faal otot ppt

8/12/2019 faal otot ppt

1/110

Muscles Physiology


2/110

Muscle Overview

The three types of muscle tissue are skeletal,

cardiac, and smooth

These types differ in structure, location, function,

and means of activation


3/110

Muscle Similarities

Skeletal and smooth muscle cells are elongated and

are called muscle fibers

Muscle contraction depends on two kinds of

myofilamentsactin and myosin

Muscle terminology is similar

Sarcolemmamuscle plasma membrane

Sarcoplasmcytoplasm of a muscle cell


4/110

Skeletal Muscle Tissue

Packaged in skeletal muscles that attach to and

cover the bony skeleton

Has obvious stripes called striations

Is controlled voluntarily (i.e., by conscious control)

Contracts rapidly but tires easily

Is responsible for overall body motility

Is extremely adaptable and can exert forces ranging

from a fraction of an ounce to over 70 pounds


5/110

Cardiac Muscle Tissue

Occurs only in the heart

Is striated like skeletal muscle but is not voluntary

Contracts at a fairly steady rate set by the hearts

pacemaker

Neural controls allow the heart to respond tochanges in bodily needs


6/110

Smooth Muscle Tissue

Found in the walls of hollow visceral organs, such

as the stomach, urinary bladder, and respiratory

passages

Forces food and other substances through internal

body channels

It is not striated and is involuntary


7/110

Functional Characteristics of Muscle Tissue

Excitability, or irritabilitythe ability to receive

and respond to stimuli

Contractilitythe ability to shorten forcibly

Extensibilitythe ability to be stretched or extended

Elasticitythe ability to recoil and resume theoriginal resting length


8/110

Muscle Function

Skeletal muscles are responsible for all locomotion

Cardiac muscle is responsible for coursing the blood

through the body

Smooth muscle helps maintain blood pressure, and

squeezes or propels substances (i.e., food, feces)

through organs

Muscles also maintain posture, stabilize joints, and

generate heat


9/110

Skeletal Muscle


10/110

Skeletal Muscle

Each muscle is a discrete organ composed of muscle

tissue, blood vessels, nerve fibers, and connectivetissue

The three connective tissue sheaths are:

Endomysiumfine sheath of connective tissuecomposed of reticular fibers surrounding eachmuscle fiber

Perimysiumfibrous connective tissue thatsurrounds groups of muscle fibers called fascicles

Epimysiuman overcoat of dense regular

connective tissue that surrounds the entire muscle


11/110

Skeletal Muscle

Figure 9.2 (a)


12/110

Skeletal Muscle: Nerve and Blood Supply

Each muscle is served by one nerve, an artery, and

one or more veins

Each skeletal muscle fiber is supplied with a nerveending that controls contraction

Contracting fibers require continuous delivery of

oxygen and nutrients via arteries

Wastes must be removed via veins


13/110

Skeletal Muscle: Attachments

Most skeletal muscles span joints and are attached to

bone in at least two places

When muscles contract the movable bone, themuscles insertion moves toward the immovable

bone, the muscles origin

Muscles attach:

Directlyepimysium of the muscle is fused to theperiosteum of a bone

Indirectlyconnective tissue wrappings extendbeyond the muscle as a tendon or aponeurosis


14/110

Microscopic Anatomy of a Skeletal Muscle Fiber

Each fiber is a long, cylindrical cell with multiple

nuclei just beneath the sarcolemma

Fibers are 10 to 100 m in diameter, and up to

hundreds of centimeters long

Each cell is a syncytium produced by fusion ofembryonic cells


15/110

Microscopic Anatomy of a Skeletal Muscle Fiber

Sarcoplasm has numerous glycosomes and a uniqueoxygen-binding protein called myoglobin

Fibers contain the usual organelles, myofibrils,sarcoplasmic reticulum, and T tubules


16/110

Myofibrils

Myofibrils are densely packed, rodlike contractile

elements

They make up most of the muscle volume

The arrangement of myofibrils within a fiber is such

that a perfectly aligned repeating series of dark Abands and light I bands is evident


17/110

Myofibrils

Figure 9.3 (b)


18/110

Sarcomeres

The smallest contractile unit of a muscle

The region of a myofibril between two successive Z

discs

Composed of myofilaments made up of contractile

proteins

Myofilaments are of two typesthick and thin


19/110

Sarcomeres

Figure 9.3 (c)


20/110

Myofilaments: Banding Pattern

Thick filamentsextend

the entire length of an Aband

Thin filamentsextend

across the I band andpartway into the A band

Z-disccoin-shaped sheet

of proteins (connectins)that anchors the thin

filaments and connects

myofibrils to one another


21/110


Thin filaments do not

overlap thick filaments

in the lighter H zone

M lines appear darker

due to the presence of

the protein desmin


22/110


Figure 9.3 (c, d)


23/110

Ultrastructure of Myofilaments: Thick Filaments

Thick filaments are

composed of the proteinmyosin

Each myosin molecule has

a rodlike tail and twoglobular heads

Tailstwo interwoven,

heavy polypeptide chains

Headstwo smaller,light polypeptide chains

called cross bridges


24/110

Ultrastructure of Myofilaments: Thick Filaments

Figure 9.4 (a)(b)


25/110

Ultrastructure of Myofilaments: Thin Filaments

Thin filaments are chiefly composed of the proteinactin

Each actin molecule is a helical polymer of globular

subunits called G actin

The subunits contain the active sites to which myosin

heads attach during contraction

Tropomyosin and troponin are regulatory subunits

bound to actin


26/110

Ultrastructure of Myofilaments: Thin Filaments


27/110

Arrangement of the Filaments in a Sarcomere

Longitudinal section within one sarcomere

S l i R i l (SR)


28/110

Sarcoplasmic Reticulum (SR)

SR is an elaborate, smooth endoplasmic reticulum that

mostly runs longitudinally and surrounds each myofibril

Paired terminal cisternae form perpendicular cross

channels

Functions in the regulation of intracellular calcium

levels

Elongated tubes called T tubules penetrate into the cells

interior at each A bandI band junction

T tubules associate with the paired terminal cisternae to

form triads

S l i R ti l (SR)


29/110

Sarcoplasmic Reticulum (SR)

Figure 9.5

T T b l


30/110

T Tubules

T tubules are continuous with the sarcolemma

They conduct impulses to the deepest regions of themuscle

These impulses signal for the release of Ca2+from

adjacent terminal cisternae

T i d R l ti hi


31/110

Triad Relationships

T tubules and SR provide tightly linked signals for

muscle contraction

A double zipper of integral membrane proteinsprotrudes into the intermembrane space

T tubule proteins act as voltage sensors

SR foot proteins are receptors that regulate Ca2+

release from the SR cisternae

Slidi Fil t M d l f C t ti


32/110

Sliding Filament Model of Contraction

Thin filaments slide past the thick ones so that the

actin and myosin filaments overlap to a greater

degree

In the relaxed state, thin and thick filaments overlap

only slightly

Upon stimulation, myosin heads bind to actin andsliding begins

Slidi Fil t M d l f C t ti


33/110

Sliding Filament Model of Contraction

Each myosin head binds and detaches several times

during contraction, acting like a ratchet to generate

tension and propel the thin filaments to the center of

the sarcomere

As this event occurs throughout the sarcomeres, the

muscle shortens

Sk l t l M l C t ti


34/110

Skeletal Muscle Contraction

In order to contract, a skeletal muscle must:

Be stimulated by a nerve ending

Propagate an electrical current, or action potential,

along its sarcolemma

Have a rise in intracellular Ca2+levels, the final

trigger for contraction

Linking the electrical signal to the contraction is

excitation-contraction coupling

N Sti l f Sk l t l M l


35/110

Nerve Stimulus of Skeletal Muscle

Skeletal muscles are stimulated by motor neurons ofthe somatic nervous system

Axons of these neurons travel in nerves to muscle

cells

Axons of motor neurons branch profusely as they

enter muscles

Each axonal branch forms a neuromuscular junction

with a single muscle fiber

Ne rom sc lar J nction


36/110

Neuromuscular Junction

The neuromuscular junction is formed from:

Axonal endings, which have small membranous

sacs (synaptic vesicles) that contain the

neurotransmitter acetylcholine(ACh)

The motor end plate of a muscle, which is a specific

part of the sarcolemma that contains ACh receptors

and helps form the neuromuscular junction

Though exceedingly close, axonal ends and muscle

fibers are always separated by a space called the

synaptic cleft



37/110


Figure 9.7 (a-c)



38/110


When a nerve impulse reaches the end of an axon at

the neuromuscular junction:

Voltage-regulated calcium channels open and allow

Ca2+to enter the axon

Ca2+inside the axon terminal causes axonal

vesicles to fuse with the axonal membrane



39/110


This fusion releases ACh into the synaptic cleft via

exocytosis

ACh diffuses across the synaptic cleft to ACh

receptors on the sarcolemma

Binding of ACh to its receptors initiates an action

potential in the muscle

Destruction of Acetylcholine


40/110

Destruction of Acetylcholine

ACh bound to ACh receptors is quickly destroyed

by the enzyme acetylcholinesterase

This destruction prevents continued muscle fiber

contraction in the absence of additional stimuli

Action Potential


41/110

Action Potential

A transient depolarization event that includes

polarity reversal of a sarcolemma (or nerve cell

membrane) and the propagation of an action

potential along the membrane

Role of Acetylcholine (Ach)


42/110

Role of Acetylcholine (Ach)

ACh binds its receptors at the motor end plate

Binding opens chemically (ligand) gated channels

Na+and K+diffuse out and the interior of the

sarcolemma becomes less negative

This event is called depolarization

Depolarization


43/110

Depolarization

Initially, this is a local electrical event called end

plate potential

Later, it ignites an action potential that spreads in all

directions across the sarcolemma

Action Potential: Electrical Conditions of a


44/110

The outside

(extracellular) face

is positive, while

the inside face isnegative

This difference in

charge is the restingmembrane potential

Figure 9.8 (a)


Polarized Sarcolemma



45/110

The predominantextracellular ion isNa+

The predominantintracellular ion isK+

The sarcolemma isrelativelyimpermeable toboth ions

Figure 9.8 (a)


Polarized Sarcolemma

Action Potential: Depolarization and Generation


46/110

An axonal terminal of

a motor neuron

releases ACh andcauses a patch of the

sarcolemma to

become permeable to

Na+ (sodium channels

open)

Figure 9.8 (b)


of the Action Potential



47/110

Na+enters the cell,and the resting

potential is

decreased(depolarization

occurs)

If the stimulus isstrong enough, an

action potential is

initiatedFigure 9.8 (b)


of the Action Potential

Action Potential: Propagation of the Action


48/110

Polarity reversal ofthe initial patch ofsarcolemmachanges the

permeability of theadjacent patch

Voltage-regulated

Na+channels nowopen in the adjacentpatch causing it todepolarize

Figure 9.8 (c)


Potential



49/110

Thus, the actionpotential travels

rapidly along the

sarcolemma

Once initiated, the

action potential is

unstoppable, andultimately results in

the contraction of a

muscleFigure 9.8 (c)


Potential

Action Potential: Repolarization


50/110


Immediately after the

depolarization wavepasses, thesarcolemmapermeability changes

Na+channels closeand K+channels open

K+

diffuses from thecell, restoring theelectrical polarity ofthe sarcolemma

Figure 9.8 (d)



51/110


Repolarization occurs

in the same directionas depolarization, andmust occur before themuscle can be

stimulated again(refractory period)

The ionic

concentration of theresting state isrestored by theNa+-K+pump

Figure 9.8 (d)

Excitation-Contraction Coupling


52/110

Excitation Contraction Coupling

Once generated, the action potential:

Is propagated along the sarcolemma

Travels down the T tubules

Triggers Ca2+release from terminal cisternae

Ca2+binds to troponin and causes:

The blocking action of tropomyosin to cease

Actin active binding sites to be exposed



53/110


Myosin cross bridges alternately attach and detach

Thin filaments move toward the center of the

sarcomere

Hydrolysis of ATP powers this cycling process

Ca2+

is removed into the SR, tropomyosin blockageis restored, and the muscle fiber relaxes



54/110


Figure 9.9

Role of Ionic Calcium (Ca2+) in the Contraction


55/110

At low intracellular Ca2+concentration:

Tropomyosin blocks the

binding sites on actin

Myosin cross bridges

cannot attach to binding

sites on actin

The relaxed state of the

muscle is enforced

Role of Ionic Calcium (Ca ) in the Contraction

Mechanism

Figure 9.10 (a)



56/110

Figure 9.10 (b)

At higher intracellular Ca2+

concentrations:

Additional calcium binds

to troponin (inactive

troponin binds two Ca2+)

Calcium-activated

troponin binds an

additional two Ca2+at a

separate regulatory site


Mechanism



57/110

Calcium-activated

troponin undergoes a

conformational change

This change moves

tropomyosin away fromactins binding sites

Figure 9.10 (c)


Mechanism



58/110

Myosin head can

now bind and cycle

This permitscontraction (sliding

of the thin filaments

by the myosin crossbridges) to begin

Figure 9.10 (d)


Mechanism

Sequential Events of Contraction


59/110

q

Cross bridge formationmyosin cross bridge

attaches to actin filament

Working (power) strokemyosin head pivots and

pulls actin filament toward M line

Cross bridge detachmentATP attaches to myosin

head and the cross bridge detaches

Cocking of the myosin head energy fromhydrolysis of ATP cocks the myosin head into the

high-energy state

Sequential Events of Contraction


60/110

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 P i,

cocking of the myosin head occurs

Myosin head

(high-energy

configuration)

Thick

filament

Myosin head

(low-energy

configuration)

ADP and Pi(inorganicphosphate) released

q

Figure 9.11

Thin filament

Contraction of Skeletal Muscle Fibers


61/110

Contractionrefers to the activation of myosins

cross bridges (force-generating sites)

Shortening occurs when the tension generated by thecross bridge exceeds forces opposing shortening

Contraction ends when cross bridges become

inactive, the tension generated declines, andrelaxation is induced

Contraction of Skeletal Muscle (Organ Level)


62/110

( g )

Contraction of muscle fibers (cells) and muscles

(organs) is similar

The two types of muscle contractions are:

Isometric contractionincreasing muscle tension

(muscle does not shorten during contraction)

Isotonic contractiondecreasing muscle length(muscle shortens during contraction)

Isotonic and Isometric Contractions


63/110

Motor Unit: The Nerve-Muscle Functional Unit


64/110

A motor unit is a motor neuron and all the muscle

fibers it supplies

The number of muscle fibers per motor unit can varyfrom four to several hundred

Muscles that control fine movements (fingers, eyes)

have small motor units



65/110



66/110

Large weight-bearing muscles (thighs, hips) have

large motor units

Muscle fibers from a motor unit are spread throughout

the muscle; therefore, contraction of a single motor

unit causes weak contraction of the entire muscle

Muscle Spindles


67/110

Are composed of 3-10 intrafusal muscle fibers that

lack myofilaments in their central regions, arenoncontractile, and serve as receptive surfaces

Muscle spindles are wrapped with two types ofafferent endings: primary sensory endings of type Iafibers and secondary sensory endings of type II

fibers

These regions are innervated by gamma () efferentfibers

Note: contractile muscle fibers are extrafusal fibers

and are innervated by alpha () efferent fibers

Muscle Spindles


68/110

Figure 13.15

Operation of the Muscle Spindles


69/110

Stretching the muscles activates the muscle spindle

There is an increased rate of action potential in Ia

fibers

Contracting the muscle reduces tension on the

muscle spindle

There is a decreased rate of action potential on Iafibers

Operation of the Muscle Spindles


70/110

Figure 13.16

Muscle Twitch


71/110

A muscle twitch is the response of a muscle to a

single, brief threshold stimulus

The three phases of a muscle twitch are:

Latent period

first few milli-seconds after

stimulation

when excitation-contraction

coupling is

taking placeFigure 9.13 (a)

Muscle Twitch


72/110

Period of contractioncross bridges actively form

and the muscle shortens

Period of relaxation

Ca2+is reabsorbed

into the SR, and

muscle tension

goes to zero

Figure 9.13 (a)

Graded Muscle Responses


73/110

Graded muscle responses are:

Variations in the degree of muscle contraction

Required for proper control of skeletal movement

Responses are graded by:

Changing the frequency of stimulation

Changing the strength of the stimulus

Muscle Response to Varying Stimuli


74/110

A single stimulus results in a single contractile

responsea muscle twitch

Frequently delivered stimuli (muscle does not have

time to completely relax) increases contractile force

wave summation

Figure 9.14

Muscle Response to Varying Stimuli


75/110

More rapidly delivered stimuli result in incomplete

tetanus

If stimuli are given quickly enough, complete

tetanus results

Figure 9.14

Muscle Response: Stimulation Strength


76/110

Threshold stimulusthe stimulus strength at whichthe first observable muscle contraction occurs

Beyond threshold, muscle contracts more vigorously

as stimulus strength is increased

Force of contraction is precisely controlled by

multiple motor unit summation

This phenomenon, called recruitment, brings more

and more muscle fibers into play

Stimulus Intensity and Muscle Tension


77/110

Figure 9.15 (a, b)

Treppe: The Staircase Effect


78/110

Staircaseincreased contraction in response to

multiple stimuli of the same strength

Contractions increase because:

There is increasing availability of Ca2+in thesarcoplasm

Muscle enzyme systems become more efficient

because heat is increased as muscle contracts

Treppe: The Staircase Effect


79/110

Figure 9.16


80/110

Smooth muscle

Smooth muscle


81/110

Nonstriated

Lack sarcomeres

Thin filaments anchored to dense bodies

Involuntary

Structure of smooth muscle


82/110

Shape of muscle fiber

spindle shaped 1-5 m in diameter

20-500 m in length

A single nucleus present in the central thick portion. Sarcolemma (cell membrane).

Cytoplasm appears homogenous without striations.

Fewer mitochondria as compared to the skeletal

muscle. Metabolism mostly glycolytic.

Actin, Myosin & Tropomyosin but NO Troponin



83/110

Dense bodies present attached to the cell membranes OR

dispersed throughout the cell

Dense bodies serve the same purpose as the Z-discs

Attached to the dense bodies are numerous numbers of

Actin filaments

Interspersed between the actin filaments are Myosin

filaments (their diameter twice as much as actin

filaments)Usually, 5-10 times as many actin filaments as Myosin

filaments

Smooth Muscle Tissue


84/110

Figure 10.23

Smooth Muscle


85/110

Innervated by autonomic nervous system (ANS)

Visceral or unitary smooth muscle

Only a few muscle fibers innervated in each group

Impulse spreads through gap junctions Contracts as a unit

Often autorhythmic

Multiunit:

Cells or groups of cells act as independent units

Errector pili of skin and iris of eye

Functional characteristics of smooth muscle


86/110

Contract when calcium ions interact with

calmodulin Activates myosin light chain kinase

Functions over a wide range of lengths

Plasticity Multi-unit smooth muscle cells are innervated by

more than one motor neuron

Visceral smooth muscle cells are not always

innervated by motor neuronsNeurons that innervate smooth muscle are not

under voluntary control

Oblique arrangement of sarcomeres


87/110

Smooth Muscle Cell


88/110

Sidepolar cross-bridges


89/110

Myosin filaments have sidepolar cross-bridges

Bridges on one side hinge in one direction & on the other side in the oppositedirection

Allows myosin to pull an actin filament in one direction while simultaneouslypulling it in the other direction on the other side

Allow smooth muscle to contract 80% as compared to only 30 % in theskeletal muscle

(force of contraction in skeletal muscle is limited because of the presence of

the z-disc, against which the thick filament will abutt against and cannotmove any further)

Calcium Pump: pumps Ca back into the SR if present for relaxation totake place. But it is very slow so that duration of cont. is longer.


90/110



91/110

Neuromuscular Junction:

Does not occur in smooth muscleInstead the

autonomic nervesmake diffuse junctions that

secrete NT into the matrix coating of smooth muscle

a few micrometers away from the muscle fiber

Also the axons supplying them do not have terminalbuttons but varicositieson their terminal axons that

contain the vesicles containing the NT

Neurotransmitter (NT)

Apart from Ach, norepinephrinecan also bereleased

Instead of synaptic clefts, smooth muscles have

contact junctions



92/110

Single unit

Multi unit

Classification of smooth muscles

MULTI UNIT


93/110

SINGLE UNIT

1. Muscles of visceral organs.e.g. GIT, uterus, ureters &some of the smaller bloodvessels.

2. Form a sheet or bundles oftissue.

3. Cell membranes show gapjunctions that allows AP topass rapidly from cell to cell.

4. AP spreads rapidlythroughout the sheet of cellscells contract as a single unit.

MULTI-UNIT

1. Iris & Ciliary body of the

eye, large arteries,Piloerector muscles

2. Showing discrete, individualsmooth muscle fibers.

3. Smooth muscle cells notelectrically linked. Eachmuscle fiber innervated by asingle nerve ending. NTitself can spread and lead to

an AP.4. Selective activation of each

muscle fiber that can thencontract independently of

each other.

Single-Unit Muscle


94/110

Properties of Single-Unit Smooth Muscle


95/110

Gap junctions

Pacemaker cells

with spontaneous

depolarizations

Innervation to few cells

Tone = level of

contraction withoutstimulation

Increases/decreases

in tension

Graded Contractions

No recruitment

Vary intracellular

calcium

Stretch Reflex

Relaxation in

response to suddenor prolonged stretch

Multi-Unit Muscle


96/110

M lti Si l U it M l


97/110

Multi vs. Single-Unit Muscle

Comparisons Types of Muscle


98/110

Single muscle twitch


99/110

Single muscle contraction (muscle twitch) developsmore slowly & relaxes even more slowly longer

sustained contraction without fatigue

Advantage:This ability allows the walls of the organsto maintain tension with a continued load .e.g.urinary bladder filled with urine

A TYPICAL SMOOTH MUSCLE HAS A TOTALCONTRACTION TIME OF 1-3 SECONDS (about30 times as long as single skeletal muscle

contraction)

Single muscle twitch


100/110

Action potential


101/110

In the normal resting state, the membrane potential isabout -50 to -60 mv.

The AP of visceral smooth muscle is of 2 types:

Typical spike potentials: (similar to skeletalmuscles) -mostly seen in the unitary smooth

muscles

AP with Plateaus: Starts like a typical spikepotential but repolarization delayed for severalhundred to as many as 1000 msec -accounts forthe prolonged contraction that occurs in certainorgans

Action potential - Slow wave potentials


102/110

Without an external stimulus membrane potential isoften associated with a basic slow wave rhythm. This is

itself not an AP but a local property of the smoothmuscle fibers.

Cause:

Waxing & waning of the pumping of Na ions Conductance of the ion channels increase &decrease rhythmically

When the peak of the slow wave reaches about -35 mv,

threshold is reached and an AP develops & leads to acontraction at peak of the slow waves an AP canoccur Pacemaker waves

Slow wave potentials Pacemaker potentials


103/110


104/110

When unitary (visceral) smooth m. is stretched,

spontaneous AP is usually generated, because:1. Normal slow potentials caused by stretch

2. Overall in membran negativity caused by stretch

Role of calcium


105/110

Poorly developed SR

Presence of small invaginations abut the SR whichrelease Ca when AP reaches it.

Smooth muscle contraction is highly dependent on

Extracellular Calcium concentration

The main source of Calcium ions in smooth muscle is togreater extent ECF and to a lesser extent SR as

compared to the skeletal muscles where greatest source

of Calcium is SR.

Calcium plays the main role in the prolongedcontraction process.

Smooth muscle contraction sequence


106/110

Binding of Ach to the receptors

Increased Influx of Ca into the cell from the following sources:1. ECF thru Ca channels

2. Ca released from SR

3. Stretch-activated Ca channels when memb. Deformed

4. Chemical-gated Ca channels by NT & hormones

Ca binds to Calmodulin

Ca-Calmodulinactivates the enzyme: Myosin light chain kinase MLCK or

simply Myosin kinase

Phosphorylation of myosin, using energy & Pi from ATP

Increased ATPase activity & binding of myosin to actin

Contraction of smooth muscle

Smooth Muscle Contraction


107/110

Smooth muscle relaxation sequence


108/110

Dephosphorylation of Myosin by myosin phosphatase/ MLCP

Decreases its ATP activity

Ca removed from cytoplasm using Ca-Na antiport protein & Ca-ATPase

Calmodulin releases Ca & uncomplexes from MK

MK is phosphorylated by Protein kinase, inactivating it

Relaxation OR sustained contraction

Smooth Muscle Relaxation


109/110

Latch system


110/110

It is a state in which the dephosphrylated myosin

remains attached to actin for prolonged period oftime. This produces sustained contraction without

consuming ATP & thus enables the smooth muscle

to sustain long-term maintenance of tone without

fatigue. E.g. urinary bladder full of urine.

Documents

faal otot ppt