physiology of muscle
DESCRIPTION
Physiology of Muscle. Humaryanto. TIPE OTOT. Otot Skeletal (lurik/striata) Otot Jantung (lurik/striata) Otot Polos (polos) (GI, VU, Vascular). Extrafusal Muscle Fibers. Striate muscle Force for limb movements flexion - closes joint extension - opens joint Contract or relax ~. - PowerPoint PPT PresentationTRANSCRIPT
Physiology of MusclePhysiology of Muscle
HumaryantoHumaryanto
TIPE OTOTTIPE OTOT
Otot SkeletalOtot Skeletal (lurik/striata)(lurik/striata)
Otot JantungOtot Jantung (lurik/striata)(lurik/striata)
Otot Polos (polos)Otot Polos (polos)
(GI, VU, Vascular)(GI, VU, Vascular)
Extrafusal Muscle FibersExtrafusal Muscle Fibers
Striate muscleStriate muscle
Force for limb Force for limb movements movements – flexion - closes jointflexion - closes joint– extension - opens jointextension - opens joint
Contract or relax ~Contract or relax ~
OTOT SKELETALOTOT SKELETAL
40%40% BB tubuh BB tubuh
FungsiFungsi : mengatur posisi : mengatur posisi dan gerak rangkadan gerak rangka
Melekat ke tulang melalui Melekat ke tulang melalui tendotendo
OrigoOrigo : perlekatan pada : perlekatan pada bag. proksimal, bersifat bag. proksimal, bersifat stasionerstasioner
InsersioInsersio : perlekatan pada : perlekatan pada bag. distal, bersifat mobilbag. distal, bersifat mobil
TIPE OTOT SKELETALTIPE OTOT SKELETAL
Berdasarkan kecepatan kontraksi dan daya Berdasarkan kecepatan kontraksi dan daya tahan terhadap fatigue.tahan terhadap fatigue.
Fast-twitch glycolitic fibers (putih)Fast-twitch glycolitic fibers (putih)Fast-twitch oxidative fibers (merah)Fast-twitch oxidative fibers (merah)Slow twitch oxidative fibers (merah)Slow twitch oxidative fibers (merah)
Setiap orang punya 3 tipe otot, tapi berbeda Setiap orang punya 3 tipe otot, tapi berbeda pada komposisi dominanpada komposisi dominan
(Jauhari Johan vs John Murray/ Ben Johnson)(Jauhari Johan vs John Murray/ Ben Johnson)
Type 1 FibersType 1 FibersSlow fibersSlow fibers
dark reddark red
– slow, sustained contraction slow, sustained contraction – slow to fatigue slow to fatigue
Aerobic metabolism Aerobic metabolism – many capillaries & mitochondriamany capillaries & mitochondria– oxygen required for ATP synthesis oxygen required for ATP synthesis – myoglobin myoglobin
gives dark red appearance ~gives dark red appearance ~
Type 2b FibersType 2b FibersFast fatigable fibersFast fatigable fibers
white fiberswhite fibers
– rapid, brief contraction rapid, brief contraction – fast to fatiguefast to fatigue– produce about 10x force of Type 1 produce about 10x force of Type 1
Anaerobic metabolism Anaerobic metabolism – fewer capillaries & mitochondriafewer capillaries & mitochondria– ATP generated by glycolysisATP generated by glycolysis– lactic acid buildup ~lactic acid buildup ~
Type 2a FibersType 2a Fibers
Fast fatigue-resistant fibersFast fatigue-resistant fiberspale redpale red
– properties intermediate to types 1 & 2bproperties intermediate to types 1 & 2b– rapid, brief contraction rapid, brief contraction – slow to fatigueslow to fatigue– produce least force produce least force
Aerobic & Anaerobic metabolism Aerobic & Anaerobic metabolism – many capillaries & mitochondria ~many capillaries & mitochondria ~
Neuromuscular JunctionNeuromuscular Junction
Synapse between neuron & effectorSynapse between neuron & effector
Cholinergic (ACh)Cholinergic (ACh)– nicotinic receptorsnicotinic receptors
Motor end-plateMotor end-plate– postsynaptic membranepostsynaptic membrane– folds packed with receptorsfolds packed with receptors
increased surface area ~increased surface area ~
Global view of a Global view of a neuromuscular neuromuscular junction:junction:1. 1. Axon2. Motor end-plate2. Motor end-plate3. 3. Muscle fiber4. 4. Myofibril
Detailed view of a Detailed view of a neuromuscular junction:neuromuscular junction:1. 1. Presynaptic terminal terminal2. 2. Sarcolemma3. Synaptic vesicle3. Synaptic vesicle4. Nicotinic acetylcholine 4. Nicotinic acetylcholine receptorreceptor5. Mitochondrion 5. Mitochondrion
Mechanism of action Mechanism of action
Upon the arrival of an action potential at the axon Upon the arrival of an action potential at the axon terminal, voltage-dependent calcium channels open and terminal, voltage-dependent calcium channels open and Ca2+ ions flow from the extracellular fluid into the motor Ca2+ ions flow from the extracellular fluid into the motor neuron's cytosol. This influx of Ca2+ triggers neuron's cytosol. This influx of Ca2+ triggers excitation-excitation-contraction couplingcontraction coupling, a biochemical cascade that , a biochemical cascade that causes neurotransmitter-containing vesicles to fuse to causes neurotransmitter-containing vesicles to fuse to the motor neuron's cell membrane and release the motor neuron's cell membrane and release acetylcholine into the synaptic cleft.acetylcholine into the synaptic cleft.Acetylcholine diffuses across the synaptic cleft and binds Acetylcholine diffuses across the synaptic cleft and binds to the nicotinic acetylcholine receptors that dot the motor to the nicotinic acetylcholine receptors that dot the motor end plate.end plate.The receptors are ligand-gated ion channels, and when The receptors are ligand-gated ion channels, and when bound by acetylcholine, they open, allowing sodium and bound by acetylcholine, they open, allowing sodium and potassium ions to flow in and out of the muscle's cytosol, potassium ions to flow in and out of the muscle's cytosol, respectively.respectively.
Mechanism of action Mechanism of action
Because of the differences in electrochemical gradients Because of the differences in electrochemical gradients across the plasma membrane, more sodium moves in across the plasma membrane, more sodium moves in than potassium out, producing a local depolarization of than potassium out, producing a local depolarization of the motor end plate known as an end-plate potential the motor end plate known as an end-plate potential (EPP).(EPP).This depolarization spreads across the surface of the This depolarization spreads across the surface of the muscle fiber into transverse tubules, eliciting the release muscle fiber into transverse tubules, eliciting the release of calcium from the sarcoplasmic reticulum, thus of calcium from the sarcoplasmic reticulum, thus initiating muscle contraction.initiating muscle contraction.The action of acetylcholine is terminated when the The action of acetylcholine is terminated when the enzyme acetylcholinesterase degrades the enzyme acetylcholinesterase degrades the neurotransmitter and the unhydrolysed neurotransmitter neurotransmitter and the unhydrolysed neurotransmitter diffuses awaydiffuses away
Neurotransmitters and Neurotransmitters and NeuromodulatorsNeuromodulators
Neuromodulators modify the postsynaptic cell's response to Neuromodulators modify the postsynaptic cell's response to neurotransmitters or change the presynaptic cell's synthesis, release or neurotransmitters or change the presynaptic cell's synthesis, release or metabolism of the neurotransmitter. metabolism of the neurotransmitter.
Acetylcholine (Ach)Acetylcholine (Ach)Major neurotransmitter. Fibers that release ACh are called cholinergic Major neurotransmitter. Fibers that release ACh are called cholinergic fibers. Acetylcholine is degraded by the enzyme, acetylcholinesterase. fibers. Acetylcholine is degraded by the enzyme, acetylcholinesterase.
Biogenic Amines Biogenic Amines Biogenic amines are neurotransmitters containing an amino group. Biogenic amines are neurotransmitters containing an amino group. Catecholamines such as dopamine, norepinephrine and epinephrine, Catecholamines such as dopamine, norepinephrine and epinephrine, serotonin. Nerve fibers that release epinephrine and norepinephrine are serotonin. Nerve fibers that release epinephrine and norepinephrine are called adrenergic and noradrenergic fibers respectively. called adrenergic and noradrenergic fibers respectively.
Neurotransmitters and Neurotransmitters and NeuromodulatorsNeuromodulators
Amino Acid Neurotransmitters Amino Acid Neurotransmitters Amino acid neurotransmitters are the most prevalent Amino acid neurotransmitters are the most prevalent neurotransmitters in CNS. Glutamate, aspartate GABA (gamma neurotransmitters in CNS. Glutamate, aspartate GABA (gamma aminobutyric acid), glycine, aminobutyric acid), glycine,
Neuropeptides Neuropeptides Neuropeptides are composed of two or more amino acids. Neurons Neuropeptides are composed of two or more amino acids. Neurons releasing neuropeptides are called releasing neuropeptides are called peptidergicpeptidergic. Beta-endorphin, . Beta-endorphin, dynorphin, enkephalins. dynorphin, enkephalins. Nitric oxide, ATP, adenine also act as neurotransmitters. Nitric oxide, ATP, adenine also act as neurotransmitters.
Neuroeffector Communication Neuroeffector Communication Many neurons of peripheral nervous system end at neuroeffector Many neurons of peripheral nervous system end at neuroeffector junctions on muscle and gland cells. Neurotransmitters released by junctions on muscle and gland cells. Neurotransmitters released by these efferent neurons then activate the target cell. these efferent neurons then activate the target cell.
Muscle ContractionMuscle Contraction
AP generated in muscle fiber (cell)AP generated in muscle fiber (cell)
Ca++ released from internal stores Ca++ released from internal stores
Muscle fiber contractsMuscle fiber contracts– continues while Ca++ & ATP availablecontinues while Ca++ & ATP available
RelaxationRelaxation– Ca++ sequestered by active transport ~Ca++ sequestered by active transport ~
Muscle Fiber StructureMuscle Fiber Structure
MultinucleatedMultinucleated– fusion of multiple precursor cellsfusion of multiple precursor cells
Sarcolemma Excitable membrane Sarcolemma Excitable membrane
Myofibrils: contractile unitsMyofibrils: contractile units
Sarcopasmic reticulum (SR)Sarcopasmic reticulum (SR)– sequesters Ca++ sequesters Ca++
T tubulesT tubules– AP from sarcolemma to SR AP from sarcolemma to SR – like inside-out axons ~like inside-out axons ~
Miofibril Miofibril struktur kontraksi otot struktur kontraksi otot
1 Serat otot, tdd: ribuan miofibril1 Serat otot, tdd: ribuan miofibril1 miofibril tdd: 1 miofibril tdd: Aktin & miosinAktin & miosin (protein kontraksi) (protein kontraksi)Troponin & tropomiosinTroponin & tropomiosin (protein pengatur) (protein pengatur)Titin & nebulinTitin & nebulin (protein asessoris besar) (protein asessoris besar)MiosinMiosin thick filament, punya kepala thick filament, punya kepala
Motor protein, E kimia Motor protein, E kimia E mekanik, mgd ATP-ase E mekanik, mgd ATP-ase (hidrolisis)(hidrolisis)
AktinAktin thin filament, melekat troponin & tropomiosin thin filament, melekat troponin & tropomiosinTitinTitin molekul elastis (protein terbesar) molekul elastis (protein terbesar)
stabilitas & elastisistas ototstabilitas & elastisistas ototNebulinNebulin penyanggah aktin penyanggah aktin
SarcolemmaMyofibrils
Sarcoplasmic Reticulum
T tubules
Myofibril: structure & Myofibril: structure & functionfunction
SarcomeresSarcomeres– repeating sectionsrepeating sectionsZ linesZ lines
dividers between sarcomeresdividers between sarcomeres
thin filaments anchored to Z linesthin filaments anchored to Z lines– actin & troponinactin & troponinThick filaments between thin filamentsThick filaments between thin filaments– myosinmyosinContraction:filaments slide by each Contraction:filaments slide by each other ~other ~
Sarcomere
Z line Z lineThin filaments
ThickFilaments
KONTRAKSI OTOTKONTRAKSI OTOTMenghasilkan force / gaya Menghasilkan force / gaya muscle tension muscle tensionMelawan beban/ loadMelawan beban/ loadMemerlukan energi (dari ATP)Memerlukan energi (dari ATP)
Pencetus kontraksi ototPencetus kontraksi otot1. Neuromuscular junction : 1. Neuromuscular junction :
Rangsang somatik Rangsang somatik rangsang listrik rangsang listrik2. Excitation-contraction coupling2. Excitation-contraction coupling
Potensial aksi Potensial aksi signal Ca++ signal Ca++ siklus kontr-relaks siklus kontr-relaks
SIKLUS KONTRAKSI DAN RELAKSASI SIKLUS KONTRAKSI DAN RELAKSASI Sliding filaments theorySliding filaments theory
ContractionContractionExcitation-contraction couplingExcitation-contraction coupling
Myosin “heads” crossbridges w/ actinMyosin “heads” crossbridges w/ actin– Ca++ dependentCa++ dependent– binds to troponin, reveals binding sitebinds to troponin, reveals binding site
Myosin head rotatesMyosin head rotates– ““ratchets” actin inward ~ratchets” actin inward ~
ContractionContractionATP binds to myosin ---> detachmentATP binds to myosin ---> detachment– cocks myosin ---> binds againcocks myosin ---> binds again– rigor mortis: no ATPrigor mortis: no ATP
fibers remain crosslinkedfibers remain crosslinked
Repeats as long as Ca++ presentRepeats as long as Ca++ present– sequestered via active transport ~sequestered via active transport ~
SLIDING FILAMENT THEORYSLIDING FILAMENT THEORY
Serat Serat otot memendekotot memendek (overlapping thick & thin filament) (overlapping thick & thin filament)Sliding aktin terhadap miosinSliding aktin terhadap miosinGaya dari crossbridge miosin mendorong aktin Gaya dari crossbridge miosin mendorong aktin ((power strokepower stroke))Crossbridge miosin mendorong aktin Crossbridge miosin mendorong aktin menuju pusatmenuju pusat sarkomersarkomerSetelah Setelah power stroke power stroke kepala miosin melepas aktin untuk kepala miosin melepas aktin untuk mengikat bagian aktin yang lain, demikian seterusnya mengikat bagian aktin yang lain, demikian seterusnya jadi siklus.jadi siklus.
Analogi : Analogi : menarik tambangmenarik tambang..
In the absence of calcium ions, tropomyosin In the absence of calcium ions, tropomyosin blocks access to the mysosin binding site of blocks access to the mysosin binding site of actin. actin. When calcium binds to troponin, the positions of When calcium binds to troponin, the positions of troponin and tropomyosin are altered on the the troponin and tropomyosin are altered on the the thin flament and myosin then has access to its thin flament and myosin then has access to its binding site on actin. binding site on actin. Myosin hydolyzes ATP and undergoes a Myosin hydolyzes ATP and undergoes a conformational change into a high-energy state. conformational change into a high-energy state. The head group of myosin binds to actin forming The head group of myosin binds to actin forming a cross-bridge between the thick and thin a cross-bridge between the thick and thin filaments. filaments.
Role of CaRole of Ca+2+2 in Muscle Contraction in Muscle Contraction
Ca+2
Ca++
Ca++
* Actin-binding sites are exposed as a result of Ca+2 binding to troponin complex that causes a conformational shift of tropomyosin
The energy stored by myosin is released, and The energy stored by myosin is released, and ADP and inorganic phosphate dissociate from ADP and inorganic phosphate dissociate from myosin. myosin.
The resulting relaxation of the myosin molecule The resulting relaxation of the myosin molecule entails rotation of the globular head, which entails rotation of the globular head, which induces longitudinal sliding of the filaments. induces longitudinal sliding of the filaments.
When the calcium level decreases, troponin When the calcium level decreases, troponin locks tropomyosin in the blocking position and locks tropomyosin in the blocking position and the thin filament slides back to the resting state. the thin filament slides back to the resting state.
Sliding-Filament MechanismSliding-Filament Mechanism
Muscle contraction is produced by cross bridge cycles. Muscle contraction is produced by cross bridge cycles. A cycle has 4 steps: A cycle has 4 steps: (1) Energizing of myosin cross bridge (1) Energizing of myosin cross bridge A + M•ATP —> A + M*•ADP•Pi (ATP is energizer here) A + M•ATP —> A + M*•ADP•Pi (ATP is energizer here) (2) Attachment of cross bridge to a thin filament (2) Attachment of cross bridge to a thin filament A + M*•ADP•Pi —> A•M*•ADP•Pi A + M*•ADP•Pi —> A•M*•ADP•Pi (3) Movement of cross bridge, producing tension (3) Movement of cross bridge, producing tension A•M*•ADP•Pi —> A•M + ADP + Pi A•M*•ADP•Pi —> A•M + ADP + Pi (4) Detachment of cross bridge from thin filament (4) Detachment of cross bridge from thin filament A•M + ATP —> A + M•ATP (ATP is modulator here) A•M + ATP —> A + M•ATP (ATP is modulator here)
Movement of the cross bridges make the overlapping Movement of the cross bridges make the overlapping thick and thin filaments slide past each other (they do not thick and thin filaments slide past each other (they do not change in length) to produce a contraction. change in length) to produce a contraction.
Actin MyofilamentActin Myofilament
During contraction, calcium binds to troponin
Covers actin-bindingsites at rest
Cross-Bridge FormationCross-Bridge Formation
Cross-Bridge CycleCross-Bridge Cycle
Cross-bridge Cycle
This animation by Mike Geeves, Laboratory of Molecular Biology in the UK and the Cambridge Institute for Medical Research
SIKLUS KONTRAKSISIKLUS KONTRAKSI
1.1. Rigor state: Rigor state: Kepala miosin terikat dg molekul G-aktin.Kepala miosin terikat dg molekul G-aktin.2.2. ATP menempel ke miosin, kepala miosin lepas dari ATP menempel ke miosin, kepala miosin lepas dari
aktin.aktin.3.3. Hidrolisis ATP: Hidrolisis ATP: jadi ADP + Pi (masih menempel) jadi ADP + Pi (masih menempel) 4.4. Miosin melekat ke G-aktin yang baruMiosin melekat ke G-aktin yang baru, energi dari , energi dari
pecahnya ATP, saat ada potensial energi di kepala pecahnya ATP, saat ada potensial energi di kepala miosin untuk power stroke.miosin untuk power stroke.
5.5. Pi lepas & power strokePi lepas & power stroke: Kepala miosin berotasi : Kepala miosin berotasi mendorong aktin mendekati pusat sarkomer mendorong aktin mendekati pusat sarkomer (crossbridge tilting)(crossbridge tilting)
6.6. ADP lepasADP lepas: kepala miosin tetap melekat ke aktin, siap : kepala miosin tetap melekat ke aktin, siap untuk siklus berikut bila ada ATP yang baruuntuk siklus berikut bila ada ATP yang baru
Excitation-Contraction CouplingExcitation-Contraction Coupling
Excitation-Contraction CouplingExcitation-Contraction Coupling
Excitation-Contraction (EC) Coupling:1. An AP travels down a motor (somatic neuron).2. The AP causes the release of the neurotransmitter
acetylcholine into the synapse at the neuromuscular junction.
3. The acetylcholine binds to the acetylcholine receptors on the muscle fiber and cause an EPSP.
4. If the EPSP reaches threshold, an AP is produced on the sarcolemma of the muscle fiber. Meanwhile, the acetylcholine attached to the receptor is destroyed.
5. The AP travels rapidly along the sarcolemma and enters the fiber at every t-tubule.
Excitation-Contraction CouplingExcitation-Contraction Coupling
6. As the AP travels through the t-tubule, it causes the Ca++ gates to open and Ca++ flows from the SR into the sarcoplasm. The Ca++ gates close when the AP ends.
7. The increased [Ca++] in the sarcoplasm results in Ca++ binding to troponin. This induces an allosteric change, the tropomyosin is pulled out of the way and steric inhibition is removed. The result is crossbridges begin to form, rotate and break (provided there is plenty of ATP).
8. Cross-bridge cycling continues as long as sarcoplasmic [Ca++] remains high.
9. However, if the Ca++ gates close, the action of the Ca++ ATPase (pump) begins to predominate and sarcoplasmic [Ca++]] drops. When it drops low enough, the troponin loses its Ca++ and changes shape the next time a crossbridge is not in the way. Steric inhibition is quickly re-established and the muscle contraction is over.
Exitation-Contraction CouplingExitation-Contraction Coupling
Dirangsang oleh asetilkolin/achetylcholineDirangsang oleh asetilkolin/achetylcholine
TahapTahap::
Asetilkolin (Ach) lepas dari motor neuron Asetilkolin (Ach) lepas dari motor neuron somatiksomatik
Ach merangsang potensial aksi serat ototAch merangsang potensial aksi serat otot
PA, m’rsg Ca++ lepas dr Ret.SarkoplasmaPA, m’rsg Ca++ lepas dr Ret.Sarkoplasma
Ca++ me’ikat troponin dan m’rsg kontraksiCa++ me’ikat troponin dan m’rsg kontraksi
DHP:
Dihydropiridine
Saat PA:
Ca 100x
Relaksasi:
Ca masuk RS krn enzim
Ca-ATP-ase
PERIODE KONTRAKSI/ TWITCHPERIODE KONTRAKSI/ TWITCH
1.1. Periode LatenPeriode Laten
(Antara potensial aksi-kontraksi)(Antara potensial aksi-kontraksi)
2. Periode kontraksi2. Periode kontraksi
3. Periode relaksasi3. Periode relaksasi
Lama periode kontraksi tergantung tipe ototLama periode kontraksi tergantung tipe otot
SUMBER ENERGI KONTRAKSISUMBER ENERGI KONTRAKSI
ATP (Adenosine Tri Phosphate)ATP (Adenosine Tri Phosphate)1.1. Kontraksi: gerakan crossbridgeKontraksi: gerakan crossbridge2.2. Relaksasi: Ca++ masuk lagi ke RSRelaksasi: Ca++ masuk lagi ke RS3.3. Relaksasi: melepas ikatan aktin dan miosinRelaksasi: melepas ikatan aktin dan miosin4.4. Diluar periode kontraksi : restore Na-KDiluar periode kontraksi : restore Na-K
SUMBER ATPSUMBER ATP1.1. Konversi posfo-kreatin (8 twitch)Konversi posfo-kreatin (8 twitch)2.2. An-aerobik glikolisisAn-aerobik glikolisis3.3. Posforilasi-oksidatifPosforilasi-oksidatif
KELELAHAN OTOTKELELAHAN OTOT
Fatigue:Fatigue:
Kondisi dimana otot tidak mampu lagi Kondisi dimana otot tidak mampu lagi melakukan / mempertahankan kontraksimelakukan / mempertahankan kontraksi
Jenis FatigueJenis Fatigue::Sentral: SSPSentral: SSPPerifer: NM-Junction – elemen kontraksiPerifer: NM-Junction – elemen kontraksi
E/ >> E/ >> elemen kontraksi elemen kontraksi
Lelah Sentral SSP Psikologis
Refleks Proteksi
Asidosis
(as. Laktat)
NM-Junction Pelepasan Neurotransmitter dan sensitivitas reseptor
Ggn.
Neuromuskuler
(Ach )
Kelelahan
Perifer
Excitation-contraction coupling
Perubahan membran potensial
Gangguan elektrolit (Hipokalemia)
Ca++ signal Pelepasan Ca & interaksi dg troponin
Pi
Kontraksi-relaksasi
PCr, ATP, glikogen
H+, Pi, laktat
Pi
Daya kontraksi (tension) maksimal tjd pada Daya kontraksi (tension) maksimal tjd pada panjang sarokomere yang optimalpanjang sarokomere yang optimal
Tension juga meningkat bila stimulus dilakukan Tension juga meningkat bila stimulus dilakukan berulang kali sebelum mencapai relaksasi berulang kali sebelum mencapai relaksasi maksimum (Stimulus Summation)maksimum (Stimulus Summation)
Akan tetapi, bila stimulus (potensial aksi) berlangsung terus menerus dg cepat (frekuensi tinggi), tanpa fase relaksasi terjadi Tetanus
Tetanus
-Komplet/ fused
-Inkomplet / unfused
Muscle Adaptation to ExerciseMuscle Adaptation to Exercise
Increased amount of contractile activity Increased amount of contractile activity (exercise) increases size (hypertrophy) of (exercise) increases size (hypertrophy) of muscle fibers and capacity for ATP production. muscle fibers and capacity for ATP production. Low intensity exercise affects oxidative fibers, Low intensity exercise affects oxidative fibers, increasing the number of mitochondria and increasing the number of mitochondria and capillaries. capillaries. High intensity exercise affects glycolytic fibers, High intensity exercise affects glycolytic fibers, increasing their diameter by an increased increasing their diameter by an increased synthesis of actin and myosin filaments, and an synthesis of actin and myosin filaments, and an increased synthesis of glycolytic enzymes. increased synthesis of glycolytic enzymes.
Speed of Muscle Contraction Varies by Fiber Type
MOTOR UNITMOTOR UNIT
Unit dasar kontraksiUnit dasar kontraksi, tdd: bbrp serat otot + motor , tdd: bbrp serat otot + motor neuron somatikneuron somatikMotor neuron mencetuskan potensial aksi Motor neuron mencetuskan potensial aksi kontraksi 1 motor unit.kontraksi 1 motor unit.1 motor neuron 1 motor neuron bbrp otot; 1 serat otot bbrp otot; 1 serat otot dipersyarafi 1 neurondipersyarafi 1 neuronOtot kecil (gerak halus; tangan, wajah) Otot kecil (gerak halus; tangan, wajah) 1 motor unit = 3-5 serat otot1 motor unit = 3-5 serat ototOtot besar (gerak kasar; tungkai, trunkus) Otot besar (gerak kasar; tungkai, trunkus) 1 motor unit = 100an- 1000an serat otot1 motor unit = 100an- 1000an serat otot
Motor Pool Motor Pool all a motor neurons that innervate a single all a motor neurons that innervate a single muscle muscle
An a motor neuron and An a motor neuron and all the muscle fibers that it innervates all the muscle fibers that it innervates
1:3 to 1:1001:3 to 1:100
fewer muscle fibers ---> finer controlfewer muscle fibers ---> finer control– 3 types3 types based on speed of contraction & fatigue based on speed of contraction & fatigue
~~
Motor Pools & Motor UnitsMotor Pools & Motor Units
Types of Motor UnitsTypes of Motor UnitsMost muscle contain both slow- & fast-Most muscle contain both slow- & fast-twitch fibers twitch fibers – ratio depends on functionratio depends on function
e.g. ankle extensorse.g. ankle extensors– Soleus active during standing Soleus active during standing
hi ratio of slow fibers hi ratio of slow fibers – Medial Gastrocnemius: active during running Medial Gastrocnemius: active during running
& jumping& jumping
hi ratio of fast fibers ~hi ratio of fast fibers ~
Variasi gradasi, gaya & durasi kontrksi Variasi gradasi, gaya & durasi kontrksi ditentukan oleh : ditentukan oleh :
Jumlah & jenis motor unit yang aktif Jumlah & jenis motor unit yang aktif (‘Recruitment’ dikontrol oleh SSP)(‘Recruitment’ dikontrol oleh SSP) Kontraksi lemah Kontraksi lemah SSP m’rsg sedikit motor unit SSP m’rsg sedikit motor unit Motor unit yang t’rsg Ix nilai ambang rendah Motor unit yang t’rsg Ix nilai ambang rendah slow- slow-
twitchtwitch Stimulus Stimulus m’rsg motor neuron dg nilai ambang tinggi m’rsg motor neuron dg nilai ambang tinggi
fast-twitch fast-twitch Jumlah motor unit Jumlah motor unit daya kontraksi daya kontraksi Asynchronous RecruitmentAsynchronous Recruitment
Pada kontraksi lama, SSP m’rsg bbrp motor unit scr Pada kontraksi lama, SSP m’rsg bbrp motor unit scr bergantian bergantian 1 serat kontraksi, serat lain istirahat 1 serat kontraksi, serat lain istirahatHanya terjadi pada kontraksi sub-maksimal, why ?Hanya terjadi pada kontraksi sub-maksimal, why ?
BIOMEKANIKA GERAK BIOMEKANIKA GERAK TUBUHTUBUH
Fs otot: menggerakkan rangkaFs otot: menggerakkan rangka
KONTRAKSI ISOTONIK (Iso;=, teinein; stretch)KONTRAKSI ISOTONIK (Iso;=, teinein; stretch)Kontraksi Kontraksi gaya + menggerakkan beban gaya + menggerakkan beban Sarkomer menarik beban dan serat elastisSarkomer menarik beban dan serat elastisKonsentrikKonsentrik arah gerak = pemendekan otot arah gerak = pemendekan ototEksentrikEksentrik arah gerak = pemanjangan otot arah gerak = pemanjangan otot
>> m’rusak otot (DOMS)>> m’rusak otot (DOMS)KONTRAKSI ISOMETRIK (Iso;=, metric;ukuran)KONTRAKSI ISOMETRIK (Iso;=, metric;ukuran)Kontraksi Kontraksi gaya + tanpa menggerakkan beban gaya + tanpa menggerakkan beban Sarkomer otot hanya menarik serat elastisSarkomer otot hanya menarik serat elastis
USAHA OTOTUSAHA OTOTLever/ lengan Lever/ lengan dibentuk oleh rangkadibentuk oleh rangkaFulcrum/ sumbu Fulcrum/ sumbu dibentuk sendidibentuk sendi
W = F x dW = F x d WW (otot) = W (otot) = W (beban) (beban)
Insersi bisep 5 cm dari sikuInsersi bisep 5 cm dari sikuPanjang lengan 20 cmPanjang lengan 20 cmBerat beban 5 kgBerat beban 5 kg
Berapa usaha otot bisep Berapa usaha otot bisep mengangkat beban ?mengangkat beban ?
Semakin dekat insersi ke fulcrum Semakin dekat insersi ke fulcrum Gerak semakin luasGerak semakin luas
Refleks Otot SkeletalRefleks Otot Skeletal
Berfungsi utkBerfungsi utk::1.1. Mengatur keseimbanganMengatur keseimbangan2.2. Gerak spesifik (keselamatan)Gerak spesifik (keselamatan)3.3. Optimalisasi gerakOptimalisasi gerakKomponen RefleksKomponen Refleks1.Reseptor sensoris (proprioceptors)1.Reseptor sensoris (proprioceptors)
Spindle otot, organ tendo Golgi & reseptor sendiSpindle otot, organ tendo Golgi & reseptor sendi2. Neuron sensoris (transfer input)2. Neuron sensoris (transfer input)3. SSP3. SSP4. Motor neuron somatik (alfa motor neuron)4. Motor neuron somatik (alfa motor neuron)5. Serat otot (serat ekstrafusal5. Serat otot (serat ekstrafusal) )
Reseptor SendiReseptor Sendi
Terdapat di kapsul sendi dan ligamenTerdapat di kapsul sendi dan ligamen
Distimulasi oleh distorsi mekanik krn Distimulasi oleh distorsi mekanik krn perubahan sudut, beban dan posisi sendi perubahan sudut, beban dan posisi sendi & tulang& tulang
Pusat pengaturan di cerebellumPusat pengaturan di cerebellum
Spindle OtotSpindle Otot
Reseptor regangan ototReseptor regangan ototMengirim impuls ke Med. Spinalis & otakMengirim impuls ke Med. Spinalis & otakResponsif thd perubahan panjang ototResponsif thd perubahan panjang otot1 otot memiliki bbrp spindle otot, kec, 1 otot memiliki bbrp spindle otot, kec, rahangrahangTerletak di sisi dalam otot ekstrafusal, Terletak di sisi dalam otot ekstrafusal, mengelilingi otot intrafusalmengelilingi otot intrafusalAkibat dari rangsangan menghasilkan Akibat dari rangsangan menghasilkan refleks kontraksirefleks kontraksi
Organ Tendo GolgiOrgan Tendo Golgi
Terletak di sambungan tendo dan ototTerletak di sambungan tendo dan otot
Responsif terhadap tegangan ototResponsif terhadap tegangan otot
Menghasilkan refleks relaksasiMenghasilkan refleks relaksasi
Terdiri dari ujung syaraf bebasTerdiri dari ujung syaraf bebas
Refleks menghambat interneuron di MS, Refleks menghambat interneuron di MS, interneuron menghambat alfa motor interneuron menghambat alfa motor neuron sehingga kontraksi berkurang.neuron sehingga kontraksi berkurang.
Knee Jerk reflexes; Knee Jerk reflexes;
merangsang spindle ototmerangsang spindle otot
Flexion reflexes;Flexion reflexes;
menghindari bahayamenghindari bahaya
Movement Disorders of Movement Disorders of MuscleMuscle
Duchenne’s Muscular Duchenne’s Muscular DystrophyDystrophy
Muscular DystrophiesMuscular Dystrophies– wasting away of muscleswasting away of muscles– metabolic / structural abnormalitiesmetabolic / structural abnormalities
Duchenne’sDuchenne’s– best understoodbest understood– young boys ~young boys ~
Duchenne’s Muscular Duchenne’s Muscular DystrophyDystrophy
CauseCause– hereditary - maternal X chromosome hereditary - maternal X chromosome – single gene ---> proteinsingle gene ---> protein
dystrophindystrophin– maybe involved in Ca++ regulationmaybe involved in Ca++ regulation
TreatmentTreatment– Inject dystrophin or mRNAInject dystrophin or mRNA– Gene therapy promising for muscles ~Gene therapy promising for muscles ~
Myasthenia GravisMyasthenia Gravis
Severe muscle weaknessSevere muscle weakness– rapid fatigue following exerciserapid fatigue following exercise
Develops in people of all agesDevelops in people of all ages– Most common: women in 30sMost common: women in 30s– Risk of respiratory paralysisRisk of respiratory paralysis
Autoimmune disorderAutoimmune disorder– body develops antibodies for ACh-Rbody develops antibodies for ACh-R– reduces synaptic transmission ~reduces synaptic transmission ~
Myasthenia Gravis: Myasthenia Gravis: Treatment Treatment
AChE inhibitors AChE inhibitors – ¯ degradation of ACh¯ degradation of ACh– narrow therapeutic windownarrow therapeutic window– too much ACh ---> paralysistoo much ACh ---> paralysis
Reduce immune responseReduce immune response– remove thymusremove thymus– filtering antibodies from blood filtering antibodies from blood
temporary ~temporary ~