fisio otot fkunja2010 | our mini digital library

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Physiology of Muscle

Humaryanto

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TIPE OTOT

Otot Skeletal

(lurik/striata)

Otot Jantung

(lurik/striata)

Otot Polos (polos)

(GI, VU, Vascular)

(3)

Extrafusal Muscle Fibers

Striate muscle

Force for limb

movements

–

_{flexion - closes joint}

–

_{extension - opens joint}

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OTOT SKELETAL

40%

40% BB tubuh BB tubuh Fungsi

Fungsi : mengatur posisi : mengatur posisi dan gerak rangka

dan gerak rangka

Melekat ke tulang melalui

tendo

Origo

Origo : perlekatan pada : perlekatan pada bag. proksimal, bersifat

bag. proksimal, bersifat

stasioner

Insersio

Insersio : perlekatan pada : perlekatan pada bag. distal, bersifat mobil

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TIPE OTOT SKELETAL

Berdasarkan kecepatan kontraksi dan daya

tahan terhadap fatigue.



_{Fast-twitch glycolitic fibers (putih)}



_{Fast-twitch oxidative fibers (merah)}



_{Slow twitch oxidative fibers (merah)}

Setiap orang punya 3 tipe otot, tapi berbeda

pada komposisi dominan

(Jauhari Johan vs John Murray/ Ben Johnson)

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Type 1 Fibers

Slow fibers

dark red dark red

– slow, sustained contraction _{slow, sustained contraction}

– slow to fatigue _{slow to fatigue}

Aerobic metabolism

– many capillaries & mitochondria_{many capillaries & mitochondria}

– oxygen required for ATP synthesis _{oxygen required for ATP synthesis}

– myoglobin _myoglobin

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Type 2b Fibers

Fast fatigable fibers

white fibers white fibers

– _{rapid, brief contraction}_{rapid, brief contraction} – _{fast to fatigue}_{fast to fatigue}

– _{produce about 10x force of Type 1}_{produce about 10x force of Type 1}

Anaerobic metabolism

– _{fewer capillaries & mitochondria}_{fewer capillaries & mitochondria} – _{ATP generated by glycolysis}_{ATP generated by glycolysis}

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Type 2a Fibers

Fast fatigue-resistant fibers

pale red pale red

–

properties intermediate to types 1 & 2b

_{properties intermediate to types 1 & 2b}

–

_{rapid, brief contraction}

–

_{slow to fatigue}

–

produce least force

_{produce least force}

Aerobic & Anaerobic metabolism

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Neuromuscular Junction

Synapse between neuron & effector

Cholinergic (ACh)

–

_{nicotinic receptors}

Motor end-plate

–

_{postsynaptic membrane}

–

_{folds packed with receptors}

increased surface area ~

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Global view of a Global view of a neuromuscular

neuromuscular

junction:

1.

1. AxonAxon

2. Motor end-plate

3.

3. Muscle fiberMuscle fiber 4.

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Detailed view of a

neuromuscular junction:

1.

1. PresynapticPresynaptic terminal terminal 2.

2. SarcolemmaSarcolemma 3. Synaptic vesicle

3. Synaptic vesicle

4. Nicotinic acetylcholine

receptor

5. Mitochondrion

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Mechanism of action

Upon the arrival of an action potential at the axon terminal, Upon the arrival of an action potential at the axon terminal,

voltage-dependent calcium channels open and Ca2+ ions voltage-dependent calcium channels open and Ca2+ ions

flow from the extracellular fluid into the motor neuron's flow from the extracellular fluid into the motor neuron's

cytosol. This influx of Ca2+ triggers

cytosol. This influx of Ca2+ triggers excitation-contraction excitation-contraction coupling

coupling, a biochemical cascade that causes , a biochemical cascade that causes

neurotransmitter-containing vesicles to fuse to the motor neurotransmitter-containing vesicles to fuse to the motor

neuron's cell membrane and release acetylcholine into the neuron's cell membrane and release acetylcholine into the

synaptic cleft. synaptic cleft.

Acetylcholine diffuses across the synaptic cleft and binds to Acetylcholine diffuses across the synaptic cleft and binds to

the nicotinic acetylcholine receptors that dot the motor end the nicotinic acetylcholine receptors that dot the motor end

plate. 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,

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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 initiating of calcium from the sarcoplasmic reticulum, thus initiating

muscle contraction. 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

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Neurotransmitters and

Neuromodulators

Neuromodulators modify the postsynaptic cell's response to

neurotransmitters or change the presynaptic cell's synthesis, release or

metabolism of the neurotransmitter.

Acetylcholine (Ach)

Major neurotransmitter. Fibers that release ACh are called cholinergic fibers.

Acetylcholine is degraded by the enzyme, acetylcholinesterase.

Biogenic Amines

Biogenic amines are neurotransmitters containing an amino group.

Catecholamines such as dopamine, norepinephrine and epinephrine,

serotonin. Nerve fibers that release epinephrine and norepinephrine are

called adrenergic and noradrenergic fibers respectively.

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Neurotransmitters and

Neuromodulators

Amino Acid Neurotransmitters

Amino acid neurotransmitters are the most prevalent

neurotransmitters in CNS. Glutamate, aspartate GABA (gamma

aminobutyric acid), glycine,

Neuropeptides

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.

Neuroeffector Communication

Many neurons of peripheral nervous system end at neuroeffector

junctions on muscle and gland cells. Neurotransmitters released by

these efferent neurons then activate the target cell.

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Muscle Contraction

AP generated in muscle fiber (cell)

Ca++ released from internal stores

Muscle fiber contracts

–

_{continues while Ca++ & ATP available}

Relaxation

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Muscle Fiber Structure

Multinucleated

– fusion of multiple precursor cells_{fusion of multiple precursor cells}

Sarcolemma Excitable membrane

Myofibrils: contractile units

Sarcopasmic reticulum (SR)

– sequesters Ca++ _{sequesters Ca++}

T tubules

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Miofibril



struktur kontraksi otot

1 Serat otot, tdd: ribuan miofibril

1 miofibril tdd:

Aktin & miosin

Aktin & miosin (protein kontraksi) (protein kontraksi) Troponin & tropomiosin

Troponin & tropomiosin (protein pengatur) (protein pengatur) Titin & nebulin

Titin & nebulin (protein asessoris besar) (protein asessoris besar) Miosin

Miosin  thick filament, punya kepala thick filament, punya kepala

Motor protein, E kimia

Motor protein, E kimia  E mekanik, mgd ATP-ase (hidrolisis) E mekanik, mgd ATP-ase (hidrolisis)

Aktin

Aktin  thin filament, melekat troponin & tropomiosin thin filament, melekat troponin & tropomiosin Titin

Titin  molekul elastis (protein terbesar) molekul elastis (protein terbesar)



 stabilitas & elastisistas ototstabilitas & elastisistas otot Nebulin

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Sarcolemma

Myofibrils

Sarcoplasmic

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Myofibril: structure &

function

Sarcomeres

– repeating sections_{repeating sections}

Z lines

dividers between sarcomeres

thin filaments anchored to Z lines

– actin & troponin_{actin & troponin}

Thick filaments between thin filaments

– myosin_myosin

Contraction:filaments slide by each

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Sarcomere

Z line

Thin filaments

Z line

Thick

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KONTRAKSI OTOT

Menghasilkan force / gaya

Menghasilkan force / gaya  muscle tension muscle tension Melawan beban/ load

Melawan beban/ load

Memerlukan energi (dari ATP)

Pencetus kontraksi otot

1. Neuromuscular junction :

Rangsang somatik

Rangsang somatik  rangsang listrik rangsang listrik 2. Excitation-contraction coupling

2. Excitation-contraction coupling

Potensial aksi

Potensial aksi  signal Ca++ signal Ca++  siklus kontr-relaks siklus kontr-relaks

SIKLUS KONTRAKSI DAN RELAKSASI



(28)

Contraction

Excitation-contraction coupling

Myosin “heads” crossbridges w/ actin

–

_{Ca++ dependent}

–

_{binds to troponin, reveals binding site}

Myosin head rotates

(29)

Contraction

ATP binds to myosin ---> detachment

–

cocks myosin ---> binds again

_{cocks myosin ---> binds again}

–

_{rigor mortis: no ATP}

fibers remain crosslinked

Repeats as long as Ca++ present

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SLIDING FILAMENT THEORY

Serat

Serat otot memendekotot memendek (overlapping thick & thin filament) (overlapping thick & thin filament) Sliding aktin terhadap miosin

Sliding aktin terhadap miosin

Gaya dari crossbridge miosin mendorong aktin

(

(power strokepower stroke))

Crossbridge miosin mendorong aktin

Crossbridge miosin mendorong aktin menuju pusatmenuju pusat sarkomer

sarkomer

Setelah

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.

Analogi :

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(32)

In the absence of calcium ions, tropomyosin

blocks access to the mysosin binding site of

actin.

When calcium binds to troponin, the positions of

troponin and tropomyosin are altered on the the

thin flament and myosin then has access to its

binding site on actin.

Myosin hydolyzes ATP and undergoes a

conformational change into a high-energy state.

The head group of myosin binds to actin forming

a cross-bridge between the thick and thin

filaments.

(33)

Role 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

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(35)

The energy stored by myosin is released, and

ADP and inorganic phosphate dissociate from

myosin.

The resulting relaxation of the myosin molecule

entails rotation of the globular head, which

induces longitudinal sliding of the filaments.

When the calcium level decreases, troponin

locks tropomyosin in the blocking position and

the thin filament slides back to the resting state.

(36)

(37)

Sliding-Filament Mechanism

Muscle contraction is produced by cross bridge cycles.

A cycle has 4 steps:

(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

A•M*•ADP•Pi —> A•M + ADP + Pi A•M*•ADP•Pi —> A•M + ADP + Pi

(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

thick and thin filaments slide past each other (they do not

change in length) to produce a contraction.

(38)

Actin Myofilament

During

contraction,

calcium binds to troponin

(39)

Cross-Bridge Formation

(40)

Cross-Bridge Cycle

(41)

Cross-bridge Cycle

This animation by Mike Geeves,

(42)

SIKLUS 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.

3.

3. Hidrolisis ATP: _{Hidrolisis ATP:}jadi ADP + Pi (masih menempel) _{jadi ADP + Pi (masih menempel)}

4.

4. Miosin melekat ke G-aktin yang baru_{Miosin melekat ke G-aktin yang baru}, energi dari _{, energi dari}

pecahnya ATP, saat ada potensial energi di kepala

miosin untuk power stroke.

5.

5. Pi lepas & power stroke_{Pi lepas & power stroke}: Kepala miosin berotasi _{: Kepala miosin berotasi}

mendorong aktin mendekati pusat sarkomer

(crossbridge tilting)

6.

6. ADP lepas_{ADP lepas}: kepala miosin tetap melekat ke aktin, siap _{: kepala miosin tetap melekat ke aktin, siap}

untuk siklus berikut bila ada ATP yang baru

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Excitation-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

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Excitation-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

(46)

(47)

Exitation-Contraction Coupling

Dirangsang oleh asetilkolin/achetylcholine

Tahap

:

Asetilkolin (Ach) lepas dari motor neuron

somatik

Ach merangsang potensial aksi serat otot

PA, m’rsg Ca++ lepas dr Ret.Sarkoplasma

Ca++ me’ikat troponin dan m’rsg kontraksi

(48)

DHP:

Dihydropiridine

Saat PA: Ca  100x

Relaksasi: Ca masuk RS krn enzim

(49)

PERIODE KONTRAKSI/ TWITCH

1.

1. Periode Laten

_{Periode Laten}

(Antara potensial aksi-kontraksi)

2. Periode kontraksi

3. Periode relaksasi

Lama periode kontraksi tergantung tipe otot

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SUMBER ENERGI KONTRAKSI

ATP (Adenosine Tri Phosphate)

1.

Kontraksi: gerakan crossbridge

_{Kontraksi: gerakan crossbridge}

2.

Relaksasi: Ca++ masuk lagi ke RS

_{Relaksasi: Ca++ masuk lagi ke RS}

3.

Relaksasi: melepas ikatan aktin dan miosin

_{Relaksasi: melepas ikatan aktin dan miosin}

4.

Diluar periode kontraksi : restore Na-K

_{Diluar periode kontraksi : restore Na-K}

SUMBER ATP

1.

Konversi posfo-kreatin (8 twitch)

_{Konversi posfo-kreatin (8 twitch)}

2.

An-aerobik glikolisis

_{An-aerobik glikolisis}

3.

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KELELAHAN OTOT

Fatigue:

Kondisi dimana otot tidak mampu lagi

melakukan / mempertahankan kontraksi

Jenis Fatigue

:



_{Sentral: SSP}



_{Perifer: NM-Junction – elemen kontraksi}

E/ >>

(54)

Lelah Sentral SSP Psikologis

Refleks Proteksi

Asidosis (as. Laktat)

NM-Junction  Pelepasan

Neurotransmitter dan sensitivitas reseptor

(55)

Daya kontraksi (tension) maksimal tjd pada

(56)

Tension juga meningkat bila stimulus dilakukan

berulang kali sebelum mencapai relaksasi

maksimum (Stimulus Summation)

Akan tetapi, bila stimulus (potensial aksi) berlangsung terus menerus dg cepat

(frekuensi tinggi), tanpa fase relaksasi  terjadi Tetanus

Tetanus

-Komplet/ fused

(57)

Muscle Adaptation to Exercise

Increased amount of contractile activity

(exercise) increases size (hypertrophy) of

muscle fibers and capacity for ATP production.

Low intensity exercise affects oxidative fibers,

increasing the number of mitochondria and

capillaries.

High intensity exercise affects glycolytic fibers,

increasing their diameter by an increased

synthesis of actin and myosin filaments, and an

increased synthesis of glycolytic enzymes.

(58)

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MOTOR UNIT

Unit dasar kontraksi

, tdd: bbrp serat otot + motor

neuron somatik

Motor neuron mencetuskan potensial aksi



kontraksi 1 motor unit.

1 motor neuron



bbrp otot; 1 serat otot

dipersyarafi 1 neuron

Otot kecil (gerak halus; tangan, wajah)



1 motor unit = 3-5 serat otot

Otot besar (gerak kasar; tungkai, trunkus)



1 motor unit = 100an- 1000an serat otot

(60)

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

all the muscle fibers that it innervates all the muscle fibers that it innervates

1:3 to 1:100

fewer muscle fibers ---> finer control

– _{3 types}_{3 types} _{based on speed of contraction & fatigue}_{based on speed of contraction & fatigue}

_~

Motor Pools & Motor Units

(61)

Types of Motor Units

Most muscle contain both slow- &

fast-twitch fibers

twitch fibers

– _{ratio depends on function}_{ratio depends on function}

e.g. ankle extensors

– _{Soleus active during standing}_{Soleus active during standing}

hi ratio of slow fibers

– _{Medial Gastrocnemius: active during running &}_{Medial Gastrocnemius: active during running &}

jumping

hi ratio of fast fibers ~

(62)

(63)

Variasi gradasi, gaya & durasi kontrksi



ditentukan oleh :

Jumlah & jenis motor unit yang aktif

(‘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-twitch

twitch

 _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 Recruitment

Pada kontraksi lama, SSP m’rsg bbrp motor unit scr

bergantian

bergantian  1 serat kontraksi, serat lain istirahat 1 serat kontraksi, serat lain istirahat

Hanya terjadi pada kontraksi sub-maksimal, why ?

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BIOMEKANIKA GERAK TUBUH

Fs otot: menggerakkan rangka

KONTRAKSI ISOTONIK (Iso;=, teinein; stretch)

Kontraksi

Kontraksi  gaya + menggerakkan beban gaya + menggerakkan beban



 Sarkomer menarik beban dan serat elastisSarkomer menarik beban dan serat elastis Konsentrik

Konsentrik arah gerak = pemendekan otot arah gerak = pemendekan otot

Eksentrik

Eksentrik arah gerak = pemanjangan otot arah gerak = pemanjangan otot



 >> m’rusak otot (DOMS)>> m’rusak otot (DOMS)

KONTRAKSI ISOMETRIK (Iso;=, metric;ukuran)

Kontraksi

Kontraksi  gaya + tanpa menggerakkan beban gaya + tanpa menggerakkan beban