Transcript No Slide Title

Human Anatomy & Physiology
Muscle Tissue
Chapter 11
By
Abdul Fellah, Ph.D.
11-1
Muscle Tissue
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Types and characteristics of muscular tissue
Microscopic anatomy of skeletal muscle
Nerve-Muscle relationship
Behavior of skeletal muscle fibers
Behavior of whole muscles
Muscle metabolism
Cardiac and smooth muscle
11-2
Introduction to Muscle
• Movement is a fundamental characteristic
of all living things
• Cells capable of shortening and
converting the chemical energy of ATP
into mechanical energy
• Types of muscle
– skeletal, cardiac and smooth
• Physiology of skeletal muscle
– basis of warm-up, strength, endurance and
fatigue
11-3
Characteristics of Muscle
• Responsiveness (excitability)
– to chemical signals, stretch and electrical
changes across the plasma membrane
• Conductivity
– local electrical change triggers a wave of
excitation that travels along the muscle fiber
• Contractility -- shortens when stimulated
• Extensibility -- capable of being stretched
• Elasticity -- returns to its original resting
length after being stretched
11-4
Skeletal Muscle
• Voluntary striated muscle attached to
bones
• Muscle fibers (myofibers) as long as 30
cm
• Exhibits alternating light and dark
transverse bands or striations
– reflects overlapping arrangement of
internal contractile proteins
• Under conscious
control (voluntary)
11-5
Connective Tissue Elements
• Attachments between muscle and bone
– endomysium, perimysium, epimysium, fascia,
tendon
• Collagen is extensible and elastic
– stretches slightly under tension and recoils
when released
• protects muscle from injury
• returns muscle to its resting length
• Elastic components
– parallel components parallel muscle cells
– series components joined to ends of muscle11-6
The Muscle Fiber
11-7
Muscle Fibers
• Multiple flattened nuclei inside cell
membrane
– fusion of multiple myoblasts during
development
– unfused satellite cells nearby can multiply to
produce a small number of new myofibers
• Sarcolemma has tunnel-like infoldings or
transverse (T) tubules that penetrate the
cell
– carry electric current to cell interior
11-8
Muscle Fibers 2
• Sarcoplasm is filled with
– myofibrils (bundles of myofilaments)
– glycogen for stored energy and myoglobin
for binding oxygen
• Sarcoplasmic reticulum = smooth ER
– network around each myofibril
– dilated end-sacs (terminal cisternea) store
calcium
– triad = T tubule and 2 terminal cisternea
11-9
Thick Filaments
• Made of 200 to 500 myosin molecules
– 2 entwined polypeptides (golf clubs)
• Arranged in a bundle with heads directed
outward in a spiral array around the
bundled tails
– central area is a bare zone with no heads
11-10
Thin Filaments
• Two intertwined strands fibrous (F) actin
– globular (G) actin with an active site
• Groove holds tropomyosin molecules
– each blocking 6 or 7 active sites of G actins
• One small, calcium-binding troponin
molecule on each tropomyosin molecule
11-11
Elastic Filaments
• Springy proteins called titin
• Anchor each thick filament to Z disc
• Prevents overstretching of sarcomere
11-12
Regulatory and Contractile Proteins
• Myosin and actin are contractile proteins
• Tropomyosin and troponin = regulatory proteins
– switch that starts and stops shortening of muscle cell
– contraction activated by release of calcium into
sarcoplasm and its binding to troponin,
11-13
– troponin moves tropomyosin off the actin active sites
Overlap of Thick and Thin Filaments
11-14
Striations = Organization of Filaments
• Dark A bands (regions) alternating with lighter I bands (regions)
– anisotrophic (A) and isotropic (I) stand for the way these regions affect
polarized light
• A band is thick filament region
– lighter, central H band area
contains no thin filaments
• I band is thin filament region
– bisected by Z disc protein called
connectin, anchoring elastic and thin
filaments
– from one Z disc (Z line) to the next is a sarcomere
11-15
Striations and Sarcomeres
11-16
Relaxed and Contracted
Sarcomeres
• Muscle cells shorten because their individual
sarcomeres shorten
– pulling Z discs closer together
– pulls on sarcolemma
• Notice neither thick nor thin filaments change
length during shortening
• Their overlap changes as sarcomeres shorten
11-17
Nerve-Muscle Relationships
• Skeletal muscle must be stimulated by
a nerve or it will not contract
• Cell bodies of somatic motor neurons
in brainstem or spinal cord
• Axons of somatic motor neurons =
somatic motor fibers
– terminal branches supply one muscle fiber
• Each motor neuron and all the muscle
fibers it innervates = motor unit
11-18
Motor Units
• A motor neuron and the muscle
fibers it innervates
– dispersed throughout the muscle
– when contract together causes
weak contraction over wide area
– provides ability to sustain longterm contraction as motor units
take turns resting (postural
control)
• Fine control
– small motor units contain as few
as
20 muscle fibers per nerve fiber
– eye muscles
• Strength control
– gastrocnemius muscle has 1000
fibers per nerve fiber
11-19
Neuromuscular Junctions (Synapse)
• Functional connection between
nerve fiber and muscle cell
• Neurotransmitter (acetylcholine/ACh) released
from
nerve fiber stimulates muscle cell
• Components of synapse (NMJ)
– synaptic knob is swollen end of nerve fiber (contains
ACh)
– junctional folds region of sarcolemma
• increases surface area for ACh receptors
• contains acetylcholinesterase that breaks down ACh and
causes relaxation
– synaptic cleft = tiny gap between nerve and muscle
cells
– Basal lamina = thin layer of collagen and glycoprotein
over all of muscle fiber
11-20
The Neuromuscular Junction
11-21
Neuromuscular Toxins
• Pesticides (cholinesterase inhibitors)
– bind to acetylcholinesterase and prevent it
from degrading ACh
– spastic paralysis and possible suffocation
• Tetanus or lockjaw is spastic paralysis
caused by toxin of Clostridium bacteria
– blocks glycine release in the spinal cord and
causes overstimulation of the muscles
• Flaccid paralysis (limp muscles) due to
curare that competes with ACh
– respiratory arrest
11-22
Electrically Excitable Cells
• Plasma membrane is polarized or charged
– resting membrane potential due to Na+ outside
of cell and K+ and other anions inside of cell
– difference in charge across the membrane =
resting membrane potential (-90 mV cell)
• Stimulation opens ion gates in membrane
– ion gates open (Na+ rushes into cell and K+
rushes out of cell)
• quick up-and-down voltage shift = action potential
– spreads over cell surface as nerve signal
11-23
Muscle Contraction and
Relaxation
• Four actions involved in this process
– excitation = nerve action potentials lead to
action potentials in muscle fiber
– excitation-contraction coupling = action
potentials on the sarcolemma activate
myofilaments
– contraction = shortening of muscle fiber
– relaxation = return to resting length
• Images will be used to demonstrate the
steps of each of these actions
11-24
Excitation of a Muscle Fiber
11-25
Excitation (steps 1 and 2)
• Nerve signal opens voltage-gated calcium channels.
Calcium stimulates exocytosis of synaptic vesicles
containing ACh = ACh release into synaptic cleft.
11-26
Excitation (steps 3 and 4)
Binding of ACh to receptor proteins opens Na+ and K+
channels resulting in jump in RMP from -90mV to +75mV
11-27
forming an end-plate potential (EPP).
Excitation (step 5)
Voltage change in end-plate region (EPP) opens nearby
voltage-gated channels producing an action potential 11-28
Excitation-Contraction Coupling
11-29
Excitation-Contraction Coupling (steps 6 and 7)
Action potential spreading over sarcolemma enters T
tubules -- voltage-gated channels open in T tubules
causing calcium gates to open in SR
11-30
Excitation-Contraction Coupling (steps 8 and 9)
• Calcium released by SR binds to troponin
• Troponin-tropomyosin complex changes shape
11-31
and exposes active sites on actin
Contraction (steps 10 and 11)
• Myosin ATPase in myosin head hydrolyzes an
ATP molecule, activating the head and “cocking”
it in an extended position
11-32
• It binds to actin active site forming a cross-bridge
Contraction (steps 12 and 13)
• Power stroke =
myosin head releases
ADP and phosphate as
it flexes pulling the thin
filament past the thick
• With the binding of more
ATP, the myosin head
extends to attach to a
new active site
– half of the heads are bound to a thin
filament at one time preventing slippage
– thin and thick filaments do not become
shorter, just slide past each other (sliding
filament theory)
11-33
Relaxation (steps 14 and 15)
Nerve stimulation ceases and acetylcholinesterase
removes ACh from receptors. Stimulation of the
muscle cell ceases.
11-34
Relaxation (step 16)
• Active transport needed to pump calcium
back into SR to bind to calsequestrin
• ATP is needed for muscle relaxation as well
as muscle contraction
11-35
Relaxation (steps 17 and 18)
• Loss of calcium from sarcoplasm moves
troponin-tropomyosin complex over active sites
– stops the production or maintenance of tension
• Muscle fiber returns to its resting length due to
recoil of series-elastic components and
11-36
contraction of antagonistic muscles
Rigor Mortis
• Stiffening of the body beginning 3 to 4 hours
after death
• Deteriorating sarcoplasmic reticulum releases
calcium
• Calcium activates myosin-actin cross-bridging
and muscle contracts, but can not relax.
• Muscle relaxation requires ATP and ATP
production is no longer produced after death
• Fibers remain contracted until myofilaments
decay
11-37
Length-Tension Relationship
• Amount of tension generated depends on length
of muscle before it was stimulated
– length-tension relationship (see graph next slide)
• Overly contracted (weak contraction results)
– thick filaments too close to Z discs and can’t slide
• Too stretched (weak contraction results)
– little overlap of thin and thick does not allow for very
many cross bridges too form
• Optimum resting length produces greatest force
when muscle contracts
– central nervous system maintains optimal length
producing muscle tone or partial contraction
11-38
Length-Tension Curve
11-39
Muscle Twitch in Frog
• Threshold = voltage
producing an action
potential
– a single brief stimulus at
that voltage produces a
quick cycle of contraction
and relaxation called a
twitch (lasting less than
1/10 second)
• A single twitch contraction
is not strong enough to do
any useful work
11-40
Muscle Twitch in Frog 2
• Phases of a twitch contraction
– latent period (2 msec delay)
• only internal tension is generated
• no visible contraction occurs since
only elastic components are being
stretched
– contraction phase
• external tension develops as muscle
shortens
– relaxation phase
• loss of tension and return
to resting length as calcium returns to SR
11-41
Contraction Strength of Twitches
• Threshold stimuli produces twitches
• Twitches unchanged despite increased
voltage
• “Muscle fiber obeys an all-or-none law”
contracting to its maximum or not at all
– not a true statement since twitches vary in
strength
• depending upon, Ca2+ concentration, previous stretch
of the muscle, temperature, pH and hydration
• Closer stimuli produce stronger twitches
11-42
Recruitment and Stimulus Intensity
• Stimulating the whole nerve with higher and
higher voltage produces stronger contractions
• More motor units are being recruited
– called multiple motor unit summation
– lift a glass of milk versus a whole gallon of milk
11-43
Twitch and Treppe Contractions
• Muscle stimulation at variable frequencies
– low frequency (up to 10 stimuli/sec)
• each stimulus produces an identical twitch response
– moderate frequency (between 10-20 stimuli/sec)
• each twitch has time to recover but develops more
tension than the one before (treppe phenomenon)
– calcium was not completely put back into SR
– heat of tissue increases myosin ATPase efficiency
11-44
Incomplete and Complete Tetanus
• Higher frequency stimulation (20-40 stimuli/second)
generates gradually more strength of contraction
– each stimuli arrives before last one recovers
• temporal summation or wave summation
– incomplete tetanus = sustained fluttering contractions
• Maximum frequency stimulation (40-50 stimuli/second)
– muscle has no time to relax at all
– twitches fuse into smooth, prolonged contraction called
complete tetanus
– rarely occurs in the body
11-45
Isometric and Isotonic Contractions
• Isometric muscle contraction
– develops tension without changing length
– important in postural muscle function and
antagonistic muscle joint stabilization
• Isotonic muscle contraction
– tension while shortening = concentric
– tension while lengthening = eccentric
11-46
Muscle Contraction Phases
• Isometric and isotonic phases of lifting
– tension builds though the box is not moving
– muscle begins to shorten
– tension maintained
11-47
ATP Sources
• All muscle contraction depends on ATP
• Pathways of ATP synthesis
– anaerobic fermentation (ATP production limited)
• without oxygen, produces toxic lactic acid
– aerobic respiration (more ATP produced)
• requires continuous oxygen supply, produces H2O and CO211-48
Immediate Energy Needs
• Short, intense exercise (100
m dash)
– oxygen need is supplied by
myoglobin
• Phosphagen system
– myokinase transfers Pi groups
from one ADP to another
forming ATP
– creatine kinase transfers Pi
groups from creatine
phosphate to make ATP
• Result is power enough for 1
minute brisk walk or 6
seconds of sprinting
11-49
Short-Term Energy Needs
• Glycogen-lactic acid system takes over
– produces ATP for 30-40 seconds of
maximum activity
• playing basketball or running around baseball
diamonds
– muscles obtain glucose from blood and
stored glycogen
11-50
Long-Term Energy Needs
• Aerobic respiration needed for prolonged
exercise
– Produces 36 ATPs/glucose molecule
• After 40 seconds of exercise, respiratory and
cardiovascular systems must deliver enough
oxygen for aerobic respiration
– oxygen consumption rate increases for first 3-4
minutes and then levels off to a steady state
• Limits are set by depletion of glycogen and
blood glucose, loss of fluid and electrolytes
11-51
Fatigue
• Progressive weakness from use
– ATP synthesis declines as glycogen is
consumed
– sodium-potassium pumps fail to maintain
membrane potential and excitability
– lactic acid inhibits enzyme function
– accumulation of extracellular K+
hyperpolarizes the cell
– motor nerve fibers use up their acetylcholine
11-52
Endurance
• Ability to maintain high-intensity
exercise for >5 minutes
– determined by maximum oxygen uptake
• VO2 max is proportional to body size, peaks at
age 20, is larger in trained athlete and males
– nutrient availability
• carbohydrate loading used by some athletes
– packs glycogen into muscle cells
– adds water at same time (2.7 g water with each
gram/glycogen)
» side effects include “heaviness” feeling
11-53
Oxygen Debt
• Heavy breathing after strenuous exercise
– known as excess postexercise oxygen consumption
(EPOC)
– typically about 11 liters extra is consumed
• Purposes for extra oxygen
– replace oxygen reserves (myoglobin, blood
hemoglobin, in air in the lungs and dissolved in
plasma)
– replenishing the phosphagen system
– reconverting lactic acid to glucose in kidneys and
liver
– serving the elevated metabolic rate that occurs as
long as the body temperature remains elevated by
exercise
11-54
Slow- and Fast-Twitch Fibers
• Slow oxidative, slow-twitch fibers
– more mitochondria, myoglobin and
capillaries
– adapted for aerobic respiration and
resistant to fatigue
– soleus and postural muscles of the
back (100msec/twitch)
11-55
Slow and Fast-Twitch Fibers
• Fast glycolytic, fast-twitch fibers
– rich in enzymes for phosphagen and
glycogen-lactic acid systems
– sarcoplasmic reticulum releases calcium
quickly so contractions are quicker (7.5
msec/twitch)
– extraocular eye muscles, gastrocnemius
and biceps brachii
• Proportions genetically determined
11-56
Strength and Conditioning
• Strength of contraction
– muscle size and fascicle arrangement
• 3 or 4 kg / cm2 of cross-sectional area
– size of motor units and motor unit recruitment
– length of muscle at start of contraction
• Resistance training (weight lifting)
– stimulates cell enlargement due to synthesis of
more myofilaments
• Endurance training (aerobic exercise)
– produces an increase in mitochondria, glycogen and
density of capillaries
11-57
Cardiac Muscle 1
• Thick cells shaped like a log with uneven,
notched ends
• Linked to each other at intercalated discs
– electrical gap junctions allow cells to stimulate their
neighbors
– mechanical junctions keep the cells from pulling
apart
• Sarcoplasmic reticulum less developed but
large T tubules admit Ca+2 from extracellular
fluid
• Damaged cells repaired by fibrosis, not mitosis
11-58
Cardiac Muscle 2
• Autorhythmic due to pacemaker cells
• Uses aerobic respiration almost
exclusively
– large mitochondria make it resistant to
fatigue
– very vulnerable to interruptions in oxygen
supply
11-59
Smooth Muscle
• Fusiform cells with one nucleus
– 30 to 200 microns long and 5 to 10 microns
wide
– no striations, sarcomeres or Z discs
– thin filaments attach to dense bodies
scattered throughout sarcoplasm and on
sarcolemma
– SR is scanty and has no T tubules
• calcium for contraction comes from extracellular
fluid
• If present, nerve supply is autonomic
– releases either ACh or norepinephrine
11-60
Types of Smooth Muscle
• Multiunit smooth muscle
– largest arteries, iris, pulmonary air
passages, arrector pili muscles
– terminal nerve branches synapse on
myocytes
– independent contraction
11-61
Types of Smooth Muscle
• Single-unit smooth muscle
– most blood vessels and viscera as circular
and longitudinal muscle layers
– electrically coupled by gap junctions
– large number of cells contract as a unit
11-62
Stimulation of Smooth Muscle
11-63
Stimulation of Smooth Muscle
• Involuntary and contracts without nerve
stimulation
– hormones, CO2, low pH, stretch, O2 deficiency
– pacemaker cells in GI tract are autorhythmic
• Autonomic nerve fibers have beadlike
swellings called varicosities containing
synaptic vesicles
– stimulates multiple myocytes at diffuse
junctions
11-64
Features of Contraction and Relaxation
• Calcium triggering contraction is
extracellular
– calcium channels triggered to open by voltage,
hormones, neurotransmitters or cell stretching
• calcium ions bind to calmodulin
• activates light-chain myokinase which activates
myosin ATPase
• power stroke occurs when ATP hydrolyzed
• Thin filaments pull on intermediate filaments
attached to dense bodies on the plasma
membrane
– shortens the entire cell in a twisting fashion
11-65
Features of Contraction and Relaxation
• Contraction and relaxation very slow in
comparison
– slow myosin ATPase enzyme and slow
pumps that remove Ca+2
• Uses 10-300 times less ATP to maintain
the same tension
– latch-bridge mechanism maintains tetanus
(muscle tone)
• keeps arteries in state of partial contraction
(vasomotor tone)
11-66
Contraction of Smooth Muscle
11-67
Responses to Stretch 1
• Stretch opens mechanically-gated calcium
channels causing muscle response
– food entering the esophagus brings on
peristalsis
• Stress-relaxation response necessary for
hollow organs that gradually fill (urinary
bladder)
– when stretched, tissue briefly contracts then
relaxes
11-68
Responses to Stretch 2
• Must contract forcefully when greatly
stretched
– thick filaments have heads along their
entire length
– no orderly filament arrangement -- no Z
discs
• Plasticity is ability to adjust tension to
degree of stretch such as empty
bladder is not flabby
11-69
Muscular Dystrophy
• Hereditary diseases - skeletal muscles
degenerate and are replaced with adipose
• Disease of males
– appears as child begins to walk
– rarely live past 20 years of age
• Dystrophin links actin filaments to cell
membrane
– leads to torn cell membranes and necrosis
• Fascioscapulohumeral MD -- facial and
shoulder muscle only
11-70
Myasthenia Gravis
• Autoimmune disease - antibodies attack
NMJ and bind ACh receptors in clusters
– receptors removed
– less and less sensitive to ACh
• drooping eyelids and double vision, difficulty
swallowing, weakness of the limbs, respiratory
failure
• Disease of women between 20 and 40
• Treated with cholinesterase inhibitors,
thymus removal or immunosuppressive
agents
11-71
Myasthenia Gravis
Drooping eyelids and weakness of muscles
of eye movement
11-72