2-storing reddish pigment, and capillaries
 red muscle  white muscle  fiber diameter varies as do the cell’s allocations of mitochondria, blood capillaries, & sarcoplasmic reticulum
 contraction velocity & resistance to fatigue also differ btn fibers.
 1. Slow Oxidative
 Type I, slow-twitch, or fatigue resistant fibers.
 increased mitos, increased myoglobin, increased blood capillaries
 look red & have high capacity to generate ATP aerobically, but slowly
 slow contraction velocity
 postural muscles - neck - highly resistant to fatigue
 increase in % w/ age
 2. Fast Oxidative
 Type IIA, fast-twitch A, or fatigue resistant fibers.
 increased # of mitos, increased myoglobin, increased capillaries
 look red to pink in color & have a high capacity to generate ATP aerobically
 fast contraction velocity
 fairly resistant to fatigue
 sprinters leg muscles
 3. Fast Glycolitic
 Type IIB, fast-twitch B, or fatigable fibers
 decreased myoglobin, decreased mitos, decreased capillaries
 contain lg amts of glycogen used to generate ATP anaerobically
 appears white in color
 fatigue easily
 contraction strong and rapid
 arm muscles
 In general:
o Most skeletal muscles contain a mixture of all three.
o The proportion varies w/ the usual action of the muscle.
o But all fibers in any one motor unit are the same type