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79 Cards in this Set

  • Front
  • Back
Muscle Overview
3 types of muscle tissue are skeletal, cardiac & smooth

~These types differ in structure, location, function & means of activation
Muscle Similarities
~Skeletal & smooth muscle cells are elongated & are called muscle fibers
~Muscle contraction depends on 2 kinds of myofilaments –Actin & myosin
~Muscle terminology is similar
a)Sarcolemma –Muscle plasma membrane
b)Sarcoplasm –Cytoplasm of a muscle cell
c)Prefixes –Myo, mys & sarco all refer to muscle
Skeletal Muscle Tissue
~Packaged in skeletal muscles that attach to & cover bony skeleton

~Has obvious stripes called striations

~Is controlled voluntarily (by conscious control)

~Contracts rapidly but tires easily

~Is responsible for overall body motility

~Is extremely adaptable & can exert forces ranging from a fraction of an ounce to over 70 pounds
Cardiac Muscle Tissue
~Occurs only in heart

~Is striated like skeletal muscle but is not voluntary

~Contracts at a fairly steady rate set by heart’s pacemaker

~Neural controls allow heart to respond to changes in bodily needs
Smooth Muscle Tissue
~Found in walls of hollow visceral organs, such as stomach, urinary bladder & respiratory passages

~Forces food & other substances through internal body channels

~It is not striated & is involuntary
*Functional Characteristics of Muscle Tissue(4)
1~Skeletal muscles are responsible for all locomotion

2~Cardiac muscle is responsible for coursing blood through body

3~Smooth muscle helps maintain blood pressure & squeezes or propels substances (food, feces) through organs

4~Muscles also maintain posture, stabilize joints & generate heat
Skeletal Muscle & 3 connective tissue sheaths
~Each muscle is a discrete organ composed of muscle tissue, blood vessels, nerve fibers & connective tissue

~Connective tissue sheaths are:
1)Endomysium –Fine sheath of connective tissue composed of reticular fibers surrounding each muscle fiber
2)Perimysium – Fibrous connective tissue that surrounds groups of muscle fibers called fascicles
3)Epimysium –An overcoat of dense regular connective tissue that surrounds entire muscle
Skeletal Muscle: Nerve & Blood Supply
~Each muscle is served by 1 nerve, an artery & one or more veins

~Each skeletal muscle fiber is supplied w a nerve ending that controls contraction

~Contracting fibers require continuous delivery of oxygen & nutrients via arteries

~Wastes must be removed via veins
Skeletal Muscle: Attachments(2 ways)
~Most skeletal muscles span joints & are attached to bone in at least 2 places

~When muscles contract movable bone, muscle’s insertion moves toward immovable bone, muscle’s origin

~Muscles attach:
1)Directly –Epimysium of muscle is fused to periosteum of a bone
2)Indirectly –Connective tissue wrappings extend beyond muscle as a tendon or aponeurosis
Microscopic Anatomy of a Skeletal Muscle Fiber
~Each fiber is a long, cylindrical cell w multiple nuclei just beneath sarcolemma

~Fibers are 10 to 100 u?m in diameter & up to 100s of centimeters long

~Each cell is a syncytium produced by fusion of embryonic cells

~Sarcoplasm has numerous glycosomes and a unique oxygen-binding protein called myoglobin

~Fibers contain the usual organelles, myofibrils, sarcoplasmic reticulum & T tubules
Myofibrils
~Myofibrils are densely packed, rodlike contractile elements & make up most of muscle volume

~Arrangement of myofibrils within a fiber is such that a perfectly aligned repeating series of dark A bands & light I bands is evident
Sarcomeres
~Smallest contractile unit of a muscle

~Region of a myofibril between 2 successive Z discs

~Composed of myofilaments (2 types – thick & thin) made up of contractile proteins
Myofilaments: Banding Pattern
~Thick filaments –Extend entire length of an A band

~Thin filaments –Extend across I band & partway into A band

~Z-disc – coin-shaped sheet of proteins (connectins) that anchors thin filaments & connects myofibrils to 1 another

~Thin filaments do not overlap thick filaments in lighter H zone

~M lines appear darker due to presence of protein desmin
Ultrastructure of Myofilaments: Thick Filaments
~Thick filaments are composed of protein myosin

~Each myosin molecule has a rod-like tail & 2 globular heads:
1)Tails –2 interwoven, heavy polypeptide chains
2)Heads –2 smaller, light polypeptide chains called cross bridges
Ultrastructure of Myofilaments: Thin Filaments
~Thin filaments are chiefly composed of protein actin

~Each actin molecule is a helical polymer of globular subunits called G actin

~Subunits contain active sites to which myosin heads attach during contraction

~Tropomyosin & troponin are regulatory subunits bound to actin
Arrangement of Filaments in a Sarcomere
~Longitudinal section within 1 sarcomere
*Sarcoplasmic Reticulum (SR)
~SR is an elaborate, smooth endoplasmic reticulum that mostly runs longitudinally & surrounds each myofibril
~Paired terminal cisternae form perpendicular cross channels
~Functions in regulation of intracellular calcium levels
~Elongated tubes called T tubules penetrate into cell’s interior at each A band–I band junction
~T tubules associate w paired terminal cisternae to form triads
*T Tubules
~T tubules are continuous w sarcolemma

~They conduct impulses to deepest regions of muscle

~These impulses signal for release of Ca2+ from adjacent terminal cisternae
Triad Relationships
~T tubules & SR provide tightly linked signals for muscle contraction

~A double zipper of integral membrane proteins protrudes into intermembrane space

~T tubule proteins act as voltage sensors

~SR foot proteins are receptors that regulate Ca2+ release from SR cisternae
*Sliding Filament Model of Contraction
~Thin filaments slide past thick ones so that actin & myosin filaments overlap to a greater degree

~In relaxed state, thin & thick filaments overlap only slightly

~Upon stimulation, myosin heads bind to actin & sliding begins

~Each myosin head binds & detaches several times during contraction, acting like a ratchet to generate tension & propel thin filaments to center of sarcomere

~As this event occurs throughout sarcomeres, muscle shortens
Skeletal Muscle Contraction
~In order to contract, a skeletal muscle must:

1~Be stimulated by a nerve ending

2~Propagate an electrical current, or action potential, along its sarcolemma

3~Have a rise in intracellular Ca2+ levels, final trigger for contraction

~Linking electrical signal to contraction is excitation-contraction coupling
*Nerve Stimulus of Skeletal Muscle
~Skeletal muscles are stimulated by motor neurons of somatic nervous system
~Axons of these neurons travel in nerves to muscle cells
~Axons of motor neurons branch profusely as they enter muscles
~Each axonal branch forms a neuromuscular junction with a single muscle fiber
*Neuromuscular Jx (Formed from 2) & 5 Things happen when nerve impulse reaches end of axon at neuromuscular jx
1)Axonal endings, which have small membranous sacs (synaptic vesicles) that contain neurotransmitter acetylcholine (ACh)
2)Motor end plate of a muscle, which is a specific part of sarcolemma that contains ACh receptors & helps form neuromuscular jx
~Though exceedingly close, axonal ends & muscle fibers are always separated by a space called synaptic cleft
1)Voltage-regulated calcium channels open & allow Ca2+ to enter axon
2)Ca2+ inside axon terminal causes axonal vesicles to fuse w axonal membrane
3)This fusion releases ACh into synaptic cleft via exocytosis
4)ACh diffuses across synaptic cleft to ACh receptors on sarcolemma
5)Binding of ACh to its receptors initiates an action potential in muscle
*Destruction of Acetylcholine
~ACh bound to ACh receptors is quickly destroyed by enzyme acetylcholinesterase

~This destruction prevents continued muscle fiber contraction in absence of additional stimuli
*Action Potential
~A transient depolarization event that includes polarity reversal of a sarcolemma (or nerve cell membrane) & propagation of an action potential along membrane
*Role of Acetylcholine (Ach)
~ACh binds its receptors at motor end plate

~Binding opens chemically (ligand) gated channels

~Na+ and K+ diffuse out & interior of sarcolemma becomes less negative (event is called depolarization)
Depolarization
~Initially, this is a local electrical event called end plate potential

~Later, it ignites an action potential that spreads in all directions across sarcolemma
Action Potential: Electrical Conditions of a Polarized Sarcolemma
~Outside (extracellular) face is positive, while inside face is negative

~This difference in charge is Resting membrane potential

~Predominant extracellular ion is Na+

~Predominant intracellular ion is K+

~Sarcolemma is relatively impermeable to both ions
Action Potential: Depolarization & Generation of Action Potential
~An axonal terminal of a motor neuron releases ACh & causes a patch of sarcolemma to become permeable to Na+ (sodium channels open)

~Na+ enters cell & resting potential is decreased (depolarization occurs)

~If stimulus is strong enough, an action potential is initiated
Action Potential: Propagation of Action Potential
~Polarity reversal of initial patch of sarcolemma changes permeability of adjacent patch

~Voltage-regulated Na+ channels now open in adjacent patch causing it to depolarize

~Thus, the action potential travels rapidly along sarcolemma

~Once initiated, action potential is unstoppable & ultimately results in contraction of a muscle
Action Potential: Repolarization
~Immediately after depolarization wave passes, sarcolemma permeability changes

~Na+ channels close & K+ channels open

~K+ diffuses from cell, restoring electrical polarity of sarcolemma

~Repolarization occurs in same direction as depolarization & must occur before muscle can be stimulated again (refractory period)

~Ionic concentration of resting state is restored by
Na+-K+ pump
Excitation-Contraction Coupling
~Once generated, action potential:
1)Is propagated along sarcolemma
2)Travels down T tubules
3)Triggers Ca2+ release from terminal cisternae

~Ca2+ binds to troponin & causes:
1)blocking action of tropomyosin to cease
2)Actin active binding sites to be exposed

~Myosin cross bridges alternately attach & detach

~Thin filaments move toward center of sarcomere

~Hydrolysis of ATP powers this cycling process

~Ca2+ is removed into SR, tropomyosin blockage is restored, & muscle fiber relaxes
*Role of Ionic Calcium (Ca2+) in Contraction Mechanism
~At low intracellular Ca2+ concentration:
1)Tropomyosin blocks binding sites on actin
2)Myosin cross bridges cannot attach to binding sites on actin
3)Relaxed state of muscle is enforced

~At higher intracellular Ca2+ concentrations:
1)Additional calcium binds to troponin (inactive troponin binds two Ca2+)
2)Calcium-activated troponin binds an additional two Ca2+ at a separate regulatory site

~Calcium-activated troponin undergoes a conformational change
~This change moves tropomyosin away from actin’s binding sites
~Myosin head can now bind & cycle which permits contraction (sliding of thin filaments by myosin cross bridges) to begin
Sequential Events of Contraction(4)
1~Cross bridge formation –Myosin cross bridge attaches to actin filament

2~Working (power) stroke –Myosin head pivots & pulls actin filament toward M line

3~Cross bridge detachment –ATP attaches to myosin head & cross bridge detaches

4~“Cocking” of myosin head –Energy from hydrolysis of ATP cocks myosin head into high-energy state
*Contraction of Skeletal Muscle Fibers
~Contraction –Refers to activation of myosin’s cross bridges (force-generating sites)

~Shortening occurs when tension generated by cross bridge exceeds forces opposing shortening

~Contraction ends when cross bridges become inactive, tension generated declines & relaxation is induced
Contraction of Skeletal Muscle (Organ Level) (2 types)
~Contraction of muscle fibers (cells) & muscles (organs) is similar

~2 types of muscle contractions are:
1)Isometric contraction –Increasing muscle tension (muscle does not shorten during contraction)
2)Isotonic contraction –Decreasing muscle length (muscle shortens during contraction)
*Motor Unit: Nerve-Muscle Functional Unit
~A motor unit is a motor neuron & all muscle fibers it supplies

~# of muscle fibers per motor unit can vary from 4 to several 100

~Muscles that control fine movements (fingers, eyes) have small motor units
*Motor Unit: Nerve-Muscle Functional Unit
~Large weight-bearing muscles (thighs, hips) have large motor units

~Muscle fibers from a motor unit are spread throughout muscle; therefore, contraction of a single motor unit causes weak contraction of entire muscle
Muscle Twitch (3 phases)
~A muscle twitch is response of a muscle to a single, brief threshold stimulus

~There are 3 phases to a muscle twitch:
1)Latent period
2)Period of contraction
3)Period of relaxation
Phases of a Muscle Twitch
1~Latent period –First few msec after stimulus; EC coupling taking place

2~Period of contraction –Cross bridges form; muscle shortens

3~Period of relaxation – Ca2+ reabsorbed; muscle tension goes to zero
*Muscle Twitch Comparisons
Graded Muscle Responses
~Graded muscle responses are:
1)Variations in degree of muscle contraction
2)Required for proper control of skeletal movement

~Responses are graded by:
1)Changing frequency of stimulation
2)Changing strength of stimulus
Muscle Response: Stimulation Strength
~Threshold stimulus –Stimulus strength at which 1st observable muscle contraction occurs

~Beyond threshold, muscle contracts more vigorously as stimulus strength is increased

~Force of contraction is precisely controlled by multiple motor unit summation

~This phenomenon, called recruitment, brings more & more muscle fibers into play
*Stimulus Intensity & Muscle Tension
Size Principle
Treppe: Staircase Effect
~Staircase –Increased contraction in response to multiple stimuli of same strength

~Contractions increase because:
1)There is increasing availability of Ca2+ in sarcoplasm
2)Muscle enzyme systems become more efficient because heat is increased as muscle contracts
*Muscle Tone
~Muscle tone:
1)Constant, slightly contracted state of all muscles, which does not produce active movements
2)Keeps muscles firm, healthy, & ready to respond to stimulus

~Spinal reflexes account for muscle tone by:
1)Activating 1 motor unit & then another
2)Responding to activation of stretch receptors in muscles & tendons
*Isotonic Contractions
~Muscle changes in length (decreasing angle of joint) & moves load

~2 types of isotonic contractions are:
1)Concentric contractions –Muscle shortens & does work
2)Eccentric contractions –Muscle contracts as it lengthens
*Isometric Contractions
~Tension increases to muscle’s capacity, but muscle neither shortens nor lengthens

~Occurs if load is greater than tension muscle is able to develop
*Muscle Metabolism: Energy for Contraction
~ATP is only source used directly for contractile activity

~As soon as available stores of ATP are hydrolyzed (4-6 seconds), they are regenerated by:
1)interaction of ADP w creatine phosphate (CP)
2)Anaerobic glycolysis
3)Aerobic respiration
*Muscle Metabolism: Anaerobic Glycolysis
~When muscle contractile activity reaches 70% of maximum:
1)Bulging muscles compress blood vessels
2)Oxygen delivery is impaired
3)Pyruvic acid is converted into lactic acid

~The lactic acid:
1)Diffuses into bloodstream
2)Is picked up & used as fuel by liver, kidneys & heart
3)Is converted back into pyruvic acid by liver
*Muscle Fatigue
~State of physiological inability to contract
~Occurs when:
a)ATP production fails to keep pace w ATP use
b)There is a relative deficit of ATP, causing contractures
c)Lactic acid accumulates in muscle
d)Ionic imbalances are present

~Intense exercise produces rapid muscle fatigue (w rapid recovery)

~Na+-K+ pumps cannot restore ionic balances quickly enough

~Low-intensity exercise produces slow-developing fatigue

~SR is damaged & Ca2+ regulation is disrupted
*Oxygen Debt
~Vigorous exercise causes dramatic changes in muscle chemistry

~For a muscle to return to a resting state:
1)Oxygen reserves must be replenished
2)Lactic acid must be converted to pyruvic acid
3)Glycogen stores must be replaced
4)ATP & CP reserves must be resynthesized

~Oxygen debt –Extra amount of O2 needed for above restorative processes
Heat Production During Muscle Activity
~Only 40% of energy released in muscle activity is useful as work

~Remaining 60% is given off as heat

~Dangerous heat levels are prevented by radiation of heat from skin & sweating
*Force of Muscle Contraction
~Force of contraction is affected by:
1)# of muscle fibers contracting -the more motor fibers in a muscle, the stronger the contraction
2)Relative size of muscle- the bulkier the muscle, the greater its strength
3)Degree of muscle stretch –Muscles contract strongest when muscle fibers are 80-120% of their normal resting length
Length Tension Relationships
Muscle Fiber Type: Functional Characteristics
~Speed of contraction –Determined by speed in which ATPases split ATP (2 types of fibers are slow & fast)

~ATP-forming pathways:
1)Oxidative fibers –Use aerobic pathways
2)Glycolytic fibers –Use anaerobic glycolysis

~These 2 criteria define 3 categories –Slow oxidative fibers, fast oxidative fibers & fast glycolytic fibers
Muscle Fiber Type: Speed of Contraction
~Slow oxidative fibers contract slowly, have slow acting myosin ATPases & are fatigue resistant

~Fast oxidative fibers contract quickly, have fast myosin ATPases & have moderate resistance to fatigue

~Fast glycolytic fibers contract quickly, have fast myosin ATPases & are easily fatigued
Load & Contraction
Effects of Aerobic Exercise
~Aerobic exercise results in an increase of:
1)Muscle capillaries
2)# of mitochondria
3)Myoglobin synthesis
*Effects of Resistance Exercise
1~Muscle hypertrophy

2~Increased mitochondria, myofilaments & glycogen stores
Overload Principle
~Forcing a muscle to work promotes increased muscular strength

~Muscles adapt to increased demands

~Muscles must be overloaded to produce further gains
Smooth Muscle
~Composed of spindle-shaped fibers w a diameter of 2-10 u?m & lengths of several hundred u?m

~Lack coarse connective tissue sheaths of skeletal muscle but have fine endomysium

~Organized into 2 layers (longitudinal & circular) of closely apposed fibers

~Found in walls of hollow organs (except heart)

~Have essentially same contractile mechanisms as skeletal muscle
Peristalsis
~When longitudinal layer contracts, organ dilates & contracts

~When circular layer contracts, organ elongates

~Peristalsis –Alternating contractions & relaxations of smooth muscles that mix & squeeze substances through lumen of hollow organs
Innervation of Smooth Muscle
~Smooth muscle lacks neuromuscular jx

~Innervating nerves have bulbous swellings called varicosities

~Varicosities release neurotransmitters into wide synaptic clefts called diffuse jx
Microscopic Anatomy of Smooth Muscle
~SR is less developed than in skeletal muscle & lacks a specific pattern

~T tubules are absent

~Plasma membranes have pouchlike infoldings called caveoli

~Ca2+ is sequestered in extracellular space near caveoli, allowing rapid influx when channels are opened

~There are no visible striations & no sarcomeres

~Thin & thick filaments are present
Proportion & Organization of Myofilaments in Smooth Muscle
~Ratio of thick to thin filaments is much lower than in skeletal muscle

~Thick filaments have heads along their entire length

~There is no troponin complex

~Thick & thin filaments are arranged diagonally, causing smooth muscle to contract in a corkscrew manner

~Noncontractile intermediate filament bundles attach to dense bodies (analogous to Z discs) at regular intervals
Contraction of Smooth Muscle
~Whole sheets of smooth muscle exhibit slow, synchronized contraction

~They contract in unison, reflecting their electrical coupling w gap jx

~Action potentials are transmitted from cell to cell
Contraction of Smooth Muscle
~Some smooth muscle cells:
1)Act as pacemakers & set contractile pace for whole sheets of muscle
2)Are self-excitatory & depolarize without external stimuli
Contraction Mechanism
~Actin & myosin interact according to sliding filament mechanism

~Final trigger for contractions is a rise in intracellular Ca2+

~Ca2+ is released from SR & from extracellular space

~Ca2+ interacts w calmodulin & myosin light chain kinase to activate myosin
Role of Calcium Ion
~Ca2+ binds to calmodulin & activates it

~Activated calmodulin activates kinase enzyme

~Activated kinase transfers phosphate from ATP to myosin cross bridges

~Phosphorylated cross bridges interact w actin to produce shortening

~Smooth muscle relaxes when intracellular Ca2+ levels drop
Special Features of Smooth Muscle Contraction
1~Slow, prolonged contractile activity

2~Low energy requirements

3~Response to stretch
Response to Stretch
~Smooth muscle exhibits a phenomenon called
stress-relaxation response in which:
1)Smooth muscle responds to stretch only briefly & then adapts to its new length
2)New length, however, retains its ability to contract
3)This enables organs such as stomach & bladder to temporarily store contents
*Hyperplasia
~Certain smooth muscles can divide & increase their # by undergoing hyperplasia

~This is shown by estrogen’s effect on uterus:
1)At puberty, estrogen stimulates synthesis of more smooth muscle, causing uterus to grow to adult size
2)During pregnancy, estrogen stimulates uterine growth to accommodate increasing size of growing fetus
Types of Smooth Muscle: Single Unit
~Cells of single-unit smooth muscle, commonly called visceral muscle:
1)Contract rhythmically as a unit
2)Are electrically coupled to one another via gap junctions
3)Often exhibit spontaneous action potentials
4)Are arranged in opposing sheets & exhibit stress-relaxation response
Types of Smooth Muscle: Multiunit (5-where found) & 5-characteristics)
~Multiunit smooth muscles are found:
1)In large airways to lungs
2)In large arteries
3)In arrector pili muscles
4)Attached to hair follicles
5)In internal eye muscles

~Their characteristics include:
1)Rare gap jx
2)Infrequent spontaneous depolarizations
3)Structurally independent muscle fibers
4)A rich nerve supply, which, w a number of muscle fibers, forms motor units
5)Graded contractions in response to neural stimuli
Muscular Dystrophy
~Muscular dystrophy –Group of inherited muscle-destroying diseases where muscles enlarge due to fat & connective tissue deposits but muscle fibers atrophy

~Duchenne muscular dystrophy (DMD):
1)Inherited, sex-linked disease carried by females & expressed in males (1/3500)
2)Diagnosed between ages of 2-10
3)Victims become clumsy & fall frequently as their muscles fail
4)Progresses from extremities upward & victims die of respiratory failure in their 20s
5)Caused by a lack of cytoplasmic protein dystrophin
6)There is no cure, but myoblast transfer therapy shows promise
Developmental Aspects
~Muscle tissue develops from embryonic mesoderm called myoblasts

~Multinucleated skeletal muscles form by fusion of myoblasts

~Growth factor agrin stimulates clustering of ACh receptors at newly forming motor end plates

~As muscles are brought under control of somatic nervous system, #s of fast & slow fibers are also determined

~Cardiac & smooth muscle myoblasts do not fuse but develop gap jx at an early embryonic stage
Developmental Aspects: Regeneration
~Cardiac & skeletal muscle become amitotic but can lengthen & thicken

~Myoblastlike satellite cells show very limited regenerative ability

~Cardiac cells lack satellite cells

~Smooth muscle has good regenerative ability
Developmental Aspects: After Birth
~Muscular development reflects neuromuscular coordination

~Development occurs head-to-toe, & proximal-to-distal

~Peak natural neural control of muscles is achieved by midadolescence

~Athletics & training can improve neuromuscular control
Developmental Aspects: Male & Female
~There is a biological basis for greater strength in men than in women

~Women’s skeletal muscle makes up 36% of their body mass

~Men’s skeletal muscle makes up 42% of their body mass

~Differences are due primarily to male sex hormone testosterone

~With more muscle mass, men are generally stronger than women but body strength per unit muscle mass is same in both sexes
Developmental Aspects: Age Related
~With age, connective tissue increases & muscle fibers decrease

~Muscles become stringier & more sinewy

~By age 80, 50% of muscle mass is lost (sarcopenia) but regular exercise can reverse

~Aging of cardiovascular system affects every organ in body

~Atherosclerosis may block distal arteries, leading to intermittent claudication & causing severe pain in leg muscles
*Muscle Function
~Skeletal muscles are responsible for all locomotion

~Cardiac muscle is responsible for coursing blood through body

~Smooth muscle helps maintain blood pressure & squeezes or propels substances (food, feces) through organs

~Muscles also maintain posture, stabilize joints & generate heat
*Muscle Response to Varying Stimuli
~A single stimulus results in a single contractile response –A muscle twitch

~Frequently delivered stimuli (muscle does not have time to completely relax) increases contractile force –Wave summation

~More rapidly delivered stimuli result in incomplete tetanus

~If stimuli are given quickly enough, complete tetanus results