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 A primary tissue type, divided into
 Skeletal muscle
 Cardiac muscle
 Smooth muscle
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 Are attached to the skeletal system
 Allow us to move
 The muscular system
 Includes only skeletal muscles
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 Organization of Connective Tissues
 Muscles have three layers of connective tissues
 Epimysium:
– exterior collagen layer
– connected to deep fascia
– Separates muscle from surrounding tissues
 Perimysium:
– surrounds muscle fiber bundles (fascicles)
– contains blood vessel and nerve supply to fascicles
 Endomysium:
– surrounds individual muscle cells (muscle fibers)
– contains capillaries and nerve fibers contacting muscle cells
– contains myosatellite cells (stem cells) that repair damage
 Muscle attachments

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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)
 Nerves
 Skeletal muscles are voluntary muscles, controlled by nerves of the central nervous system (brain and spinal cord)
 Blood Vessels
 Muscles have extensive vascular systems that
 Supply large amounts of oxygen
 Supply nutrients
 Carry away wastes
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 Internal Organization of Muscle Fibers
 The sarcolemma
 The cell membrane of a muscle fiber (cell)
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Surrounds the sarcoplasm (cytoplasm of muscle fiber)
 A change in transmembrane potential begins contractions
 Transverse tubules (T tubules)
 Transmit action potential through cell
 Allow entire muscle fiber to contract simultaneously
 Have same properties as sarcolemma
 Myofibrils
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Lengthwise subdivisions within muscle fiber
 Made up of bundles of protein filaments ( myofilaments )
 Myofilaments are responsible for muscle contraction
 Types of myofilaments:
– thin filaments :
» made of the protein actin
– thick filaments :
» made of the protein myosin
 Sarcoplasmic reticulum (SR)
 A membranous structure surrounding each myofibril
 Helps transmit action potential to myofibril
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Similar in structure to smooth endoplasmic reticulum
 Forms chambers ( terminal cisternae ) attached to T tubules

 Triad
 Is formed by one T tubule and two terminal cisternae
 Cisternae:
– concentrate Ca 2+ ( via ion pumps)
– release Ca 2+ into sarcomeres to begin muscle contraction
 Sarcomeres
 The contractile units of muscle
 Structural units of myofibrils
 Form visible patterns within myofibrils
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Muscle striations
 A striped or striated pattern within myofibrils:
– alternating dark, thick filaments (A bands) and light, thin filaments (I bands)
 Sarcomeres
 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 two ends of sarcomere
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Zone of overlap:
– the densest, darkest area on a light micrograph
– where thick and thin filaments overlap
 The H Band:
– 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
 Transverse tubules encircle the sarcomere near zones of overlap
 Ca 2+ released by SR causes thin and thick filaments to interact
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 Is caused by interactions of thick and thin filaments
 Structures of protein molecules determine interactions
 Four Thin Filament Proteins

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F-actin (Filamentous actin)
 Is two twisted rows of globular G-actin
 The active sites on G-actin strands bind to myosin
 Nebulin
 Holds F-actin strands together
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Tropomyosin
 Is a double strand
 Prevents actin –myosin interaction
 Troponin
 A globular protein
 Binds tropomyosin to G-actin
 Controlled by Ca 2+
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 Ca 2+ binds to receptor on troponin molecule
 Troponin –tropomyosin complex changes
 Exposes active site of F-actin
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 Contain twisted myosin subunits
 Contain titin strands that recoil after stretching
 The mysosin molecule
 Tail:
– binds to other myosin molecules
 Head:
– made of two globular protein subunits
– reaches the nearest thin filament
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 During contraction, myosin heads
 Interact with actin filaments, forming cross-bridges
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Pivot, producing motion
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 Sliding filament theory
 Thin filaments of sarcomere slide toward M line, alongside thick filaments
 The width of A zone stays the same
 Z lines move closer together
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The process of contraction
 Neural stimulation of sarcolemma:
– causes excitation
–contraction coupling
 Cisternae of SR release Ca 2+ :
– which triggers interaction of thick and thin filaments
– consuming ATP and producing tension

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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 )
 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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 Generated by increase in sodium ions in sarcolemma
 Travels along the T tubules
 Leads to excitation –contraction coupling
 Excitation –contraction coupling:
– action potential reaches a triad:
» releasing Ca 2+
» triggering contraction
– requires myosin heads to be in “cocked” position:
» loaded by ATP energy
 Five Steps of the Contraction Cycle
 Exposure of active sites
 Formation of cross-bridges
 Pivoting of myosin heads
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Detachment of cross-bridges
 Reactivation of myosin
 Fiber Shortening
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As sarcomeres shorten, muscle pulls together, producing tension
 Contraction Duration
 Depends on
 Duration of neural stimulus
 Number of free calcium ions in sarcoplasm
 Availability of ATP
 Relaxation
 Ca 2+ concentrations fall

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Ca 2+ detaches from troponin
 Active sites are re-covered by tropomyosin
 Sarcomeres remain contracted
 Rigor Mortis
 A fixed muscular contraction after death
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Caused when
 Ion pumps cease to function; ran out of ATP
 Calcium builds up in the sarcoplasm
 Skeletal muscle fibers shorten as thin filaments slide between thick filaments
 Free Ca 2+ in the sarcoplasm triggers contraction
 SR releases Ca 2+ when a motor neuron stimulates the muscle fiber
 Contraction is an active process
 Relaxation and return to resting length are passive
 The all –or–none principle
 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
 Tension of a Single Muscle Fiber
 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
 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
 Three Phases of Twitch
 Latent period before contraction

 The action potential moves through sarcolemma
 Causing Ca 2+ release
 Contraction phase
 Calcium ions bind
 Tension builds to peak
 Relaxation phase
 Ca 2+ levels fall
 Active sites are covered
 Tension falls to resting levels
 Treppe
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A stair-step increase in twitch tension
 Repeated stimulations immediately after relaxation phase
 Stimulus frequency <50/second
 Causes a series of contractions with increasing tension
 Wave summation
 Increasing tension or summation of twitches
 Repeated stimulations before the end of relaxation phase:
– stimulus frequency >50/second
 Causes increasing tension or summation of twitches
 Incomplete tetanus
 Twitches reach maximum tension
 If rapid stimulation continues and muscle is not allowed to relax, twitches reach maximum level of tension
 Complete Tetanus
 If stimulation frequency is high enough, muscle never begins to relax, and is in continuous contraction
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 Depends on
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Internal tension produced by muscle fibers
 External tension exerted by muscle fibers on elastic extracellular fibers
 Total number of muscle fibers stimulated
 Motor units in a skeletal muscle
 Contain hundreds of muscle fibers
 That contract at the same time
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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 are produced by slowly increasing the size or number of motor units stimulated
 Maximum tension
 Achieved when all motor units reach tetanus
 Can be sustained only a very short time

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Sustained tension
 Less than maximum tension
 Allows motor units rest in rotation
 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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 Isotonic contraction
 Isometric contraction
 Two Types of Skeletal Muscle Tension
 Isotonic Contraction
 Skeletal muscle changes length:
– resulting in motion
 If muscle tension > load (resistance):
– muscle shortens ( concentric contraction )
 If muscle tension < load (resistance):
– muscle lengthens ( eccentric contraction )
 Isometric contraction
 Skeletal muscle develops tension, but is prevented from changing length
Note : iso = same, metric = measure
 Resistance and Speed of Contraction
 Are inversely related
 The heavier the load (resistance) on a muscle
 The longer it takes for shortening to begin
 And the less the muscle will shorten
 Muscle Relaxation
 After contraction, a muscle fiber returns to resting length by
 Elastic forces
 Opposing muscle contractions
 Gravity
 Elastic Forces
 The pull of elastic elements (tendons and ligaments)
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Expands the sarcomeres to resting length
 Opposing Muscle Contractions
 Reverse the direction of the original motion
 Are the work of opposing skeletal muscle pairs
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 Can take the place of opposing muscle contraction to return a muscle to its resting state

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 ATP and CP Reserves
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Adenosine triphosphate (ATP)
 The active energy molecule
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Creatine phosphate (CP)
 The storage molecule for excess ATP energy in resting muscle
 Energy recharges ADP to ATP
 Using the enzyme creatine phosphokinase (CPK or CK)
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When CP is used up, other mechanisms generate ATP
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 Cells produce ATP in two ways
 Aerobic metabolism of fatty acids in the mitochondria
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Anaerobic glycolysis in the cytoplasm
 Aerobic metabolism
 Is the primary energy source of resting muscles
 Breaks down fatty acids
 Produces 34 ATP molecules per glucose molecule
 Anaerobic glycolysis
 Is the primary energy source for peak muscular activity
 Produces two ATP molecules per molecule of glucose
 Breaks down glucose from glycogen stored in skeletal muscles
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 At peak exertion
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Muscles lack oxygen to support mitochondria
 Muscles rely on glycolysis for ATP
 Pyruvic acid builds up, is converted to lactic acid
 Muscle Fatigue
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When muscles can no longer perform a required activity, they are fatigued
 Results of Muscle Fatigue
 Depletion of metabolic reserves
 Damage to sarcolemma and sarcoplasmic reticulum
 Low pH (lactic acid)
 Muscle exhaustion and pain
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 The time required after exertion for muscles to return to normal
 Oxygen becomes available
 Mitochondrial activity resumes

 The Cori Cycle
 The removal and recycling of lactic acid by the liver
 Liver converts lactic acid to pyruvic acid
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Glucose is released to recharge muscle glycogen reserves
 Oxygen Debt
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After exercise or other exertion
 The body needs more oxygen than usual to normalize metabolic activities
 Resulting in heavy breathing
 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
 Heat Production and Loss
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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
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Thyroid hormones
 Epinephrine
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 Power
 The maximum amount of tension produced
 Endurance
 The amount of time an activity can be sustained
 Power and endurance depend on
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The types of muscle fibers
 Physical conditioning
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 Fast fibers
 Slow fibers
 Intermediate fibers
 Fast fibers
 Contract very quickly
 Have large diameter, large glycogen reserves, few mitochondria
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Have strong contractions, fatigue quickly
 Slow fibers

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Are slow to contract, slow to fatigue
 Have small diameter, more mitochondria
 Have high oxygen supply
 Contain myoglobin (red pigment, binds oxygen)
 Intermediate fibers
 Are mid-sized
 Have low myoglobin
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Have more capillaries than fast fibers, slower to fatigue
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 White muscle
 Mostly fast fibers
 Pale ( e.g., chicken breast)
 Red muscle
 Mostly slow fibers
 Dark ( e.g., chicken legs)
 Most human muscles
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Mixed fibers
 Pink
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 Muscle growth from heavy training
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Increases diameter of muscle fibers
 Increases number of myofibrils
 Increases mitochondria, glycogen reserves
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 Lack of muscle activity
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Reduces muscle size, tone, and power
 Physical Conditioning
 Improves both power and endurance
 Anaerobic activities ( e.g., 50-meter dash, weightlifting):
– use fast fibers
– fatigue quickly with strenuous activity
 Improved by:
– frequent, brief, intensive workouts
– hypertrophy
 Improves both power and endurance
 Aerobic activities (prolonged activity):
– supported by mitochondria
– require oxygen and nutrients
 Improved by:
– repetitive training (neural responses)

– cardiovascular training
 What you don’t use, you lose
 Muscle tone indicates base activity in motor units of skeletal muscles
 Muscles become flaccid when inactive for days or weeks
 Muscle fibers break down proteins, become smaller and weaker
 With prolonged inactivity, fibrous tissue may replace muscle fibers
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 Unlike skeletal muscle, cardiac muscle cells ( cardiocytes )
 Are small
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Have a single nucleus
 Have short, wide T tubules
 Have no triads
 Have SR with no terminal cisternae
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Are aerobic (high in myoglobin, mitochondria)
 Have intercalated discs
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 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
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Conduct action potentials
 Coordination of cardiocytes
 Because intercalated discs link heart cells mechanically, chemically, and electrically, the heart functions like a single, fused mass of cells
 Four Functions of Cardiac Tissue
 Automaticity
 Contraction without neural stimulation
 Controlled by pacemaker cells
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Variable contraction tension
 Controlled by nervous system
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Extended contraction time

 Ten times as long as skeletal muscle
 Prevention of wave summation and tetanic contractions by cell membranes
 Long refractory period
 Smooth Muscle in Body Systems
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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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 Nonstriated tissue
 Different internal organization of actin and myosin
 Different functional characteristics
 Eight Characteristics of Smooth Muscle Cells
 Long, slender, and spindle shaped
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Have a single, central nucleus
 Have no T tubules, myofibrils, or sarcomeres
 Have no tendons or aponeuroses
 Have scattered myosin fibers
 Myosin fibers have more heads per thick filament
 Have thin filaments attached to dense bodies
 Dense bodies transmit contractions from cell to cell
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 Excitation –contraction coupling
 Length –tension relationships
 Control of contractions
 Smooth muscle tone
 Excitation –contraction coupling
 Free Ca 2+ in cytoplasm triggers contraction
 Ca 2+ binds with calmodulin :
– in the sarcoplasm
– activates myosin light
–chain kinase
 Enzyme breaks down ATP, initiates contraction

 Length –Tension Relationships
 Thick and thin filaments are scattered
 Resting length not related to tension development
 Functions over a wide range of lengths ( plasticity )
 Control of contractions
 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
 Smooth muscle tone
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Maintains normal levels of activity
 Modified by neural, hormonal, or chemical factors