Download lecture #11

THE MUSCULAR SYSTEM:
SKELETAL MUSCLE TISSUE
AND MUSCLE
ORGANIZATION
Muscle Tissue: Functions
• 1. producing body movements
– integrated action of skeletal muscle, joints and bones
• 2. stabilizing body positions
– skeletal muscle contraction stabilizes joints and bones
– postural muscles contract continuously when awake
• 3. storing and moving substances in the body
– contraction of ring-like smooth muscle sphincters – storage of
material in an organ
– storage of glucose within skeletal muscle
– movement of blood by cardiac muscle and by smooth muscle
within the blood vessels
– movement of food through the GI tract by smooth muscles within
abdominal viscera
Properties of Muscles
Electrical excitability
-ability to respond to stimuli by producing electrical signals
such as action potentials
-two types of stimuli: 1. autorhythmic electrical signals
2. chemical stimuli
Contractility
-ability to contract when stimulated by an AP
-isometric contraction: tension develops, length doesn’t change
-isotonic contraction: tension develops, muscle shortens
Extensibility
-ability to stretch without being damaged
-allows contraction even when stretched
Elasticity
-ability to return to its original length and shape
Gross Anatomy
•muscles are really groups of fascicles
•the fascicles are groups of muscle fibers
•muscle fiber is considered to be an individual muscle
cell
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muscles are covered superficially by a superficial fascia
layer (or subcutaneous layer/hypodermis)
three layers of connective tissue surround the muscle &
partition it into bundles and fibers
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these layers further strengthen and protect muscle
outermost layer = epimysium
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Epimysium
Perimysium
Endomysium
encircles the entire muscle
next layer = perimysium
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divides the muscle into bundles of 10 to 100 individual
muscle fibers
fibers = muscle cell
give meat its “grain” because the fascicles are visible
both epimysium and perimysium are dense irregular
connective tissue
•next layer = endomysium (areolar connective tissue)
– penetrates the fasicles and separates them
into individual muscle fibers
– skeletal muscle fibers are controlled by
lower motor/somatic motor neurons =
neuromuscular junction
•the muscle fiber is made up of fused muscle cells
-these muscle cells have a unique
cytoskeleton made up of myofibrils
•each myofibril is comprised of
repeating units of protein filaments = sarcomeres
Skeletal Muscle development
• Large, multinucleated cells
– embryonic development - muscle fibers arise from fusion of a hundred or more
mesodermal cells called myoblasts – organized into muscle fibers
– once fused, these muscle cells lose the ability of undergo mitosis
– number of muscle cells predetermined before birth
– myoblasts develop from stem cells
• adult – these stem cells are called satellite cells
• also can come from bone marrow stem cells?
muscle fibers
The muscle cell: contents
• Plasma membrane = sarcolemma
• nuclei
• organelles
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golgi, lyososome
mitochondria
sarcoplasmic reticulum
T-tubules
• Cytoplasm = sarcoplasm
– cytoskeleton
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microtubules
intermediate filaments (desmin)
actin
myosin
other structural proteins
– cytosol
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water
ions
glycogen (glucose)
myoglobin (oxygen)
creatine phosphate (ATP)
Microanatomy of Muscle Fibers
• New terminology
– Cell membrane = sarcolemma
• plasma membrane that surrounds a single muscle fiber
– Cytoplasm = sarcoplasm
• substantial amounts of glycogen - can be broken into
glucose
• contains myoglobin - binds oxygen needed for muscle
ATP production
• Internal membrane system =
sarcoplasmic reticulum
• encircles each myofibril
• have dilated end sacs =
terminal cisternae
• stores calcium when at rest
• releases it during contraction
• calcium release is triggered
by an AP
• Invaginations of the plasma
membrane = T tubules
• open to the outside of the
fiber and continuous with
the sarcolemma
• filled with interstitial fluid
• action potentials travel
along the sarcolemma and
the T tubules
• allows for the even and
quick spread of an action
potential
Microanatomy of
Muscle Fibers
M line
Sarcomere
Structure
•sarcomere = regions of myosin (thick myofilament) and actin (thin
myofilament)
•bounded by the Z line
•about 1.6 to 2.0 um in length
•typical myofibril has about 10,000 sarcomeres
•comprised of an A band, an H zone, and 2 halves of an I band
Sarcomere structure
• I band – region of thin filaments only
– split in half by the Z line
• Z line – denotes the sarcomere
– comprised of proteins called connectins (e.g. actinin) that interconnect the
thin filaments from sarcomere to sarcomere
– also connect to a structural protein called titin
• keeps thick and thin filaments in proper alignment and resists extreme
stretching forces
– connected to adjacent myofibrils by intermediate filaments (e.g. desmin)
• results in the sarcomeres from adjacent myofibrils aligning with each other =
striated appearance
• M line – made up of a protein called the M line protein
– binds an enzyme for ATP storage called creatine kinase
– helps in the positioning of the thick filaments between the thin filaments
(binds myosin)
• A band – length of the thick filament
– contains the “zone of overlap” between thin and thick filaments
The Proteins of
Muscle
• Myofibrils are built of 3
kinds of protein
– contractile proteins
• myosin and actin
– regulatory proteins which
turn contraction on & off
• troponin and tropomyosin
– structural proteins which
provide proper alignment,
elasticity and extensibility
• E.g. titin, nebulin and
dystrophin
Structural Proteins of Muscle
• Nebulin, an inelastic protein
helps align the thin filaments.
•Dystrophin links thin
filaments to sarcolemma and
transmits the tension generated
to the tendon.
•Titin anchors thick filament
to the M line and the Z line.
Contractile proteins of muscle: Actin
•two forms of actin – G-actin and F-actin
•the G-actin “beads” are assembled together (using ATP) to form two linear chains of
actin called F-actin
•these two chains are wrapped around a core “rod” of nebulin to form a helix
•F-actin filament is associated with the regulatory proteins troponin and
tropomyosin = THIN FILAMENT
Contractile proteins of muscle: Myosin
• myosin thick myofilament is a bundle of myosin molecules
• each myosin protein is made up of two heavy chains - each with a
globular “head” with a site to bind ATP and a site to bind actin
• also associated with the heads are 4 light chains
– play a role in myosin’s assembly and ability to hydrolyze ATP
Contraction: The Sliding Filament Theory
• Contraction:
– Active process
– Elongation is passive
– Amount of tension produced is proportional to degree
of overlap of thick and thin filaments
• SF Theory:
– Explains how a muscle fiber exerts tension
– Four step process
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Active sites on actin
Crossbridge formation
Cycle of attach, pivot, detach, return
Troponin and tropomyosin control contraction
myosin binding site or
-calcium binds to troponin and exposes sites that can interact with myosin
- Ca+2 binds to troponin & causes troponin-tropomyosin complex to move & reveal
myosin binding sites on actin
-ATP binding, hydrolysis and ADP release changes the conformation of the head (“power
stroke”) and causes actin to “slide” along the myosin myofilaments
-shortens the distance between the Z lines
Contracted Sarcomere
CHECK OUT THESE ANIMATIONs!!!
http://highered.mcgrawhill.com/sites/0072495855/student_view0/chapter10/animatio
n__myofilament_contraction.html
http://www.youtube.com/watch?v=EdHzKYDxrKc
http://www.youtube.com/watch?v=Vlchs4omFDM
Sarcoplasmic Reticulum and Calcium
release
• the SR wraps around each A and I band
– segmented with T-tubules between each SR segment
• each segment forms saclike regions at the ends = lateral sacs (terminal cisternae)
Sarcoplasmic Reticulum and Calcium
release
•
on the lateral sac of the SR is an orderly arrangement of proteins = foot proteins (ryanodine
receptors)
– serve as Ca release channels
– 50% of the foot proteins of the SR are “zipped” together with voltage-sensing proteins found on the
T-tubule (dihydropyridine receptors)
– when an AP travels down the T-tubule – the local depolarization activates these DHP receptors
which then open the foot proteins on the SR
– the opening of these foot proteins triggers the SR to open the remaining foot proteins that are not
connected to the T-tubule
– efflux of calcium into the sarcoplasm
foot proteins
T-tubule
SR
The Neuromuscular Junction
• end of neuron (synaptic terminal or
axon bulb) is in very close association
with a single muscle fiber (cell)
•nerve impulse leads to release of
neurotransmitter (acetylcholine) from the
synaptic end terminal
• AcH binds to receptors on myofibril
surface (ligand-gated Na+ channels)
• binding leads to influx of sodium ions
and depolarization of the membrane
potential of the sarcolemma
• creation of an action potential that travels
through the muscle cell – eventual
contraction
• Acetylcholinesterase breaks down ACh
• Limits duration of contraction
Muscle Contraction: A summary
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ACh released from synaptic vesicles at each neuromuscular junction
Binding of ACh to muscle cell of the NMJ
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Generation of action potential in sarcolemma
Conduction of impulse along T-tubules
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Ca binds to troponin and “pulls it away” from the actin filament
Cross-bridge formation with myosin
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AP results in release of Ca by the SR
SR is in close physical association with each A and I band
Exposure of active sites on actin
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AP flows along the outside of the muscle cell via the sarcolemma
enters the inside of the muscle cell via T-tubules
close association of T-tubules with the sarcoplasmic reticulum (SR)
Release of Calcium ions by SR
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entrance of Na ions and depolarization
requires hydrolysis of ATP  ADP
Release of ADP
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pivoting of myosin head
sliding filaments & contraction
• called excitation-contraction coupling –
describes the events linking generation
of an AP (excitation) to the contraction
of the muscle
The Events in Muscle Contraction
CHECK OUT THIS
ANIMATION!!!
http://www.blackwellpublishing.co
m/matthews/myosin.html
Relaxation
• Acetylcholinesterase (AChE) breaks down ACh within the synaptic
cleft
• Muscle action potential ceases
• Ca+2 release channels (foot proteins) close
• Active transport pumps Ca2+ back into storage in the
sarcoplasmic reticulum
– Ca ATPase pumps
– the rate of pumping Ca back into the SR is slower than the rate of efflux
– so as long as the muscle is being stimulated via the T-tubules – more Ca in
the sarcoplasm
• Tropomyosin-troponin complex recovers binding site on the actin
Rigor Mortis
• Rigor mortis is a state of muscular rigidity
that begins 3-4 hours after death and lasts
about 24 hours
• After death, Ca+2 ions leak out of the SR
and allow myosin heads to bind to actin
• Since ATP synthesis has ceased,
crossbridges cannot detach from actin until
proteolytic enzymes begin to digest the
decomposing cells.
Length of Muscle Fibers: Length Tension
relationship
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Normally
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Optimal overlap of thick & thin filaments
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produces greatest number of crossbridges and the
greatest amount of tension
optimal length = lo (muscle length at which maximum
force is generated)
optimal length = point A
As stretch muscle (past optimal length)
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resting muscle length remains between 70 to 130% of
the optimum
length of the muscle fiber is greater than lo
fewer cross bridges exist & less force is produced =
point B
when muscle is stretched to about 70% than lo of its
(point C) the actin filaments are completely pulled out
from between the myosin – no cross-bridges possible
If muscle is overly shortened (less than optimal)
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length of the muscle fiber is less than lo
thick filaments crumpled by Z discs and the actin
filaments overlap – poor cross-bridge formation
fewer cross bridges exist & less force is produced =
point D
even less calcium released from the SR - ??
A
B
D
C
Levers
Motor Units
• Each skeletal fiber has only ONE
NMJ
• MU = Somatic neuron + all the
skeletal muscle fibers it innervates
• Number and size indicate precision of
muscle control
• Muscle twitch
– Single momentary contraction in one
muscle fiber
– too small to generate any significant
force
– Response to a single stimulus
• All-or-none theory
– Either contracts completely or not at
all
• Motor units are grouped together to provide a greater force & delay fatigue
• in a whole muscle they fire asynchronously
• some fibers are active others are relaxed
• delays muscle fatigue so contraction can be sustained
•
Muscle fibers of different motor units are intermingled so that net distribution of force
applied to the tendon remains constant even when individual muscle groups cycle
between contraction and relaxation.
Neural control of Motor Units
• 1. input from the motor cortex
– axons originating from neuronal cell bodies within the primary motor cortex
descend directly to synapse with motor neurons in the SC
– part of the corticospinal motor system (lecture 8)
• 2. input from the brain stem
– extrapyramidal motor system
– involves many regions of the brain
– final link is the brain stem
Neural control of Motor Units
• 3. input from afferent neurons
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at the level of the SC
by interneurons within the SC = spinal reflex
afferent information is needed to control skeletal muscle activity
the CNS must know the position of your body prior to initiating movement
and must know how the movement is progressing = prioprioceptive input
– comes from information from your eyes, joints, inner ear and from the
muscles themselves (prioprioceptors)
– muscle spindles and tendon organs within the muscle monitor changes in
muscle length and tension (see lecture 9)
Motor Tone
• Resting muscle contracts random motor
units
– Constant tension created on tendon
– Resting tension – muscle tone
• Stabilizes bones and joints
• controlled by proprioceptors
Muscle Metabolism
• Production of ATP:
-contraction requires huge amounts of ATP
-muscle fibers produce ATP three ways:
1. Creatine phosphate
2. Aerobic metabolism
3. Anaerobic metabolism
Creatine Phosphate
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Muscle fibers at rest produce more ATP then they need for resting metabolism
Excess ATP within resting muscle used to form creatine phosphate or phosphocreatine
Creatine phosphate: 3-6 times more plentiful than ATP within muscle
the first storehouse of energy used upon the onset of contraction when additional ATP is
needed
Sustains maximal contraction for 15 sec (used for 100 meter dash)
– or about 8 muscle twitches
– creatine phosphate breakdown is favored by muscles undergoing explosive movements
•
formed through the combination of creatine and ATP
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when energy is required – CP splits up into creatinine and a high energy phosphate group
the phosphate group is added to ADP to recreate ATP
creatine phosphate and reconversion both catalyzed by creatine kinase
CK is linked to the M line in sarcomeres
Anaerobic Cellular Respiration
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Muscles deplete creatine – make ATP in
anaerobically via glycolysis
glucose  2 pyruvic acid
if enough O2 is available to the muscle 
pyruvic acid made during glycolysis enters the
citric acid cycle and electron transport chain to
make ATP
BUT: if insufficient oxygen is present only
glycolysis is performed
– glucose is broken down into two pyruvic acid
molecules to yield 2 ATP
– BUT in low oxygen this pyruvic acid is further
processed to the by-product = lactic acid
•
Glycolysis can continue anaerobically to
provide ATP for 30 to 40 seconds of maximal
activity (200 meter race)
http://www.indstate.edu/thcme/mwking/oxidative-phosphorylation.html
Aerobic Cellular Respiration
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aerobic respiration produces ATP for any activity lasting over 30 seconds
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if sufficient oxygen is available, pyruvic acid enters the mitochondria to generate ATP, water and heat via the
electron transport chain
fatty acids and amino acids can also be used by the mitochondria
can provide 90% of ATP energy if activity lasts more than 10 minutes is intensity level is moderate
oxygen levels must be sufficient!!!!!
Each glucose = 36 ATP
Fatty acids = ~100 ATP
Sources of oxygen – diffusion from blood, released by myoglobin (hemoglobin-like molecule of muscle
cells)
Muscle Fatigue
• Inability to contract after prolonged activity
– central and peripheral fatigue
– central fatigue is feeling of tiredness and a desire to stop
(protective mechanism)
• Factors that contribute to muscle fatigue
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depletion of creatine phosphate
decline of Ca+2 within the sarcoplasm
insufficient oxygen or glycogen
accumulation of extracellular K ions
drop in pH within muscle cell
buildup of lactic acid
buildup of ADP and inorganic phosphate from ATP hydrolysis
insufficient release of acetylcholine from motor neurons
Isotonic and Isometric Contraction
• Isotonic contractions = a load is moved
– concentric contraction = a muscle shortens to produce force and
movement
– eccentric contractions = a muscle lengthens while maintaining
force and movement
• Isometric contraction = no movement occurs
– tension is generated without muscle shortening
– maintaining posture & supports objects in a fixed position
• Atrophy
– wasting away of muscles
– caused by disuse (disuse atrophy) or severing of the
nerve supply (denervation atrophy)
– the transition to connective tissue can not be reversed
• Hypertrophy
– increase in the diameter of muscle fibers
– resulting from very forceful, repetitive muscular
activity and an increase in myofibrils, SR &
mitochondria
Exercise-Induced Muscle Damage
• Intense exercise can cause muscle damage
– electron micrographs reveal torn sarcolemmas,
damaged myofibrils an disrupted Z discs
– increased blood levels of myoglobin & creatine
phosphate found only inside muscle cells
• Delayed onset muscle soreness
– 12 to 48 Hours after strenuous exercise
– stiffness, tenderness and swelling due to
microscopic cell damage
Three Types of Muscle Fibers
• Fast fibers = fast twitch glycolytic
• Slow fibers = slow twitch oxidative
• Intermediate fibers = fast twitch oxidative-glycolytic
• Fibers of one motor unit all the same type
• Percentage of fast versus slow fibers is genetically determined
• Proportions vary with the usual action of the muscle
- neck, back and leg muscles have a higher proportion of postural,
slow oxidative fibers
- shoulder and arm muscles have a higher proportion of fast
glycolytic fibers
Fast Fibers
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Large in diameter
Contain densely packed myofibrils
Large glycogen reserves
pump calcium into their SRs faster – faster twitches (single cell contraction rates)
high ATPase activity – faster cross-bridge/contraction potential
fatigue very quickly
Fast Fibers
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Fast twitch oxidative-glycolytic (fast-twitch A)
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red in color (lots of mitochondria, myoglobin & blood vessels)
higher ability to produce ATP via aerobic metabolism
highly vascularized
split ATP at very fast rate; used for walking and sprinting
lower resistance to fatigue
Fast twitch glycolytic (fast-twitch B)
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white in color (few mitochondria & BV, low myoglobin)
higher concentration of enzymes for glycolysis
need less oxygen to function
anaerobic movements for short duration; used for weight-lifting
fatigue faster also
• Slow fibers
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Half the diameter of fast fibers
Three times longer to contract
low ATPase activity, low glycogen content
high resistance to fatigue
higher ability to produce ATP via aerobic metabolism
many mitochondria
highly vascularized
continue to contract for long periods of time
• e.g. marathon runners
Muscle Adaptation
• long-term adaptive changes can occur with exercise depending on the
pattern of neuronal discharge
• 1. improvement of oxidative capacity
– regular aerobic activity
– induces metabolic changes in the oxidative fibers
– increases number of mitochondria and capillaries to the fast and slow
oxidative fibers
– more efficient use of oxygen – prolonged activity without fatigue
• 2. muscle hypertrophy
– increased by regular bursts of short, anaerobic, high-intensity exercise
– increases the diameter of the muscle fiber – increase synthesis of myosin
and actin
– exercise triggers the activation of specific genes that direct the synthesis
of actin and myosin
– also a role for muscle stem cells?
• 3. influence of testosterone
– makes muscle fibers thicker
– promotes the synthesis of myosin and actin
Smooth muscle
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slowest of contraction and relaxation of all three types of muscle
lowest O2 consumption rates
require less energy to contract
generates force over longer periods of time
– maximum tension with only 25-30% of cross-bridges “active”
• can still generate tension even when over-stretched
Characteristics of Smooth Muscle
• fibers have more variety
– with differing properties
– vascular, gastrointestinal, urinary, respiratory, reproductive, ocular
– single model of smooth muscle function is impossible
• anatomy is distinct
– fibers are arranged in oblique bundles (“lattice-like) so that contractile
forces are generated in multiple directions
• contraction is controlled by hormones, paracrines and NTs
• variable electrical properties
– do NOT always respond to an AP with a twitch
• multiple pathways can influence contraction and relaxation
– some paths illicit contraction, others inhibit
Smooth muscle
• three filaments: myosin, actin and intermediate sized
filaments (don’t participate in contraction)
– forms of actin, myosin are specific to smooth muscle
– more actin vs. skeletal muscle
– express tropomyosin only
• have no sarcomeric structure
– do not have Z lines
– the actin and myosin filaments are organized in a lattice-like
pattern rather than parallel to each other
– have dense bodies
•
•
•
•
same proteins as found in Z lines
positioned throughout the cell and attach to the internal surface of the PM
held in place by the cytoskeleton of the cell
act as an anchor for actin filaments
• no T-tubule structure and poorly developed
sarcoplasmic reticulum
– neural excitation differs from skeletal muscle cells
– AP travels along the PM of the smooth muscle cell –
opens calcium channels in the PM – flows in from the
ECF
– this increased calcium from the ECF triggers the
opening of ryanodine Ca receptors on the SR – these
act as calcium channels also
• can still generate tension even when overstretched
– the nonstretched length of smooth muscle is shorter
than skeletal
– therefore it can be stretched quite a distance before the
optimal length is reached
– important for the contractile ability of hollow organs
and blood vessels
• turned on by calcium-dependent
phosphorylation of myosin
– since there is no troponin – how does the cell
prevent cross-bridge formation at rest?
– lightweight chains of proteins – myosin light
chain proteins – attach to the head of myosin
– increasing cytosolic calcium initiates a series of
biochemical events that phosphorylates the
myosin light chain – this allows an interaction
between actin and myosin
– so there is two forms of myosin in muscle cells
(skeletal too!) – myosin heavy and myosin light
– myosin light chains have no function in skeletal
muscle contraction
Smooth muscle
• organized as multi-unit or single-unit smooth muscles
– multi-unit – exhibits neural-like properties
• muscle fibers within the muscle contract as a unit
• multiple units per muscle
• each unit is stimulated by nerves to contract – similar to skeletal muscle motor
units
• so multi-unit smooth muscle is neurogenic – “nerve produced”
• supplied by the ANS
– single unit – muscle fibers within the muscle contract as a separate, single
unit
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•
•
•
found in cell walls of organs and blood vessels
cells are linked by gap junctions for spread of AP
interconnected cells form a functional syncytium
myogenic – self excitable
– clusters of cells exhibit spontaneous electrical activity without neural stimulation
» clusters are specialized to initiate an AP BUT are not specialized to contract
– their membrane potential fluctuates automatically without any external influence
– two type of spontaneous depolarizations: pacemaker and slow-wave potentials
Smooth muscle
• smooth muscle tone:
– single-unit smooth muscle interconnection ensures that the entire
muscle contracts upon initiation of an AP by a unit
– can’t vary the number of muscle fibers contracting
– BUT can vary the tension
• varying the cytosolic calcium can alter the number of eventual crossbridges that form – alters strength of contraction
• many single units have sufficient calcium within their cytosol to ensure
a low level of constant contraction = tone
• smooth muscle activity:
– innervated by the ANS
– does not initiate the contraction
– but modifies the rate and strength of contraction of single-unit
smooth muscle
– also can be modified by: hormones, muscle stretch, drugs
• all act by modifying the permeability of the PM to calcium in the ECF
Smooth muscle
•
•
•
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slowest of contraction and relaxation of all three types of muscle
lowest O2 consumption rates
requires less energy to contract
generates force over longer periods of time
– maximum tension with only 25-30% of cross-bridges “active”
• can still generate tension even when over-stretched
Characteristics of Smooth Muscle
• fibers have more variety
– single model of smooth muscle function is impossible
• anatomy is distinct
– fibers are arranged in oblique bundles (“lattice-like) so that contractile
forces are generated in multiple directions
• contraction is controlled by hormones, paracrines and NTs
– ACh, NE, Epi etc…
• variable electrical properties
– do NOT always respond to an AP with a twitch
• multiple pathways can influence contraction and relaxation
– some paths illicit contraction, others inhibit contraction
• three filaments: myosin, actin and intermediate sized filaments (don’t
participate in contraction)
– forms of actin, myosin are specific to smooth muscle – myosin and actin are longer than
SKM
– more actin vs. skeletal muscle
– express tropomyosin only
• have no sarcomeric structure
– do not have Z lines
– the actin and myosin filaments are organized in a lattice-like pattern rather than
parallel to each other
– actin is anchored to dense bodies located at the cell surface
•
•
•
•
have the same proteins as found in Z lines
positioned throughout the cell and attach to the internal surface of the PM
held in place by the cytoskeleton of the cell
act as an anchor for actin filaments
• no T-tubule structure and poorly developed sarcoplasmic reticulum
– SO: neural excitation differs from skeletal muscle cells
– AP travels along the PM of the smooth muscle cell
• intracellular calcium levels
trigger contraction
– AP travels along the PM of the
smooth muscle cell
– opens calcium channels in the PM
– calcium flows in from the ECF
– this increased intracellular
calcium from the ECF triggers
the opening of ryanodine/foot Ca
receptors on the SR
– more Ca flows into the smooth
muscle cell cytoplasm
– intracellular calcium levels
increase further
AP
• contraction is turned on by calcium-dependent phosphorylation of
myosin
– since there is no troponin – how does the cell regulate cross-bridge
formation
– ANSWER: lightweight chains of proteins – myosin light chain proteins –
attach to the head of myosin
– increasing cytosolic calcium initiates a series of biochemical events that
phosphorylates the myosin light chain – this allows an interaction
between actin and myosin
Smooth muscle contraction: A summary
– influx of calcium into cell
– increase in intracellular Ca levels
– activates a calcium-dependent kinase
called calmodulin/CaM
– CaM activates another kinase called
myosin light chain kinase/MLCK
– MLCK phosphorylates the myosin light
chain
– this phosphorylation allows crossbridging to actin
Smooth muscle
• organized as multi-unit or single-unit smooth muscles
– multi-unit – exhibits neural-like properties
•
•
•
•
muscle fibers within the muscle contract as a unit
fibers are not linked electrically
each muscle cell must be closely associated with an axon terminal
SO: each unit/cell is stimulated by nerves to contract (i.e. neurogenic –
“nerve produced”) – similar to skeletal muscle motor units
• nerves are part of the ANS
• allows for fine control of contractions
• found in iris and ciliary body, parts of male reproductive tract and in the uterus
(becomes single unit as pregnancy proceeds!)
– single unit – muscle fibers within the muscle contract as a separate, single unit
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myogenic = contraction originates from the property of the muscle cell itself
also called visceral SM
most SM are single-unit
found in cell walls of organs and blood vessels
cells are linked by gap junctions for spread of AP from one cell to the next
all muscle cells contract as a result
amount of calcium that enters the cell determines the force of the contraction
Myogenic, Single-unit SM
– some single-unit SM cells exhibit spontaneous electrical activity
without neural stimulation
» these cells are specialized to initiate an action potential BUT are
not specialized to contract
» their resting membrane potential is unstable - fluctuates
automatically without any external influence
» so they spontaneously depolarize
» two types of spontaneous depolarizations: pacemaker and slowwave potentials (both are due to ion channels that
spontaneously open and close)
• slow wave
– exhibit cyclic depolarization and repolarization
– might not reach the threshold level and might not contract
• pacemaker
– always reach their threshold potential
– create regular rhythms of contraction and relaxation
• smooth muscle tone:
– single-unit smooth muscle interconnection ensures that the entire muscle
contracts upon initiation of an AP by a unit
– can’t vary the number of muscle fibers contracting
– BUT can vary the tension
• many single units have sufficient calcium within their cytosol to ensure a low
level of constant contraction = tone
• smooth muscle activity:
– innervated by the ANS and its neurotransmitters – AcH and NE
– does not initiate the contraction
– but modifies the rate and strength of contraction of single-unit smooth
muscle
– also can be modified by: hormones, muscle stretch, drugs
• all act by modifying the permeability of the PM to calcium in the ECF