151 Muscle Phys

8/4/2019 151 Muscle Phys

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Muscle Fiber Anatomy

Sarcolemma - cell membrane

Surrounds the sarcoplasm(cytoplasm of fiber) Contains many of the same organelles seen in other cells

An abundance of the oxygen-binding protein myoglobin

Punctuated by openings called the transverse tubules (T-tubules)

Narrow tubes that extend into the sarcoplasm at right angles to thesurface

Filled with extracellular fluid

Myofibrils -cylindrical structures within muscle fiber

Are bundles of protein filaments (=myofilaments)

Two types of myofilaments

1. Actin filaments (thin filaments)

2. Myosin filaments (thick filaments)

At each end of the fiber, myofibrils are anchored to the inner surface of thesarcolemma

When myofibril shortens, muscle shortens (contracts)

Myofibrils surrounded bysarcoplasmic Reticulum, a calcium-

containing network of tubules


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Sarcoplasmic Reticulum (SR)

SR is an elaborate, smooth endoplasmicreticulum that mostly runs longitudinallyand surrounds each myofibril

Form chambers called terminal cisternae

on either side of the T-tubules A single T-tubule and the 2 terminal

cisternae form a triad

SR has Ca++ pumps that function to pumpCa++ out of the sarcoplasm back into theSR


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Sarcoplasmic Reticulum (SR) SR is an elaborate, smooth endoplasmic

reticulum that mostly runs longitudinallyand surrounds each myofibril

Form chambers called terminal cisternae

on either side of the T-tubules A single T-tubule and the 2 terminal

cisternae form a triad

SR has Ca++ pumps that function to pumpCa++ out of the sarcoplasm back into theSR


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Sarcoplasmic Reticulum (SR)

Figure 9.5


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Structure of Actin and Myosin


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Actin (Thin)

Myofilaments

Two strands of fibrous (F) actin forma double helix extending the lengthof the myofilament; attached ateither end at sarcomere.

Composed of G actin monomerseach of which has an active site

Actin site can bind myosinduring muscle contraction.

Tropomyosin: an elongated proteinwinds along the groove of the F actin

double helix. Troponin is composed of three

subunits: Tn-I site: binds to actin

Tn-T site: binds to tropomyosin

Tn-C site: binds to calcium ions

The tropomyosin/troponin complexregulates the interaction betweenactive sites on G actin and myosin.


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Myosin (Thick)Myofilament

Many elongated myosin moleculesshaped like golf clubs.

Molecule consists of two heavy myosinmolecules wound together to form a

rod portion lying parallel to the myosinmyofilament and two heads that extendlaterally.

Myosin heads

1. Can bind to active sites on the actinmolecules to form cross-bridges.

2. Attached to the rod portion by ahinge region that can bend andstraighten during contraction.

3. Have ATPase activity: activity thatbreaks down adenosinetriphosphate (ATP), releasing

energy. Part of the energy is used tobend the hinge region of the myosinmolecule during contraction


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Sarcomeres

Z disk: filamentous network ofprotein. Serves as attachment foractin myofilaments

Striated appearance

I bands: from Z disks to ends ofthick filaments

A bands: length of thick filaments

H zone: region in A band whereactin and myosin do not overlap

M line: middle of H zone; delicate

filaments holding myosin in place In muscle fibers, A and I bands of

parallel myofibrils are aligned.

Titin filaments: elastic chains ofamino acids; make muscles

extensible and elastic


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Striations and Sarcomeres


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Nerve-Muscle Relationships

Skeletal muscle must be stimulated by a motorneuron or it will not contract

Cell bodies of somatic motor neurons in

brainstem or spinal cordAnterior horn motor neurons (AHMN)

Axons of these AHMNs form terminal brancheswith synaptic bulbs

Each terminal branch supplies one muscle fiber

Each motor neuron and all the muscle fibers itinnervates = motor unit


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White Matter: Pathway

Generalizations


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Descending (Motor) Pathways

Descending tracts deliver motorimpulses from thebrain to the spinal cord

Motor pathways involve two neurons Upper motor neuron (UMN)

Originates (cell body) in brain Its axons form the projection tracts of the brain

Synapses with LMN in spinal cord

Lower motor neuron (LMN): AHMN Originates (cell body) in anterior horn

Myelinated axon exits cord via ventral root and enters spinalnerve

Its synaptic knobs form the neuromuscular junction (aka,myoneural junction)


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Pyramidal (Corticospinal) Tracts

Originate in theprecentral gyrus of brain (aka, primary motor area)

I.e., cell body of the UMN located in precentral gyrus

Pyramidal neuron is the UMN

Its axon forms the corticospinal tract

UMN synapses in the anterior horn with LMN Some UMN decussate in pyramids = Lateral corticospinal tracts

Others decussate at other levels of s.c. = Anterior corticospinal tracts

LMN (anterior horn motor neurons)

Exits spinal cord via anterior root

Activates skeletal muscles Regulates fast and fine (skilled) movements


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Corticospinal

tracts

1. Location of UMN cell

body in cerebral cortex2. Decussation of UMN

axon in pyramids or atlevel of exit of LMN

3. Synapse of UMN andLMN occurs in anterior

horn of s.c.4. LMN axon exits via

anterior root

1.

2.

4.

3.


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Motor Units Def: A motor neuron and all the

muscle fibers it innervates Fibers aredispersed throughout the

muscle

When contracted together cause a weakcontraction over wide area

provides ability to sustain long-termcontraction as motor units take turnsresting (postural control)

Fine control of muscles small motor units contain as few as

4-6 muscle fibers per nerve fiber Extraocular muscles (move eyeball)

Strength control Gastrocnemius muscle has 1000-1500

muscle fibers per nerve fiber


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Neuromuscular Junctions (Synapse)

Functional connection between nerve fiber andmuscle cell Neurotransmitter (acetylcholine/ACh) released from

nerve fiber stimulates muscle fiber

Components of synapse (NMJ) synaptic knob is swollen end of axon terminal contains ACh

Motor end plate: region of sarcolemma that abuts thesynaptic knob; highly folded

increases surface area allowing for more ACh receptors contain acetylcholinesterase that breaks down ACh and causes

relaxation

synaptic cleft = tiny gap between synaptic knob andsarcolemma of muscle fiber


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The Neuromuscular Junction


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Muscle Fibers are Excitable

Sarcolemma is polarized or charged resting membrane potential due to Na+ outside of cell and K+

and other anions inside of cell

difference in charge across the membrane = resting

membrane potential (-90 mV cell) Stimulation (ACh binding to cholinergic receptors)

opens ion gates in sarcolemma ion gates open (Na+ rushes into cell and K+ rushes out of

cell) quick up-and-down voltage shift = action potential

spreads over cell surface as an action potential


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Muscle Contraction and Relaxation

Four actions involved in this process Excitation = nerve action potentials lead to

action potentials in muscle fiber

Excitation-contraction coupling = actionpotentials on the sarcolemma activatemyofilaments

Contraction = shortening of muscle fiber

Relaxation = return to resting length

Images will be used to demonstrate thesteps of each of these actions


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Explains the relationship between thick andthin filaments as contraction proceeds

Cyclic process beginning with calcium release

from SR Calcium binds to troponin

Troponin moves, moving tropomyosin and

exposing actin active site Myosin head forms cross bridge and bends

toward H zone (pulling actin inward)

ATP allows release of cross bridge

Sliding Filament Theory


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Changes in the appearance of aSarcomere during the Contraction of a

Skeletal Muscle Fiber


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Created when muscles contract

Series of steps that begin with excitation at

the neuromuscular junction Calcium release

Thick/thin filament interaction

Muscle fiber contraction Tension

Tension


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Excitation-Contraction Coupling


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Myosin cross bridge attaches to the

actin myofilament

1

2

3

4 Working strokethe myosin head pivots and

bends as it pulls on the actin filament, sliding it

toward the M line

As new ATP attaches to the myosin head,

the cross bridge detaches

As ATP is split into ADP and Pi,

cocking of the myosin head occurs

Myosin head (high-energy

configuration)

Thick

filament

Myosin head

(low-energy

configuration)

ADP and Pi (inorganic

phosphate) released

Sequential Events of Contraction

Thin filament


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Rigor Mortis

Stiffening of the body beginning 3 to 4 hours after death

Deteriorating sarcoplasmic reticulum releases calcium

Calcium activates myosin-actin cross-bridging and muscle

contracts, but can not relax. Muscle relaxation requires ATP and ATP production is no

longer produced after death

Fibers remain contracted until myofilaments decay


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Functions of ATP in SkeletalMuscle Contraction

1. Hydrolysis of ATP by myosin- energizes the cross-bridges, providing energy for

force generation.

1. Binding of ATP to myosin- dissociates cross-bridges bound to actin.

1. Energizes Ca++ pumps that actively transport Ca++back into the sarcoplasmic reticulum- lowers cytosolic calcium levels leading to relaxation

1. Runs the Na+-K+ pump in the sarcolemma- maintains the resting membrane potential of the

sarcolemma


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The Effect of Sarcomere Lengthon Tension

Amount of tension (force) generated by the muscledepends on length of muscle before it was stimulated length-tension relationship (see graph next slide)

Overly contracted (weak contraction results)- See Fig. 1 on left side on next slide

thick filaments too close to Z discs and cant slide Too stretched (weak contraction results)

Fig. 3 on right side on next slide

little overlap of thin and thick filaments does not allow for verymany cross bridges too form

Optimum resting length (Lo) produces greatest force when

muscle contracts Fig. 2 in center

central nervous system maintains optimal length producing

muscle tone or partial contraction

Th Eff t f S


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The Effect of SarcomereLength on Tension

Active tension: force appliedto an object to be lifted when amuscle contracts

Load - the object beingacted upon by the muscle

Stretchedmuscle- not enoughcross-bridging

Crumpled muscle-myofilaments crumpled, cross-bridges can't contract


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Muscle Twitch

A muscle twitch is the response of a muscle fiber to asingle, brief threshold stimulus

The three phases of a muscle twitch are:

Latent period (2 msec delay)

No visible contraction occurs; no tension developed Processes of excitation-contraction coupling occurring

Contraction phase External tension develops as muscle shortens

Not all skeletal muscle fibers have same contraction time Fast twitch fibers = 10 msec; Slow twitch fibers = 100 msec

Relaxation phase Loss of tension and return to resting length as calcium returns to

SR


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Muscle Twitch

Threshold = voltage producingan action potential

a single brief stimulus atthat voltage produces a

quick cycle of contractionand relaxation called atwitch (lasting less than 1/10second = 100 msc)

A single twitch contraction isnot strong enough to do anyuseful work

Figure 9.13 (a)

The Twitch and the Development


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The Twitch and the Developmentof Tension


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Effects of Repeated Stimulations


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Twitch and Treppe Contractions

Muscle stimulation at variable frequencies

low frequency (up to 10 stimuli/sec)- Fig A above each stimulus produces an identical twitch response

moderate frequency (between 10-20 stimuli/sec) each twitch has time to recover but develops more tension

than the one before (treppe phenomenon)

calcium was not completely put back into SR

heat of tissue increases myosin ATPase efficiency


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Incomplete and Complete Tetanus

Higher frequency stimulation (20-40 stimuli/second) generatesgradually more strength of contraction (Fig A)

each stimuli arrives before last one recovers

temporal summation or wave summation

incomplete tetanus = sustained fluttering contractions

Maximum frequency stimulation (40-50 stimuli/second) (Fig. B) muscle has no time to relax at all

twitches fuse into smooth, prolonged contraction called complete tetanus

rarely occurs in the body


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Motor Units Def: A motor neuron and all the

muscle fibers it innervates Fibers are dispersed throughout the

muscle

Provides ability to sustain long-termcontraction as motor units take turnsresting (postural control)

Fine control of muscles small motor units contain as few as

4-6 muscle fibers per nerve fiber

Extraocular muscles (move eyeball)

Strength control Gastrocnemius muscle has 1200-1500

muscle fibers per nerve fiber

S i l I i


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Stimulus Intensity

and Muscle Tension

Muscle contracts morevigorously as stimulus strengthis increased

Force of contraction preciselycontrolled by MMUS

Multiple Motor UnitSummation or recruitment

Recruitment brings moreand more motor units intoplay

Note that as the stimulusintensity increases (Fig. 1)more and more motor unitsare stimulated (Fig.2) and thusthe strength of muscle

contraction increases (Fig. 3).

The Arrangement of Motor Units


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Figure 10.17

The Arrangement of Motor Unitsin a Skeletal Muscle


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Force of Muscle Contraction

The force of contraction is affected by: The relative size of the muscle

Larger muscles have larger and more muscle fibers

Larger fibers can generate more force than smaller fibers

More muscle fibers can generate more force than fewer fibers

The number of muscle fibers contracting Greater numbers of motor units generate more force than

smaller numbers of motor units

Degree of muscle stretch Muscles contract strongest when muscle fibers are 80-120% of

their normal resting length


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Force of Muscle Contraction

Figure 9.20 (a)


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Isometric and Isotonic Contractions

Isometric muscle contraction Tension (force) does not exceed resistance (load) important in postural muscle function

Isotonic muscle contraction Tension exceeds resistance

tension while shortening = concentric

tension while lengthening = eccentric

l i i


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Muscle contraction requireslarge amounts of energy

ATP provides immediate energy for muscle contrac-tions. Produced from three sources Creatine phosphate (CP)

Most rapid method of ATP generation

Only 1 ATP per CP used Aerobic respiration

Requires oxygen and breaks down glucose to produce ATP,carbon dioxide and water

Most efficient method

Generates 36 ATP per glucose molecule

Anaerobic respiration (Glycolysis) Occurs in absence of oxygen

Results in breakdown of glucose to yield ATP and lactic acid

Muscle Metabolism: Energy for


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Muscle Metabolism: Energy forContraction

Figure 9.18


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Short-Term Energy Needs

Creatine phosphate system

ADP + CP creatine kinase C + ATP

CP levels quickly exhausted during intense contractions

Able to sustain maximum contractions for 8-10 seconds

CP (creatine phosphate) regenerated during resting conditions(ATP + CCP + ADP)

Glycogen-lactic acid system takes over

produces ATP for 30-40 seconds of maximum activity

playing basketball or running around baseball diamonds muscles obtain glucose from blood and stored glycogen


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Long-Term Energy Needs

Aerobic respiration needed for prolonged exercise Produces 36 ATPs/glucose molecule

After 40 seconds of exercise, respiratory and

cardiovascular systems must deliver enough oxygen foraerobic respiration oxygen consumption rate increases for first 3-4 minutes and

then levels off to a steady state

Limits are set by depletion of glycogen and blood glucose,loss of fluid and electrolytes


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Fatigue

Progressive weakness from useATP synthesis declines as glycogen is consumed

Sodium-potassium pumps fail to maintain

membrane potential and excitability Lactic acid buildup inhibits enzyme function

Accumulation of extracellular K+ hyperpolarizesthe cell

Motor nerve fibers use up their acetylcholine


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Oxygen Debt

Vigorous exercise causes dramatic changes inmuscle chemistry

For a muscle to return to a resting state: Oxygen reserves must be replenished

Lactic acid must be converted to pyruvic acid

Glycogen stores must be replaced

ATP and CP reserves must be resynthesized

Oxygen debt the extra amount of O2 needed

for the above restorative processes


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Begins immediately after activity ends

Oxygen debt (excess post-exerciseoxygen consumption)

Amount of oxygen required during restingperiod to restore muscle to normal

conditions

Recovery period

E d
http://en.wikipedia.org/wiki/Miguel_Indurain


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Endurance Ability to maintain high-intensity exercise for >5

minutes: determined byVO2 max orMaximal oxygen uptake

maximum capacity of an individual's body to transport andutilize oxygen during incremental exercise

Measured as the millilitres of oxygen per kilogram of

bodyweight per minute (ml/kg/min)

average young untrained male will have a VO2 max of

approximately 3.5 litres/minute and 45 ml/kg/min

Miguel Indurain is reported to have had a VO2 max of 88.0 at his

peak

average young untrained female will score a VO2 max of

approximately 2.0 litres/minute and 38 ml/kg/min

To calculate yours go to: http://health.drgily.com/walking-test-peak-aerobic-capacity.php

Nutrient availability
http://en.wikipedia.org/wiki/Miguel_Indurainhttp://en.wikipedia.org/wiki/Miguel_Indurainhttp://en.wikipedia.org/wiki/Miguel_Indurainhttp://en.wikipedia.org/wiki/Miguel_Indurainhttp://en.wikipedia.org/wiki/Miguel_Indurainhttp://en.wikipedia.org/wiki/Miguel_Indurainhttp://en.wikipedia.org/wiki/Miguel_Indurainhttp://en.wikipedia.org/wiki/Miguel_Indurainhttp://en.wikipedia.org/wiki/Miguel_Indurainhttp://en.wikipedia.org/wiki/Miguel_Indurainhttp://en.wikipedia.org/wiki/Miguel_Indurainhttp://en.wikipedia.org/wiki/Incremental_exercisehttp://en.wikipedia.org/wiki/Miguel_Indurainhttp://en.wikipedia.org/wiki/Miguel_Indurainhttp://en.wikipedia.org/wiki/Kilogramhttp://en.wikipedia.org/wiki/Miguel_Indurainhttp://en.wikipedia.org/wiki/Miguel_Indurainhttp://en.wikipedia.org/wiki/Miguel_Indurainhttp://en.wikipedia.org/wiki/Miguel_Indurainhttp://en.wikipedia.org/wiki/Miguel_Indurainhttp://en.wikipedia.org/wiki/Miguel_Indurainhttp://en.wikipedia.org/wiki/Miguel_Indurainhttp://en.wikipedia.org/wiki/Miguel_Indurainhttp://en.wikipedia.org/wiki/Miguel_Indurainhttp://en.wikipedia.org/wiki/Kilogramhttp://en.wikipedia.org/wiki/Incremental_exercise


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Types of Skeletal Muscle Fibers

Skeletal muscle cells are specialized into 2main types in humans and primates

Specialization allows either High work rates (power output)

Long duration contractions

2 cell types are differentiated on whether gene

for a slow or fast myosin isoenzyme isexpressed in the cell i.e. cell will have a moderate or a high ATPase

activity or recycling time

M l P f


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Muscle Performance:Types of skeletal muscle fibers

Slow-twitch or high-oxidative Contract more slowly Moderate power output Consume ATP at moderate rates High capillary density (rich blood supply) More mitochondria Smaller in diameter

Minimize diffusion distances for oxygen and nutrients

Large amount of myoglobin.

More fatigue-resistant than fast-twitch If blood supply adequate, great endurance

Postural muscles, more in lower than upper limbs. Darkmeat of chicken.


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Slow and Fast Fibers

Fast-twitch or low-oxidative Respond rapidly to nervous stimulation Maximal ATP consumption can be met only byglycolysis Contain myosin that can break down ATP more rapidly than

that in slow-twitch fibers Less blood supply (paler in color) Fewer and smaller mitochondria than slow-twitch Fatigue rapidly as glycogen is depleted Lower limbs in sprinter, upper limbs of most people White meat in chicken.

Distribution of fast-twitch and slow-twitch

Most muscles have both but varies for each muscle


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Strength and Conditioning

Strength of contraction muscle size and fascicle arrangement

3 or 4 kg / cm2 of cross-sectional area

size of motor units and motor unit recruitment

length of muscle at start of contraction

Resistance training (weight lifting) stimulates cell enlargement due to synthesis of more myofilaments

Endurance training (aerobic exercise) produces an increase in mitochondria, glycogen and density of

capillaries

Atrophy: decrease in muscle size


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Smooth Muscle

Composed of spindle-shaped fibers witha diameter of 2-10 m and lengths of

several hundred m Often organized into two layers(longitudinal and circular) of closelyapposed fibers

Found in walls of hollow organs (exceptthe heart)


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Microscopic Anatomy of

Smooth Muscle SR is less developed than in skeletal muscle and lacks aspecific pattern

T tubules are absent

There is no troponin complex Plasma membranes have pouchlike infoldings called

caveoli Ca2+ is sequestered in the extracellular space near the

caveoli, allowing rapid influx when channels are opened

There are no visible striations and no sarcomeres Thin and thick filaments are present

Proportion and Organization of


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Thick filaments have heads along theirentire length

There is no troponin complex

Thick and thin filaments are arrangeddiagonally, causing smooth muscle tocontract in a corkscrew manner

Noncontractile intermediate filamentbundles attach to dense bodies (analogousto Z discs) at regular intervals

opo o O g o oMyofilaments in Smooth Muscle

Proportion and Organization of Myofilaments in


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Figure 9.26

Proportion and Organization of Myofilaments inSmooth Muscle


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Stimulation of Smooth Muscle

Involuntary and contracts without nervestimulation

Hormones, CO2, low pH, stretch, O2 deficiency Autonomic nerve fibers have beadlike

swellings called varicosities containing

synaptic vesicles stimulates multiple myocytes at diffuse junctions


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Innervation of Smooth Muscle

Figure 9.25


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Contraction of Smooth Muscle

Whole sheets of smooth muscle exhibit slow,synchronized contraction

They contract in unison, reflecting theirelectrical coupling with gap junctions

Action potentials are transmitted from cell tocell

Some smooth muscle cells:Act as pacemakers and set the contractile pace forwhole sheets of muscle

Are self-excitatory and depolarize without externalstimuli


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Contraction Mechanism

Actin and myosin interact according to thesliding filament mechanism

The final trigger for contractions is a rise inintracellular Ca2+

Ca2+ is released from the SR and from theextracellular space

Ca2+ interacts with calmodulin and myosinlight chain kinase to activate myosin

R l f C l i I


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Role of Calcium Ion

Ca2+

binds to calmodulin and activates it Activated calmodulin activates the kinase

enzyme

Activated kinase transfers phosphate from ATP

to myosin cross bridges Phosphorylated cross bridges interact with actin

to produce shortening

Smooth muscle relaxes when intracellular Ca2+

levels drop See Fig 9.24 in text


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Response to Stretch

Smooth muscle exhibits a phenomenoncalled stress-relaxation response in

which: Smooth muscle responds to stretch onlybriefly, and then adapts to its new length

The new length, however, retains its ability

to contract This enables organs such as the stomach

and bladder to temporarily store contents


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Hyperplasia

Certain smooth muscles can divide andincrease their numbers by undergoinghyperplasia

This is shown by estrogens effect on the uterusAt puberty, estrogen stimulates the synthesis of

more smooth muscle, causing the uterus to grow toadult size

During pregnancy, estrogen stimulates uterinegrowth to accommodate the increasing size of thegrowing fetus


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Types of Smooth Muscle:

Single Unit The cells of single-unit smooth muscle,

commonly called visceral muscle:

Contract rhythmically as a unit (as one)Are electrically coupled to one another via

gap junctions

Often exhibit spontaneous action potentialsAre arranged in opposing sheets and exhibit

stress-relaxation response


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Types of Smooth Muscle:

Multiunit Multiunit smooth muscles are found:

In large airways to the lungs

In large arteries In arrector pili muscles

Attached to hair follicles

In the internal eye muscles

Multi-unit smooth muscle cells are innervatedby more than one motor neuron

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151 Muscle Phys