Y khoa, y dược - Muscles and muscle tissue: Part A

9 Muscles and Muscle Tissue: Part AThree Types of Muscle TissueSkeletal muscle tissue:Attached to bones and skinStriated Multi-nucleatedVoluntary (i.e., conscious control)Powerful Three Types of Muscle TissueCardiac muscle tissue:Only in the heart Striated Single nucleatedInvoluntaryAutorhythmicThree Types of Muscle TissueSmooth muscle tissue:In the walls of hollow organs, e.g., stomach, urinary bladder, and airwaysNot striatedInvoluntarySingle nucleated Table 9.3Special Characteristics of Muscle TissueExcitability (responsiveness or irritability): ability to receive and respond to stimuliContractility: ability to shorten when stimulatedExtensibility: ability to be stretched Elasticity: ability to recoil to resting lengthMuscle FunctionsMovement of bones or fluids (e.g., blood)Maintaining posture and body position Stabilizing jointsHeat generation (especially skeletal muscle)Skeletal MuscleEach muscle is served by one artery, one nerve, and one or more veinsSkeletal MuscleConnective tissue sheaths of skeletal muscle:Epimysium: dense regular connective tissue surrounding entire muscle Perimysium: fibrous connective tissue surrounding fascicles (groups of muscle fibers)Endomysium: fine areolar connective tissue surrounding each muscle fiberFigure 9.1BonePerimysiumEndomysium(between individualmuscle fibers)Muscle fiberFascicle(wrapped by perimysium)EpimysiumTendonEpimysiumMuscle fiberin middle ofa fascicleBlood vesselPerimysiumEndomysiumFascicle(a)(b)Skeletal Muscle: AttachmentsMuscles attach:Directly—epimysium of muscle is fused to the periosteum of bone or perichondrium of cartilageIndirectly—connective tissue wrappings extend beyond the muscle as a ropelike tendon or sheetlike aponeurosisTable 9.1Microscopic Anatomy of a Skeletal Muscle FiberCylindrical cell, up to 30 cm longMultiple peripheral nucleiMany mitochondriaGlycosomes for glycogen storageMyoglobin for O2 storageAlso contain myofibrils, sarcoplasmic reticulum, and T tubulesMyofibrilsDensely packed, rodlike elements Exhibit striations: perfectly aligned repeating series of dark A bands and light I bandsNucleusLight I bandDark A bandSarcolemmaMitochondrion(b) Diagram of part of a muscle fiber showing the myofibrils. Onemyofibril is extended afrom the cut end of the fiber.MyofibrilSarcomereSmallest contractile unit (functional unit) of a muscle fiberThe region of a myofibril between two successive Z discsComposed of thick and thin myofilaments made of contractile proteinsFeatures of a SarcomereThick filaments: run the entire length of an A bandThin filaments: run the length of the I band and partway into the A bandZ disc: coin-shaped sheet of proteins that anchors the thin filaments and connects myofibrils to one anotherH zone: lighter midregion where filaments do not overlap M line: line of protein myomesin that holds adjacent thick filaments togetherFigure 9.2c, dI bandI bandA bandSarcomereH zoneThin (actin)filamentThick (myosin)filamentZ discZ discM line(c)Small part of one myofibril enlarged to show the myofilamentsresponsible for the banding pattern. Each sarcomere extends fromone Z disc to the next.Z discZ discM lineSarcomereThin (actin)filamentThick(myosin)filamentElastic (titin)filaments(d)Enlargement of one sarcomere (sectioned lengthwise). Notice the myosin heads on the thick filaments.Ultrastructure of Thick FilamentComposed of the protein myosinMyosin tails contain: 2 interwoven, heavy polypeptide chainsMyosin heads contain: 2 smaller, light polypeptide chains that act as cross bridges during contraction Binding sites for actin of thin filamentsBinding sites for ATPATPase enzymesUltrastructure of Thin FilamentTwisted double strand of fibrous protein F actinF actin consists of G (globular) actin subunits G actin bears active sites for myosin head attachment during contractionTropomyosin and troponin: regulatory proteins bound to actinFigure 9.3Flexible hinge regionTailTropomyosinTroponinActinMyosin headATP-bindingsiteHeadsActive sitesfor myosinattachment Actinsubunits Actin-binding sitesThick filamentEach thick filament consists of manymyosin molecules whose heads protrude at opposite ends of the filament.Thin filamentA thin filament consists of two strandsof actin subunits twisted into a helix plus two types of regulatory proteins(troponin and tropomyosin).Thin filamentThick filamentIn the center of the sarcomere, the thickfilaments lack myosin heads. Myosin heads are present only in areas of myosin-actin overlap.Longitudinal section of filamentswithin one sarcomere of a myofibril Portion of a thick filamentPortion of a thin filamentMyosin moleculeActin subunits Sarcoplasmic Reticulum (SR)Network of smooth endoplasmic reticulum surrounding each myofibrilPairs of terminal cisternae form perpendicular cross channelsFunctions in the regulation of intracellular Ca2+ levelsT TubulesContinuous with the sarcolemmaPenetrate the cell’s interior at each A band–I band junctionAssociate with the paired terminal cisternae to form triads that encircle each sarcomereFigure 9.5MyofibrilMyofibrilsTriad:Tubules ofthe SRSarcolemmaSarcolemmaMitochondriaI bandI bandA bandH zoneZ discZ discPart of a skeletalmuscle fiber (cell) • T tubule• Terminalcisternaeof the SR (2) M lineTriad RelationshipsT tubules conduct impulses deep into muscle fiber Integral proteins protrude into the intermembrane space from T tubule and SR cisternae membranesT tubule proteins: voltage sensorsSR foot proteins: gated channels that regulate Ca2+ release from the SR cisternaeContractionThe generation of force Does not necessarily cause shortening of the fiberShortening occurs when tension generated by cross bridges on the thin filaments exceeds forces opposing shorteningSliding Filament Model of ContractionIn the relaxed state, thin and thick filaments overlap only slightlyDuring contraction, myosin heads bind to actin, detach, and bind again, to propel the thin filaments toward the M lineAs H zones shorten and disappear, sarcomeres shorten, muscle cells shorten, and the whole muscle shortensFigure 9.6IFully relaxed sarcomere of a muscle fiberFully contracted sarcomere of a muscle fiberIAZZHIIAZZ12Requirements for Skeletal Muscle ContractionActivation: neural stimulation at aneuromuscular junctionExcitation-contraction coupling: Generation and propagation of an action potential along the sarcolemmaFinal trigger: a brief rise in intracellular Ca2+ levelsEvents at the Neuromuscular Junction Skeletal muscles are stimulated by somatic motor neurons Axons of motor neurons travel from the central nervous system via nerves to skeletal musclesEach axon forms several branches as it enters a muscle Each axon ending forms a neuromuscular junction with a single muscle fiberFigure 9.8NucleusActionpotential (AP)Myelinated axonof motor neuronAxon terminal ofneuromuscular junctionSarcolemma ofthe muscle fiberCa2+Ca2+Axon terminalof motor neuronSynaptic vesiclecontaining AChMitochondrionSynapticcleft Fusing synaptic vesicles1 Action potential arrives ataxon terminal of motor neuron. 2 Voltage-gated Ca2+ channels open and Ca2+ enters the axon terminal.Figure 9.8Neuromuscular JunctionSituated midway along the length of a muscle fiberAxon terminal and muscle fiber are separated by a gel-filled space called the synaptic cleftSynaptic vesicles of axon terminal contain the neurotransmitter acetylcholine (ACh)Junctional folds of the sarcolemma contain ACh receptors Events at the Neuromuscular JunctionNerve impulse arrives at axon terminalACh is released and binds with receptors on the sarcolemmaElectrical events lead to the generation of an action potentialPLAYA&P Flix™: Events at the Neuromuscular JunctionFigure 9.8NucleusActionpotential (AP)Myelinated axonof motor neuronAxon terminal ofneuromuscular junctionSarcolemma ofthe muscle fiberCa2+Ca2+Axon terminalof motor neuronSynaptic vesiclecontaining AChMitochondrionSynapticcleft Junctionalfolds ofsarcolemmaFusing synaptic vesiclesAChSarcoplasm ofmuscle fiberPostsynaptic membraneion channel opens;ions pass.Na+K+Ach–Na+K+Degraded AChAcetyl-cholinesterasePostsynaptic membraneion channel closed;ions cannot pass.1 Action potential arrives ataxon terminal of motor neuron. 2 Voltage-gated Ca2+ channels open and Ca2+ enters the axon terminal.3 Ca2+ entry causes some synaptic vesicles to release their contents (acetylcholine)by exocytosis.4 Acetylcholine, aneurotransmitter, diffuses across the synaptic cleft and binds to receptors in the sarcolemma.5 ACh binding opens ionchannels that allow simultaneous passage of Na+ into the musclefiber and K+ out of the muscle fiber.6 ACh effects are terminated by its enzymatic breakdown in the synaptic cleft by acetylcholinesterase.Destruction of AcetylcholineACh effects are quickly terminated by the enzyme acetylcholinesterase Prevents continued muscle fiber contraction in the absence of additional stimulationEvents in Generation of an Action PotentialLocal depolarization (end plate potential):ACh binding opens chemically (ligand) gated ion channelsSimultaneous diffusion of Na+ (inward) and K+ (outward)More Na+ diffuses, so the interior of the sarcolemma becomes less negativeLocal depolarization – end plate potentialEvents in Generation of an Action PotentialGeneration and propagation of an action potential:End plate potential spreads to adjacent membrane areasVoltage-gated Na+ channels openNa+ influx decreases the membrane voltage toward a critical thresholdIf threshold is reached, an action potential is generatedEvents in Generation of an Action PotentialLocal depolarization wave continues to spread, changing the permeability of the sarcolemmaVoltage-regulated Na+ channels open in the adjacent patch, causing it to depolarize to thresholdEvents in Generation of an Action PotentialRepolarization:Na+ channels close and voltage-gated K+ channels openK+ efflux rapidly restores the resting polarityFiber cannot be stimulated and is in a refractory period until repolarization is completeIonic conditions of the resting state are restored by the Na+-K+ pumpFigure 9.9Na+Na+Open Na+ChannelClosed Na+ChannelClosed K+ChannelOpen K+ChannelAction potential++++++++++++Axon terminalSynapticcleftAChAChSarcoplasm of muscle fiberK+2 Generation and propagation ofthe action potential (AP) 3Repolarization1 Local depolarization: generation of the end plate potential on the sarcolemmaK+K+Na+K+Na+WaveofdepolarizationFigure 9.9, step 1Na+Na+Open Na+ChannelClosed K+ChannelK+Na+K+Action potential++++++++++++Axon terminalSynapticcleftAChAChSarcoplasm of muscle fiberK+1 Local depolarization: generation of the end plate potential on the sarcolemma1WaveofdepolarizationFigure 9.9, step 2Na+Na+Open Na+ChannelClosed K+ChannelK+Na+K+Action potential++++++++++++Axon terminalSynapticcleftAChAChSarcoplasm of muscle fiberK+ Generation and propagation of the action potential (AP)1 Local depolarization: generation of the end plate potential on the sarcolemma21WaveofdepolarizationFigure 9.9, step 3Na+Closed Na+ChannelOpen K+ChannelK+Repolarization3Figure 9.9Na+Na+Open Na+ChannelClosed K+ChannelAction potential++++++++++++Axon terminalSynapticcleftAChAChSarcoplasm of muscle fiberK+2 Generation and propagation ofthe action potential (AP) 3Repolarization1 Local depolarization: generation of the end plate potential on the sarcolemmaK+K+Na+K+Na+WaveofdepolarizationClosed Na+ChannelOpen K+ChannelFigure 9.10Na+ channelsclose, K+ channelsopenK+ channelscloseRepolarizationdue to K+ exitThresholdNa+channelsopenDepolarizationdue to Na+ entryExcitation-Contraction (E-C) CouplingSequence of events by which transmission of an AP along the sarcolemma leads to sliding of the myofilamentsLatent period:Time when E-C coupling events occurTime between AP initiation and the beginning of contractionEvents of Excitation-Contraction (E-C) Coupling AP is propagated along sarcomere to T tubulesVoltage-sensitive proteins stimulate Ca2+ release from SR Ca2+ is necessary for contractionFigure 9.11, step 1Axon terminalof motor neuronMuscle fiberTriad One sarcomere Synaptic cleftSetting the stageSarcolemmaAction potentialis generatedTerminal cisterna of SR AChCa2+ Figure 9.11, step 2 Action potential is propagated alongthe sarcolemma and down the T tubules.Steps in E-C Coupling:TroponinTropomyosinblocking active sitesMyosinActinActive sites exposed and ready for myosin bindingCa2+Terminal cisterna of SRVoltage-sensitivetubule proteinT tubuleCa2+releasechannelMyosincross bridgeCa2+Sarcolemma Calcium ions are released. Calcium binds to troponin andremoves the blocking action oftropomyosin. Contraction beginsThe aftermath1234Figure 9.11, step 3Steps inE-C Coupling:Terminal cisterna of SRVoltage-sensitivetubule proteinT tubuleCa2+releasechannelCa2+Sarcolemma Action potential ispropagated along thesarcolemma and downthe T tubules.1Figure 9.11, step 4Steps inE-C Coupling:Terminal cisterna of SRVoltage-sensitivetubule proteinT tubuleCa2+releasechannelCa2+Sarcolemma Action potential ispropagated along thesarcolemma and downthe T tubules. Calciumions arereleased.12Figure 9.11, step 5TroponinTropomyosinblocking active sitesMyosinActinCa2+The aftermathFigure 9.11, step 6TroponinTropomyosinblocking active sitesMyosinActinActive sites exposed and ready for myosin bindingCa2+ Calcium binds totroponin and removesthe blocking action oftropomyosin.The aftermath3Figure 9.11, step 7TroponinTropomyosinblocking active sitesMyosinActinActive sites exposed and ready for myosin bindingCa2+Myosincross bridge Calcium binds totroponin and removesthe blocking action oftropomyosin. Contraction beginsThe aftermath34Figure 9.11, step 8 Action potential is propagated alongthe sarcolemma and down the T tubules.Steps in E-C Coupling:TroponinTropomyosinblocking active sitesMyosinActinActive sites exposed and ready for myosin bindingCa2+Terminal cisterna of SRVoltage-sensitivetubule proteinT tubuleCa2+releasechannelMyosincross bridgeCa2+Sarcolemma Calcium ions are released. Calcium binds to troponin andremoves the blocking action oftropomyosin. Contraction beginsThe aftermath1234Role of Calcium (Ca2+) in ContractionAt low intracellular Ca2+ concentration:Tropomyosin blocks the active sites on actinMyosin heads cannot attach to actinMuscle fiber relaxesRole of Calcium (Ca2+) in ContractionAt higher intracellular Ca2+ concentrations:Ca2+ binds to troponin Troponin changes shape and moves tropomyosin away from active sitesEvents of the cross bridge cycle occur When nervous stimulation ceases, Ca2+ is pumped back into the SR and contraction endsCross Bridge CycleContinues as long as the Ca2+ signal and adequate ATP are presentCross bridge formation—high-energy myosin head attaches to thin filamentWorking (power) stroke—myosin head pivots and pulls thin filament toward M line Cross Bridge CycleCross bridge detachment—ATP attaches to myosin head and the cross bridge detaches“Cocking” of the myosin head—energy from hydrolysis of ATP cocks the myosin head into the high-energy stateFigure 9.121ActinCross bridge formation.Cocking of myosin head.The power (working) stroke.Cross bridge detachment.Ca2+Myosincross bridgeThick filamentThin filamentADPMyosinPiATPhydrolysisATPATP243ADPPiADPPiFigure 9.12, step 1ActinCross bridge formation.Ca2+Myosincross bridgeThick filamentThin filamentADPMyosinPi1Figure 9.12, step 3The power (working) stroke.ADPPi2Figure 9.12, step 4Cross bridge detachment.ATP3Figure 9.12, step 5Cocking of myosin head.ATPhydrolysisADPPi4Figure 9.121ActinCross bridge formation.Cocking of myosin head.The power (working) stroke.Cross bridge detachment.Ca2+Myosincross bridgeThick filamentThin filamentADPMyosinPiATPhydrolysisATPATP243ADPPiADPPi