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SampleOnly–TOPIC1_WithoutImages Whatisphysiology? Thestudyofnormalfunctioninalivingstate, Whatisexercisephysiology? Thestudyofacuteresponsesandchronicadaptationstoexercise. Someexercisephysiologistsstudytheaffectsofexerciseonpathology. Thiscanbeverydifferentinindividualsduetotrainingstatusandathlete types.(strengthvsendurance) MUSCLE MuscleàFascicleàFibre(cell)àMyofibrilàSarcomere ConnectiveTissueLayers Fascia–superficial(underskin),encapsulatesallbodytissues(eg.Muscleand bone) Epimysium–Surroundsindividualwholemuscles,itisthick. Perimysium–Surroundseachfascicle,containsbloodvessels,motoraxons andmusclespindles. Endomysium–surrounds1-2musclefibres,providesbasementmembrane (frameworkforregeneration) Sarcolemma=cell/fibremembrane(lipidbilayer) This image cannot currently be displayed. Aboveis1sarcomere.Thisshowsthecontractileelementofactinandmyosin thatcausemusclecontraction Thestep-wiseprocessofeacheventsequencethatleadstoskeletalmuscle contraction. 1.Neuromuscularcontraction 2.Excitation-contractioncoupling 3.Cross-bridgecycle Step1:NeuromuscularTransmission Themotorunitconsistsofasomaticmotoneuronandthemusclefibresit innervates.Thereisasynapsecausedbyaactionpotentialbetweenthe motoneuronandmusclefibreattheneuromuscularjunctionwhichoccursat themotor-end-plate.Theactionpotentialopensvoltagegatedcalcium channelswhichcausesthereleaseofacetylcholine(ACh).AChthendiffuses acrossandbindswithareceptoronthemusclecell.TheNicotiniccholinergic receptorsallowforaninflowofsodiumandoutflowofpotassiumwhich generatesacurrentacrossthemembranewithinthemotorendplate.When thiscurrentgetsbigenoughitwilldriftoutsidethemotorendplateandcause anactionpotentialwithinamusclecell. t This image cannot currently be displayed. Summary; Theactionpotentialwillthenrunalongthesurfaceofthecellmembraneand deepintothecellthroughTransversetubules(T-tubules)whicharelocated alongsidethezlinesofthesarcomere.TheTtubulesfunctiontorapidlyand evenlydistributeactionpotentials.Calciumionsarestoredinthesarcoplasmic reticulumofthemusclecellwhichisamembranenetworksurroundingeach myofibril.Thesehavetwodistinctregions.Firstlytheterminalcisternaewhich aresaclikestructuresneartheZ-line/I-bandwhichreleasescalciumintothe cytosolandformaTRIADwiththeT-tubules.Thesecondregionisthe LongitudinaltubuleswhicharelocatedneartheA-bandandareresponsible fortheuptakeofcalcium. TransverseTubules(T-tubules) • Invaginationsofthesarcolemmathatappearlikeperforatingholes • Penetratedeepintoeachmusclefibreallowingactionpotentialsto quicklyreacheachmyofibrilandthereforesarcomere. • Thereare2persarcomere,atA-Ijunctions. SarcoplasmicReticulum(Ca2Storage) • Membranenetworksurroundingeachmyofibril • Twodistinctregions o TerminalCisternae–saclikestructuresneartheZ-line/I-band thatreleaseCa2intocytosolandformsaTRIADwiththeTtubules. o Longitudinaltubules–locatedaroundtheA-bandregionand responsibleforuptakeofCa2fromcytosol. Step2:Exciting-ContractionCoupling Theprocessofactionpotentialtransductiontoprovideanintracellularsignal (increasedCa2)andsubsequentmusclecellcontraction ThisprocessfocusesmostcommonlyonthelinkbetweentheT-tubuleand sarcoplasmicreticulumcalciumrelease.Themechanismisnotentirely understoodbutmuchmoreisunderstoodaboutthefunctionandinteraction ofkeycomponentsincludingtheT-tubulevoltagesensor(Dihydropyridine receptor–DHP)andSRCa2channelreleasemechanism(Ryanodinereceptor). Wheneveraproteindetectssomethingitchangesitstructure,thereforewhen theDHPreceptorsdetectaactionpotentialtheywillchangetheirstructure whichwillthencausethecalciumgatedchannels(ryanodinereceptors)to open.Calciumisthenreleasedintothecell. This image cannot currently be displayed. This image cannot currently be displayed. Step2Complete–theintracellularmusclefibreenvironmentnowhasahigh calciumconcentrationwhichcantriggermyofilamentinteractionstoproduce forceandcellshortening. TheMyofilaments/ContractileProteins Thethickmyosinfilamentiscentrallylocatedwithinthesarcomereandmade upofaround300smallermyosinmolecules.Thesehaveaprotrudinghead segmentwhichcontainactinbindingsites.Thetailsegmenthasflexiblehinge regionsandallcombinetoformthemyofilament.(ImageBelowLeft). This image cannot currently be displayed. This image cannot currently be displayed. ThethinactinfilamentareconnectedtoZ-linesatoneendandapparentfree floatingendislocatedcentrally.Tropomyosinliesoverthemyosinbinding sitespreventingconstantcontraction.Thetroponincomplexregulatesthe abilityforthemuscletocontract.Partofthistroponincomplexhastheability tobindtocalcium.Whenthishappenstropomyosintwistsaroundtheactin filament,andexposesthemyosinbindingsites.(ImageAboveRight). Musclestensionorforceisproducedonlywhenmyosinreleasesenergy obtainedviaATPhydrolysis,andactinandmyosinexistinaboundstate.This processformsthebasisoftheslidingfilamenttheoryandismostcommonly describedbythecross-bridgecyclewhichdescribestheinteractionsbetween themyofilamentcontractileproteins,intracellularCa2ionsandATPhydrolysis. ForceProduction-FourMajorSteps • Rest:myosinisinanenergizedstatefollowingATPhydrolysis • Bound:Actinandmyosinbindatspecificsites • PowerStroke:energyreleaseand“cellshortening” • Detachment:ActinandmyosindetachfollowingATPbinding Step3–Thecrossbridgecycle 1. Atrestmyosinisenergized,ATPhasbeencleavedtoADP,P,andenergy, energyisstoredwithinthemyosinprotein. 2. Ca2bindstotroponin-C 3. Themyosinbindingsiteonactinbecomesexposed 4. Myosinbecomesboundtoactin 5. Piisreleasedfrommyosinuponbindingwithactin 6. Myosinreleasesenergythroughthepowerstroke 7. Actinisdraggedtowardstheinteriorofthesarcomere–thisappearance providesthebasisofslidingfilamenttheory 8. Sarcomerelengthincreases,translationtowholemuscleshorteningor CONTRACTION 9. ADPisreleasedfrommyosinduringthepowerstroke 10.AfterpowerstrokemyosinbindsanewmoleculeofATP 11.Actinandmyosindetach 12.ATPhydrolysisoccurstore-energisemyosin 13.Myosinheadreturnstotheresting“cranked”position 14.IfahighCa2ismaintainthecrossbridgecyclecontinues This image cannot currently be displayed. Summary 1.AttheneuromuscularjunctionanactionpotentialisreleasedviaAChwithin themotorendplate.Thiscausesandinflowofsodiumandanoutflowof potassiumgeneratingacurrent. 2.Whenthiscurrentisbigenoughtheactionpotentialwilltraveloutsidethe motorendplateanddownT-tubulesinthesarcoplasmicreticulum. 3.Voltagesensorsarethenactivatedandcalciumisreleasedintothemuscle cell. 4.Calciumbindstothetroponinofactinfilamentscausingtropomyosinto twistaroundtheactinfilamentandexposemyosinbindingsites. 5.Crossbridgecyclethenoccursasmyosinmoleculeheadsbindwiththe myosinbindingsiteontheactin,pullingactinfilamentstogetherand shorteningthesarcomere. 6.ActiveCa2removalthencausesmusclerelaxation. 7.Returntorestingstate.Thiscrossbridgecycleprocesswillcontinueifaction potentialscontinue.