Transcript Chp 9 skeletal muscle notes.ppt

Chapter 9
Skeletal muscle tissue
Muscle Tissue
• Three types of muscle tissue:
– Skeletal muscle, cardiac muscle, smooth
muscle
– Composes 40-50% of weight of the adult
• 700 skeletal muscles in the muscular system
skeletal muscle - voluntary, striated muscle attached to
one or more bones
voluntary – usually subject to conscious control
Functions of Skeletal Muscle
• Functions of Skeletal Muscle
– Body movement
• contraction of muscles attached to bones
– Maintenance of posture
• stabilizes joints and helps maintain the body’s posture
– Protection and support
• muscles arranged along the walls of abdominal and pelvic cavity
• protect the internal organs and support normal position
– Storage and movement of materials
• sphincters, circular muscle bands
– contract and relax to regulate passage of material
– allow voluntary expulsion of feces and urine
– Heat production
• produced by energy required for muscle contraction
• continuously generate heat to maintain body temperature
• shiver when cold to generate heat
Characteristics Skeletal Muscle Tissue
• Characteristics
– Excitability
• responsive to nervous system stimulation
• neurons secreting neurotransmitters that bind to muscle cells
– Conductivity
• electrical change traveling along plasma membrane
• initiated in response to neurotransmitter binding
– Contractility
• contractile proteins within muscle cells
• slide past each other tension used to pull on bones of skeleton
– Elasticity
• due to protein fibers acting like compressed coils
• muscle returns to original length
– Extensibility
• lengthening of a muscle cell
Anatomy of Skeletal Muscle: Gross Anatomy
•
Skeletal muscle
–
–
–
–
–
Composed of thousands
of muscle cells
Typically as long as the
entire muscle
Often referred to as
muscle fibers
Organized into bundles,
termed fascicles
Muscle composed of
fibers, connective
tissue, blood vessels,
nerves
Anatomy of Skeletal Muscle: Gross Anatomy
• Connective tissue components
– Three concentric layers of connective tissue:
For protection, blood vessels, nerves, and attachment
– Epimysium
•
layer of dense irregular connective tissue
•
surrounds whole skeletal muscle
– Perimysium
•
dense irregular tissue surrounding the fascicles
•
contains extensive blood vessels and nerves supplying fibers
– Endomysium
•
innermost connective tissue layer
•
delicate areolar connective tissue
•
surrounds and electrically insulates each muscle fiber
•
protein fibers
– help bind together neighboring muscle fibers
Connective tissue components
–
–
–
–
Tendon
•
cordlike structure composed of dense regular connective tissue
•
formed by the three connective tissue layers
•
attach the muscle to bone, skin or another muscle
Aponeurosis
•
thin, flattened sheet of dense irregular tissue
•
formed from the three connective tissue layers
Deep fascia
•
additional sheet of dense irregular connective tissue- fills spaces
•
external to the epimysium
•
separates and binds together muscles with similar functions
•
contains nerves, blood vessels, and lymph vessels
Superficial fascia
•
superficial to deep fascia
•
composed of areolar and adipose connective tissue
•
separates muscles from skin
Gross Anatomy
• Blood vessels and nerves
–
–
–
Skeletal muscles vascularized by
extensive blood vessels
Deliver oxygen and nutrients,
removing waste products
Innervated by motor neurons
•
extend from brain and spinal
cord to muscle fibers
•
have long extensions called
axons
•
junction termed the
neuromuscular junction
Skeletal Muscle
• skeletal muscle - voluntary, striated
muscle attached to one or more
bones
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
• striations - alternating light
dark transverse bands
and
Nucleus
Muscle fiber
– results from an overlapping of internal
contractile proteins
• voluntary – usually subject
conscious control
Endomysium
to
Striations
© Ed Reschke
• muscle cell, muscle fiber, (myofiber)
as long as 30 cm
Figure 11.1
11-10
Anatomy of Skeletal Muscle:
Microscopic Anatomy
• Multinucleated
cell
–
–
Elongated cells
extending length
of muscle
Satellite cells
•
myoblasts
remaining,
unfused, in
adult skeletal
tissue
•
may be
stimulated to
differentiate if
tissue injured
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Myoblasts
Muscle fiber
Myoblasts fuse
to form a skeletal
muscle fiber.
Satellite cell
Muscle fiber
Satellite cell
Nuclei
Microscopic Anatomy
• Sarcolemma and T-tubules
–
–
–
Plasma membrane of a skeletal muscle fiber
•
sarcolemma
Invaginations of the sarcolemma
•
T-tubules, or transverse tubules
Na+/ K+ pumps along sarcolemma and T-tubules
•
create concentration gradients for Na+ and K+
•
three Na+ pumped out while two K+ pumped in
•
resting membrane potential maintained by pumps
– inside of cell relatively negative in comparison to outside
– responsible for excitability of skeletal muscle fibers
– Voltage-gated Na+ channels and voltage-gated K+ channels
Anatomy of Skeletal Muscle:
Microscopic Anatomy
• Sarcoplasmic reticulum
–
–
–
–
Internal membrane complex
Similar to smooth endoplasmic reticulum
Surround bundles of contractile proteins
Terminal cisternae
•
blind sacs of sarcoplasmic reticulum
•
serve as reservoirs for calcium ions
•
combine in twos with central T-tubule to form triads
Structure and Organization of a Skeletal Muscle Fiber:
Sarcolemma and T-Tubules (Figure 10.3 b)
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Interstitial fluid
– K+
+
+ + +
+ + +
–
– – –
– – –
+
+
– –
– –
+
+
+
+
+
– –
– –
+
+
+
–
in
– Na+
–
2K+
+
Sarcolemma
Sarcoplasm
(b) Sarcolemma and T-tubules
Voltage-gated
K+ channel
–
3 Na+ out
Voltage-gated
Na+ channel
Na+/K+
pump
+
T-tubule
• Sarcoplasmic
reticulum (continued)
– Ca2+ pumps embedded in
sarcoplasmic reticulum
• move Ca2+ into
sarcoplasmic reticulum
– Voltage-gated Ca2+ channels
• open to release Ca2+ from
sarcoplasmic reticulum
into sarcoplasm
• causes muscle
contraction
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
SR membrane
Ca2+
Ca2+ pump
Voltage-gated
Ca2+ channel
Calmodulin
Calsequestrin
Sarcoplasm
Terminal cisterna
(c) Sarcoplasmic reticulum
(Figure 10.3c)
Anatomy of Skeletal Muscle:
Microscopic Anatomy
• Muscle fibers and myofibrils
–
–
Myofibrils
•
long cylindrical structures
•
extend length of muscle fiber
•
compose 80% of volume of muscle fiber
•
each fiber with hundreds to thousands
Myofilaments
•
bundles of protein filaments
•
takes many to extend length of myofibril
•
two types: thick and thin
Structure and Organization of a Skeletal Muscle Fiber
(Figure 10.3 a)
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Muscle
Fascicle
Muscle fiber
Triad
Sarcoplasmic
reticulum
T-tubule
Terminal
cisternae
Sarcolemma
Nucleus
Myofibrils
Sarcomere
Myofilaments
Nucleus
Openings into
T-tubules
Sarcoplasm
Nucleus
(a) Skeletal muscle fiber
Mitochondrion
Anatomy of Skeletal Muscle:
Microscopic Anatomy
Muscle fibers and myofibrils
• Thick filaments A bands
–
•
Assembled from bundles of protein molecules, myosin
•
each myosin protein with two intertwined strands
•
each strand with a globular head and elongated tail
•
head with a binding site for actin (thin filaments)
•
head with site where ATP attaches and is split
Thin filaments I bands
–
–
–
Primarily composed of two strands of protein, actin
Two strands twisted around each other
Globular actin with myosin binding site
•
where myosin head attaches during contraction
Anatomy of Skeletal Muscle:
Microscopic Anatomy
Muscle fibers and myofibrils
• Thin filaments
–
–
Tropomyosin
•
twisted “stringlike” protein
•
cover small bands of the actin strands
•
covers myosin binding sites in a noncontracting muscle
Troponin
•
globular protein attached to tropomyosin
•
binding site for Ca2+
•
together form troponin-tropomyosin complex
•
http://www.youtube.com/watch?v=Ct8AbZn_A8A
•
http://www.youtube.com/watch?v=EdHzKYDxrKc
Molecular Structure of Thick and Thin Filaments
(Figure 10.4)
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Muscle fiber
Myofibril
Myofilaments
Myosin molecule
Heads
Actin binding site
ATP and ATPase binding site
Tail
Myosin heads
(a) Thick filament
Troponin
Tropomyosin
G-actin
(b) Thin filament
F-actin
Myosin binding site
Ca2+ binding site
Anatomy of Skeletal Muscle:
Microscopic Anatomy
• Organization of a sarcomere
–
–
–
–
•
Myofilaments arranged in repeating units, sarcomeres
Number varies with length of myofibril
Composed of overlapping thick and thin filaments
Delineated at both ends by Z discs
•
specialized proteins perpendicular to myofilaments
•
anchors for thin filaments
Overlapping filaments (continued)
–
–
–
Form alternating patterns of light and dark regions
Appears striated under a microscope
•
due to size and density differences between thick and thin
filaments
Each thin filament with three thick filaments
•
form triangle at its periphery
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 – alternating lighter band – I stands for isotropic
• the way the bands reflect polarized light
– z disc – provides anchorage for thin filaments and elastic filaments
• bisects I band
– sarcomere – the segment of the myofibril from one z disc to the next
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
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
11-22
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
11-23
Structure of a Sarcomere (Figure 10.5 a)
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Muscle fiber
Sarcomeres
I band
A band
I band
Myofibril
Z disc
H zone
M line
Sarcomere
(a)
Z disc
Myofilaments
Structure of a Sarcomere (Figure 10.5 b)
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Sarcomere
Z disc
Connectin
Z disc
Thick filament
Thin filament
M line
Thin filament
H zone
I band
(b)
A band
I band
Structure of a Sarcomere (Figure 10.5 c)
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Transverse
sectional plane
M line
Thick filaments
and accessory
proteins
(c)
H zone
Thick filaments
A band
Thick filaments
Thin filaments
I band
Thin filaments
Connectin
Z disc
Thin filaments
Connectin
and accessory
proteins
Microscopic Anatomy
• Mitochondria and other structures associated with
energy production
–
–
–
–
–
Muscle with high ATP requirement
Abundant mitochondria for aerobic cellular respiration
Glycogen stores for immediate fuel molecule
Creatinine phosphate
•
molecule unique to muscle tissue
•
provides fibers means of supplying ATP anaerobically
Myoglobin
•
molecule unique to muscle tissue
•
reddish globular protein similar to hemoglobin
•
binds oxygen when muscle at rest
•
releases it during muscular contraction
•
provides additional oxygen to enhance aerobic cellular respiration
Innervation of Skeletal Muscle Fibers
• Motor unit
–
–
Motor neuron nerve cells
•
transmit nerve signals from brain or spinal cord
•
have axons that branch
•
individually innervate numerous skeletal muscle fibers
•
single motor neuron + fibers it controls = motor unit
Varied number of fibers a neuron innervates
•
small motor units less than five muscle fibers
•
large motor units with several thousand
•
inverse relationship between size of motor unit and degree
of control
– e.g., small motor units innervating eye
– need greater control
– e.g., large motor units innervating lower limbs
– need less precise control
• Neuromuscular junctions
–
–
–
•
Location where motor neuron
innervates muscle
Usually mid-region of muscle
fiber
Has synaptic knob, motor end
plate, synaptic cleft
Synaptic knob
–
–
–
–
The expanded tip of the axon
Axon enlarged and flattened in
this region
Houses synaptic vesicles, small
membrane sacs
•
filled with neurotransmitter,
acetylcholine (ACh)
Has Ca2+ pumps embedded in
plasma membrane
•
establish calcium gradient,
with more outside the neuron
Neuromuscular junctions
• Motor end plate
–
–
–
•
Specialized region of sarcolemma
Has numerous folds
•
increase surface area covered by
knob
Has vast numbers of ACh receptors
•
plasma membrane protein channels
•
opened by binding of ACh
•
allow Na+ entry and K+ exit
Synaptic cleft
–
–
–
Narrow fluid-filled space
Separates synaptic knob and motor end
plate
Acetylcholinesterase enzyme that
breaks down ACh molecules
•
after their release into synaptic cleft
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Neuromuscular
junction
Structure and
Organization
of a
Neuromuscular
Junction
(Figure
10.7a)
Synaptic knob
Nerve signal
Synaptic
cleft
Endomysium
Sarcolemma
(a)
Motor end
plate
Myofilaments
Myofibril
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Ca2+ pump
Interstitial fluid
Ca2+
Voltage-gated
Ca2+ channels
Structure and
Organization
of a
Neuromuscular
Junction
(Figure
10.7b)
Synaptic knob
Vesicle
with ACh
Synaptic
cleft
ACh
Sarcolemma
Sarcoplasm
–Na+
Ach receptor
K+
Junction fold
Motor end plate
(b)
Overview of Events in Skeletal Muscle Contraction
(Figure 10.8)
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1 NEUROMUSCULAR JUNCTION: EXCITATION OF A SKELETAL MUSCLE FIBER
Release of neurotransmitter acetycholine (ACh) from synaptic vesicles and
subsequent binding of Ach to Ach receptors.
2 SARCOLEMMA, T-TUBULES, AND SARCOPLASMIC
Neuromuscular
junction
Synaptic vesicle (contains ACh)
Action potential
1
Muscle
fiber
T-tubule
ACh
Ach receptor
Terminal
cisterna
of SR
Sarcoplasmic
reticulum
RETICULUM: EXCITATION-CONTRACTION COUPLING
ACh binding triggers propagation of an action potential
along the sarcolemma and T-tubules to the sarcoplasmic
reticulum, which is stimulated to release Ca2+.
2
Ca2+
Sarcolemma
Sarcomere
Ca2+
3
Thin filament
Ca2+
3 SARCOMERE: CROSSBRIDGE CYCLING
Ca2+ binding to troponin triggers sliding of thin
filaments past thick filaments of sarcomeres;
sarcomeres shorten, causing muscle contraction.
Thick filament
Excitation of a Skeletal Muscle Fiber
• First physiological event
– Muscular fiber excitation by motor neuron
– Occurs at neuromuscular junction
– Results in release of ACh and subsequent binding of ACh receptors
1.Calcium entry at synaptic knob
– Nerve signal propagated down motor axon
– Triggers opening of voltage-gated Ca2+ channels
– Movement of calcium down concentration gradient
• from interstitial fluid into synaptic knob
– Binding of calcium with proteins on synaptic vesicles
Excitation of a Skeletal Muscle Fiber
2.Release of ACh from synaptic knob
– Merging of synaptic vesicles with synaptic knob membrane
• triggered by binding of Ca2+
– Exocytosis of ACh into synaptic cleft
– About 300 vesicles per nerve signal
Binding of ACh at motor end plate
– Diffusion of ACh across synaptic cleft
– Binds with ACh receptors within motor end plate
– Causes excitation of muscle fiber
– http://www.youtube.com/watch?v=CepeYFvqmk4
– http://www.youtube.com/watch?v=y7X7IZ_ubg4
Neuromuscular Junction: Excitation of a Skeletal Muscle
Fiber (Figure 10.9)
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1
NEUROMUSCULAR JUNCTION: EXCITATION OF A SKELETAL MUSCLE FIBER
1a Ca2+ entry at synaptic knob
A nerve signal is propagated down a motor axon and triggers
the entry of Ca2+ into the synaptic knob.
Nerve signal
Ca2+ binds to proteins in synaptic vesicle membrane.
Voltage-gated
Ca2+ channel
Synaptic knob
Ca2+
1a
Synaptic vesicles
(contain ACh)
Ca2+
Synaptic
vesicle
ACh
Interstitial
fluid
1b
Synaptic cleft
1b Release of ACh from synaptic knob
Calcium binding triggers synaptic vesicles to merge
with the synaptic knob plasma membrane and ACh
is exocytosed into the synaptic cleft.
ACh
1c
1c Binding of ACh to ACh receptor at motor end plate
ACh receptor
ACh diffuses across the fluid-filled synaptic cleft in the
motor end plate to bind with ACh receptors.
Motor end plate
Skeletal Muscle Contraction—Neuromuscular
Junction: Excitation of a Skeletal Muscle Fiber
Clinical View: Myasthenia Gravis
–
–
–
–
–
–
–
Autoimmune disease, primarily in women
Antibodies binding ACh receptors in neuromuscular junctions
Receptors removed from muscle fiber by endocytosis
Results in decreased muscle stimulation
Rapid fatigue and muscle weakness
Eye and facial muscles often involved first
May be followed by swallowing problems, limb weakness
Skeletal Muscle Contraction—Sarcolemma, T-Tubules,
Sarcoplasmic Reticulum: Excitation-Contraction Coupling
• Development of an end-plate potential at the
motor end plate
–
–
–
–
–
–
–
Binding of ACh to ACh receptors on motor end plate
Receptors stimulated to open
Allows Na+ to rapidly diffuse into muscle fiber
Allows K+ to slowly diffuse out
Net gain of positive charge inside fiber
Reverses electrical charge difference at motor end plate
Can be stimulated again almost immediately
• Binding of ACh at motor end plate
– Diffusion of ACh across synaptic cleft
– Binds with ACh receptors within motor end plate
– Causes excitation of muscle fiber
• Initiation and propagation of action potential
along the sarcolemma and T-tubules
– Action potential
• first, inside of sarcolemma becoming relatively positive
– due to influx of Na+ from voltage-gated channels
– termed depolarization
• then, inside of sarcolemma returning to resting potential
– due to outflux of K+ from voltage-gated channels
– termed repolarization
– Action potential propagated along sarcolemma and T-tubules
• inflow of Na+ at initial portion of sarcolemma
• causes adjacent regions to experience electrical changes
• initiate voltage-gated Na+ channels in this region to open
• action potential propagated down the sarcolemma and t-tubules
– Refractory period
• time between depolarization and repolarization
• muscle unable to be restimulated
Excitation-Contraction Coupling
• Release of calcium from the sarcoplasmic reticulum
– Opening of voltage-gated Ca2+ channels
• found in terminal cisternae of sarcoplasmic reticulum
• triggered by action potential
– Diffusion of Ca2+ out of cisternae
– Diffusion of Ca2+ into sarcoplasm
– Now interacts with thick and thin filaments
– Binding of Ca2+ and crossbridge cycling
– Results in muscle contraction
• Calcium binding
–
–
–
–
Binding of calcium to subunit of troponin
Induces conformation change in troponin
Troponin-tropomyosin complex moved
Myosin binding sites of actin exposed
Skeletal Muscle Fiber: Excitation-Contraction Coupling
(Figure 10.10)
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
2
SARCOLEMMA, T-TUBULES, AND SARCOPLASMIC RETICULUM:
EXCITATION-CONTRACTION COUPLING
Interstitial fluid
+
+
+
+
– –
– –
– –
– –
– –
– –
– –
– –
– –
– –
+
Release of Ca2+ from the
sarcoplasmic reticulum
Ca2+
When the action potential reaches
the sarcoplasmic reticulum, it
triggers the opening of
voltage-gated Ca2+ channels
located in the terminal cisternae
of the sarcoplasmic reticulum
Ca2+ diffuses out of the cisternae
sarcoplasmic reticulum into the
sarcoplasm.
2c
Ca2+
Ca2+
Terminal cisterna
Ca2+
+
– –
– –
– –
– –
– –
– –
–
– – –
Second, voltage-gated K+ channels open, and K+ moves
out to cause repolarization.
+
+
– – –
The result is a reversal in the electrical charge difference across the
membrane of a muscle fiber at the motor end plate, which is called
an end-plate potential (EPP). (The inside which was negative is now
positive.)
First, voltage-gated Na+ channels open, and Na+ moves
in to cause depolarization.
+
+
Development of an end-plate potential (EPP) at the motor end plate
Binding of ACh to ACh receptors in the motor end plate triggers the opening
of these chemically gated ion channels. Na+ rapidly diffuses into and K+
slowly diffuses out of the muscle fiber.
An action potential is propagated along the sarcolemma
and T-tubules.
+
+
2a
+
+
Motor end plate
+
+
Sarcoplasm
Initiation and propagation of an action potential
along sarcolemma and T-tubules
T-tubule
Voltage-gated
Ca2+ channels
2c
K+
+
+
+
+
+
+
+
+
+
+
+
+
2b
Terminal cisterna
of sarcoplasmic
reticulum
Voltage-gated
K+ channel
Voltage-gated
Na+ channel
+
+
ACh
+
+
ACh
receptor
+
+
K+
+
+
2a
Na+
Sarcolemma
+
+
Na+
+
+
+
EPP
2b
– –
Synaptic
cleft
Voltage-gated
K+ channel
– –
Voltage-gated
Na+ channel
Sarcolemma
• Crossbridge cycling
– Four repeating steps will continue as long as Ca+ is present
1) Crossbridge formation
• myosin heads in the ready position
• attach to exposed myosin binding sites on actin
• results in formation of a crossbridge between thick and thin filament
2) Power stroke
• swiveling of the myosin head, termed power stroke
• pulls thin filaments a small distance past thick filaments
• ADP and Pi released
3) Release of myosin head
• binding of ATP to binding site of myosin head
• causes release of myosin head from actin
4) Reset myosin head
• ATP split into ADP and Pi by ATPase
– enzyme on myosin head
• provides energy to “cock” the myosin head
– http://www.youtube.com/watch?v=gJ309LfHQ3M
Muscle Contraction
• Sliding Filament Theory
– Ca ions cause ACH released
– membrane becomes permeable to Na +
deplorization
– Na + flows in K + flows out
– Ca + released from sarcoplasmic reticulum
– Ca + causes actin filament troponin –tropomyosin
covers to be uncovered
– myosin forms cross bridges connecting to actin
filament
– sarcomere shortens
Excitation (steps 1 and 2)
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Nerve signal
Motor
nerve
fiber
Ca2+ enters
synaptic knob
Synaptic
knob
Sarcolemma
Synaptic
vesicles
ACh
Synaptic
cleft
ACh
receptors
1 Arrival of nerve signal
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
• ACh released into synaptic cleft
11-44
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.
• Na+ enters shifting RMP goes from -90mV to +75mV, then K+ exits and RMP
returns to -90mV - quick voltage shift is called an end-plate potential (EPP).
11-45
Excitation (step 5)
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
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 surface.
11-46
Sarcomere Shortening (Figure 10.12)
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Relaxed sarcomere
Z disc
Connectin
Relaxed sarcomere
Thick filament
Thin filament
Z disc
Thin filament
M line
Z disc
H zone
I band
Z disc
M line
H zone
A band
I band
I band
A band
I band
(a) Relaxed skeletal muscle
Contraction
Z disc
Contraction
M line
Z disc
Z disc
(b) Fully contracted skeletal muscle
M line
A band
A band
Fully contracted
sarcomere
Fully contracted
sarcomere
a, b(right): © Dr. H. E. Huxley
Z disc
Clinical View: Muscular Paralysis and Neurotoxins
– Tetanus
• form of spastic paralysis
• caused by toxin produced by Clostridium tetani
• blocks release of inhibitory neurotransmitter in spinal cord
• results in overstimulation of muscles
• penetrating wound with soil prone to developing C. tetani infection
• routine vaccination against this life-threatening condition
– Botulism
• potentially fatal muscular paralysis
• caused by toxin produced by Clostridium botulinum
• prevents release of ACh at synaptic knobs
• most cases from ingesting toxin in canned foods
– temperatures not high enough to kill spores
• toxin can be injected for temporary diminishing of wrinkles
Clinical View: Muscular Paralysis and Neurotoxins
• 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
• flaccid paralysis – a state in which the muscles are limp and cannot contract
– curare – compete with ACh for receptor sites, but do not stimulate the
muscles
– plant poison used by South American natives to poison blowgun darts
Muscle Relaxation
• Relaxation- nerve impulse stops
– acetylcholinesterase break down ACh
– Na + flows out K + flows in- repolarization
- Ca + reabsorbed
– covers on actin fibers reform
– cross bridges released
- A and I bands relax
• All or None Response
– sarcomere lengthens
– each muscle cell and fiber contracts fully or not at all
• Muscle Twitch
– quick brief jerky movement
• Tetanus
– smooth substained contraction
Physiology of Skeletal Muscle Contraction:
Skeletal Muscle Relaxation
• Events in muscle relaxation
–
–
–
–
–
–
–
–
–
Termination of the nerve signal in the motor neuron
Prevents further release of ACh
Continual hydrolysis of ACh from receptor by acetylcholinesterase
Ceasing of end plate potential
No further action potential generated
Closure of voltage-gated calcium channels in SR
calcium transported back into storage
Return of troponin to its original shape
Tropomyosin now moving over myosin binding sites on actin
• prevents crossbridge formation
– Returns to original relaxed position
• through natural elasticity of muscle fiber
Relaxation
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AChE
ACh
14 Cessation of nervous stimulation
and ACh release
15 ACh breakdown by
acetylcholinesterase (AChE)
• nerve stimulation & ACh release stop
• AChE breaks down ACh & fragments reabsorbed into synaptic knob
• stimulation by ACh stops
11-52
Relaxation
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Terminal cisterna
of SR
Ca2+
Ca2+
16 Reabsorption of calcium ions by
sarcoplasmic reticulum
• Ca+2 pumped back into SR by active transport. Ca+2 binds to calsequestrin
while in storage in SR
• ATP is needed for muscle relaxation as well as muscle contraction.
11-53
Relaxation
• 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
• muscle fiber returns to its
resting length
– due to recoil of elastic
components & contraction of
antagonistic muscles
Ca2+
Loss of calcium ions from troponin
Tropomyosin
ATP
18
Return of tropomyosin to position
blocking active sites of actin
11-54
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
Ca+2 activates myosin-actin cross-bridging
muscle contracts, but can not relax.
• muscle relaxation requires ATP, and ATP production is no longer
produced after death
– fibers remain contracted until myofilaments begins to decay
• rigor mortis peaks about 12 hours after death, then diminishes
over the next 48 to 60 hours
11-55
• Three ways to generate ATP in skeletal muscle fiber:
1)Immediate supply via the phosphagen system
– Creatinine phosphate
• can supply ATP in skeletal muscle only
– Creatinine kinase
• transfer Pi from creatine phosphate to ADP
• provides an additional 10 to 15 seconds of energy
2)Short-term supply via anaerobic cellular respiration
– ATP provided by anaerobic cellular respiration
• occurs in cytosol does not require oxygen
• glucose from glycogen or through the blood
• 2 ATP released per glucose molecule
3)Long-term supply via aerobic cellular respiration
– Occurs within mitochondria Requires oxygen
– Energy used to generate ATP by oxidative phosphorylation
– 34 net ATP produced
Phosphagen System (Figure 10.14)
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ATP
ATPase
ADP + Pi
2 ADP
ADP
ATP
(a)
Creatine kinase
ADP + CP
ADP + Creatine
ADP
ADP
Pi
ATP
(b)
CP
Creatine
kinase
Myokinase
ATPase
ADP
Myokinase
ADP + AMP
AMP
ATP
(c)
Creatine
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
11-58
Metabolic Processes for Generating ATP (Figure 10.15)
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Glycolysis
Glucose
NADH
2
ATP
(a) Short-term energy supply
(anaerobic cellular respiration)
2 pyruvate
Insufficient oxygen
Cytosol
Lactic acid
Oxygen
Outer mitochondrial membrane
Mitochondrion
Pyruvate
Outer membrane compartment
NADH
Acetyl CoA
CO2
Inner mitochondrial membrane
Mitochondrial matrix
NADH
FADH2
(b) Long-term energy supply
(aerobic cellular respiration)
e–
CO2
Citric
acid
cycle
e–
H+ O2
H2O
e– Electron e–
transport chain
2
ATP
32
ATP
ATP synthetase
(oxidative phosphorylation)
H+
Skeletal Muscle Metabolism: Supplying
Energy for Skeletal Muscle Contraction
Energy supply and varying intensity of exercise
• ATP source dependent on intensity and duration
– E.g., in a 50-meter sprint
• ATP supplied primarily by phosphagen system
– 400-meter sprint
• ATP supplied initially by phosphagen system
• then primarily by anaerobic cellular respiration
– 1500-meter run
• ATP supplied by all three
• primarily supplied by aerobic processes after first minute
Utilization of Immediate, Short-Term, and
Long-Term Energy Sources (Figure 10.16)
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50 meters: 5–6 seconds
1500 meters: 5–6 minutes
400 meters: 50–60 seconds
Phosphagen system = immediate energy source
Anaerobic cellular respiration = short-term energy source
Aerobic cellular respiration = long-term energy source
1500-meter track
Skeletal Muscle Metabolism: Oxygen Debt
• Oxygen debt
– Amount of additional oxygen that must be inhaled following exercise
– Needed to restore pre-exercise conditions
– Additional oxygen required to
• replace oxygen on hemoglobin and myoglobin
• replenish glycogen
• replenish ATP and creatine phosphate in phosphagen system
• convert lactic acid back to glucose (in the liver)
Skeletal Muscle Fiber Types: Criteria for
Classification of Muscle Fiber Types
• Muscle fibers categorized by:
– type of contraction generated
– the primary means used for supplying ATP
Type of contraction generated
• Characteristic of contractions
– Differ in power, speed, and duration
– Power related to diameter of muscle fiber
• larger muscle fibers producing more powerful contraction
Skeletal Muscle Fiber Types
– Fast-twitch fibers extrinsic eye muscles, gastrocnemius and biceps
brachii use anaerobic cellular respiration
• have fast variant of myosin ATPase
• initiate contraction more quickly following stimulation
• produce contraction of shorter duration
• produce a strong contraction
• greater power and speed than slow-twitch 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
– Slow-twitch fibers soleus of calf and postural muscles of the back
• have slow variant of myosin ATPase
• red, or type I fibers
• abundant mitochondria, myoglobin and capillaries - deep red color
• adapted for aerobic respiration and fatigue resistance
– relative long twitch lasting about 100 msec
– soleus of calf and postural muscles of the back
• Variation of muscle fiber
types in individuals
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
– Long distance runners
• higher proportion of slowoxidative fibers in legs
– Sprinters
• higher percentage of fastglycolytic fibers
– Determined primarily by genes
– Determined partially by training
FO
SO
FO
FO
FG
FO
FG
SO
FG
SO
FO
SO
FG
© Gladden Willis/ Visuals Unlimited
Muscle Twitch
• Periods of the twitch
– Latent period
• period after stimulus before
contraction begins
• no change in fiber length
• time needed to initiate tension
in fiber
– Contraction period
• begins as power strokes pull
thin filaments
• increasing muscle tension
• shorter duration than relaxation
period
– Relaxation period
• begins with release of
crossbridges
• decreasing muscle tension
Contraction
phase
Latent
period
Time of
stimulation
Relaxation
phase
Muscle Twitch (Figure 10.18)
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
Muscle Twitch
Latent
period
Pivot
Weight
Hardware
detecting change
of length of muscle
Muscle tension
Muscle
Electrodes
Contraction
period
Stimulus
Voltage
Frequency
Time (msec)
Relaxation
period
Factors Affecting Skeletal Muscle Tension
Within the Body: Muscle Tone
• Muscle tone
–
–
–
–
–
–
–
Resting tension in a muscle
Generated by involuntary nervous stimulation of muscle
Some motor units stimulated randomly at any time
Change continuously so units not fatigued
Tension called the resting muscle tone
Do not generate enough tension for movement
Decreases during deep sleep
Isometric and Isotonic Contractions
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
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
– muscle is producing internal tension while an external resistance causes it to
stay the same length or become longer
– can be a prelude to movement when tension is absorbed by elastic
component of muscle
– important in postural muscle function and antagonistic muscle joint
stabilization
isotonic muscle contraction
– muscle changes in length with no change in tension
– concentric contraction – muscle shortens while maintains tension
11-69
– eccentric contraction – muscle lengthens as it maintains tension
Factors Affecting Skeletal Muscle Tension Within
the Body: Isometric and Isotonic Contractions
Clinical View: Isometric Contraction and
Increase in Blood Pressure
– Sustained isometric contractions
• associated with increase in blood pressure
– May be a concern for those with baseline high blood pressure
– E.g., shoveling snow
• general peripheral constriction (from cold) elevates pressure
• isometric contractions also increasing pressure
• Muscle fatigue
Muscle Fatigue
– Reduced ability to produce muscle tension
– Decrease in glycogen stores
• primary cause during excessive exercise
• Other causes of muscle fatigue
– Problems of excitation at the neuromuscular junction
• insufficient free Ca2+ at neuromuscular junction
• decreased number of synaptic vesicles
– Problems with crossbridge cycling
• increased phosphate ion concentration
– interferes with Pi release from myosin head
– slows rate of cycling
• lower Ca2+ available for release from sarcoplasmic reticulum
– less available to bind to troponin
• both produce weaker muscle contraction
Effects of Exercise and Aging on
Skeletal Muscle: Effects of Exercise
• Changes in muscle from a sustained exercise
program
–
–
Hypertrophy
•
increase in skeletal muscle size
•
results from repetitive stimulation of fibers
•
results in
– more mitochondria
– larger glycogen reserves
– increased ability to produce ATP
– more myofibrils that contain larger number of myofilaments
Hyperplasia
•
increase in the number of muscle fibers
•
may occur in a limited way with exercise
Effects of Exercise and Aging on
Skeletal Muscle: Effects of Exercise
• Changes in muscle from lack of exercise
–
Atrophy
•
decreasing muscle fiber size
•
results from lack of exercise
•
can arise from temporary reduction in muscle use
– e.g., individuals in a cast
•
initially reversible, but dead fibers not replaced
•
with extreme atrophy, loss of muscle function permanent
– muscle replaced with connective tissue
Effects of Exercise and Aging on
Skeletal Muscle
Clinical View: Anabolic steroids as performanceenhancing compounds
–
–
–
–
–
Synthetic substances that mimic testosterone
Require prescription for legal use
Stimulate manufacture of muscle proteins
Popular performance enhancers
Side effects include
• increased risk of heart disease and stroke
• kidney damage and liver tumors
• testicular atrophy, breast development in males
• acne, high blood pressure, aggressive behavior
• growth of facial hair and menstrual irregularities in women
Effects of Exercise and Aging on
Skeletal Muscle: Effects of Aging
• Loss of muscle mass with age
– Slow loss begins in person’s mid-30s
• as a result of decreased activity
– Decreased size and power of skeletal muscle
– Loss in fiber number and diameter
– Decreased oxygen storage capacity
– Muscle strength and endurance impaired
– Decreased circulatory supply to muscles with exercise
– Muscle mass often replaced by dense regular connective tissue
• termed fibrosis
• decreases flexibility of muscle
• can restrict movement and circulation
– Reduced decline in muscular performance
• with attention to physical fitness throughout life