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Chapter 9: Muscles & Muscle Tissue
Objectives
Overview of Muscle Tissues
1. Compare and contrast the three basic types of muscle tissue.
2. List four important functions of muscle tissue.
Skeletal Muscle
3. Describe the gross structure of a skeletal muscle.
4. Describe the microscopic structure and functional roles of the myofibrils, sarcoplasmic reticulum, and T tubules of skeletal muscle fibers.
5. Describe the sliding filament model of muscle contraction.
6. Explain how muscle fibers are stimulated to contract by describing events that occur at the neuromuscular
junction.
7. Describe how an action potential is generated.
8. Follow the events of excitation-contraction coupling that lead to cross bridge activity.
9. Define motor unit and muscle twitch, and describe the events occurring during the three phases of a muscle
twitch.
10. Explain how smooth, graded contractions of a skeletal muscle are produced.
11. Differentiate between isometric and isotonic contractions.
12. Describe three ways in which ATP is regenerated during skeletal muscle contraction.
13. Define EPOC and muscle fatigue. List possible causes of muscle fatigue.
14. Describe factors that influence the force, velocity, and duration of skeletal muscle contraction.
15. Describe three types of skeletal muscle fibers and explain the relative value of each type.
16. Compare and contrast the effects of aerobic and resistance exercise on skeletal muscles and on other body
systems.
Smooth Muscle
17. Compare the gross and microscopic anatomy of smooth muscle cells to that of skeletal muscle cells.
18. Compare and contrast the contractile mechanisms and the means of activation of skeletal and smooth muscles.
19. Distinguish between unitary and multi unit smooth muscle structurally and functionally.
Developmental Aspects of Muscles
20. Describe embryonic development of muscle tissues and the changes that occur in skeletal muscles with age.
Suggested Lecture Outline
I. Overview of Muscle Tissues (pp. 276–278; Table 9.1)
A. Types of Muscle Tissue (p. 277; Table 9.1) Review Chapter 4 – Muscle Histology
1. Skeletal muscle is associated with the bony skeleton and consists of large cells that bear striations and are
under voluntary control.
2. Cardiac muscle occurs only in the heart and consists of small cells that are striated and under involuntary
control.
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3. Smooth muscle is found in the walls of hollow organs and consists of small, elongated cells that are not striated and are under involuntary control.
B. Special Characteristics of Muscle Tissue (p. 277)
1. Excitability, or responsiveness, is the ability to receive and respond to a stimulus: action potential (impulses); autorhythmic (pace maker) & chemical (neurotransmitter)
2. Contractility is the ability to contract forcibly when stimulated. Muscles only act by shortening; generating
tension
3. Extensibility is the ability to be stretched, within limits, without being damaged.
4. Elasticity is the ability to resume the cells’ original length once stretched; recoil
C. Muscle Functions (pp. 277–278; Table 9.1)
1. Movement of body & contents: Muscles produce movement by acting on the bones of the skeleton, pumping blood, or propelling substances throughout hollow organ systems, including fluid in lymph & blood vessels. Examples:
a. Cardiac muscle – shunts blood thru contractions
b. Smooth muscle
i. Vessel diameter – vasoconstriction & vasodilation
ii. GI – peristalsis; Urinary System – urine transport
iii. Reproductive – gametes fertilization; ovulation
c. Skeletal muscle – promote flow of lymph & venous return via respiratory & skeletal pump
2. Stabilize position: Muscles aid in maintaining posture by adjusting the position of the body with respect to
gravity.
3. Muscles stabilize joints by exerting tension around the joint.
4. Thermoregulation: Muscles generate heat as a function of their cellular metabolic processes.
a. Thermogenesis – skeletal muscle promote shivering to generate heat; smooth muscle vasoconstriction
b. Heat reduction – smooth muscle vasodilation
5. Storage & Special Functions: Muscles enclose and protect internal organs, form valves (sphincters) that regulate passage of substances in the body, control the size of the pupil of the eye, and attach to hair follicles as
arrector pili muscles.
II. Skeletal Muscle (pp. 278–305; Figs. 9.1–9.24; Tables 9.1–9.3)
A. Gross Anatomy of Skeletal Muscle (pp. 278–279; Fig. 9.1; Tables 9.1, 9.3)
1. Each muscle has a nerve and blood supply that allows neural control and ensures adequate nutrient delivery
and waste removal. Well supplied; somatic motor neurons & many capillaries
2. Connective tissue sheaths are found at various structural levels of each muscle: endomysium surrounds each
muscle fiber (myocyte), perimysium surrounds groups of muscle fibers (fascicle), and epimysium surrounds
whole muscles.
3. Skeletal muscles span joints and cause movement to occur from the movable attachment (the muscle’s insertion) toward the less movable attachment (the muscle’s origin).
4. Muscle attachments may be direct, in which the epimysium fuses with the periosteum or perichondrium; or
indirect, in which the connective tissue wrappings of the muscle extend into a ropelike or sheetlike structure
that attaches to the bone, cartilage, or fascia. Fascia – DICT; allows free movement; carries VAN; fills in
spaces
a. Indirect attachments are the most common because they are durable and are small in size, conserving
space across joints.
5. Sub Q (hypodermis) Areolar CT with adipose – pathway for VAN; insulates & protects muscle
B. Microscopic Anatomy of a Skeletal Muscle Fiber (pp. 279–285; Figs. 9.2–9.5; Tables 9.1, 9.3)
1. Skeletal muscle fibers are large, cylindrical cells with multiple nuclei (along periphery) beneath the sarcolemma, or plasma membrane; wrapped by endomysium
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2. Sarcoplasm, the cytoplasm of a muscle cell, is similar to other types of cells, except it has large amounts of
glycosomes, for glycogen storage, and myoglobin, an oxygen binding pigment similar to hemoglobin. Also
contains nuclei, SR, & mitochondria.
3. Myofibrils account for roughly 80% of cellular volume and contain the contractile elements of the muscle
cell.
4. Striations are due to a repeating series of dark A bands and light I bands.
5. Myofilaments make up the myofibrils and consist of thick (myosin) and thin (actin) filaments.
6. Striations, alternating dark A bands and light I bands, extend the length of each myofibril.
a. Each A band has a lighter central region, the H zone, which is bisected vertically by an M line.
b. Each I band is bisected vertically by a Z disc, and the region extending from one Z disc to the next forms a
sarcomere, the smallest contractile unit of a muscle cell.
7. There are two types of myofilaments in muscle cells: thick filaments composed of bundles of myosin, and
thin filaments composed of strands of actin.
a. Each myosin filament consists of myosin molecules that have a rod-like tail attached to two globular
heads that form cross bridges with actin during contraction. Myosin heads (“golf clubs”); titin to z disc; M
line, A band.
b. Actin filaments consist of polymerized G actin subunits that have active sites that bind myosin heads during contraction.
8. Thin filaments (Actin) also have a set of regulatory proteins: tropomyosin, that wrap around actin filaments,
stabilizing it and blocking myosin binding sites; and troponin, which binds to both actin and tropomyosin,
and binds calcium ions.
a. Review of Muscle Proteins
i. Contractile – generate force; actin & myosin (motor protein)
ii. Regulatory – switches contraction on & off; troponin (affinity for Ca2+) & tropomyosin (covers myosinbinding sites)
iii. Structural – proper alignment, elasticity & extensibility, linkage; titin, α-Actinin, Myomesin, Nebulin,
& Destrophin (MD)
9. The sarcoplasmic reticulum, a smooth endoplasmic reticulum (SER) that regulates the availability of calcium
ions (5K more), surrounds each myofibril, and forms terminal cisterns at the A band–I band junction.
10. T tubules are infoldings of the sarcolemma that run between the terminal cisterns and increases surfave area, forming triads, that conduct electrical impulses into the cell to cause release of calcium ions from the
terminal cisterns. Filled with interstitial fluid; ensures entire fiber is stimulated by impulse simultaneously.
11. Synaptic vesicles – in end bulbs containing neurotransmitters acetylcholine (ACh)
12. Synaptic cleft – space or “gap” between cells.
C. The sliding filament model of muscle contraction states that during contraction, the thin filaments slide past
the thick filaments. Overlap between the myofilaments increases and the sarcomere shortens (p. 285; Fig. 9.6).
D. Physiology of Skeletal Muscle Fibers (pp. 285–293; Figs. 9.7–9.12; Table 9.1)
1. The neuromuscular junction (NMJ) is a connection between an axon terminal of a somatic motor neuron
and a muscle fiber that is the route of electrical stimulation of the muscle cell.
2. A nerve impulse causes the release of acetylcholine (ACh) from the axon terminal to the synaptic cleft, which
binds to receptors on the junctional folds of the muscle cell, triggering a series of electrical events on the
sarcolemma.
3. After acetylcholine binds to ACh receptors, an enzyme in the synaptic cleft, acetylcholinesterase, breaks
down acetylcholine to acetic acid and choline, to prevent continued contraction in the absence of stimulation.
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4. Generation and propagation of an action potential across the sarcolemma occurs when an end plate potential, generated when ACh binds to ACH receptors, reaches threshold, causing voltage-gated sodium channels to open causing depolarization.
5. Repolarization restores the resting polarity to the sarcolemma and is accomplished by diffusion of potassium
ions out of the cell.
a. During repolarization, the muscle cell is in a refractory period and may not be depolarized until repolarization is complete.
6. Excitation-contraction coupling is the sequence of events by which an action potential on the sarcolemma
results in the sliding of the myofilaments. – cause & effect relationship
a. A nerve impulse reaches the axon terminal, causing the release of ACh to the synaptic cleft. Impulse
causes VGCa2+ channel to open = Ca2+ diffuse into synaptic end bulb release Ach (via exocytosis of synaptic
vesicles)
b. ACh binds to ACh receptors (ligand-gated) in the sarcolemma, and a net influx of sodium ions causes the
generation of an end plate potential. AchE is always present in synaptic cleft to rapidly remove XS Ach
i. The acetate enters the blood, where it can be used in energy metabolism
ii. The choline is recycled into the presynaptic nerve.
What would result if AchE was absent?
c. Voltage Ligand- gated sodium channels open, allowing the generation and propagation of an action potential on the sarcolemma. (depolarization to threshold causing muscle action potential)
d. Transmission of the action potential along the T tubules, stimulating the voltage-gated Ca2+ channels release of calcium ions (due to diffusion) from the sarcoplasmic reticulum to the cytosol.
e. As calcium levels in the cytosol increase, calcium binds to troponin, which causes tropomyosin to slide
away from the binding sites for myosin on the actin filaments.
f. Contraction Cycle: Energized myosin heads bind to actin (forming a cross bridge) and perform a power
stroke, causing actin to slide over myosin. Causing muscle shortening aka: contraction); myosin heads detach.
What must you have to continue contractions? How is NRMP reestablished? What is myas
thenia gravis?
7. Toxins affecting NMJ
a. Transmitter Release Inhibitors
Botulism - poisoning usually occurs in people who have eaten improperly preserved foods; the toxin can
be destroyed by heating
a. Blocks Ach release
b. Causes ___________ paralysis; potentially fatal respiratory arrest
Tetanus toxin – inhibits CNS synapses that release the inhibitory transmitters, glycine and gammaaminobutyric acid (GABA)
a. Results in excessive Ach release from motor neurons
b. Causes ___________ paralysis and potentially fatal paralytic convulsions ("lockjaw")
8. Receptor Inhibitor
Cobra toxin & curare (African arrow poison)
a. Blocks Ach receptors
b. Cause flaccid paralysis, potentially fatal respiratory arrest
c. Synthetic curare used for relaxant during surgery
9. Acetylcholinesterase Inhibitors
1. Nerve gas and insecticides
a. Cause potentially fatal paralytic convulsions
E. Contraction of a Skeletal Muscle (pp. 293–298; Figs. 9.13–9.18)
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1. A motor unit consists of a motor neuron and all the muscle fibers it innervates. It is smaller in muscles that
exhibit fine control. Contract in unison.
Factors affecting muscle contractile force
a. Size & number of muscle fibers contracting
b. Rate of motor neuron firing
c. Optimal starting sarcomere length
2. The muscle twitch is the response of a muscle to a single action potential on its motor neuron or rate of motor neuron firing; typical myogram wave; has three phases:
a. Latent period – corresponding to the lag between stimulation and excitation-contraction coupling (In
other words: NMJ to release of Ca2+ via SR)
b. Contraction period (contraction cycle)
c. Relaxation period
3. Muscle contractions are smooth and vary in strength, leading to different kinds of graded muscle responses.
a. Wave summation occurs when impulses reach the muscle in rapid succession, preventing the cell
from relaxing between stimulation events, ultimately causing contraction to become sustained, a
condition called tetanus.
i. Increases contractile force (staircase or "treppe" effect) due to combination of tautness of elastic
components and partially contracted filaments
ii. Too much causes tetanus (incomplete=20 to 30/sec; complete=80-100)
b. Multiple motor unit summation (recruitment) involves the response of a muscle to increasing stimulus
voltage: smaller stimuli result in contraction of the smallest motor units, and as voltage increases, larger,
more forceful motor units respond, leading to progressively greater contractile force. Results in smooth
motion & delays fatigue
4. Muscle tone is due to reflexive neural stimulation, resulting in muscles exhibiting slight contraction, even
when at rest, which keeps muscles firm, healthy, and ready to respond. Ex: Postural, GI & vessel tone.
5. Isotonic contractions produce uniform tension in a muscle, once a load has been overcome, and result in
movement occurring at the joint and a change of length of muscles.
a. Concentric isotonic contractions result when muscle generates force when it shortens, while in eccentric
isotonic contractions (aka: “negatives”), the muscle generates force as it lengthens. Ex: bicep curls; wall
squats
6. Isometric contractions result in increases in muscle tension, but no lengthening or shortening of the muscle
occurs, and often are used to maintain posture or joint stability while movement occurs at other joints. Ex:
attempt to lift a baby grand piano or “sitting on the wall”; load is greater than the effort.
F. Muscle Metabolism (pp. 298–301; Figs. 9.19–9.20)
1. Muscles contain very little stored ATP, and consumed ATP is replenished rapidly through phosphorylation by
creatine phosphate, anaerobic glycolysis, and aerobic respiration.
2. Creatine-phosphate – uses creatine phosphokinase (CPK or CK) – As muscle metabolism transitions to
meet higher demand during vigorous exercise, consumed ATP is regenerated by transferring a
phosphate to consumed ATP from creatine phosphate, a molecule unique to muscle tissue. .
a. Creatine – synthesize in liver, kidneys, & pancreas the transported to muscle
b. 3 to 6 times more plentiful than ATP
c. First source of energy; delivers ~ 15-30 sec max. activity
3. As stored ATP and creatine phosphate are consumed, ATP is produced by breaking down blood glucose or stored glycogen in glycolysis, an anaerobic pathway that precedes both aerobic and anaerobic respiration. Glycolysis – First step of cellular respiration – No O2 required; occurs in cytosol
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If adequate oxygen is not available to support aerobic respiration, anaerobic glycolysis converts the pyruvate formed from glycolysis into lactic acid. Liver converts lactic acid into glucose
a. This pathway produces only about 5% the ATP from each glucose compared to the aerobic pathway, but
ATP production occurs 2½ times faster. Delivers 30-40 sec max. activity. Net ATP = 2; aka: “fermentation”
b. Most of the lactic acid produced is released to the bloodstream and taken to the liver, heart, or kidneys
for use, but the lactic acid that remains in the muscle contributes to muscle soreness, trigger points &
muscle spasms following exercise. Ex: sprints & heavy exercise; EPOC (see below)
4. Aerobic respiration aka: Oxidative pathway; provides most of the ATP during light to moderate activity, includes glycolysis, along with reactions that occur within the mitochondria, and produces 32 ATP per glucose,
as well as water, and CO2, which will be lost from the body in the lungs. Includes Acetyl CoA Formation,
Kreb’s Cycle, & ETC. C6H12O6 + 6O2  36 ATP + 6CO2 + 6O2 + heat. Utilizes amino acids, fatty acids, or pyruvic
acid; most efficient use of glucose. Glucose circulates in blood; stored as glycogen in liver & muscle. Oxygen –
hemoglobin and myoglobin
5. Muscles function aerobically as long as there is adequate oxygen and nutrient delivery to support it, but
when exercise demands for ATP exceed the production ability of aerobic reactions, the cell will switch to anaerobic pathways.
6. Muscle fatigue is the physiological inability to contract, and results from ionic imbalances that interfere with
normal excitation-contraction coupling.
7. Excess post-exercise oxygen consumption (EPOC) aka. “oxygen debt” – is the extra oxygen the body requires following exercise to replenish oxygen on myoglobin, reconvert lactic acid to pyruvic acid, replace
stored glycogen, and restore ATP and creatine phosphate reserves.
8. Muscle activity produces excess energy that is lost from the body as heat: excess body heat can be lost
through sweating and radiant heat loss from skin, while heat production through shivering can be used to
warm the body when it is too cold.
G. Force of Muscle Contraction (pp. 301–302; Figs. 9.21–9.22)
1. As the number of muscle fibers stimulated increases, force of contraction increases.
2. Large muscle fibers generate more force than smaller muscle fibers.
3. As the rate of stimulation increases, contractions sum up, ultimately producing tetanus, allowing the external tension generated by the connective tissue elements to approach internal tension generated by the
muscle fibers, increasing contractile force.
4. The length-tension relationship optimizes the overlap between the thick and thin filaments that produces optimal contraction.
H. Velocity and Duration of Contraction (pp. 302–304; Figs. 9.23–9.24; Tables 9.2–9.3)
1. There are three muscle fiber types: slow oxidative fibers, fast glycolytic fibers, and fast oxidative fibers.
a. Slow oxidative (SO) fibers contract slowly, rely mostly on aerobic respiration, and are highly fatigue resistant. Smallest in size; high amount of myoglobin, mitochondria, and capillaries. Ex: Postural muscles
b. Fast glycolyic (FG) fibers contract rapidly, use anaerobic respiration, depend heavily on glycogen, but
fatigue quickly. Largest; low amount of myoglobin, mitochondria, and capillaries. Ex: Arm muscles
Hypertrophy – d/t synthesis of actin & myosin
c. Fast oxidative fibers (FOG) are a less common, intermediate type of fiber that provide rapid contraction,
but have excellent capillary penetration for oxygen and nutrient delivery, and rely on aerobic respiration.
high amount of myoglobin, mitochondria, Ex: Sprinter's legs
2. All muscles have varying amounts of all fiber types and, while the proportion of each type is a genetically influenced trait, that proportion can be modified by specific types of exercise.
3. As the load on a muscle increases, velocity and duration of contraction decreases.
4. Recruitment of additional motor units increases velocity and duration of contraction.
I. Adaptations to Exercise (pp. 304–305)
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1. Aerobic exercise promotes an increase in capillary penetration, the number of mitochondria, and synthesis
of myoglobin, leading to higher efficiency and endurance, while possibly converting fast glycolytic fibers to
fast oxidative fibers.
2. Resistance exercise, such as weight lifting or isometric exercise, promotes an increase in the number of mitochondria, myofilaments and myofibrils, and glycogen storage, producing hypertrophied cells that may
change from fast oxidative to fast glycolytic fibers.
III. Smooth Muscle (pp. 305–311; Figs. 9.25–9.28; Table 9.3)
A. Microscopic Structure of Smooth Muscle Fibers (pp. 305–307; Figs. 9.25–9.27; Table 9.3)
1. Smooth muscle cells are small, spindle-shaped cells with one central nucleus, and lack the coarse connective
tissue coverings of skeletal muscle. Involuntary; two types:
a. Visceral (single-unit) – skin, small vessels, hollow organs
i. Autorhythmic
ii. Gap junctions (Review Chapter 4) = contracting fibers in unison
b. Multiunit – large arteries, airways, arrector pili, pupillary muscles, ciliary muscle of lens
i. Own motor unit = contraction single fiber
2. Smooth muscle cells are usually arranged into sheets of opposing fibers, forming a longitudinal layer and a
circular layer.
3. Contraction of the opposing layers of muscle leads to a rhythmic form of contraction, called peristalsis,
which propels substances through the organs. Corkscrew contractions.
4. Smooth muscle lacks neuromuscular junctions, but has varicosities: numerous bulbous swellings that release
neurotransmitters to a wide synaptic cleft.
5. Smooth muscle cells have a less developed sarcoplasmic reticulum, sequestering large amounts of calcium in
extracellular fluid within caveolae in the cell membrane. No T tubules
6. Smooth muscle has no striations, no sarcomeres, a lower ratio of thick to thin filaments compared with skeletal muscle, and has tropomyosin but no troponin.
7. Smooth muscle fibers contain longitudinal bundles of noncontractile intermediate filaments anchored to the
sarcolemma and surrounding tissues via dense bodies (instead of Z discs.
B. Contraction of Smooth Muscle (pp. 307–309; Fig. 9.28; Table 9.3)
1. Mechanism of Contraction
a. Smooth muscle fibers exhibit slow, synchronized contractions due to electrical coupling by gap junctions.
b. Like skeletal muscle, actin and myosin interact by the sliding filament mechanism; contraction is triggered
by a rise in intracellular calcium level, and the process is energized by ATP.
c. During excitation-contraction coupling, calcium ions enter the cell from the extracellular space, bind to
calmodulin, and activate an enzyme, myosin light chain kinase, powering the cross bridging cycle.
d. Smooth muscle contracts more slowly and consumes less ATP than skeletal muscle. Long term
tone – sustain pressure; Stress–relaxation response
2. Regulation of Contraction
a. Autonomic nerve endings release either acetylcholine (Ach) or norepinephrine, which may result in excitation of certain groups of smooth muscle cells, and inhibition of others.
b. Hormones and local factors, such as lack of oxygen, histamine, excess carbon dioxide, or low pH, act as
signals for contraction.
3. Special Features of Smooth Muscle Contraction
a. Smooth muscle initially contracts when stretched (or distended), but contraction is brief, and then the
cells relax to accommodate the stretch.
b. Because the muscle filaments have an irregular overlapping pattern, smooth muscle stretches more and
generates more tension when stretched than skeletal muscle.
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c. Hyperplasia, an increase in cell number through division, is possible in addition to hypertrophy, an increase in individual cell size.
C. Types of Smooth Muscle (p. 309)
1. Unitary smooth muscle, called visceral muscle, is the most common type of smooth muscle. It contracts
rhythmically as a unit, is electrically coupled by gap junctions, and exhibits spontaneous action potentials.
2. Multi unit smooth muscle is located in large airways to the lungs, large arteries, arrector pili muscles in hair
follicles, and the iris of the eye. It consists of cells that are structurally independent of each other, has motor
units, and is capable of graded contractions.
IV. Cardiac Muscle – refer to p. 357 Table 10.5. Compare & contrast to skeletal muscle.
A. Intercalated disc – desmosomes & gap junctions
B. Lacks ________________.
C. 10-15 time longer contraction – Why?
D. Autorhythmic – 75 bpm
E. Mitochondria larger & more numerous – How does this affect oxygen requirements?
F. Discuss reasons for physiologic & pathologic hypertrophy.
V. Developmental Aspects of Muscles (pp. 312–313, 315; Fig. 9.29)
A. Nearly all muscle tissue develops from specialized mesodermal cells called myoblasts (p. 312).
B. Skeletal muscle fibers form through the fusion of several myoblasts, and are actively contracting by week 7 of
fetal development (p. 312; Fig. 9.29).
C. Myoblasts of cardiac and smooth muscle do not fuse but form gap junctions at a very early stage (p. 312).
D. Muscular development in infants is mostly reflexive at birth, and progresses in a head-to-toe and proximal-todistal direction (p. 312).
E. Women have relatively less muscle mass than men due to the effects of the male sex hormone testosterone,
which accounts for the difference in strength between the sexes (p. 312).
F. Muscular dystrophy is characterized by atrophy and degeneration of muscle tissue. Enlargement of muscles is
due to fat and connective tissue deposit (pp. 312, 315).
G. Aging and Muscles – 30-50 years of age. List the results of aging musculature and the type of exercise program recommended to slow or reverse these changes.
1. General skeletal muscle fiber atrophy with age
a. Less myoglobin, mitochondria, fibrils, glycogen, ATP synth/ muscle fiber
b. Less blood flow
c. Less elasticity
i. Increased fibrosis & adipose in muscles (accumulation of fibrous connective tissue)
d. Sarcopenia – Aging Skeletal Muscle: Physiologic Changes and the Effects of Training
e. Less heat dissipation from skin (overheating)
f. Less satellite cells to help recover from injury
g. 30-50% decline in muscle performance by age _________
i. Rate of decline mostly constant
ii. Conditioning affects the duration of "quality" performance, not rate of decline
VI. Muscular Disorders
A. Myasthenia gravis – means _________________________; progressive disorder; 75% thymus abnormality
1. Face/neck muscles affected first; diplopia, "ptosis", difficulty with deglutition & mastication
2. Spreads to chest & limbs; usually not fatal (5-10% respiratory failure)
3. Affects females 2X males; ages ____________
4. Autoimmune disorder
a. Anti-AchR autoantibodies
b. Loss of AchR in motor end plate
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c. Inability to stimulate muscles leads to ____________ paralysis
5. Treatment & RX
a. Neostigmine (AchE inhibitors)
b. Prednisone (immunosuppressive)
c. Plasmaphoresis (filter out anti-AchR)
d. Thymectomy
B. Muscular Dystrophy – progressive muscle degeneration/atrophy
1. Appears early (2-5 yrs old); by 12 unable to walk
2. Facial & cardiac muscles usually affected last
3. Continuous progression of degeneration
a. Average lifespan about 20yrs; respiratory or cardiac failure
4. Many forms of MD – Duchenne MD (DMD) more severe form; Becker MD milder than DMD
Duchenne MD - most common form
a. X-linked inherited disorder; most common in boys
b. Caused by defective dystrophin gene; results in:
i. Continual Ca2+ leakage from SR
ii. XS Ca2+ activates catabolic enzymes inside fibers resulting in muscle fibers degeneration
c. Use of gene therapy to replace dystrophin show promise
d. Induce utrophin - experimental
C. Fibromyalgia – non-inflammatory painful CT disorder of musculoskeletal system; idiopathic
1. More common in females (15X) than males
2. Severe morning pain & stiffness in limbs
3. Several characteristic "tender points" key to diagnostic features
4. Overall fatigue, restlessness, poor sleep, depression
a. Typically treat with stress reduction, regular exercise, PT, NSAIDs (aspirin, acetaminophen, & ibuprofen)
Define Muscle spasm, cramps; tics vs. tremors, fasciculation vs. fibrillation.
Review Homeostatic Imbalances, A Closer Look captions throughout the chapter and At-the-Clinic & Medical Terminology located
in all chapters.
This is only a general outline. There may be material that has been discussed in lecture that is not included in this outline and there may be material
on this outline that has not been discussed in lecture. Any material discussed in lecture or listed in this outline is "fair game" for the test.
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