Download An Introduction to Muscle Tissue

An Introduction to Muscle Tissue
 Muscle Tissue
 A primary tissue type, divided into
 Skeletal muscle
 Cardiac muscle
 Smooth muscle
 Skeletal Muscles
 Are attached to the skeletal system
 Allow us to move
 The muscular system
 Includes only skeletal muscles
Functions of Skeletal Muscles
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Produce skeletal movement
Maintain body position
Support soft tissues
Guard openings
Maintain body temperature
Store nutrient reserves
Skeletal Muscle Structures
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Muscle tissue (muscle cells or fibers)
Connective tissues
Nerves
Blood vessels
 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
 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
Skeletal Muscle Fibers
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Are very long
Develop through fusion of mesodermal cells (myoblasts)
Become very large
Contain hundreds of nuclei
 Internal Organization of Muscle Fibers
 The sarcolemma
 The cell membrane of a muscle fiber (cell)
 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
 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
 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 Ca2+ (via ion pumps)
– release Ca2+ into sarcomeres to begin muscle contraction
 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)
 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
 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
 Ca2+ released by SR causes thin and thick filaments to interact
 Muscle Contraction
 Is caused by interactions of thick and thin filaments
 Structures of protein molecules determine interactions
 Four Thin Filament Proteins
 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
 Tropomyosin
 Is a double strand
 Prevents actin–myosin interaction
 Troponin
 A globular protein
 Binds tropomyosin to G-actin
 Controlled by Ca2+
 Initiating Contraction
 Ca2+ binds to receptor on troponin molecule
 Troponin–tropomyosin complex changes
 Exposes active site of F-actin
 Thick Filaments
 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
 Myosin Action
 During contraction, myosin heads
 Interact with actin filaments, forming cross-bridges
 Pivot, producing motion
 Skeletal Muscle Contraction
 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
 The process of contraction
 Neural stimulation of sarcolemma:
– causes excitation–contraction coupling
 Cisternae of SR release Ca2+:
– which triggers interaction of thick and thin filaments
– consuming ATP and producing tension
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)
 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)
 Action Potential
 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 Ca2+
» triggering contraction
– requires myosin heads to be in “cocked” position:
» loaded by ATP energy
The Contraction Cycle
 Five Steps of the Contraction Cycle
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Exposure of active sites
Formation of cross-bridges
Pivoting of myosin heads
Detachment of cross-bridges
Reactivation of myosin
 Fiber Shortening
 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
 Ca2+ concentrations fall
 Ca2+ detaches from troponin
 Active sites are re-covered by tropomyosin
 Sarcomeres remain contracted
 Rigor Mortis
 A fixed muscular contraction after death
 Caused when
 Ion pumps cease to function; ran out of ATP
 Calcium builds up in the sarcoplasm
The Contraction Cycle
 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 are passive
Tension Production
 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 Ca2+ release
 Contraction phase
 Calcium ions bind
 Tension builds to peak
 Relaxation phase
 Ca2+ levels fall
 Active sites are covered
 Tension falls to resting levels
 Treppe
 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
 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
 Motor units in a skeletal muscle
 Contain hundreds of muscle fibers
 That contract at the same time
 Controlled by a single motor neuron
 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
 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
 Two Types of Skeletal Muscle Tension
 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)
 Expands the sarcomeres to resting length
 Opposing Muscle Contractions
 Reverse the direction of the original motion
 Are the work of opposing skeletal muscle pairs
 Gravity
 Can take the place of opposing muscle contraction to return a
muscle to its resting state
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
 ATP and CP Reserves
 Adenosine triphosphate (ATP)
 The active energy molecule
 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)
 When CP is used up, other mechanisms generate ATP
 ATP Generation
 Cells produce ATP in two ways
 Aerobic metabolism of fatty acids in the mitochondria
 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
 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
 Muscle Fatigue
 When muscles can no longer perform a required activity, they are fatigued
 Results of Muscle Fatigue
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Depletion of metabolic reserves
Damage to sarcolemma and sarcoplasmic reticulum
Low pH (lactic acid)
Muscle exhaustion and pain
 The Recovery Period
 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
 Glucose is released to recharge muscle glycogen reserves
 Oxygen Debt
 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
 Active muscles produce heat
 Up to 70% of muscle energy can be lost as heat, raising body temperature
 Hormones and Muscle Metabolism
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Growth hormone
Testosterone
Thyroid hormones
Epinephrine
 Muscle Performance
 Power
 The maximum amount of tension produced
 Endurance
 The amount of time an activity can be sustained
 Power and endurance depend on
 The types of muscle fibers
 Physical conditioning
Muscle Fiber Types
 Three Types of Skeletal Muscle Fibers
 Fast fibers
 Slow fibers
 Intermediate fibers
 Fast fibers
 Contract very quickly
 Have large diameter, large glycogen reserves, few mitochondria
 Have strong contractions, fatigue quickly
 Slow fibers
 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
 Have more capillaries than fast fibers, slower to fatigue
 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
 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
 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
Cardiac Muscle Tissue
 Structure of Cardiac Tissue
 Cardiac muscle is striated, found only in the heart
 Seven Characteristics of Cardiocytes
 Unlike skeletal muscle, cardiac muscle cells (cardiocytes)
 Are small
 Have a single nucleus
 Have short, wide T tubules
 Have no triads
 Have SR with no terminal cisternae
 Are aerobic (high in myoglobin, mitochondria)
 Have intercalated discs
 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
 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
 Variable contraction tension
 Controlled by nervous system
 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
 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”
 Structure of Smooth Muscle
 Nonstriated tissue
 Different internal organization of actin and myosin
 Different functional characteristics
 Eight Characteristics of Smooth Muscle Cells
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Long, slender, and spindle shaped
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
Smooth Muscle Tissue
 Functional Characteristics of Smooth Muscle
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Excitation–contraction coupling
Length–tension relationships
Control of contractions
Smooth muscle tone
 Excitation–contraction coupling
 Free Ca2+ in cytoplasm triggers contraction
 Ca2+ 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
 Maintains normal levels of activity
 Modified by neural, hormonal, or chemical factors