Biokimia Muscle

MuscleBME 5010 - Engineering Physiology

Objectives - Skeletal Muscle

Define the function of skeletal muscleDiscuss the hierarchical structure of skeletal muscleDescribe the mechanism of contraction at amolecular level, including the role of ATP and calciumList the steps in neural stimulation of musclecontractionDefine the three types of muscle fiber contractionDiscuss the following relationships:n Frequency-muscle tensionn Length-muscle tensionn Load-shortening velocity

Objectives - Skeletal Muscle

Discuss the three types of energy metabolism whichoccur in muscle

Define muscle fatigue and give theories for itsoccurrence

Define the three types of muscle fibers

Discuss how whole-muscle tension and shorteningvelocity is regulated by the nervous system

Explain how exercise or lack of activity affects muscle

Describe the benefits and drawbacks of the leversystem of movement based on muscle and bone

Skeletal Muscle

Most are attached to bone

Responsible for supporting and moving the skeleton

Generally voluntary control

Skeletal Muscle Structure

Myoblasts (undifferentiated, mononucleated cells)fuse during fetal development to form a single,cylindrical, multi-nucleated cell called a muscle fiberwhich is no longer able to dividen Muscle fibers are between 10 and 100 µm in

diameter and up to 20 cm longMuscle fibers are grouped into cylindrical bundlesand eventually a whole muscle by connective tissueMuscles are connected to bones by tendonsDestroyed muscle fibers are replaced byundifferentiated satellite cells located in theconnective tissue surrounding muscle cells

Muscle Microstructure

Skeletal and cardiacmuscle show a striatedstructure under themicroscopeStriated pattern is due tothe arrangement of thickand thin filaments intomyofibrils which run thelength of muscle fiberwithin the cytoplasmOne unit of repeatingpattern within a muscle cellis called a sarcomere


See Figure 11-4 in Vander, Sherman, and LucianoThick filaments: myosinn Located in the middle of the sarcomeren Wide, dark band of myosin called the A bandn Held together by proteins within the cytoplasm (not

free-floating)Thin filaments: actin along with troponin andtropomyosinn Located at either end of the sarcomere, with one

end of each filament anchored to the Z line andthe other end overlapping the myosin filaments


Sarcomeres are bounded by Z-lines on both ends

The light bands of the muscle fiber contain only thinfilaments

n Called the I band

n Divided in half by a Z-line

Molecular Mechanism ofContraction

Contraction: turning on of cross-bridges withinmuscle fibers

Relaxation: turning off of cross-bridges, reducingtension

In order for muscle shortening to occur, the cross-bridge induced force must exceed an external,opposing force

The current theory of muscle contraction is called thesliding filament mechanism

Sarcomeres in Contraction andRelaxation

Relaxation

Contraction

Sliding Filament TheoryMyosin is a linear molecule with a globular endn All myosin molecules have their linear portion

directed parallel to the myofibril axis and towardsthe center of the sarcomere

n The globular end has a binding site for actin and asecond site for ATPase (an enzyme that breaksdown ATP)w This globular portion is termed the cross-bridge

Actin is a globular molecule that forms a double helixn Actin is wrapped by a molecule of tropomyosin

which covers binding sites for the cross-bridgesn The tropomyosin is held in this blocking position by

molecules of troponin, which have a binding site forcalcium

Sliding Filament Mechanism*

(1) Calcium is released by the sarcoplasmicreticulum of the muscle cells

(2) Calcium ion binds to troponin molecule of thinfilament

(3) Troponin moves tropomyosin molecule awayfrom cross-bridge binding sites of actin

(4) ATP molecules bound to myosin are hydrolizedby ATPase to produce an energized myosin molecule

n M•ATP --> M*•ADP•Pi

Sliding Filament Mechanism(5) The cross-bridge of the energized myosinmolecule binds to actin and triggers the release of theenergy stored in the myosinn A + M*•ADP•Pi --> A•M*•ADP•Pi --> A•M + ADP +

Pi

(6) Energy release corresponds to movement ofbound cross-bridge in a rowing motion, bringing theactin molecules towards the center of the sarcomere(7) An ATP molecule binds to the myosin moleculeand releases the cross-bridge attachment

n A•M + ATP --> A + M•ATP(8) Myosin molecule is then ready to bind to anotheractin site and steps 4 through 7 are repeated as longas calcium is present

Excitation-Contraction Coupling

Sequence of events by whichan action potential at theplasma membrane leads tocross-bridge activitySkeletal muscle plasmamembrane is excitable andcapable of generating andpropagating action potentials ina similar way to nerve cellsA muscle action potential lasts1 to 2 ms and is followed by100 ms or more of mechanicalactivity within the muscle due toan increase in cytosolic calcium

Action potential due to Na+ channels

Force

Time 30 ms

Action Potential and CalciumConcentration

In resting muscles, the cytosolic calciumconcentration is very low (10 -7 mol/L)Following an action potential, there is a rapidincrease in cytosolic calcium due to release ofcalcium stores from the cellular sarcoplasmicreticulumWithin a muscle fibre, the myofibrils are surroundedby sleeves of sarcoplasmic reticulum (SR)(See Fig 11-15)n At the end of each segment of SR are enlarged

regions called lateral sacs or terminal cisternaewhich contain the stored calcium

Action Potential and CalciumConcentration

A transverse tubule (or T tubule) crosses a musclefiber even with each A-I junction, between adjacentlateral sacs, and connects to the plasma membranen Action potentials along the plasma membrane are

conducted into the center of the cell by the Ttubules

When an action potential passes a lateral sac,calcium channels are opened and calcium is releasedinto the cytosolic fluid surrounding the myofibrilsA positive feed-back loop is set-up, as initiallyreleased calcium binds to calcium channels of thelateral sacs and causes more channels to openAs Ca2+ concentration rises, Ca2+ binds to loweraffinity sites on the channels and causes them toclose and end ion release

Calcium Concentration and MuscleRelaxation

Contraction of myofibrils will continue as long asthere is an elevated cytosolic calcium concentrationand binding to troponin

Calcium is returned to the SR by active transport inthe presence of ATP

n The time required to remove the calciumdetermines the length of time of mechanicalactivity, not the duration of the action potential

n Note: this a third role for ATP in musclecontraction

Muscle Membrane ExcitationActivated by stimulation of nerve fibers to a skeletalmuscle (motor neurons)The axon of a motor neuron branches into multiplebranches, with each forming a single junction with amuscle fibern A single motor neuron innervates many muscle fibers,

but each muscle fiber is controlled by only one motorneuron

A motor unit is defined as a motor neuron plus themuscle fibers it innervatesn Muscle fibers in a single motor unit are scattered

throughout a single musclen An action potential produced in a motor neuron

causes all of the muscle fibers in its motor unit tocontract

Muscle Membrane Excitation

The area of the plasma membrane under the terminalportion of an axon is the motor end plate

The junction of the axon with the motor end plate iscalled the neuromuscular junction

Muscle Membrane ExcitationMechanism*

(1) An action potential arriving at an axon terminal openscalcium channels in the axon, allowing calcium to diffuse intothe axon(2) The calcium triggers the release by exocytosis ofacetylcholine into the extracellular cleft separating the axonterminal and the motor end plate(3) Acetylcholine binds to receptor sites on the motor endplate, opening ion channels which allow sodium ions to enterand potassium ions to exit(4) Ion movement results in a local depolarization of themembrane, triggering an action potential which propagatesalong the membrane(5) Acetylcholinesterase breaks down acetylcholine, ionchannels close, and the membrane repolarizes

Single Fiber Contraction

Whether or not muscle contraction leads to muscleshortening depends on the relationship betweenmuscle tension and external loads

Note that muscle fibers only shorten when stimulated-- there are no inhibitory impulses nor anymechanisms to actively lengthen the fibers

n Lengthening occurs when an external force isgreater than the generated muscle force


Isometric contraction: muscle develops tension but doesnot shorten or lengthenn Occurs when: (1) a muscle supports a load in a

constant position; or (2) attempts to move a load thatis greater than the muscle tension and that isexternally supported

n Cross-bridges generate a tension but are not able toshorten myofibrils

Isotonic contraction: load on muscle remains constantbut the muscle is shorteningn ie. lifting an objectn Cross-bridges cause tension and myofibril shortening


Lengthening contraction: muscle lengthens whileconstant tension is being maintained

n Occurs when an unsupported load on a muscle isgreater than the generated tension, such aslowering an object

n While bound to the actin, the cross-bridges arepulled towards the ends of the sarcomere insteadof stroking towards the middle


Twitch: response of a musclefiber to a single actionpotentialLatent period: time betweenaction potential and initialgeneration of tension(isometric) or shortening(isotonic)Contraction time: timebetween initial generation oftension and generation ofpeak tensionn Contraction time can differ

between muscle fibers,ranging from 10 ms for fastfibers to 100 ms or morefor slow fibers

Latent Period

Contraction Time

Time

Ten

sion


Tension often increases before shortening occurs, asthe tension must first overcome any external load(including that of bones, etc.)

Time

Ten

sion

Shor

teni

ng

Single Fiber Contraction -Tension:Frequency

Due to time difference betweenthe duration of an actionpotential and the duration ofmechanical response in themyofibrils, multiple actionpotentials can be applied to amuscle fiber before relaxationoccursThe mechanical activity of amuscle fiber is subject tosummationn A subsequent action

potential can result in agenerated tension higherthan the peak tension of asingle action potential


Maintained contraction resulting from a repetitivestimulus is called tetanusn This occurs when the frequency of stimulation is

such to not allow complete relaxation of the musclein between action potentials

n A maximal tetanic tension exists for each musclefiber, which is approximately 3 to 5x greater than theisometric twitch tension

The tension produced by each sarcomere at any timedepends on the number of cross-bridges which arebound to actin and are “rowing”A single action potential releases enough calcium tosaturate the troponin molecules


Almost immediately after the action potential, calcium ispumped back into the SR and the Ca2+ concentrationdecreases resulting in fewer actin sites being available forbindingMaximal tension takes time to develop as there is a finitetime required for the molecular reactions and responsesDuring a single twitch, the maximal number of actin sitesdoes not stay available long enough for the time lags to beovercome and maximal tension to be developedDuring tetanic contraction, successive action potentialsrelease calcium before the concentration can be returnedto resting levels, allowing the maximal number of actinsites to be made available for contraction and maximumtension develops

Single Fiber Contraction -Tension:Length

See Figure 11-25The length of the muscle fiber before contractioninfluences the maximal contraction that can be developedn The length at which a muscle fiber generates its

maximal tetanic tension is termed the optimal lengthWhen the fiber length is less than 60 percent of its optimallength, no tension is developed on stimulationn The actin molecules cannot move further towards the

center of the sarcomereWhen the fiber length is greater than 175 percent of itsoptimal length, no tension is developed on stimulationn The actin and myosin fibrils no longer overlap

Single Fiber Contraction -Tension:Length

At rest, most skeletal fibers are near their optimallengths

Length of a relaxed fiber can be altered by externallyapplied loads or the contraction of other muscles

n Due to limits caused by the attachment of musclesto bone, muscle fiber length rarely varies by morethan 30 percent from optimal

n Muscles can therefore always contract

Single Muscle Contraction -Load:Velocity

The velocity at which a muscle shortens while undergoingmaximal tetanic stimulation decreases with increasingloadsn Maximum velocity at zero loadn Zero velocity when external load is equal to maximal

isometric tensionn At loads greater than maximal isometric tension, the

fiber will lengthen at a velocity which increases withincreasing load and at very high loads fibers will break

Shortening velocity is determined by the rate at whichindividual cross-bridges cyclen Increasing the load decreases the rate at which the

cross-bridge “rows” and generates force

Single Fiber Contraction -Calcium Concentration

The generated force in a single muscle fiber isdependent on the cytosolic Ca2+ concentration in asigmoidal fashion

RelativeForce

1.0

0.0Calcium Concentration

Energy Metabolism

ATP performs three functions related to musclecontraction and relaxation

For contraction to be maintained, ATP must besupplied at a rate equal to that at which it is brokendown

ATP is generated through phosphorylation of ADP bythree mechanisms within muscle cells

n (1) Through creatine phosphate

n (2) Through oxidation in the mitochondria

n (3) Through glycolysis in the cytosol

Energy Metabolism - CreatinePhosphate

Rapid means of forming ATP at the beginning ofcontractionChemical bond between creatine and phosphate is broken,the energy released is the same as needed by ADP toattract the free phosphate group and form ATP

n CP + ADP <==> C + ATPReversible reactionDuring rest, muscle concentrations of CP build up to 5x theconcentration of ATPAfter contraction, mass action favors formation of ATPAmount of ATP formed by this mechanism is limited by theinitial concentration of creatine phosphate in the cellBeyond a few seconds of contraction, additional sources ofATP are required to maintain contraction

Energy Metabolism -Oxidation

Requires fuel plus oxygen

Predominant mechanism of ATP production duringmoderate muscular activity

Energy provided by muscle glycogen during first 5 to10 minutes of muscle contraction

For following 30 minutes or so, glucose and fattyacids brought by the blood supply contribute equallyto fuel supply

In sustained activity, fatty acids becomeprogressively dominant as the fuel for oxidation

Energy Metabolism -Glycolysis

Requires fuel but no oxygen

Contributes increasingly more to ATP productionwhen the intensity of exercise exceeds 70 percent ofmaximal rate of ATP breakdown

Produces lactic acid, which results in muscle burn

Energy Metabolism

Replenishment of glycogen and creatine phosphatewithin the cytosol after contraction has stoppedrequires additional energy to be supplied

Results in continued use of oxygen

n Evidenced by continued deep and/or rapidbreathing for a period after activity has finished

The longer and more intense the exercise, the longerit takes to replenish the stores

Muscle Fatigue

With repeated stimulation, fiber tension, contractionvelocity, and the rate of relaxation eventually slowRest allows the muscle to regain its ability to contractThe onset of muscle fatigue, its rate of development,and rate of recovery depend on the type of musclefiber and the intensity and duration of contractionn Muscle fatigue following weight lifting (short-

duration, high-intensity) can develop quickly butrecovers rapidly

n Fatigue that develops slowly with low-intensity,long-duration exercise such as long distancerunning may take up to 24 hours to recovercompletely

Muscle Fatigue - High FrequencyStimulation

Fatigue is partly caused by the increase in inorganicphosphate concentration (from ATP breakdown) andhydrogen ion concentration (from lactic acid build-up)

Pi and H+ concentration inhibit portions of the cross-bridge cycle, leading to decreased force production

n Accounts for 50 percent of force reduction

Additional fatigue is due to decreased release ofcalcium ions from the SR

Muscle Fatigue

Fatigue from long-term, continuous activity is due tochanges in activity of proteins: calcium channels, Ca-ATPase pumps in the SR, troponin, tropomyosin,actin, and myosin

Fatigue may provide a protective mechanism

n It occurs at a time when ATP breakdown exceedsATP formation

n Without fatigue, ATP concentration woulddecrease to a level resulting in continued bindingof cross bridges in rigor

Skeletal Muscle Fibers

Fibers can be identified based on

n Maximal velocity of shortening: fast vs. slow

n Major ATP forming pathway: oxidative vs. glycolitic

Three types of fibers

n Slow-oxidative fibers

n Fast-oxidative fibers

n Fast-glycolytic fibers

Fast fibers: contain myosin with high ATPase activity

Slow fibers: contain myosin with low ATPase activity


Oxidative fibersn Contain numerous mitochondrian Surrounded by numerous blood vesselsn Large amounts of myoglobin which increases the rate of

oxygen diffusion and makes muscle fibers redGlycolytic fibersn Few mitochondria but high levels of glycolitic enzymesn Large store of glycogen but little myoglobinn Surrounded by few blood vessels, larger diameter than

oxidative fibersn More overall myofibrils allow generation of higher fiber

tension


Fast-glycolitic fibers fatigue rapidly

Slow-oxidative fibers fatigue slowly

Fast-oxidative fibers have an intermediate capacity toresist fatigue

Whole Muscle

Muscles are made up of many muscle fibers organizedinto motor unitsAll fibers of a single motor unit are of a single fiber typeMost muscles are composed of all three motor unittypes mixed togethern Proportion of the three fiber types determnes the

muscle’s maximum contraction speed, strength, andfatiguability

n Back and Legs: slow-oxidative fibers predominate tosupport an upright posture for extended periods

n Arms: fast-glycolytic fibers in greater proportion toproduce large amounts of tension over short times

Muscle Tension

Depends on the amount of tension developed by eachfiber and the number of fibers contracting at any timeNervous system controls both factors to determinemuscle tension and shortening velocityThe number of fibers contracting depends on the thenumber of fibers in each motor unit and the number ofactive motor unitsn Muscles requiring fine control (eye and hand) have

motor units with very few fibers -- as few as 13 -- sothat activating a new motor unit generates a smallincrease in tension

n Coarsely controlled muscles (back and legs) havemotor units with hundreds or thousands of fibers

Muscle TensionMotor unit recruitment generally occurs in thefollowing ordern Slow-oxidativen Fast-oxidativen Fast-glycolytic

Moderate levels of exercise will thus generally notinclude high numbers of fast-glycolytic fibersn These last motor units are generally recruited after

the intensity of contraction exceeds about 40percent of the maximal tension of the muscle

Tension in a motor unit is governed by the frequencyof neural stimulation

Muscle Shortening Velocity

Recruitment also affects shortening velocity

n The type of motor units recruited play a role inshortening velocity

n An increased number of active motor units resultsin less load being carried by each motor unit (andfiber) thus allowing for higher shortening velocities

Adaptation to Exercise

Muscle reduction can occur due to:n Denervation atrophy: if the neurons to a muscle

are destroyed, the diameter of the denervatedfibers and number of contractile proteins willdecrease

n Disuse atrophy: loss of muscle diameter andcontractile proteins due to lack of use ( ie. casting)

Increased levels of activity can produce musclehypertrophy as well as changes in the chemicalcomposition of the of the fibersMuscle atrophy and hypertrophy is not throughchanges in the number of fibers, but through themetabolic capability and size of each fiber


Increased aerobic exercisen Produces an increased number of mitochondria in

oxidative fibersn Causes an increase in the number of capillaries

around the fibersIncreased “strength training”n Causes an increase in the diameter of fast-

glycolytic fibers through the production of moreactin and myosin filaments

n Increases the synthesis of glycolytic enzymes infast-glycolytic fibers


Changes in muscle occur slowly over time inresponse to repeated exercise

Stopping exercise will cause muscles to return to theoriginal state, again slowly

Lever Action of Muscles

Muscles exert tensile forces on the lever arms ofbones through tendons

Muscles act as antagonists through this tensile force

n One set of muscles acting on a limb will causeflexion (bending) while a paired set will causeextension (straightening)

Muscles and applied external forces exert momentson a lever arms about a joint (fulcrum)

Lever Action of Muscles

Lever system amplifies the velocity of movement atthe end of the lever

n ie. A 1 cm shortening of the bicep produces a 7cm movement of the hand in the same amount oftime

Short lever arm of muscles compared to supportedweight requires much greater muscle tension toovercome the external load

Smooth Muscle

BME 5010 - Engineering Physiology

Objectives

Discuss the function of smooth muscle

Describe the structure of smooth muscle and howthis relates to its function

Explain the mechanism of contraction and its control

List the types of smooth muscle and theirdifferentiating features

Smooth Muscle

Most smooth muscle surrounds hollow organs

Structure

Smooth muscle fibers are spindle-shaped cells withdiameters from 2 to 10 µmSingle nucleated cells that retain their ability to divideContain two types of filaments:n Thick, myosin containing filamentsn Thin, actin containing filaments

Actin filaments are anchored to either the plasmamembrane or to structures in the cytoplasm known asdense bodiesn Dense bodies function similarly to Z-lines in

skeletal muscle

Structure

Filaments are oriented diagonally with respect to cellaxis

Thick and thin filaments are not organized intomyofibrils or sarcomeres

n No striated pattern

Actin of thin filaments is not bound to the regulatorymolecule, troponin

Contraction

Calcium triggered cross-bridge activation is mediatedby a calcium-regulated enzyme that phosporylatesmyosin

The phosphorylated myosin is then capable ofbinding to actin and undergoing cross-bridge cycling

Smooth muscle contraction involves calcium-inducedchanges in the thick filaments, whereas skeletalmuscle regulation was through the thin filaments

Contraction Mechanism

(1) Rise in cytosolic calcium(2) Calcium binds to calmodulin (a calcium bindingprotein)(3) Calcium-calmodulin complex binds to myosinlight-chain kinase (a protein kinase) which activatesthe enzyme(4) Activated myosin light-chain kinase uses ATP tophosphorylate the myosin(5) Myosin cross-bridge binds to actin and goesthrough remainder of cross-bridge cycle (see skeletalmuscle steps 5 to 8)

Contraction

Smooth muscle has a low rate of ATP degradation, thus alow cycling rate and a slow contraction rateAn overall low rate of ATP use contributes to lack offatiguability in smooth muscleIsometric contraction of smooth muscle can be maintainedwith a very low rate of ATP useSmooth muscle relaxes when myosin is dephosphorylizedn Dephosphorylization occurs at a slower rate than

phosphorylization during contractionn When cytosolic calcium decreases, dephosphorylization

exceeds the rate of phosphorylization and the musclerelaxes

Smooth Muscle Tension

A length:tension relationship exists which isqualitatively similar to that of skeletal muscle

n Range of muscle lengths over which smoothmuscle can generate tension is greater

n Hollow organs undergo changes in volume whichalso change the muscle length

Cytosolic Calcium

In smooth muscle calcium enters the cytosol fromboth the SR and the extracellular fluidn Extracellular calcium enters through calcium

channelsThe ratio of supply from these two sources dependson the type of smooth muscleThere is no defined arrangement of the SR aroundthe filaments and no T-tubulesCalcium release is triggered by action potentialsreaching SR located near the surface of the plasmamembrane and by second messengers

Cytosolic CalciumVoltage-sensitive calcium channels in the plasma membraneopen in response to an action potential and allow fastdiffusion of ionsCalcium is returned to the SR and the extracellular fluid byactive transportn Active transport is much slower than in skeletal muscle,

allowing single twitches to last for several secondsA single action potential does not activate all cross-bridges insmooth musclen Allows tension to be graded by cytosolic calcium

concentration and therefore the degree of electricalstimulation

Some smooth muscle maintains a smooth muscle tonewithout external stimulin Due to a normal cytosolic calcium concentration which

maintains some cross-bridge activation

Membrane Activation

Cytosolic calcium concentration is governed by acombination of mechanismsn Spontaneous electrical activity in the plasma

membranen Neurotransmitters of the autonomic nervous systemn Hormonesn Local changes in extracellular fluid compositionn Stretch

Not all smooth muscle membranes are capable ofgenerating action potentialsGraded membrane potentials, in addition to actionpotentials, can govern cytosolic calcium concentrationn Graded potentials can increase or decrease calcium

Membrane Activation -- Spontaneous Electrical Activity

Some smooth fibers generate action potentials in theabsence of neural or hormonal input

Membrane does not maintain a resting potential, butgradually depolarize until reaching a threshold andproducing an action potential

n Repolarization starts process again

Potential change between the end of repolarizationand the depolarization that reaches a threshold istermed the pacemaker potential

Membrane Activation - Nerves

Autonomic nerve endings release neurotransmittersSmooth muscle does not have specialized motor end-plate regionsAxons enter the region of smooth muscle fibers andbranch, with each branch containing swollenvaricositiesn Neurotransmitters are released from vesicles in the

varicosities in response to an action potentialVaricosities from a single axon can be located alongseveral muscle fibersA single muscle fiber can be located near varicositiesbelonging to both sympathetic and parasympatheticneurons

Membrane Activation - Nerves

Some neurotransmitters cause depolarization of themembrane and increase in cytosolic calciumSome neurotransmitters cause hyperpolarization ofthe membrane and a decrease in cytosolic calcium,thus reducing contractionThe type of response depends not only on the type ofneurotransmitter, but also on the type of smoothmuscle celln Norepinephrine contracts muscle in blood vessels

but inhibits the spontaneous activity of intestinalsmooth muscle

Membrane Activation -Hormones

Smooth muscle plasma membrane containsreceptors for

Membrane-bound hormones can open or close ionchannels that change the membrane potential orrelease second messengers that affects release ofSR calcium

n Second messenger effects can occur without achange in membrane potential

Membrane Activation - LocalFactors

Local factors can affect cytosolic calciumconcentration

- paracrine agents - osmolarity

- acidity - ion composition of fluid

- oxygen concentration

Stretching opens mechanosensitive ion channels insome smooth muscle

n Leads to depolarization

n Resulting contraction resists force of stretching

Types of Smooth Muscle

Smooth muscles can be placed in one of two groupsaccording to the excitability characteristics of theplasma membrane and the conduction of electricalactivity between the muscle fibersSingle-unit smooth muscles:n membranes propagate action potentials from cell to

cell through gap junctionsn may exhibit spontaneous action potentials

Multi-unit smooth muscles:n little, if any, propagation of action potential from cell

to celln contraction dominated by neural stimulation

Single-Unit Smooth Muscle

Include muscles of intestinal tract, uterus, and smalldiameter blood vesselsWhole muscle responds to stimulation as a singleunitn Gap junctions allow an action potential occuring in

one cell to propagate to remaining cells of muscleSome of cells in muscle will act as pacemaker cellsRegulation mechanisms often target pacemaker cellsContraction can often be induced by stretching themusclen ie. uterine contraction is in response to the

increase in volume of the hollow structure

Multi-Unit Smooth Muscle

Include large airways of the lung, larger arteries, hairfollicles of skin

Each muscle fiber responds independently of itsneighbors

High levels of autonomic nerve stimulation

Contractile response of whole muscle depends onnumber of fibers activated and the frequency ofstimulation

Stretch does not induce contraction

Biokimia Muscle

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