MUSCULAR SYSTEM for B sc Nursing students

SYSTEM for B sc Nursing students

1. MUSCULARSYSTEM
Althoughbonesformtheframeworkofbody,theycannotmovebodypartsby
themselves.Motionresultsfromthealternatecontractionandrelaxationofmuscles,which
constitute40-50%ofthetotalbodyweightinadults.Musclesareclassifiedin3different
methodsbasedondifferentfactors.
1.Dependinguponstriations:-2types
a.Striatedmuscles-whichhavelargestriations.E.g.,skeletalmuscleandcardiacmuscle.
b.Non-striatedmuscles-whichdoesnothavestriations.E.g.,smoothmuscle.
2.Dependinguponcontrol:-2types
Voluntarymuscles-thatcanbecontrolledaccordingtoone’swill.E.g.,skeletalmuscle.
Involuntarymuscles-thatcannotbecontrolledaccordingtoone’swill.E.g.,cardiac
muscleandsmoothmuscle.
3.Dependinguponthelocation-3types
a.Skeletalmuscles-attachedtotheskeleton
b.Smoothmuscles-liningtheinternalorgans
c.Cardiacmuscles-seenintheheart.

3. TYPESOFSKELETALMUSCLES
REDMUSCLE(SloworTypeImuscles) WHITEMUSCLE(FastorTypeIImuscles)
1.Myoglobincontentishigh.Soitis
red
Myoglobincontentisless.Soitispale.
2.Sarcoplasmicreticulumisless
extensive.
Sracoplasmicreticulumismoreextensive.
3.Bloodvesselsaremoreextensive. Bloodvesselsarelessextensive.
4.Mitochondriaaremoreinnumber. Mitochondriaarelessinnumber
5.Responseisslowwithlonglatent
period.
Responseisrapidwithshortlatentperiod
6.Contractionislesspowerful. Contractionismorepowerful.
7.Involvedinprolongedandcontinued
activityasitundergoessustained
contraction.
Notinvolvedinprolongedandcontinued
activityasitrelaxesimmediately.
8.Fatigueoccursslowly Fatigueoccursquickly
9.Dependsuponcellularrespirationfor
ATPproduction.
DependsuponglycolysisforATPproduction.
PROPERTIESOFSKELETALMUSCLES
EXCITATION:Itisthecapacityofskeletalmusclestorespondtoastimulus.Normally
askeletalmusclecontractasaresultofstimulationbynerves.
CONDUCTION:Theactionpotentialgeneratedanypartofthemusclemembraneisnot
restrictedtothatsite.Insteaditispropagatedthroughoutthelengthofthemuscle
membrane.Thispropertyiscalledconduction.

4. CONTRACTION:Itmeansshorteningofthelengthofthemusclefibers.Thegap
betweenthetwoZlinesdecreases.Contractionisamechanicalpropertyofamuscle.
Contractionofmuscleleadstomovementsofpartsofthebodyandhelpsinworking.
Muscularcontractionisclassifiedintotwotypesbasedonchangeinthelengthof
musclefibersortensionofthemuscle:
Isotoniccontraction:Itisthetypeofmuscularcontractioninwhichthetension
remainsthesameandthelengthofthemusclefiberisaltered.Ex:Liftinga
load.
Isometriccontraction:Inwhichthelengthofthemusclefibersremainsthesame
andthetensionisincreased.Ex:Pullingawall.
REFRACTORYPERIOD:Itisdefinedastheperiodduringwhichasecondstimulus
cannotproduceafreshactionpotential.
ALLORNONELAW:Theminimumstrengthofastimulusrequiredtogeneratean
actionpotentialisknownasthresholdstimulus.Strengthofstimulusbelowthreshold
leveliscalledsubthresholdandaboveiscalledsuprathreshold.Amuscledoesn’t
respondtosub-thresholdstimulus,respondmaximallytothresholdandnottosupra
threshold.Soifitresponds,itismore.Otherwisenot.Thisiscalledallornonelaw.
STRUCTUREOFSKELETALMUSCLE
Eachskeletalmuscleisaseparateorgancomposedofhundredstothousandsofcellscalled
musclefiberswhicharelongandslenderinappearance.Afasciaisasheetorbroadbandoffibrous
connectivetissuethatsupportsandsurroundsthemusclesandotherorgansofthebody.Beneath
thefasciathemuscleiscoveredbyaconnectivetissuesheathcalledEpimysium,whichisthe
outermostlayercoveringthewholemuscle.Inthemuscle,themusclefibersarearrangedinvarious
groupsorbundleshaving10-100musclefiberscalledFascicles.Theconnectivetissuesheath

5. coveringeachfascicleiscalledPerimysium.Eachmusclefiberiscoveredbyaconnectivetissue
sheathcalledEndomysium.
STRUCTURE OF A
MUSCLEFIBER:-
The most
importantcomponentof
amuscleisthemuscle
fiber.Themultiplenucleiofamusclefiberarelocatedjustbeneaththesarcolemma,the
plasmamembraneofthemusclefiber.Thousandsoftinyinvaginationsofthesarcolemma,
calledTtubules(transversetubules)tunnelinfromthesurfacetowardsthecenterofeach
musclefiber.Ttubulesareopentotheoutsideofthefiberandthusarefilledwithinterstitial
fluid.MuscleactionpotentialsarepropagatedthroughthesarcolemmaandTtubulesquickly
spreadingthroughoutthemusclefiber.
Withinthesarcolemmaisthesarcoplasm,thecytoplasmofthemusclefiber.It
containssubstantialamountofglycogen,whichissplitintoglucosethatisusedforthe
productionofATP.Inaddition,itcontainsaredcoloredpigment,themyoglobinthatbinds
withoxygenandreleasesitintothemusclewhenmitochondrianeeditforATPproduction.
Eachmusclefibercontainslargenumberofrod-likestructurescalledmyofibrilswhich
arethecontractileunitsoftheskeletalmuscle.Theyrunparallelandextendtheentirelength
ofthemusclefiber.Theirprominentstriationsmakeanentiremusclefiberlookstriated.A

6. fluidfilledsystemofmembranoussacscalledtheSarcoplasmicreticulumencirclesthe
myofibril.Thiselaboratesystemissimilartosmoothendoplasmicreticuluminnon-muscle
cells.Inrelaxedmusclefiber,thesarcoplasmicreticulumstorescalciumions.Releaseof
calciumionsfromthesarcoplasmicreticulumtriggersmusclecontraction.
FILAMENTSANDSARCOMERE
Eachmyofibrilsconsistsofanumberoftwoalternatingbandswhicharealsocalledthe
sections.ThetwobandsareIband(Thinfilament)andAband(Thickfilament).The
filamentsinsideamyofibrildonotextendtheentirelengthofmusclefiber,insteadtheyare
arrangedincompartmentscalledsarcomereswhicharethebasicfunctionalunitofmyofibril.
Striations,arepeatingseriesofdarkandlightbandsareevidentalongthelengthofeach
myofibril.ThedarkbandsarecalledAbands(myosin)andthelightbandsarecalledlight
bandIband(actin).Ibandisdividedintotwoportionsbymeansofanarrowanddarkline
calledZlineorZdisk.TheportionofmyofibrilinbetweentwoZlinesiscalledsarcomere.
InthemiddleoftheAbandthereisalightareacalledHzone.InthemiddleofHzoneliesthe
middlepartofmyosinfilament.ThisiscalledMline.Mlineisformedbymyosinbinding
proteins.
Theelectronmicroscopicstudiesreveals,thatthesarcomereconsistsofmanythreadlike
structurescalledthemyofibrils.Myofibrilsareof2types.Actinfilamentsandmyosinfilaments.

7. A.ACTINFILAMENT:Thesearethethinfilamentswithadiameterof20Åandalengthof1μ.These
filamentsextendsfromeithersideoftheZlines.
B.MYOSINFILAMENT:Thesearethickfilamentswithadiameterof115Åandalengthof
1.5μ.ThesefilamentsaresituatedinAband.Therearesomelateralprocessesorcross
bridgesarisingfrommyosinfilaments.Thesebridgeshaveenlargedstructurescalledmyosin
heads.Themyosinheadsattachthemselvesactinfilaments.Theseheadspullstheactin
filamentsduringcontractionofthemusclebymeansofamechanismcalledsliding
mechanism.
CONTRACTILEELEMENTSOFMUSCLE:Themyosinfilamentsareformedbymyosin
molecules.Theactinfilamentsareformedbythreetypesofproteinscalledactin,
tropomyosinandtroponin.Thesefourproteinstogetherconstitutethemuscleproteinsorthe
contractileelementsofthemuscle.
MYOSINMOLECULE
Eachmyosinfilamentsconsistsofabout200myosinmolecules.Eachmyosin
moleculeismadeupof6polypeptidechainsofwhich2areheavychainsand4arelightchains.
The2heavychainstwistaroundeachothertoformadoublehelix.Thispartoftheheavy
chainsformsthetailportionofthemyosinmolecule.Attheotherend,boththechainsturn
awayinoppositedirectionsandformtheglobularheadportion.Toeachpartofthishead.
areattached2lightchains.Thus,thereare4lightchainsineachmyosinmolecule.Each
myosinheadhas2attachmentsites.Onesiteisforactinfilamentandotheroneisforone
ATPmolecule.Inthecentralpartofthemyosinfilament,i.e.intheHzone,themyosinhead
isabsent.
ACTINMOLECULE
Actinmoleculesarethemajorconstituentsofthethinactinfilaments.Eachactin
moleculeiscalledFactinanditisthepolymerofasmallproteinknownasGactin.Thereare
about300-400actinmoleculesineachactinfilament.Theactinmoleculesintheactin
filamentalsoarearrangedintheformofadoublehelix.EachFactinmoleculehasanactive
sitetowhichthemyosinheadiosattached.

8. TROPOMYOSIN
Thereareabout40-60tropomyosinmoleculessituatedalongthedoublehelixstrabdof
actinfilament.Inrelaxedconditionofthemuscle,thetropomyosinmoleculescoverallt\he
activesitesofFactinmolecule.
TROPONIN
Itisformedby3subunits:
TroponinI–AttachedtoFactin
TroponinT–Attachedtotropomyosin
TroponinC–Attachedtocalciumions.
Inadditiontothecontractileproteins,thesarcomerecontainssomemore
proteinssuchas:actinin,desmin,nebulin,titinanddystrophin.
SARCOTUBULARSYSTEM
Sarcotubularsystemisasystemofmembranousstructuresintheformofvesiclesand
tubulesinthesarcoplasmofthemusclefiber.Itsurroundsthemyofibrilsembeddedinthe
sarcoplasm.Thesarcotubularisformedmainlybytwotypesofstructures:TtubulesandL
tubulesorsarcoplasmicreticulum.
TTUBULES:Thesecarenarrowtubulesformedbytheinvaginationofthesracolemma.
Thesetubulespenetrateallthewayfromonesideofthemusclefibertootherside.
Thatis,thesetubulespenetratethemusclecellthroughandthrough.Becauseoftheir
originfromsarcolemma,theTtubulesopentotheexteriorofthemusclecell.
Therefore,theECFrunsthroughtheirlumen.
TheTtubulesareresponsibleforrapidtransmissionofimpulseintheformofactionpotential
fromsarcolemmatothemyofibrils.Whenthemuscleisstimulated,theactionpotential
developsinsarcolemmaandspreadsthroughit.SincetheTtubulesarethecontinuationof

9. thesarcolemma,theactionpotentialpassesthroughthemandreachestheinteriorofthe
musclefiberrapidly.
LTUBULES:Thesearetheclosedtubulesthatruninlongaxisofthemusclefiber
formingsarcoplasmicreticulum.Thesetubulesfromaclosedtubularsystemaround
eachmyofibrilanddonotexteriorlikeTtubules.TheLtubulescorrespondtothe
endoplasmicreticulumofothercells.Atregularintervals,throughoutthelengthofthe
myofibrils,theLtubulesdilatetoformapairoflateralsacscalledterminalcisternae.
EachpairofterminalisinclosecontactwithTtubule.TheTtubulealongwiththe
cisternaeoneithersideiscalledthetriadofskeletalmuscle.Inhumanskeletalmuscle,
thetriadaresituatedatthejunctionbetweenAbandandIband.Calciumionsare
storedinLtubuleandtheamountofcalciumionsismoreincisternae.
TheLtubulesstorealargequantityofcalciumions.Whentheactionpotential
reachesthecisternaeofLtubule,thecalciumionsarereleasedintothesarcoplasm.
Thecalciumionstriggertheprocessesinvolvedincontractionofthemuscle.The
processbywhichthecalciumionscausecontractionofmuscleiscalledexcitation
contraction
coupling.
MECHANISMOFMUSCLECONTRACTION
Themusclecontractswhenitisstimulated.Itincludesthreestages:

10. Excitation-contractioncoupling
Roleoftroponinandtropomyosin
Slidingmechanism
EXCITATION-CONTRACTIONCOUPLING:Itisaprocessthatoccursinbetweentheexcitation
andcontractionofthemuscle.Thisprocessinvolvesseriesofactivitieswhichareresponsible
forthecontractionoftheexcitedmuscle.Whentheimpulsepassesthroughamotorneuron
andreachestheneuromuscularjunction,Achisreleasedfromthemotorend-plate.Ach
causestheopeningofligandgatedchannels.So,sodiumionsentertheneuromuscular
junction.Itleadstothedevelopmentofend-platepotential.End-platepotentialcausesthe
generationofactionpotentialinthemusclefiber.Theactionpotentialspreadsover
sarcolemmaandalsointothemusclefiberthroughtheT-tubules.TheT-tubulesare
responsiblefortherapidtransmissionoftheactionpotentialintothemusclefiber.Whenthe
actionpotentialreachesthecisternaeofL-tubules,thesecisternaeareexcited.Now,the
calciumionsstoredinthecisternaearereleasedintothesarcoplasm.Thecalciumionsfrom
thesarcoplasmmovetowardstheactinfilamentstoproducethecontraction.
Thus,theCaionsformlinkorcouplingmaterialbetweentheexcitationandthecontractionof
muscle.Hence,theCaionsaresaidtoformthebasisofexcitation-contractioncoupling.
ROLEOFTROPONINANDTROPOMYOSIN:Normallytheheadofmyosinmoleculeshavea
strongtendencytogetattachedwiththeactivesiteofFactin.However,inrelaxedcondition,.
TheactivesiteofFactiniscoveredbythetropomyosin.Therefore,themyosinheadcannot
combinewithactinmolecule.LargenumberofCaionswhicharereleasedfromLtubules
duringtheexcitationofthemuscle,bindwithtroponinC.TheloadingoftroponinCwithCa
ionsproducessomechangeinthepositionoftroponinmolecule.Itinturn,pullstropomyosin
moleculeawayfromFactin.DuetothemovementoftropomyosintheactivesiteofFactinis
uncoveredandimmediatelytheheadofmyosingetsattachedtotheactin.
SLIDINGMECHANISM:Thistheoryexplainshowtheactinfilamentsslideovermyosin
filamentsandformtheactomyosincomplexduringmuscularcontraction.Itisalsocalled
Ratchettheoryorwalkalongtheory.Eachcross-bridgefromthemyosinfilamentshasgot

11. threecomponentsnamelyHinge,armandhead.AfterbindingwiththeactivesiteofFactin,the
myosinheadistiltedtowardthearmsothattheactinfilamentisdraggedalongwithit.This
tiltingofheadiscalledpowerstroke.Aftertilting,theheadimmediatelybreaksawayfromthe
activesiteandreturnstotheoriginalposition.Now,itcombineswithanewactivesiteonthe
actinmolecule.And,tiltingmovementoccursagain.Thus,theheadofthecross-bridgebend
backandforthandpull;seactinfilamentstowardsthecenterofthesarcomere.Inthisway,all
theactinfilamentsofboththeendsofthesarcomerearepulled.So,theactinfilamentsof
oppositesidesoverlapandformactomyosincomplex.Formationofactomyosincomplex
resultsincontractionofthemuscle.
Duringthecontractionofthemuscle,thefollowingchangesoccurinthesarcomere:
ThelengthofallthesarcomeresdecreasesastheZlinescomesclosetoeachother.
ThelengthoftheIbanddecreasessincetheactinfilamentsfromoppositesideoverlap
TheHzoneeitherdecreasesordisappears
ThelengthofAbandremainsthesame.
ENERGYFORMUSCLECONTRACTION:Theenergyformovementofmyosinheadisobtained
bybreakdownofATPintoADPandpi.TheheadofmyosinhasasiteforATP.When
tropomyosinmovestoexposetheactivesites,theheadisattachedtotheactivesite.Now
ATPasecleavesATPintoADPandpi,whichremainsintheheaditself.Theenergyreleased
duringthisprocessisutilizedforcontraction.Whentheheadistilted,theADPandPiare
releasedandanewATPmoleculebindswithhead.Thisprocessisrepeateduntilthemuscular
contractioniscompleted.
RELAXATIONOFTHEMUSCLE:Therelaxationofthemuscleoccurswhenthecalciumions
arepumpedbackintotheLtubules.WhencalciumionsentertheLtubules,calciumcontentin
thesarcoplasmdecreasesleadingtothereleaseofcalciumionsfromthetroponin.Itcauses
detachmentofthemyosinfromactinfollowedbytherelaxationofthemuscle.The
detachmentofmyosinfromactinobtainsenergyfromthebreakdownofATP.
NEUROMUSCULARJUNCTION

12. Neuromuscularjunctionisthejunctionbetweentheterminalbranchofthenervefiberand
musclefiber.Skeletalmusclefibersareinnervatedbythemotornervefibers.Eachnerve
fiberdividesintomanyterminalbranches.Eachterminalbranchinnervatesonemusclefiber
throughtheneuromuscularjunction.
Axonterminalandmotorendplate:Terminalbranchofnervefiberiscalledaxonterminal.
Whentheaxoncomesclosetothemusclefiber,itlosesthemyelinsheath.Sotheaxis
cylinderisexposed.Thisportionoftheaxiscylinderisexpandedlikeabulbwhichiscalled
motorendplate.
Synaptictroughorgutter:Themotorendplateinvaginatesinsidethemusclefiberandformsa
depressionwhichisknownassynaptictroughorgutter.Themembraneofthemusclefiber
belowthemotorendplateisthickened.
Synapticcleft:Themembraneofthenerveendingiscalledpre-synapticnerve.The
membraneofthemusclefiberiscalledpostsynapticmembrane.Thespacebetweenthese
twoiscalledsynapticcleft.Theaxonterminalcontainsmitochondriaandsynapticvesicles.
Thesynapticvesiclescontaintheneuromuscularsubstance,acetylcholine.TheAchis
synthesizedbymitochondriapresentintheaxonterminalandstoredinthevesicles.The
mitochondriacontainATPwhichisthesourceofenergyforthesynthesisofAch.
Subneuralclefts:Thepostsynapticmembraneisthemembraneofthemusclefiber.Itis
thrownintonumerousfoldscalledsubneuralclefts.Thepostsynapticmembranecontains
thereceptorscallednicotinicacetylcholinereceptors.

13. NEUROMUSCULARTRANSMISSION
Itisdefinedasthetransferofinformationfrommotornerveendingtothemusclefiber
throughtheneuromuscularjunction.Itisthemechanismbywhichthemotornerveimpulses
initiatemusclecontraction.Aseriesofeventstakeplaceintheneuromuscularjunction
duringthisprocess.
1.ReleaseofAch
2.ActionofAch
3.Developmentofendplatepotential
4.Developmentofminiatureendplatepotential
5.DestructionofAch.
RELEASEOFACETYLCHOLINE:Whentheactionpotentialreachestheaxonterminal,it
increasesthepermeabilityofpre-synapticmembraneforcalciumionsbyopeningthe
voltagegatedcalciumchannelsinthemembraneoftheaxonterminal.Calciumions
entertheaxonterminalfromextracellularfluid.Thecalciumionscauseburstingof
thevesicles.Actuallythecalciumionsmakethesynapticvesiclesmoveandfusewith

14. pre-synapticmembrane.Now,Achisreleasedfromthevesicles.Thisprocessis
calledexocytosis.TheAchdiffusesacrossthepre-synapticmembraneandentersthe
synapticcleft.
ACTIONOFACETYLCHOLINE:Afterenteringthesynapticcleft,theAchmolecules
bindwithnicotinicreceptorspresentinthepostsynapticmembraneandformtheAch-
receptorcomplex.Itopenstheligandgatedchannelsforsodiuminthepostsynaptic
membrane.Now,thesodiumionsfromtheextracellularfluidentertheneuromuscular
junctionthroughthischannel.Andthere,thesodiumionsproduceanelectrical
potentialcalledtheendplatepotential.
ENDPLATEPOTENTIAL:Endplatepotentialisthechangeintherestingmembrane
potentialwhenimpulsereachestheneuromuscularjunction.Therestingmembrane
potentialattheneuromuscularjunctionis-90mV.Whensodiumionsenterinside,
slightdepolarizationoccursupto-60mVwhichiscalledendplatepotential.Itcauses
thedevelopmentofactionpotentialinthemusclefiber.
MINIATUREENDPLATEPOTENTIAL:Miniatureendplatepotentialisaweakendplate
potentialinneuromuscularjunctionthatisdevelopedbythereleaseofasmallquantity
ofAchfromaxonterminal.And,eachquantumofthisneurotransmitterproducesa
weakendplatepotential.Theamplitudeofthispotentialisonlyupto0.5mV.
Miniatureendplatepotentialcannotproduceactionpotentialinthemuscle.When
moreandmorequantaofAcharereleasedcontinuously,theminiatureendplate
potentialareaddedtogetherandfinallyproduceendplatepotentialresultinginaction
potentialinthemuscle.
FATEOFACETYLCHOLINE:Achreleasedintosynapticcleftisdestroyedveryquickly.
Withinonemillisecondafterthereleaseintothesynapticcleft,itisdestroyedbythe
enzymeAchesterase.However,theAchissopotent,thateventhisshortdurationof
onemillisecondissufficienttoexcitethemusclefiber.TherapiddestructionofAch
hasgotsomeimportantfunctionalsignificance.Itpreventstherepeatedexcitationof
themusclefiberandallowsthemuscletorelax.

15. REUPTAKEPROCESS
Reuptakeisaprocessinneuromuscularjunction,bywhichadegradedproductof
neurotransmitterre-entersthepre-synapticaxonterminalwhereitisreused.Achesterase
splitsAchintoinactivecholineandacetate.Cholineistakenbackintotheaxonterminal
fromsynapticcleftbyreuptakeprocess.Thereitisreusedinsynapticvesicletoformnew
Achmolecule.
MYASTHENIAGRAVIS:Itisanautoimmunediseaseofneuromuscularjunctioncausedby
antibodiestocholinergicreceptors.Itischaracterizedbygraveweaknessofthemuscledue
totheinabilityofneuromuscularjunctiontotransmitimpulsesfromnervetothemuscle.
Causes:Itisduetothedevelopmentofauto-antibodies(IgGauto-antibodies)againstthe
receptorsofAch.Thatis,thebodydevelopsantibodiesagainstitsownAchreceptors.
TheseantibodiesdestroytheAchreceptors.So,thoughtheAchreleaseisnormal,itcannot
actbecauseofthedestructionofthereceptors.
Symptoms:
Slowandweakmuscularcontractionbecauseofthedefectiveneuromuscular
activity.
Inabilitytomaintaintheprolongedcontractionofskeletalmuscle.
Quickfatigabilitywhenthepatientattemptsrepeatedmuscularcontraction.
Weaknessandfatigabilityofarmsandlegs.
Doublevisionanddroopyeyelidsduetotheweaknessofocularmuscles.
Difficultyinswallowingduetotheweaknessofthroatmuscle.
Difficultyinspeechduetoweaknessofmusclesofspeech.
Insevereconditions,thereisparalysisofmuscles.Thepatientdiesmostlyduetothe
paralysisofrespiratorymuscles.

16. MUSCLARDYSTROPHY
Musculardystrophyisadiseasecharacterizedbyprogressivedegenerationofmuscle
fiberswithouttheinvolvementofnervoussystem.Mostlyithasahereditaryorigin.The
musclesfailtoregenerateresultinginprogressiveweaknessandconfinementtoawheelchair.
CommontypesofmusculardystrophyareDuchennemusculardystrophyandBecker’s
musculardystrophy.
DUCHENNEMUSCULARDYSTROPHY:Itisasexlinkedrecessivedisorder.Itisdueto
theabsenceofageneproductcalleddystrophinintheXchromosome.Dystrophinis
necessaryforthestabilityofsarcolemma.Thisdiseaseischaracterizedbydegenerationand
necrosisofmusclefibers.Thedegeneratedmusclefibersarereplacedbyfatandfibrous
tissue.Thecommonsymptomisthemuscularweakness.Sometimes,thereisenlargement
ofmuscles.Insevereconditions,respiratorymusclesbecomeweakresultinginbreathing
anddeath.
BECKER’SMUSCULARDYSTROPHY:Itisalsoasexlinkeddisorder.Itoccursdueto
thereductioninquantityoralterationofdystrophin.Thecommonfeaturesofthisdisorder
areslowprogressiveweaknessoflegsandpelvis,pseudo-hypertrophyofcalfmuscles,
difficultyinwalking,fatigueandmentalretardation.
RIGORMORTIS
Rigormortisreferstoafterdeathconditionofthebodywhichischaracterizedby
stiffnessofmusclesandjoints.Itoccursduetostoppageofaerobicrespirationwhich
causeschangesinthemuscles.Soonafterdeath,thecellmembranebecomeshighly
permeabletocalcium.Soalargenumbercalciumionsentersthemusclefibersand
promotestheformationofactomyosincomplexresultingincontractionofthemuscles.Few
hoursafterdeath,allthemusclesofthebodyundergoseverecontractionandbecomerigid.
Thejointsalsobecomestiffandlocked.Normallyforrelaxation,themuscleneedstodrive
outthecalciumwhichrequiresATP.Butduringcontinuesmuscularcontractionandother
cellularprocessesafterdeath,theATPmoleculesarecompletelyexhausted.NewATP

17. moleculescannotbeproducedbecauseoflackofoxygen.SointheabsenceofATP,the
musclesremainincontractedsateuntiltheonsetofcomposition.
MedicolegalimportanceofRigormortis:Rigormortisisusefulindeterminingthetimeof
death.Onsetofstiffnessstartsbetween10minutesand3hourafterdeathdependingupon
conditionofthebodyandenvironmentaltemperatureandthetimeofdeath.Ifthebodyis
activeortheenvironmentaltemperatureishighatthetimeofdeath,thestiffnesssetsin
quickly.
Thestiffnessdevelopsfirstinfacialmusclesandthenspreadstoothermuscles.Themaxim
stiffnessoccursaround12-24hoursafterdeath.Thestiffnessofmusclesandjoints
continuousfor1-3days.Afterwardsthedecompositionofgeneraltissuesstarts.Nowthe
lysosomalintracellularhydrolyticenzymesarereleased.Theseenzymeshydrolyzethe
muscleproteins,actinandmyosinresultinginthebreakdownofactomyosincomplex.It
relievesthestiffnessofthemuscles.Thisprocessiscalledresolutionofrigor.