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MUSCULAR SYSTEM
Dr. Kwame B.N. BANGA, BSc, MPhil, PhD (Biochemistry, Physiology-Pharmacology )
Senior Lecturer
Department of Pharmacology & Toxicology,
University of Ghana, College of Health Sciences,
School of Pharmacy, Legon, Accra, Ghana
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Learning Objectives
To describe muscle’s macro and micro structures
To explain the sliding-filament action of muscular
contraction
To differentiate among types of muscle fibres

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Content
 Types of muscle and functions
 Properties of muscles
 Skeletal fiber types
Excitation – contraction coupling of skeletal, cardiac
….and smooth muscles
Muscular contraction types
 Length – tension relationship of skeletal muscles
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Introduction
 The muscular system (organ system) is an extensive network
of muscle and nervous tissue which is spread throughout the
body.
 It is controlled by the central nervous system, which sends
out an assortment of signals to keep the body running
smoothly.
 There are over 650 muscles active in the human body, and
the muscular system can comprise up to 40-45% of someone's
weight.
 This complex interconnected system is essential for human
life; without it, people cannot move and perform an assortment
of bodily processes which are essential to keep the body in
working order.
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Muscular System Functions
 Body movement
 Maintenance of posture
 Respiration
 Production of body heat
 Communication
 Constriction of organs and vessels
 Heart beat
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Muscular System Functions
 The primary function of muscle is to generate
force or movement in response to a
physiological stimulus.
Skeletal muscle:
 Balance – prevention of falls
 Coordination – smoothness of movement
 Strength – moving body parts against gravity
or resistance
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3 Muscles types:
skeletal, cardiac, and smooth muscle
1. Skeletal muscle
- multiple nuclei, peripherally located; striated,
- attached to bones: locomotion and work production.
- control of breathing cycle and pump function for the venous
return
- voluntary and involuntary (reflexes)
2. Cardiac muscle
- myocardial cells: single nucleus centrally located, striations,
intercalated disks
- specific to the heart - biomechanical pump driving the
delivery of blood to the lungs and tissues.
- involuntary
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3 Muscles types:
skeletal, cardiac, and smooth muscle
3. Smooth muscle
- single nucleus centrally located, not striated, gap junctions in
visceral smooth
- walls of hollow organs, blood vessels, eye, glands, skin
- mechanical control of organ systems: digestive, urinary,
reproductive tracts, blood vessels of the circulatory system
and airway passages of the respiratory system.
- involuntary
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Properties of Muscle
 Contractility
– Ability of a muscle to shorten with force
 Excitability
– Capacity of muscle to respond to a stimulus
 Extensibility
– Muscle can be stretched to its normal resting
length and beyond to a limited degree
 Elasticity
– Ability of muscle to recoil to original resting
length after stretched
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How is muscle organized at the
tissue level?
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Skeletal Muscle Structures
 Muscle tissue (muscle cells or fibers)
 Connective tissues
 Nerves
 Blood vessels
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Organization of
Connective Tissues
 Muscles have 3 layers of connective tissues:
1. Epimysium-Exterior collagen layer
 Connected to deep fascia
 Separates muscle from surrounding tissue
2. perimysium- Surrounds muscle fiber bundles
(fascicles)
 Contains blood vessel and nerve supply to fascicles
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Organization of
Connective Tissues
3. Endomysium
 Surrounds individual muscle cells (muscle fibers)
 Contains capillaries and nerve fibers contacting
muscle cells
 Contains satellite cells (stem cells) that repair
damages
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Muscle Attachments
 Endomysium, perimysium, and epimysium
come together:
– at ends of muscles
– to form connective tissue attachment to bone
matrix
– i.e., tendon (bundle) or aponeurosis (sheet)
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Nerves
Muscle tissues are voluntary or involuntary
controlled by nerves of the central nervous
system
Blood Vessels
 Muscles have extensive vascular systems that:
– supply large amounts of oxygen
– supply nutrients
– carry away wastes
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What are the characteristics of
skeletal muscle fibers?
 Skeletal muscle cells are called fibers
 Are very long
 Develop through fusion of mesodermal cells
(myoblasts- embryonic cells)
 Become very large
 Contain hundreds of nuclei –multinucleate
 Unfused cells are satellite cells- assist in repair
after injury
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Organization of
Skeletal Muscle Fibers
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The Sarcolemma
 The cell membrane of a muscle cell
 Surrounds the sarcoplasm (cytoplasm of
muscle fiber)
 A change in transmembrane potential
begins contractions
 All regions of the cell must contract
simultaneously
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Transverse Tubules (T tubules)
 Transmit action potential – impulses
through cell
 Allow entire muscle fiber to contract
simultaneously
 Have same properties as sarcolemma
 Filled with extracellular fluid
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Myofibrils- 1-2um in diameter
 Lengthwise subdivisions within muscle fiber
 Made up of bundles of protein filaments
(myofilaments)
 Myofilaments - are responsible for muscle
contraction
2 Types of Myofilaments
 Thin filaments:
– made of the protein actin
 Thick filaments:
– made of the protein myosin
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Sarcoplasmic Reticulum (SR)
 A membranous structure surrounding each
myofibril
 Helps transmit action potential to myofibril
 Similar in structure to smooth endoplasmic
reticulum
 Forms chambers (terminal cisternae)
attached to T tubules
 function is to store and release calcium ions
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A Triad
 Is formed by 1 T tubule and 2 terminal
cisterna
Cisternae
2+
 Concentrate Ca (via ion pumps)
 Release Ca2+ into sarcomeres to begin
muscle contraction
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Organization of
Skeletal Muscle Fibers
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Structural components
of the Sarcomeres
 The contractile units of muscle
 Structural units of myofibrils
 Form visible patterns within myofibrils
Muscle Striations
A striped or striated pattern within myofibrils:
- alternating dark, thick filaments (A bands)
and light, thin filaments (I bands)
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M Lines and Z Lines
 M line:
– the center of the A band
– at midline of sarcomere
 Z lines:
– the centers of the I bands
– at 2 ends of sarcomere
Zone of Overlap
 The densest, darkest area on a light micrograph
 Where thick and thin filaments overlap
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The H Zone
 The area around the M line
 Has thick filaments but no thin filaments
Titin
 Are strands of protein
 Reach from tips of thick filaments to the Z line
 Stabilize the filaments
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Structural components
of the Sarcomeres
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Sarcomere Structure
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Sarcomere Function
 Transverse tubules encircle the sarcomere
near zones of overlap
 Ca2+ released by SR causes thin and thick
filaments to interact.
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Level 1: Skeletal Muscle
Level 2: Muscle Fascicle
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Level 3: Muscle Fiber
Level 4: Myofibril
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Level 5: Sarcomere
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3 Types of Skeletal Muscle Fibers
1. Fast fibers- Contract very quickly
• Have large diameter, large glycogen reserves, few
mitochondria
• Have strong contractions, fatigue quickly
2. Slow fibers-Are slow to contract, slow to fatigue
• Have small diameter, more mitochondria
• Have high oxygen supply
• Contain myoglobin (red pigment, binds oxygen)
3. Intermediate fibers-Are mid-sized
• Have low myoglobin
• Have more capillaries than fast fiber, slower to fatigue
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Fast versus Slow Fibers
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Comparing Skeletal
Muscle Fibers
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Muscles and Fiber Types
 White muscle:
– mostly fast fibers
– pale (e.g., chicken breast)
 Red muscle:
– mostly slow fibers
– dark (e.g., chicken legs)
 Most human muscles:
– mixed fibers
– pink
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Muscle Hypertrophy
 Muscle growth from heavy training:
– increases diameter of muscle fibers
– increases number of myofibrils
– increases mitochondria, glycogen reserves
Muscle Atrophy
 Lack of muscle activity:
– reduces muscle size, tone, and power
Hyperplasia:
 An increase in the number of cells in an organ or tissue
(excluding tumor formation) which may lead to an increase
in the volume of the organ or tissue
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Muscle Contraction
 Is caused by interactions of thick and thin
filaments
 Structures of protein molecules determine
interactions
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A Thin Filament
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4 Thin Filament Proteins
1. F actin:
–
–
is 2 twisted rows of globular G actin
the active sites on G actin strands bind to myosin
2. Nebulin:
–
holds F actin strands together
3. Tropomyosin:
–
–
is a double strand
prevents actin–myosin interaction
4. Troponin:
- a globular protein
–
–
binds tropomyosin to G actin
controlled by Ca2+
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Troponin and Tropomyosin
Initiating Contraction
Ca2+ binds to receptor on troponin
molecule
Troponin–tropomyosin complex changes
Exposes active site of F actin
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A Thick Filament
Contain twisted myosin subunits
Contain titin strands that recoil after stretching
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The Mysosin Molecule
 Tail:
– binds to other myosin molecules
 Head:
– made of 2 globular protein subunits
– reaches the nearest thin filament
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Mysosin Action
 During contraction, myosin heads:
– interact with actin filaments, forming
cross-bridges
– pivot, producing motion
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Skeletal Muscle Contraction
 Sliding filament theory:
Sliding Filaments
– thin filaments of sarcomere
slide toward M line
– between thick filaments
– the width of A zone stays the
same
– Z lines move closer together
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What are the components
of the neuromuscular
junction, and the events
involved in the neural control of
skeletal muscles?
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The Process of Contraction
 Neural stimulation of sarcolemma:
– causes excitation–contraction coupling
2+
 Cisternae of SR release Ca :
– which triggers interaction of thick and thin
filaments
– consuming ATP and producing tension
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The Neuromuscular Junction
 Is the location of neural stimulation
 Action potential (electrical signal):
– travels along nerve axon
– ends at synaptic terminal
Synaptic Terminal
 Releases neurotransmitter (acetylcholine or
ACh)
 Into the synaptic cleft (gap between synaptic
terminal and motor end plate)
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The Neurotransmitter
 Acetylcholine or ACh:
– travels across the synaptic cleft
– binds to membrane receptors on
sarcolemma (motor end plate)
– causes sodium–ion rush into sarcoplasm
– is quickly broken down by enzyme
(acetylcholinesterase or AChE)
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Action Potential
Generated by increase in sodium ions in sarcolemma
Travels along the T tubules
Leads to excitation–contraction coupling
Resting membrane potential: about -80 to -90
millivolts in skeletal fibers-the same as in large
myelinated nerve fibers.
 Duration of action potential: 1 to 5 milliseconds in
skeletal muscle-about five times as long as in large
myelinated nerves.
 Velocity of conduction: 3 to 5 m/sec-about 1/13 the
velocity of conduction in the large myelinated nerve
fibers that excite skeletal muscle.




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Excitation–Contraction
Coupling
 Action potential reaches a triad:
– releasing Ca2+
– triggering contraction
 Requires myosin heads to be in “cocked”
position:
– loaded by ATP energy
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Skeletal Muscle Contraction
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Skeletal Muscle Innervation
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Skeletal Muscle Innervation
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5 Steps of the
Contraction Cycle
1.
2.
3.
4.
5.
Exposure of active sites
Formation of cross-bridges
Pivoting of myosin heads
Detachment of cross-bridges
Reactivation of myosin
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The Contraction Cycle
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The Contraction Cycle
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The Contraction Cycle
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The Contraction Cycle
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Fiber Shortening
 As sarcomeres shorten, muscle pulls
together, producing tension
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Contraction Duration
 Depends on:
– duration of neural stimulus
– number of free calcium ions in sarcoplasm
– availability of ATP
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Relaxation
 Ca2+ concentrations fall
2+
 Ca detaches from troponin
 Active sites are recovered by tropomyosin
 Sarcomeres remain contracted
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A Review of Muscle
Contraction
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A Review of Muscle
Contraction
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KEY CONCEPT
 Skeletal muscle fibers shorten as thin filaments
slide between thick filaments
 Free Ca2+ in the sarcoplasm triggers
contraction
 SR releases Ca2+ when a motor neuron
stimulates the muscle fiber
 Contraction is an active process
 Relaxation and return to resting length is
passive
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What are the mechanisms by
which muscle fibers obtain
energy to power contractions?
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ATP and Muscle Contraction
 Sustained muscle contraction uses a lot of
ATP energy
 Muscles store enough energy to start
contraction
 Muscle fibers must manufacture more ATP
as needed
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ATP and CP Reserves
 Adenosine triphosphate (ATP):
– the active energy molecule
 Creatine phosphate (CP):
– the storage molecule for excess ATP energy in
resting muscle
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Recharging ATP
 Energy recharges ADP to ATP:
– using the enzyme creatine phosphokinase
(CPK)
 When CP is used up, other mechanisms
generate ATP
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Energy Storage in Muscle Fiber
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ATP Generation
 Cells produce ATP in 2 ways:
– aerobic metabolism of fatty acids in the
mitochondria
– anaerobic glycolysis in the cytoplasm
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Aerobic Metabolism
 Is the primary energy source of resting
muscles
 Breaks down fatty acids
 Produces 34 ATP molecules per glucose
molecule
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Anaerobic Glycolysis
 Is the primary energy source for peak
muscular activity
 Produces 2 ATP molecules per molecule
of glucose
 Breaks down glucose from glycogen stored
in skeletal muscles
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Energy Use and Muscle Activity
 At peak exertion:
– muscles lack oxygen to support mitochondria
– muscles rely on glycolysis for ATP
– pyruvic acid builds up, is converted to lactic
acid
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Muscle Metabolism
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Muscle Metabolism
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What are the structural and
functional differences between
skeletal muscle fibers and
cardiac muscle cells?
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Structure of Cardiac Tissue
 Cardiac muscle is striated,
found only in the heart
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7 Characteristics of Cardiocytes
 Unlike skeletal muscle, cardiac muscle cells
(cardiocytes):
– are small
– have a single nucleus
– have short, wide T tubules
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7 Characteristics of Cardiocytes
 have no triads
 have SR with no terminal cisternae
 are aerobic (high in myoglobin, mitochondria)
 have intercalated discs
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Intercalated Discs
 Are specialized contact points between
cardiocytes
 Join cell membranes of adjacent cardiocytes
(gap junctions, desmosomes)
Functions of Intercalated Discs
 Maintain structure
 Enhance molecular and electrical connections
 Conduct action potentials
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Coordination of Cardiocytes
 Because intercalated discs link heart cells
mechanically, chemically, and electrically,
the heart functions like a single, fused mass
of cells
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4 Functions of Cardiac Tissue
1. Automaticity:
–
–
contraction without neural stimulation
controlled by pacemaker cells
2. Variable contraction tension:
–
controlled by nervous system
3. Extended contraction time
4. Prevention of wave summation and tetanic
contractions by cell membranes
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What are the structural and
functional differences between
skeletal muscle fibers and
smooth muscle cells?
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Role of Smooth Muscle in Body
Systems
 Forms around other tissues
 In blood vessels:
– regulates blood pressure and flow
 In reproductive and glandular systems:
– produces movements
 In digestive and urinary systems:
– forms sphincters
– produces contractions
 In integumentary system:
– arrector pili muscles cause goose bumps
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Structure of Smooth Muscle
 Nonstriated tissue
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Comparing Smooth
and Striated Muscle
 Different internal organization of actin and
myosin
 Different functional characteristics
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8 Characteristics of
Smooth Muscle Cells
1. Long, slender, and spindle shaped
2. Have a single, central nucleus
3. Have no T tubules, myofibrils, or
sarcomeres
4. Have no tendons or aponeuroses
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8 Characteristics of
Smooth Muscle Cells
5. Have scattered myosin fibers
6. Myosin fibers have more heads per thick
filament
7. Have thin filaments attached to dense
bodies
8. Dense bodies transmit contractions from
cell to cell
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Functional Characteristics
of Smooth Muscle
1.
2.
3.
4.
Excitation–contraction coupling
Length–tension relationships
Control of contractions
Smooth muscle tone
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Excitation–Contraction
Coupling
 Free Ca2+ in cytoplasm triggers contraction
2+
 Ca binds with calmodulin:
– in the sarcoplasm
– activates myosin light chain kinase
 Enzyme breaks down ATP, initiates
contraction
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Length–Tension Relationships
 Thick and thin filaments are scattered
 Resting length not related to tension
development
 Functions over a wide range of lengths
(plasticity)
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Control of Contractions
 Subdivisions:
– multiunit smooth muscle cells:
• connected to motor neurons
– visceral smooth muscle cells:
• not connected to motor neurons
• rhythmic cycles of activity controlled by pacesetter
cells
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Smooth Muscle Tone
 Maintains normal levels of activity
 Modified by neural, hormonal, or chemical
factors
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Characteristics of Skeletal,
Cardiac, and Smooth Muscle
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What are the types of
muscle contractions,
and how do they differ?
2 Types of Skeletal Muscle Tension
 Isotonic contraction
 Isometric contraction
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Isotonic Contraction
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Isotonic Contraction
 Skeletal muscle changes length:
– resulting in motion
 If muscle tension > resistance:
– muscle shortens (concentric contraction)
 If muscle tension < resistance:
– muscle lengthens (eccentric contraction)
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Isometric Contraction
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Isometric Contraction
 Skeletal muscle develops tension, but is
prevented from changing length
Note: Iso = same, metric = measure
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Muscle Relaxation
 After contraction, a muscle fiber returns
to resting length by:
– elastic forces
– opposing muscle contractions
– gravity
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What is the mechanism
responsible for tension
production in a muscle fiber,
and what factors determine the
peak tension developed during
a contraction?
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Tension Production
 The all–or–none principal:
– as a whole, a muscle fiber is either contracted or
relaxed
Tension of a Single Muscle Fiber
 Depends on:
– the number of pivoting cross-bridges
– the fiber’s resting length at the time of stimulation
– the frequency of stimulation
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Tension and Sarcomere Length
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Length–Tension Relationship
 Number of pivoting cross-bridges depends on:
– amount of overlap between thick and thin fibers
 Optimum overlap produces greatest amount of
tension:
– too much or too little reduces efficiency
 Normal resting sarcomere length:
– is 75% to 130% of optimal length
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Frequency of Stimulation
 A single neural stimulation produces:
– a single contraction or twitch
– which lasts about 7–100 msec
 Sustained muscular contractions:
– require many repeated stimuli
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Tension in a Twitch
 Length of twitch depends on type of muscle
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Myogram
 A graph of twitch tension development
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3 Phases of Twitch
1. Latent period before contraction:
–
–
the action potential moves through sarcolemma
causing Ca2+ release
2. Contraction phase:
–
–
calcium ions bind
tension builds to peak
3. Relaxation phase:
–
–
–
Ca2+ levels fall
active sites are covered
tension falls to resting levels
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Treppe
 A stair-step increase in twitch tension
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Treppe
 Repeated stimulations immediately after
relaxation phase:
– stimulus frequency < 50/second
 Causes a series of contractions with
increasing tension
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Wave Summation
 Increasing tension or summation of twitches
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Figure 10–16b
Wave Summation
 Repeated stimulations before the end of
relaxation phase:
– stimulus frequency > 50/second
 Causes increasing tension or summation
of twitches
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Incomplete Tetanus
Twitches reach maximum tension
 If rapid stimulation
continues and muscle is
not allowed to relax,
twitches reach
maximum level of
tension
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Complete Tetanus
 If stimulation
frequency is high
enough, muscle
never begins to
relax, and is in
continuous
contraction
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What factors affect peak
tension production during the
contraction of an entire skeletal
muscle, and what is the
significance of the motor unit in
this process?
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Tension Produced by
Whole Skeletal Muscles
 Depends on:
– internal tension produced by muscle fibers
– external tension exerted by muscle fibers on
elastic extracellular fibers
– total number of muscle fibers stimulated
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Motor Units in a Skeletal Muscle
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Motor Units in a Skeletal
Muscle
 Contain hundreds of muscle fibers
 That contract at the same time
 Controlled by a single motor neuron
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Recruitment (Multiple
Motor Unit Summation)
 In a whole muscle or group of muscles,
smooth motion and increasing tension
is produced by slowly increasing size or
number of motor units stimulated
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Maximum Tension
 Achieved when all motor units reach
tetanus
 Can be sustained only a very short time
Sustained Tension
 Less than maximum tension
 Allows motor units to rest in rotation
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KEY CONCEPT
 Voluntary muscle contractions involve
sustained, tetanic contractions of skeletal
muscle fibers
 Force is increased by increasing the
number of stimulated motor units
(recruitment)
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Muscle Tone
 The normal tension and firmness of a
muscle at rest
 Muscle units actively maintain body
position, without motion
 Increasing muscle tone increases metabolic
energy used, even at rest
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What factors contribute to
muscle fatigue, and what are
the stages and mechanisms
involved in muscle recovery?
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Muscle Fatigue
 When muscles can no longer perform a required
activity, they are fatigued
Results of Muscle Fatigue
1. Depletion of metabolic reserves
2. Damage to sarcolemma and sarcoplasmic
reticulum
3. Low pH (lactic acid)
4. Muscle exhaustion and pain
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The Recovery Period
 The time required after exertion for
muscles to return to normal
 Oxygen becomes available
 Mitochondrial activity resumes
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The Cori Cycle
 The removal and recycling of lactic acid by the
liver
 Liver converts lactic acid to pyruvic acid
 Glucose is released to recharge muscle glycogen
reserves
Oxygen Debt
 After exercise:
– the body needs more oxygen than usual to normalize
metabolic activities
– resulting in heavy breathing
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KEY CONCEPT
 Skeletal muscles at rest metabolize fatty
acids and store glycogen
 During light activity, muscles generate ATP
through anaerobic breakdown of
carbohydrates, lipids or amino acids
 At peak activity, energy is provided by
anaerobic reactions that generate lactic acid
as a byproduct
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Heat Production and Loss
 Active muscles produce heat
 Up to 70% of muscle energy can be lost as heat,
raising body temperature
Hormones and Muscle Metabolism
 Growth hormone
 Testosterone
 Thyroid hormones
 Epinephrine
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SUMMARY (1 of 3)
 3 types of muscle tissue:
– skeletal
– cardiac
– smooth
 Functions of skeletal muscles
 Structure of skeletal muscle cells:
– endomysium
– perimysium
– epimysium
 Functional anatomy of skeletal muscle fiber:
– actin and myosin
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SUMMARY (2 of 3)
 Nervous control of skeletal muscle fibers:
– neuromuscular junctions
– action potentials
 Tension production in skeletal muscle fibers:
– twitch, treppe, tetanus
 Tension production by skeletal muscles:
– motor units and contractions
 Skeletal muscle activity and energy:
– ATP and CP
– aerobic and anaerobic energy
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SUMMARY (3 of 3)
 Skeletal muscle fatigue and recovery
 3 types of skeletal muscle fibers:
– fast, slow, and intermediate
 Skeletal muscle performance:
– white and red muscles
– physical conditioning
 Structures and functions of:
– cardiac muscle tissue
– smooth muscle tissue
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Pharmacology of the vertebrate neuromuscular junction
Prevent Depolarization
Inhibit Repolarization
Many of the proteins that are involved in synaptic transmission at the mammalian neuromuscular
junction are the targets of naturally occurring or synthetic drugs.
The antagonists are shown as minus signs highlighted in red.The agonists are shown as plus signs
highlighted in green.
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Drugs that enhance or block transmission at
the neuromuscular junction
 Drugs That Stimulate the Muscle Fiber by
Acetylcholine-Like Action.
- methacholine, carbachol, and nicotine- these Ach
agonists are not destroyed by cholinesterase or are destroyed
so slowly that their action often persists for many minutes to
several hours.
- work by causing localized areas of depolarization of motor
end plate  every time the muscle fiber recovers from a
previous contraction, these depolarized areas, by virtue of
leaking ions, initiate a new action potential  muscle spasm.
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 Drugs That Stimulate the Neuromuscular
Junction by Inactivating Acetylcholinesterase.
- neostigmine, physostigmine, pyridostigmine and
diisopropyl fluorophosphate  inactivate AChE  with
each successive nerve impulse, additional ACh accumulates and
stimulates the muscle fiber repetitively  muscle spasm
caused by minimum stimulation (it also can cause death due to
laryngeal spasm).
Neostigmine and physostigmine combine with AChE to
reversible inactivate the AChE for up to several hours.
Pyridostigmine is used in myasthenia gravis treatment.
Diisopropyl fluorophosphate (powerful "nerve" gas poison)
inactivates AChE for weeks, which makes this a particularly
lethal poison.
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 Transmission at the Neuromuscular Junction.
- curariform drugs can prevent passage of impulses from the
nerve ending into the muscle, by competing for the ACh
receptor sites. For instance, D-tubocurarine blocks the
action of ACh on the muscle fiber ACh receptors, thus
preventing sufficient increase in permeability of the muscle
membrane channels to initiate an action potential.
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Myasthenia gravis = muscle weakness
(from the Greek mys and asthenia)
 Acquired autoimmune disorder in which the spontaneous
production of anti‐AChR antibodies results in progressive loss of
muscle AChRs and degeneration of postjunctional folds.
 The most common target of these antibodies is a region of the
AChR α subunit called MIR (main immunogenic region).
 Clinical: fatigue and weakness of skeletal muscle; severe cases ‐
paralysis of the respiratory muscles  death
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Myasthenia gravis = muscle weakness
(from the Greek mys and asthenia)
 Treatment:
1. reduce the potency of the immunological attack
(immunosuppressants ‐ corticosteroids or plasmapheresis
‐removal of antibodies from the patient's serum)
2. enhance cholinergic activity within the synapse: AChE
inhibitors ‐pyridostigmine; dosage of these drugs must be carefully
monitored to prevent overexposure of the remaining AChRs to Ach
 overstimulation of the postsynaptic receptors, prolonged
depolarization of the postsynaptic membrane, inactivation of
neighboring Na+ channels, and thus synaptic blockade.
3. Some patients with myasthenia gravis have a thymus gland
tumor  removal of the thymoma leads to clinical improvement in
nearly 75% of the cases.
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THANK YOU
FOR YOUR ATTENTION
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