biokimia muscle
DESCRIPTION
Biokimia MuscleTRANSCRIPT
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
Muscle Microstructure
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
Muscle Microstructure
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
Single Fiber Contraction
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
Single Fiber Contraction
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
Single Fiber Contraction
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
Single Fiber Contraction
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
Single Fiber Contraction -Tension:Frequency
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
Single Fiber Contraction -Tension:Frequency
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
Skeletal Muscle Fibers
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
Skeletal Muscle Fibers
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
Adaptation to Exercise
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
Adaptation to Exercise
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