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Chapter 11
Lecture Outline
11-1
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Muscle Cells
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Muscle
fiber
Nucleus
A band
I band
Z disc
Openings into
transverse tubules
Mitochondria
Sarcoplasmic
reticulum
Triad:
Terminal cisternae
Transverse tubule
Figure 11.2
Sarcolemma
Sarcoplasm
Myofibrils
Myofilaments
•
•
•
•
•
•
•
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
• muscle cells are capable of converting the
chemical energy of ATP into mechanical
energy
• types of muscle
• physiology of skeletal muscle
– basis of warm-up, quickness, strength,
endurance and fatigue
11-3
Characteristics of Muscle
• responsiveness (excitability)
– to chemical signals, stretch and electrical changes
across the plasma membrane
• conductivity
• contractility
–]
• extensibility
– capable of being stretched between contractions
• elasticity
11-4
– returns to its original resting length after being stretched
Skeletal Muscle
• skeletal muscle - voluntary,
striated muscle attached to
one or more bones
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Nucleus
• striations -
Muscle fiber
• voluntary –
• muscle cell, muscle fiber,
(myofiber) as long as 30 cm
Endomysium
Striations
© Ed Reschke
Figure 11.1
11-5
Connective Tissue Elements
• tendons are attachments between muscle and bone matrix
– endomysium – connective tissue around muscle cells
– perimysium – connective tissue around muscle fascicles
– epimysium –
• collagen is somewhat extensible and elastic
– stretches slightly under tension and recoils when released
• resists excessive stretching and protects muscle from injury
• returns muscle to its resting length
• contribute to power output and muscle efficiency
11-6
Structure of a Skeletal Muscle
Fiber
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Muscle
fiber
Nucleus
A band
I band
Z disc
Openings into
transverse tubules
Mitochondria
Sarcoplasmic
reticulum
Triad:
Terminal cisternae
Transverse tubule
Sarcolemma
Myofibrils
Sarcoplasm
Myofilaments
Figure 11.2
11-7
The Muscle Fiber
•
•
•
sarcolemma – plasma membrane of a muscle fiber
sarcoplasm – cytoplasm of a muscle fiber
myofibrils – long protein bundles that occupies the main portion of the
sarcoplasm
– glycogen –
– myoglobin – red pigment – stores oxygen needed for muscle activity
•
multiple nuclei – flattened nuclei pressed against the inside of the sarcolemma
– myoblasts – stem cells that fuse to form each muscle fiber
– satellite cells – unspecialized myoblasts remaining between the muscle fiber and
endomysium
• may multiply and produce new muscle fibers to some degree
•
•
•
repair by fibrosis
mitochondria – packed in spaces between myofibrils
sarcoplasmic reticulum (SR) - smooth ER that forms a network around each
myofibril – calcium reservoir
– calcium activates the muscle contraction process
•
•
terminal cisternae – dilated end-sacs of SR which cross muscle fiber from one
side to the other
T tubules –
11-8
Thick Myofilaments
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Head
Tail
(a) Myosin molecule
Myosin head
(b) Thick filament
Figure 11.3 a-b
• made of several hundred myosin molecules
– shaped like a golf club
• two chains intertwined to form a shaft-like tail
• double globular head
– heads directed outward in a helical array around the bundle
• heads on one half of the thick filament angle to the left
• heads on the other half angle to the right
• bare zone with no heads in the middle
11-9
Thin Myofilaments
• fibrous (F) actin - two intertwined strands
– string of globular (G) actin subunits each with an
active site that can bind to head of myosin molecule
• tropomyosin molecules
• troponin molecule - small, calcium-binding protein
on each
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Tropomyosin
Troponin complex
G actin
(c) Thin filament
Figure 11.3c
11-10
Elastic Myofilaments
• titin (connectin) – huge springy protein
– flank each thick filament and anchor it to the
Z disc
– helps stabilize the thick filament
11-11
Regulatory and Contractile Proteins
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Myosin head
(b) Thick filament
Tropomyosin
Troponin complex
(c) Thin filament
• contractile proteins - myosin and actin
G actin
Figure 11.3 b-c
• regulatory proteins - tropomyosin and troponin
– like a switch that determine when the fiber can contract and when it cannot
– contraction activated by release of calcium into sarcoplasm and its binding
to troponin,
– troponin changes shape and moves tropomyosin off the active
11-12
sites on actin
Overlap of Thick and Thin Filaments
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Thick filament
Thin filament
Bare zone
(d) Portion of a sarcomere showing the overlap
of thick and thin filaments
Figure 11.3d
11-13
Accessory Proteins
• at least seven other accessory
proteins in or associated with thick or
thin filaments
– anchor the myofilaments, regulate
length of myofilaments, alignment
of myofilaments for maximum
effectiveness
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Endomysium
Linking proteins
Basal lamina
Sarcolemma
• dystrophin – most clinically important
– links actin in outermost
myofilaments to transmembrane
proteins and eventually to fibrous
endomysium surrounding the
entire muscle cell
Dystrophin
Thin filament
Thick filament
Figure 11.4
11-14
Striations
• myosin and actin are proteins that occur in all cells
– function in cellular motility, mitosis, transport of intracellular material
• organized in a precise way in skeletal and cardiac muscle
– A band – dark – A stands for anisotropic
• part of A band where thick and thin filaments overlap is especially dark
• H band in the middle of A band – just thick filaments
• M line is in the middle of the H band
– I band –
– z disc – provides anchorage for thin filaments and elastic filaments
• bisects I band
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Sarcomere
A band
I band
I band
H band
(b)
Z disc
Thick filament
Thin filament
Elastic filament
M line
Figure 11.5b
Titin
Z disc
11-15
Striations and Sarcomeres
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Nucleus
M line
Z disc
H band
A band
I band
1
I band
2
3
4
Individual myofibrils
5
Sarcomere
(a)
Visuals Unlimited
Figure 11.5a
• sarcomere – functional contractile unit of the muscle fiber
– muscle shortens because individual sarcomeres shorten
– pulls z discs closer to each other
11-16
Sarcomeres
• sarcomere - segment from Z disc to Z disc
• muscle cells shorten because their individual
sarcomeres shorten
• neither thick nor thin filaments change length
during shortening
• during shortening dystrophin & linking proteins
also pull on extracellular proteins
– transfers pull to extracellular tissue
11-17
The Nerve-Muscle Relationship
• skeletal muscle never contracts unless stimulated by a
nerve
• if nerve connections are severed or poisoned, a muscle
is paralyzed
• denervation atrophy –
• somatic motor neurons – nerve cells whose cell
bodies are in the brainstem and spinal cord that serve
skeletal muscles
• somatic motor fibers
11-18
Motor Units
•
motor unit –
•
muscle fibers of one motor unit
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– dispersed throughout the muscle
Spinal cord
– contract in unison
– produce weak contraction over wide area
– provides ability to sustain long-term
contraction as motor units take turns
contracting (postural control)
Motor
neuron 1
– effective contraction usually requires the
Motor
contraction of several motor units at once
neuron 2
•
•
•
average motor unit –
small motor units large motor units – more strength than control
– powerful contractions supplied by large
motor units – gastrocnemius – 1000
muscle fibers per neuron
– many muscle fibers per motor unit
Neuromuscular
junction
Skeletal
muscle
fibers
Figure 11.6
11-19
The Neuromuscular Junction
• synapse –
• neuromuscular junction (NMJ) - when target
cell is a muscle fiber
• each terminal branch of the nerve fiber within
the NMJ forms separate synapse with the
muscle fiber
• one nerve fiber stimulates the muscle fiber at
several points within the NMJ
11-20
Components of Neuromuscular Junction
• synaptic knob - swollen end of nerve fiber
– contains synaptic vesicles filled with acetylcholine (ACh)
• synaptic cleft • Schwann cell
• synaptic vesicles undergo exocytosis releasing ACh into synaptic cleft
• 50 million ACh receptors – proteins incorporated into muscle cell
plasma membrane
• basal lamina - thin layer of collagen and glycoprotein separates
Schwann cell and entire muscle cell from surrounding tissues
– contains acetylcholinesterase (AChE) that breaks down ACh after
contraction causing relaxation
11-21
Neuromuscular Junction
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Motor nerve fiber
Myelin
Synaptic knob
Schwann cell
Synaptic vesicles
(containing ACh)
Basal lamina
Sarcolemma
Synaptic cleft
Nucleus
ACh receptor
Junctional folds
Mitochondria
Nucleus
Sarcoplasm
Myofilaments
Figure 11.7b
11-22
(b)
Neuromuscular Junction - LM
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Motor nerve
fibers
Neuromuscular
junction
Muscle fibers
Figure 11.7a
(a)
100 µm
Victor B. Eichler
11-23
Neuromuscular Toxins
• toxins that interfere with synaptic function can paralyze the muscles
• some pesticides contain cholinesterase inhibitors
– bind to acetylcholinesterase and prevent it from degrading ACh
– spastic paralysis - a state of continual contraction of the muscles
– possible suffocation
• tetanus (lockjaw) is a form of spastic paralysis caused by toxin of
Clostridium tetani
– glycine in the spinal cord normally stops motor neurons from producing
unwanted muscle contractions
– tetanus toxin blocks glycine release in the spinal cord and causes
overstimulation and spastic paralysis of the muscles
• flaccid paralysis –
• botulism – type of food poisoning caused by a neuromuscular toxin
secreted by the bacterium Clostridium botulinum
– blocks release of ACh causing flaccid paralysis
– Botox Cosmetic injections for wrinkle removal
11-24
Electrically Excitable Cells
• muscle fibers and neurons are electrically excitable cells
– their plasma membrane exhibits voltage changes in response to stimulation
• electrophysiology - the study of the electrical activity of cells
• in an unstimulated (resting) cell
– there are more anions (negative ions) on the inside of the plasma membrane
than on the outside
– the plasma membrane is electrically polarized (charged)
– there are excess sodium ions (Na+) in the extracellular fluid (ECF)
– there are excess potassium ions (K+) in the intracellular fluid (ICF)
– also in the ICF, there are anions such as proteins, nucleic acids, and
phosphates that cannot penetrate the plasma membrane
– these anions make the inside of the plasma membrane negatively charged by
comparison to its outer surface
• voltage (electrical potential) –
• resting membrane potential – about -90mV
– maintained by sodium-potassium pump
11-25
Electrically Excitable Cells
• stimulated (active) muscle fiber or nerve cell
–
–
–
–
–
–
–
–
–
–
–
–
ion gates open in the plasma membrane
Na+ instantly diffuses down its concentration gradient into the cell
these cations override the negative charges in the ICF
depolarization - inside of the plasma membrane becomes briefly positive
immediately, Na+ gates close and K+ gates open
K+ rushes out of cell
repelled by the positive sodium charge and partly because of its concentration
gradient
loss of positive potassium ions turns the membrane negative again
(repolarization)
action potential – quick up-and-down voltage shift from the negative RMP to a
positive value, and back to the negative value again.
RMP is a stable voltage seen in a waiting muscle or nerve cell
action potential is a quickly fluctuating voltage seen in an active stimulated
cell
an action potential at one point on a plasma membrane causes another
one to happen immediately in front of it, which triggers another one a
11-26
little farther along and so forth
Muscle Contraction & Relaxation
• four major phases of contraction and relaxation
– excitation
•
– excitation-contraction coupling
– contraction
• step in which the muscle fiber develops tension and may shorten
– relaxation
11-27
Excitation of a Muscle Fiber
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Nerve signal
Ca2+ enters
synaptic knob
Motor
nerve
fiber
Sarcolemma
Synaptic
vesicles
Synaptic
knob
ACh
Synaptic
cleft
ACh
receptors
1 Arrival of nerve signal
ACh
2 Acetylcholine (ACh) release
ACh
K+
ACh receptor
Sarcolemma
Na+
4 Opening of ligand-regulated ion gate;
creation of end–plate potential
3 Binding of ACh to receptor
K+
Plasma
membrane
of synaptic
knob
Na+
Voltage-regulated
ion gates
Sarcolemma
5 Opening of voltage-regulated ion gates;
creation of action potentials
Figure 11.8
11-28
Excitation (steps 1 and 2)
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Nerve signal
Motor
nerve
fiber
Ca2+ enters
synaptic knob
Synaptic
knob
Sarcolemma
Synaptic
vesicles
ACh
ACh
receptors
1 Arrival of nerve signal
Synaptic
cleft
2 Acetylcholine (ACh) release
Figure 11.8 (1-2)
• nerve signal opens voltage-gated calcium channels in synaptic knob
• calcium stimulates exocytosis of ACh from synaptic vesicles
11-29
• ACh released into synaptic cleft
Excitation (steps 3 and 4)
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ACh
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ACh
K+
ACh receptor
Sarcolemma
Na+
4 Opening of ligand-regulated ion gate;
creation of end–plate potential
3 Binding of ACh to receptor
Figure 11.8 (3-4)
• two ACh molecules bind to each receptor protein, opening
Na+ and K+ channels.
11-30
Excitation (step 5)
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K+
Plasma
membrane
of synaptic
knob
Na+
Voltage-regulated
ion gates
Sarcolemma
5 Opening of voltage-regulated ion gates;
creation of action potentials
Figure 11.8 (5)
• voltage change (EPP) in end-plate region opens nearby voltage-gated
channels producing an action potential that spreads over muscle
11-31
surface.
Excitation-Contraction Coupling in
Skeletal Muscle
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Terminal
cisterna
of SR
T tubule
T tubule
Sarcoplasmic
reticulum
Ca2+
Ca2+
6 Action potentials propagated
down T tubules
7 Calcium released from
terminal cisternae
Figure 11.9 (6-9)
Active sites
Ca2+
Troponin
Tropomyosin
Actin Thin filament
Myosin
Ca2+
8 Binding of calcium
to troponin
9 Shifting of tropomyosin;
exposure of active sites
on actin
11-32
Excitation-Contraction Coupling
(steps 6 and 7)
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Terminal
cisterna
of SR
T tubule
T tubule
Sarcoplasmic
reticulum
Ca2+
Ca2+
6 Action potentials propagated
down T tubules
7 Calcium released from
terminal cisternae
Figure 11.9 (6-7)
• action potential spreads down into T tubules
• opens voltage-gated ion channels in T tubules and Ca+2 channels in SR
11-33
+2
• Ca enters the cytosol
Excitation-Contraction Coupling
(steps 8 and 9)
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Ca2+
Troponin
Tropomyosin
Active sites
Actin
Thin filament
Myosin
Ca2+
8 Binding of calcium
9 Shifting of tropomyosin;
to troponin
exposure of active sites
on actin
Figure 11.9 (8-9)
• troponin-tropomyosin complex changes shape and exposes active sites
11-34
on actin
Contraction (steps 10 and 11)
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Troponin
Tropomyosin
• myosin ATPase
enzyme in myosin
head hydrolyzes
an ATP molecule
• activates the head
“cocking” it in an
extended position
ADP
Pi
Myosin
10 Hydrolysis of ATP to ADP + Pi;
activation and cocking of myosin head
– ADP + Pi remain
attached
Cross-bridge:
Actin
Myosin
11 Formation of myosin–actin cross-bridge
Figure 11.10 (10-11)
• head binds to actin
active site forming
a myosin - actin
cross-bridge
11-35
Contraction (steps 12 and 13)
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• myosin head releases
ADP and Pi, flexes pulling
thin filament past thick power stroke
• upon binding more
ATP, myosin releases actin
and process is repeated
– each head performs 5 power
strokes per second
– each stroke utilizes one
molecule of ATP
ATP
13
Binding of new ATP;
breaking of cross-bridge
ADP
ADP
PPii
12
Power stroke; sliding of thin
filament over thick filament
Figure 11.10 (12-13)
11-36
Relaxation (steps 14 and 15)
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AChE
ACh
14 Cessation of nervous stimulation
and ACh release
15 ACh breakdown by
acetylcholinesterase (AChE)
Figure 11.11 (14-15)
• nerve stimulation & ACh release stop
• AChE breaks down ACh & fragments reabsorbed into synaptic
knob
11-37
Relaxation (step 16)
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Terminal cisterna
of SR
Ca2+
Ca2+
16 Reabsorption of calcium ions by
sarcoplasmic reticulum
Figure 11.11 (16)
• .
11-38
Relaxation (steps 17 and 18)
• Ca+2 removed from troponin
is pumped back into SR
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Ca2+
• tropomyosin reblocks the
active sites
ADP
Pi
17
• muscle fiber ceases to
produce or maintain tension
Loss of calcium ions from troponin
Tropomyosin
• muscle fiber returns to its
resting length
– due to recoil of elastic
components & contraction of
antagonistic muscles
Ca2+
ATP
18
Return of tropomyosin to position
blocking active sites of actin
Figure 11.11 (17-18)
11-39
Rigor Mortis
• rigor mortis - hardening of muscles and stiffening
of body beginning 3 to 4 hours after death
– deteriorating sarcoplasmic reticulum releases Ca+2
– deteriorating sarcolemma allows Ca+2 to enter cytosol
• muscle relaxation requires ATP, and ATP
production is no longer produced after death
– fibers remain contracted until myofilaments begins to
decay
11-40
Length-Tension Relationship
• Length – Tension Relationship - the amount of tension
generated by a muscle and the force of contraction depends
on how stretched or contracted it was before it was
stimulated
• if overly contracted at rest, a weak contraction results
– thick filaments too close to Z discs and can’t slide
• if too stretched before stimulated, a weak contraction
• optimum resting length produces greatest force when
muscle contracts
– muscle tone – central nervous system continually monitors and
adjusts the length of the resting muscle, and maintains a state of
partial contraction called muscle tone
– maintains optimum length and makes the muscles ideally ready for
action
11-41
Length-Tension Relationship
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Optimum resting length
(2.0–2.25µm)
z
z
Overly contracted
z
z
Overly stretched
z
z
Tension (g) generated
upon stimulation
1.0
0.5
0.0
1.0
2.0
3.0
Sarcomere length (µm) before stimulation
Figure 11.12
4.0
11-42
Behavior of Whole Muscles
• the response of a muscle to weak
electrical stimulus seen in frog
gastrocnemius - sciatic nerve
preparation
• weak, subthreshold electrical
stimulus causes no contraction
• threshold -
Relaxation
phase
Contraction
phase
Muscle tension
• myogram – a chart of the timing
and strength of a muscle’s
contraction
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Latent
period
Time of
stimulation
Time
Figure 11.13
11-43
Phases of a Twitch Contraction
• latent period - 2 msec delay between the onset of
stimulus and onset of twitch response
– time required for excitation, excitation-contraction coupling and
tensing of elastic components of the muscle
– internal tension –
• contraction phase – phase in which filaments slide and
the muscle shortens
– once elastic components are taut, muscle begins to produce
external tension – in muscle that moves a load
• relaxation phase - SR quickly reabsorbs Ca+2, myosin
releases the thin filaments and tension declines
– muscle returns to resting length
– entire twitch lasts from 7 to 100 msec
11-44
Contraction Strength of Twitches
• at subthreshold stimulus – no contraction at all
• at threshold intensity and above • not exactly true that muscle fiber obeys an all-or-none law contracting to its maximum or not at all
– electrical excitation of a muscle follows all-or-none law
– not true that muscle fibers follow the all or none law
– twitches vary in strength depending upon:
• stimulus frequency - stimuli arriving closer together produce stronger
twitches
• concentration of Ca+2 in sarcoplasm can vary the frequency
• how stretched muscle was before it was stimulated
• temperature of the muscles – warmed-up muscle contracts more strongly –
enzymes work more quickly
• lower than normal pH of sarcoplasm weakens the contraction - fatigue
• state of hydration of muscle affects overlap of thick & thin filaments
• muscles need to be able to contract with variable strengths for
different tasks
11-45
Recruitment and Stimulus
Intensity
Stimulus voltage
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Threshold
1
2
3
Stimuli to nerve
4
5
6
7
8
9
Proportion of nerve fibers excited
Tension
Maximum contraction
Figure 11.14
1
2
3
4
5
6
7
8
9
Responses of muscle
• stimulating the nerve with higher and higher voltages produces stronger
contractions
– higher voltages excite more and more nerve fibers in the motor nerve which
stimulates more and more motor units to contract
11-46
Twitch Strength & Stimulus Frequency
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Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Treppe
Twitch
Muscle twitches
Stimuli
Figure 11.15a,b
• when stimulus intensity (voltage) remains constant twitch strength can vary
with the stimulus frequency
(a)
(b)
• 10-20 stimuli per second produces treppe (staircase) phenomenon
– muscle still recovers fully between twitches, but each twitch develops more tension than
the one before
– stimuli arrive so rapidly that the SR does not have time between stimuli to completely
reabsorb all of the Ca+2 it released
– Ca+2 concentration in the cytosol rises higher and higher with each stimulus causing
subsequent twitches to be stronger
– heat released by each twitch cause muscle enzymes such as myosin ATPase to
work more efficiently and produce stronger twitches as muscle warms up
11-47
Incomplete and Complete Tetanus
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Incomplete tetanus
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Complete tetanus
Fatigue
(c)
(d)
Figure 11.15c,d
• 20-40 stimuli per second produces incomplete tetanus
–
–
–
–
–
–
–
each new stimulus arrives before the previous twitch is over
new twitch “rides piggy-back” on the previous one generating higher tension
temporal summation – results from two stimuli arriving close together
wave summation – results from one wave of contraction added to another
each twitch reaches a higher level of tension than the one before
muscle relaxes only partially between stimuli
produces a state of sustained fluttering contraction called incomplete 11-48
tetanus
Incomplete and Complete Tetanus
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Incomplete tetanus
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Complete tetanus
Fatigue
(c)
(d)
Figure 11.15c,d
• 40-50 stimuli per second produces complete tetanus
– muscle has no time to relax at all between stimuli
– twitches fuse to a smooth, prolonged contraction called complete tetanus
– a muscle in complete tetanus produces about four times the tension as a
single twitch
– rarely occurs in the body, which rarely exceeds 25 stimuli per second
– smoothness of muscle contractions is because motor units function
asynchronously
• when one motor unit relaxes, another contracts and takes over so the
muscle does not lose tension
11-49
Isometric and Isotonic Contractions
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Muscle develops
tension but does
not shorten
Muscle shortens,
tension remains
constant
Muscle lengthens
while maintaining
tension
Movement
Movement
No movement
(a) Isometric contraction
(b) Isotonic concentric contraction
(c) Isotonic eccentric contraction
Figure 11.16
•
isometric muscle contraction
•
isotonic muscle contraction
– muscle changes in length with no change in tension
– concentric contraction – muscle shortens while maintains tension
– eccentric contraction – muscle lengthens as it maintains tension
11-50
Isometric and Isotonic Phases of
Contraction
Length or Tension
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Muscle
tension
Muscle
length
Isometric
phase
Isotonic
phase
Figure 11.17
Time
• at the beginning of contraction – isometric phase
– muscle tension rises but muscle does not shorten
• when tension overcomes resistance of the load
– tension levels off
• muscle begins to shorten and move the load – isotonic phase
11-51
Muscle Metabolism
• all muscle contraction depends on ATP
• ATP supply depends on availability of:
– oxygen
– organic energy sources such as glucose and fatty acids
• two main pathways of ATP synthesis
– aerobic respiration
11-52
Modes of ATP Synthesis
During Exercise
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0
10 seconds
40 seconds
Duration of exercise
Repayment of
oxygen debt
Mode of ATP synthesis
Aerobic respiration
using oxygen from
myoglobin
Phosphagen
system
Glycogen–
lactic acid
system
(anaerobic
fermentation)
Aerobic
respiration
supported by
cardiopulmonary
function
Figure 11.18
11-53
Immediate Energy Needs
• short, intense exercise (100 m dash)
– oxygen need is briefly supplied by myoglobin for a limited amount of
aerobic respiration at onset – rapidly depleted
– muscles meet most of ATP demand by borrowing phosphate groups (Pi)
from other molecules and transferring them to ADP
• two enzyme systems control these phosphate transfers
– myokinase – transfers Pi from one ADP to another converting the
latter to ATP
– creatine kinase – obtains Pi from a phosphate-storage molecule
creatine phosphate (CP)
• fast-acting system that helps maintain the ATP level while other ATPgenerating mechanisms are being activated
– provides nearly all energy used for short bursts of intense activity
• one minute of brisk walking
• 6 seconds of sprinting or fast swimming
• important in activities requiring brief but maximum effort
– football, baseball, and weight lifting
11-54
Immediate Energy Needs
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
ADP
ADP
Pi
Myokinase
ATP
AMP
ADP
Creatine
phosphate
Pi
Figure 11.19
Creatine
Creatine
kinase
ATP
11-55
Short-Term Energy Needs
• as the phosphagen system is exhausted
• muscles shift to anaerobic fermentation
– muscles obtain glucose from blood and their
own stored glycogen
– in the absence of oxygen, glycolysis can
generate a net gain of 2 ATP for every
glucose molecule consumed
– converts glucose to lactic acid
• glycogen-lactic acid system –
11-56
Long-Term Energy Needs
• after 40 seconds or so, the respiratory and cardiovascular
systems “catch up” and deliver oxygen to the muscles fast
enough for aerobic respiration to meet most of the ATP
demands
• aerobic respiration produces 36 ATP per glucose
– efficient means of meeting the ATP demands of prolonged exercise
– one’s rate of oxygen consumption rises for 3 to 4 minutes and levels off to
a steady state in which aerobic ATP production keeps pace with demand
– little lactic acid accumulates under steady state conditions
– depletion of glycogen and blood glucose, together with the loss of fluid and
electrolytes through sweating, set limits on endurance and performance
even when lactic acid does not
11-57
Fatigue
• muscle fatigue - progressive weakness and loss of contractility from
prolonged use of the muscles
– repeated squeezing of rubber ball
– holding text book out level to the floor
• causes of muscle fatigue
– ATP synthesis declines as glycogen is consumed
– ATP shortage slows down the Na+ - K+ pumps
• compromises their ability to maintain the resting membrane potential and
excitability of the muscle fibers
– lactic acid lowers pH of sarcoplasm
• inhibits enzymes involved in contraction, ATP synthesis, and other aspects of
muscle function
– release of K+ with each action potential causes the accumulation of
extracellular K+
•
hyperpolarizes the cell and makes the muscle fiber less excitable
– motor nerve fibers use up their ACh
• less capable of stimulating muscle fibers – junctional fatigue
– central nervous system, where all motor commands originate, fatigues by
unknown processes, so there is less signal output to the skeletal muscles11-58
Endurance
• endurance – the ability to maintain high-intensity
exercise for more than 4 to 5 minutes
– determined in large part by one’s
– maximum oxygen uptake – the point at which the rate
of oxygen consumption reaches a plateau and does not
increase further with an added workload
• proportional to body size
• peaks at around age 20
11-59
Oxygen Debt
•
heavy breathing continues after strenuous exercise
– excess post-exercise oxygen consumption (EPOC) – the difference between
the resting rate of oxygen consumption and the elevated rate following exercise.
– typically about 11 liters extra is needed after strenuous exercise
– repaying the oxygen debt
•
needed for the following purposes:
– replace oxygen reserves depleted in the first minute of exercise
• oxygen bound to myoglobin and blood hemoglobin, oxygen dissolved in blood plasma
and other extracellular fluid, and oxygen in the air in the lungs
– replenishing the phosphagen system
• synthesizing ATP and using some of it to donate the phosphate groups back to creatine
until resting levels of ATP and CP are restored
– oxidizing lactic acid
• 80% of lactic acid produced by muscles enter bloodstream
• reconverted to pyruvic acid in the kidneys, cardiac muscle, and especially the liver
• liver converts most of the pyruvic acid back to glucose to replenish the glycogen stores
of the muscle.
– serving the elevated metabolic rate
• occurs while the body temperature remains elevated by exercise and consumes more
11-60
oxygen
Beating Muscle Fatigue
• Taking oral creatine increases level of creatine
phosphate in muscle tissue and increases speed of ATP
regeneration
– useful in burst type exercises – weight-lifting
– risks are not well known
• muscle cramping, electrolyte imbalances, dehydration, water
retention, stroke
• kidney disease from overloading kidney with metabolite creatinine
• carbohydrate loading –
11-61
Physiological Classes of Muscle Fibers
• slow oxidative (SO), slow-twitch, red, or type I fibers
– abundant mitochondria, myoglobin and capillaries - deep red color
• adapted for aerobic respiration and fatigue resistance
•
fast glycolytic (FG), fast-twitch, white, or type II fibers
– fibers are well adapted for quick responses, but not for fatigue resistance
– rich in enzymes of phosphagen and glycogen-lactic acid systems generate
lactic acid causing fatigue
– poor in mitochondria, myoglobin, and blood capillaries which gives pale
appearance
• SR releases & reabsorbs Ca+2 quickly so contractions are quicker
(7.5 msec/twitch)
– extrinsic eye muscles, gastrocnemius and biceps brachii
• ratio of different fiber types have genetic predisposition – born sprinter
– muscles differ in fiber types - gastrocnemius is predominantly FG for quick
movements (jumping)
– soleus is predominantly SO used for endurance (jogging)
11-62
FG and SO Muscle Fibers
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
FG
SO
Figure 11.20
11-63
Strength and Conditioning
• muscles can generate more tension than the bones and tendons can
withstand
• muscular strength depends on:
– primarily on muscle size
• a muscle can exert a tension of 3 or 4 kg / cm2 of cross-sectional area
– fascicle arrangement
– size of motor units
– multiple motor unit summation – recruitment
• when stronger contraction is required, the nervous system activates more motor
units
– temporal summation
• nerve impulses usually arrive at a muscle in a series of closely spaced action
potentials
• the greater the frequency of stimulation, the more strongly a muscle contracts
– length – tension relationship
• a muscle resting at optimal length is prepared to contract more forcefully than a
muscle that is excessively contracted or stretched
– fatigue
• fatigued muscles contract more weakly than rested muscles
11-64
Strength and Conditioning
• resistance training (weight lifting)
– growth is from cellular enlargement
– muscle fibers synthesize more myofilaments and myofibrils and
grow thicker
• endurance training (aerobic exercise)
– improves fatigue resistant muscles
– slow twitch fibers produce more mitochondria, glycogen, and
acquire a greater density of blood capillaries
– improves skeletal strength
– increases the red blood cell count and oxygen transport capacity
of the blood
– enhances the function of the cardiovascular, respiratory, and
nervous systems
11-65
Cardiac Muscle
• limited to the heart where it functions to pump blood
• required properties of cardiac muscle
– contraction with regular rhythm
– muscle cells of each chamber must contract in unison
– contractions must last long enough to expel blood
11-66
Cardiac Muscle
• characteristics of cardiac muscle cells
– striated like skeletal muscle, but myocytes (cardiocytes) are shorter
and thicker
– each myocyte is joined to several others at the uneven, notched
linkages – intercalated discs
• appear as thick dark lines in stained tissue sections
• electrical gap junctions allow each myocyte to directly stimulate its
neighbors
• mechanical junctions that keep the myocytes from pulling apart
– sarcoplasmic reticulum less developed, but T tubules are larger and
admit supplemental Ca2+ from the extracellular fluid
– damaged cardiac muscle cells repair by fibrosis
11-67
Cardiac Muscle
– can contract without need for nervous stimulation
• contains a built-in pacemaker that rhythmically sets off a wave of electrical
excitation
• wave travels through the muscle and triggers contraction of heart chambers
• autorhythmic – because of its ability to contract rhythmically and independently
– autonomic nervous system does send nerve fibers to the heart
• can increase or decrease heart rate and contraction strength
– very slow twitches - does not exhibit quick twitches like skeletal muscle
• maintains tension for about 200 to 250 msec
– uses aerobic respiration almost exclusively
• rich in myoglobin and glycogen
• has especially large mitochondria
– very adaptable with respect to fuel used
– very vulnerable to interruptions of oxygen supply
– highly fatigue resistant
11-68
Smooth Muscle
• composed of myocytes that have a fusiform shape
• there is only one nucleus, located near the middle of the cell
• no visible striations
– reason for the name ‘smooth muscle’
– thick and thin filaments are present, but not aligned with each other
• z discs are absent and replaced by dense bodies
– well ordered array of protein masses in cytoplasm
– protein plaques on the inner face of the plasma membrane
• cytoplasm contains extensive cytoskeleton of intermediate filament
– attach to the membrane plaques and dense bodies
– provide mechanical linkages between the thin myofilaments and the plasma membrane
• sarcoplasmic reticulum is scanty and there are no T tubules
• Ca2+ needed for muscle contraction comes from the ECF by way of
Ca2+ channels in the sarcolemma
• some smooth muscles lack nerve supply, while others receive autonomic
fibers, not somatic motor fibers as in skeletal muscle
• capable of mitosis and hyperplasia
• injured smooth muscle regenerates well
11-69
2 Types of Smooth Muscle
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
• multiunit smooth muscle
– occurs in some of the largest
arteries and pulmonary air
passages, in piloerector
muscles of hair follicle, and
in the iris of the eye
Autonomic
nerve fibers
Synapses
– autonomic innervation
similar to skeletal muscle
• terminal branches of a
nerve fiber synapse with
individual myocytes and
form a motor unit
• each motor unit contracts
independently of the others
(a) Multiunit
smooth muscle
Figure 11.21a
11-70
2 Types of Smooth Muscle
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
• single-unit smooth muscle
Autonomic
nerve fibers
– more widespread
– occurs in most blood vessels,
in the digestive, respiratory,
urinary, and reproductive tracts
– also called visceral muscle
– myocytes of this cell type are
electrically coupled to each
other by gap junctions
– they directly stimulate each
other and a large number of
cells contract as a single unit
Varicosities
Gap junctions
(b) Single-unit
smooth muscle
Figure 11.21b
11-71
Layers of Visceral Muscle
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Mucosa:
Epithelium
Lamina propria
Muscularis
mucosae
Muscularis externa:
Circular layer
Longitudinal
layer
Figure 11.22
11-72
Stimulation of Smooth Muscle
• smooth muscle is involuntary and can contract without nervous
stimulation
– can contract in response to chemical stimuli
• hormones, carbon dioxide, low pH, and oxygen deficiency
• in response to stretch
• single unit smooth muscle in stomach and intestines has
of contraction throughout the entire layer of muscle
that set off waves
• most smooth muscle is innervated by autonomic nerve fibers
• in single unit smooth, each autonomic nerve fibers has up to 20,000
beadlike swelling called varicosities
– each contains synaptic vesicles and a few mitochondria
– nerve fiber passes amid several myocytes and stimulates all of them at once
when it releases its neurotransmitter
• no motor end plates, but receptors scattered throughout the surface – diffuse
junctions – no one-to-one relationship between nerve fiber and myocyte
11-73
Stimulation of Smooth Muscle
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Autonomic
nerve fiber
Varicosities
Mitochondrion
Synaptic
vesicle
Single-unit
smooth muscle
Figure 11.23
11-74
Contraction and Relaxation
• contraction is triggered by Ca+2, energized by ATP, and
achieved by sliding thin past thick filaments
• contraction begins in response to Ca+2 that enters the
cell from ECF, a little internally from sarcoplasmic
reticulum
• calcium binds to calmodulin on thick filaments
– activates myosin light-chain kinase – adds phosphate to
regulatory protein on myosin head
– and myosin ATPase, hydrolyzing ATP
• enables myosin similar power and recovery strokes like skeletal
muscle
– thick filaments pull on thin ones, thin ones pull on dense bodies
and membrane plaques
– force is transferred to plasma membrane and entire cell
shortens
– puckers and twists like someone wringing out a wet towel
11-75
Contraction and Relaxation
• contraction and relaxation very slow in comparison to
skeletal muscle
–
–
–
–
–
latent period in skeletal 2 msec, smooth muscle 50 - 100 msec
tension peaks at about 500 msec (0.5 sec)
declines over a period of 1 – 2 seconds
slows myosin ATPase enzyme and slow pumps that remove Ca+2
Ca+2 binds to calmodulin instead of troponin
• latch-bridge mechanism is resistant to fatigue
– heads of myosin molecules do not detach from actin immediately
– do not consume any more ATP
– maintains tetanus tonic contraction (smooth muscle tone)
• arteries – vasomotor tone
intestinal tone
11-76
Contraction of Smooth Muscle
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Plaque
Intermediate filaments
of cytoskeleton
Actin filaments
Dense body
Myosin
(b) Contracted smooth
muscle cells
Figure 11.24
(a) Relaxed smooth muscle cells
11-77
Stretching Smooth Muscle
• stretch can open mechanically-gated calcium
channels in the sarcolemma causing contraction
– peristalsis – waves of contraction brought about by food
distending the esophagus or feces distending the colon
• propels contents along the organ
• stress-relaxation response (receptive relaxation) helps hollow organs gradually fill (urinary bladder)
11-78
Contraction and Stretching
• skeletal muscle cannot contract forcefully if overstretched
• smooth muscle contracts forcefully even when greatly stretched
• smooth muscle can be anywhere from half to twice its resting length
and still contract powerfully
• three reasons:
– there are no z discs, so thick filaments cannot butt against them and stop
contraction
– since the thick and thin filaments are not arranged in orderly sarcomeres,
stretching does not cause a situation where there is too little overlap for crossbridges to form
– the thick filaments of smooth muscle have myosin heads along their entire
length, so cross-bridges can form anywhere
• plasticity – the ability to adjust its tension to the degree of stretch
11-79
Muscular Dystrophy
• muscular dystrophy - group of hereditary diseases in which skeletal
muscles degenerate and weaken, and are replaced with fat and fibrous
scar tissue
• Duchenne muscular dystrophy is caused by a sex-linked recessive
trait (1 of 3500 live-born boys)
– most common form
– disease of males – diagnosed between 2 and 10 years of age
– mutation in gene for muscle protein dystrophin
• actin not linked to sarcolemma and cell membranes damaged during
contraction, necrosis and scar tissue results
– rarely live past 20 years of age due to affects on respiratory and cardiac
muscle – incurable
• facioscapulohumeral MD - autosomal dominant trait affecting both sexes
equally
– facial and shoulder muscles more than pelvic muscles
• limb-girdle dystrophy
– combination of several diseases of intermediate severity
– affects shoulder, arm, and pelvic muscles
11-80
Myasthenia Gravis
• autoimmune disease in which antibodies attack neuromuscular
junctions and bind ACh receptors together in clusters
– disease of women between 20 and 40
– muscle fibers then removes the clusters of receptors from the sarcolemma by
endocytosis
– fiber becomes less and less sensitive to ACh
– effects usually first appear in facial muscles
• drooping eyelids and double vision, difficulty swallowing, and weakness of the
limbs
– strabismus –
• treatments
– cholinesterase inhibitors retard breakdown of ACh allowing it to stimulate
the muscle longer
– immunosuppressive agents suppress the production of antibodies that
destroy ACh receptors
– thymus removal (thymectomy) – helps to dampen the overactive immune
response that causes myasthenia gravis
– plasmapheresis
11-81
Myasthenia Gravis
drooping eyelids and weakness of muscles of eye movement
11-82