Chapter 10

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Biology 231
Human Anatomy and Physiology
Chapter 10 Lecture Outline
Muscle Tissue – converts chemical energy to mechanical energy (contraction)
3 types of muscle:
skeletal – attaches to and moves skeleton
striated, voluntary control
cardiac – heart
striated, involuntary control (autorhythmicity)
smooth – walls of hollow organs and vessels
also associated with hair and inner eye
non-striated, involuntary control
Functions of Muscle
body movement
stabilizing body position
controlling movement of contents in hollow organs and vessels
generating heat – thermogenesis
Properties of Muscle
electrical excitability – responds to stimulus by producing an electrical signal
(action potential) which can travel (propagate) along the plasma
membrane
contractility – contracts forcefully when stimulated by an action potential
ANATOMY OF SKELETAL MUSCLE
muscle fiber (cell) – individual cell; long, multinucleate
endomysium – sheath of elastic connective tissue around individual fibers;
contains capillaries and nerve endings supplying muscle fibers
fascicle – bundle of muscle fibers (10-100)
perimysium – dense irregular connective tissue sheath around fascicle
contains blood vessels and nerves
muscle – bundle of fascicles; function together
epimysium – dense connective tissue sheath around entire muscle
tendon – dense regular connective tissue continuous with all 3 sheaths
attaches muscle to periosteum of bone
aponeurosis – broad, flat tendon sheet
Nerve and Blood Supply to Muscle:
somatic motor neurons – stimulate muscle to contract
one neuron sends branches to multiple muscle fibers
neuromuscular junction – site of communication between motor neuron and
muscle fiber
plentiful capillary supply – supply nutrients and oxygen, remove heat and waste
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Anatomy of a Muscle Fiber – formed by fusion of 100+ embryonic myoblast cells
muscle fibers cannot divide – number set at birth
sarcolemma – plasma membrane of muscle cell
T tubules – invaginations of sarcolemma into center of muscle fiber
open to interstitial space – full of interstitial fluid
sarcoplasm – cytoplasm of muscle cell
glycogen – storage form of glucose
myoglobin – red protein, binds oxygen
lots of mitochondria – ATP for contraction
sarcoplasmic reticulum – network of sacs and tubules
terminal cisterns – dilated sacs on either side of T tubules (triad)
stores calcium ions for muscle contractions
myofibrils – contractile protein fibers; have visible striations (stripes)
sarcomere – basic contractile unit of myofibril
thin filaments and thick filaments overlap to create striations
A band – appears dark
middle, thick filaments + overlap with thin
M line – center of A band; anchors thick filaments
I band – appears light
thin filaments only (ends of 2 sarcomeres)
Z lines – center of I band; separates sarcomeres
satellite cells – a few myoblasts remaining in adult muscle; help repair
damaged muscle
Muscle Proteins
3 kinds:
contractile proteins – cause sarcomere to shorten
myosin – about 300 form thick filaments
actin – thin filaments; have binding sites for myosin
regulatory proteins – switch contraction on and off
tropmyosin and troponin – form strands that cover myosin-binding sites
on thin filaments
structural proteins – align and stabilize myofibrils; give elasticity and
extensibility
titin – large protein; anchors thick filament to Z line
gives sarcomeres a degree of elasticity
CONTRACTION AND RELAXATION OF SKELETAL MUSCLE
Sliding Filament Mechanism – thick and thin filaments slide over each other;
myosin heads attach to thin filaments and pull them closer to M line;
sarcomere shortens, length of filaments doesn’t change
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Steps of Contraction
sarcoplasmic reticulum releases calcium ions
calcium ions bind to troponin on thin filament
frees myosin-binding sites on actin
Contraction Cycle:
1) myosin heads are energized – break down ATP and use energy to
become “cocked”
2) formation of cross bridges - energized myosin head binds to actin
at myosin-binding site
3) power stroke - myosin head pivots and releases ADP
pulls thin filament closer to M line
4) cross bridges detatch – occurs when ATP binds to myosin head
myosin heads “walk” up thin filament as long as ATP and calcium ions
are sufficient
pulls thin filaments towards M line, sarcomere shortens
300 myosin molecules/thick filament
Length-Tension Relationship – forcefulness of contraction depends on length of
sarcomere before contraction
optimal zone of fiber overlap = maximum tension
reduced overlap – fewer myosin heads can bind
increased overlap – fiber orientation disrupted, less binding
EXCITATION OF SKELETAL MUSCLE – electrical signal from nervous system
initiates contraction of sarcomeres; voluntary control
Neuromuscular Junction (NMJ) – site of communication (synapse) between
somatic motor neuron and muscle fiber
synaptic cleft – small gap between the neuron and muscle fiber
somatic motor neuron – axon branches end at synaptic terminals
synaptic vesicles – contain acetylcholine (ACh)
neurotransmitter – chemical released by neuron in synaptic cleft;
diffuses across cleft and binds to receptor on sarcolemma
of muscle fiber and initiates a response
muscle fiber
motor end plate – ACh receptors form ligand-gated ion channels
channels open when Ach binds to them
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Steps of Excitation
1) Release of ACh – electrical impulse in neuron causes exocytosis of
synaptic vesicles; ACh released in synaptic cleft
2) Activation of ACh receptors – ACh diffuses to motor end plate;
ACh binds to receptors; ligand-gated channels open to small
cations (mainly Na+ due to Na+/K+ pump)
3) Production of muscle action potential – Na+ flows into muscle fiber
near sarcolemma; electrical charge in cell becomes more positive;
change in charge opens voltage-gated Na+ channels in sarcolemma;
wave of electrical current travels (propagates) along the
sarcolemma and T tubules
4) Termination of ACh activity – ACh broken down rapidly by
acetylcholinesterase (AChE) in synaptic cleft
by-products taken up by neuron to be recycled
NMJ located near center of muscle fiber – action potential propagates
towards both ends rapidly
botulism – toxin prevents release of ACh (Botox)
curare – blocks ACh receptors
neostigmine – anticholinesterase agent (antidote for curare)
EXCITATION-CONTRACTION COUPLING – action potential triggers
contraction of muscle
1) Action potential travels down T tubules
2) Calcium channels in SR membrane open – triggered by action
potential; calcium ions diffuse out of SR
3) Calcium ions bind troponin on actin filaments
4) Myosin-binding sites are exposed – contraction begins
Ca ions pumped back into SR by active transport pumps using ATP
Rigor Mortis – begins 3-4 hours after death, lasts about 24 hours
no ATP synthesis
calcium ions leak out of SR – myosin heads bind and can’t detatch
ends when lysosomal enzymes digest proteins
A single nerve impulse causes a single action potential in each muscle
fiber it synapses with.
The action potential is always the same size (all-or-none) and causes
minimal contraction of the muscle fibers.
twitch – brief contraction due to a single action potential
Amount of contraction (tension) in a muscle fiber depends mainly on
frequency of nerve stimulations arriving and availability of ATP
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MUSCLE FIBER METABOLISM
Sources of ATP:
free ATP – few seconds of contraction
creatine phosphate – stores high energy phosphate groups from ATP; passes
phosphates to ADP as it accumulates during contraction (100m dash)
anaerobic cellular respiration (no oxygen used)
glycolysis – glucose is broken down into 2 pyruvic acids with a net
gain of 2 ATP/glucose molecule (400 meter dash)
(pyruvic acid converted to lactic acid, diffuses into blood, liver converts
back to glucose)
aerobic cellular respiration (oxygen required)
pyruvic acid from glycolysis enters mitochondria – completely broken
down to carbon dioxide and water
produces 36 ATP/glucose molecule
produces 95% of ATP; used in prolonged activities
(can also use lipids from adipose cells and amino acids from proteins)
Sources of Glucose:
breakdown of glycogen stores in muscle fibers
facilitated diffusion into muscle fiber from bloodstream
Sources of Oxygen:
release from myoglobin in muscle fibers
diffusion from blood capillaries
MUSCLE PERFORMANCE
motor unit – a somatic motor neuron and all of the muscle fibers it
stimulates (avg. 150)
fine movements – small motor units (2-20 fibers)
large, powerful movements – large motor units (2-3 thousand fibers)
strength of contraction depends on:
size of motor unit and frequency of stimulation
number of motor units stimulated
Myogram – record of muscle contraction
stimulus – nerve impulse resulting in an action potential
latent period –
delay before contraction begins
calcium ions released, elastic components stretch
contraction phase – sarcomeres shorten
relaxation phase – calcium pumped into SR, sarcomeres relax
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wave summation – repeated stimulations before relaxation is complete
causes stronger contraction
unfused tetanus – sustained, wavering contraction
fused tetanus – sustained, maximal contraction
occurs when no relaxation is allowed between stimulations
(treppe – “warming up” effect)
muscle fatigue – inability to contract forcefully after prolonged activity
reduced calcium release from SR and ACh from NMJ
depletion of oxygen, glycogen, and nutrients
build-up of lactic acid and ADP
damage to muscle fibers
oxygen debt and recovery – increased use of oxygen after exercise
resynthesis of glycogen, creatine phosphate and ATP
reoxidizing myoglobin
increased body temperature, heart and respiratory rates
tissue repair
delayed onset muscle soreness – 12-48 hrs after exercise
microscopic damage – torn sarcolemmas, myofibrils, and
Z discs
blood proteins seen when muscle is damaged – myoglobin,
creatine kinase (CK)
motor unit recruitment – motor units within one muscle alternately contract
and relax
delays muscle fatigue, smoothes motion
muscle tone – small degree of tension maintained when not using muscle by
alternating activity of small groups of motor units;
regulated by involuntary nerve functions
flaccid muscle – loss of nerve stimulation
Types of Muscle Contractions
Isotonic Contractions – change length of muscles to move body parts
concentric contractions – muscle shortens
eccentric contractions – muscle lengthens
Isometric Contractions – create tension equal to stretching force on muscle;
maintain posture and stabilize joints
no movement occurs
TYPES OF SKELETAL MUSCLE FIBERS
vary in content of myoglobin, capillaries, mitochondria and glycogen
variable speed of contraction cycle due to differences in ATPase
variable sources of ATP
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1) Slow Fibers
smallest diameter – least powerful
dark red - lots of myoglobin and capillaries = lots of oxygen
many mitochondria – ATP mainly from aerobic respiration
slow twitch - slow ATPase (slow contraction cycle)
slow but very resistant to fatigue – posture and endurance activities
2) Fast Fibers
largest diameter – most powerful
white - little myoglobin and few capillaries = little oxygen
few mitochondria, lots of glycogen – ATP from glycolysis
fast-twitch - fast ATPase
fast and strong but fatigue rapidly – strength and speed activities
3) Intermediate Fibers
intermediate diameter
pink - little myoglobin but more capillaries
mitochondria and glycogen – ATP from aerobic and anaerobic processes
fast-twitch - fast ATPase
intermediate properties – faster and more fatigue resistant, but less
strength and endurance
Distribution of Fibers – most muscles have all 3 types
postural muscles (back and neck) – high in slow fibers
shoulders and arms – high in fast fibers
legs (postural and active) – high in slow and intermediate fibers
motor units are composed of 1 fiber type
recruitment order – slow, intermediate, fast
ratio of fast and slow twitch fibers is genetic
Regeneration of Skeletal Muscle
muscle fibers don’t divide
satellite cells regenerate fibers to a small degree
muscle growth is due to hypertrophy (increased cell size due to more thick
and thin filaments)
significant muscle damage results in fibrosis
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Cardiac Muscle - heart
similar arrangement of myofibrils – striated
shorter, branched muscle fibers – usually one nucleus
intercalated discs – connect muscle fibers by desmosomes
have gapjunctions – allow ions to diffuse between cells
muscle action potential spreads rapidly throughout cardiac muscle fibers
autorhythmic muscle fibers (pacemaker) – contracts and relaxes 75 times/min
while resting; involuntary contractions
mainly aerobic respiration – large numbers of mitochondria
(during exercise can use lactic acid to form ATP)
prolonged contraction due to calcium channels in sarcolemma
little regenerative ability; hypertrophy due to aerobic exercise
Smooth Muscle
walls of blood vessels and hollow organs, arector pili muscles, inner eye
spindle-shaped, one nucleus
thick and thin filaments have no regular arrangement (no striations)
contractile fibers anchored to dense bodies by intermediate filaments;
contraction draws dense bodies closer together
can stretch a lot and maintain contractile function
involuntary stimulation – respond to stretching, chemicals, hormones,
autonomic nerve impulses
gap junctions connect muscle fibers – contract in unison
contractions develop slowly and last longer than in skeletal muscle
calcium ions enter mainly from interstitial fluid (little SR)
maintains smooth muscle tone
more regenerative capacity than skeletal or cardiac muscle
pericytes – stem cells around capillaries and venules
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