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Fisiologi Otot

dr. Rebecca Rumesty,


M.Biomed
Fisiologi
Fakultas Kedokteran
Universitas HKBP Nommensen
2020
Tujuan Pembelajaran
 Mengetahui Fungsi otot
 Mengetahui Mekanisme Kerja otot dalam
melakukan fungsinya
 Mengetahui faktor faktor yang mempengaruhi
otot dalam melakukan fungsinya
Pendahuluan
Struktur Otot Rangka
Motor Neuron
 Electrical characteristics of skeletal 10
muscle :
 Resting membrane potential : - 90 mV
 Duration of Action Potential : 2-4 ms
 Speed of conduction : ± 5 m/s
 Absolut refractory period : 1-3 ms

 Ionic fluxes :
 Na+ influx → depolarization
Stimulation
 K+ efflux → repolarization

Depolarization at Action
motor end-plate potential
muscle fiber

contractile
response

Single A.P → single contraction = muscle twitch


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Skeletal Muscle Contraction

 In order to contract, a skeletal muscle must be stimulated by


a nerve ending of the somatic nervous system
 Axons of this neurons branch profusely as they enter
muscles
 Each axonal branch forms a neuromuscular junction with a
single muscle fiber
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Events at Neuromuscular Junction

When a nerve impulse reaches the end of an axon at the


neuromuscular junction, Acetylcholine (Ach) release to the
synaptic cleft.
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Skeletal Muscle Contraction, cont


ACh diffuses across the synaptic cleft to ACh receptors on
the sarcolemma


Binding of ACh to its receptors  initiates an action
potential in the muscle  initiates contraction in muscle .


The process by which depolarization of the muscle fiber
initiates contraction is called Excitation-Contraction
coupling.
Dasar Molekuler Kontraksi Otot
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Sequential Events of Contraction 18

Myosin head
(high-energy
configuration)

1 Myosin cross bridge attaches to


the actin myofilament
Thin filament

Thick ADP and Pi (inorganic


filament phosphate) released

4 As ATP is split into ADP and P i, 2 Working stroke—the myosin head pivots and
cocking of the myosin head occurs bends as it pulls on the actin filament, sliding it
toward the M line

Myosin head
(low-energy
configuration)

3 As new ATP attaches to the myosin


head, the cross bridge detaches
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Skeletal Muscle Fiber Type:

Characteristics by :

Speed of contraction (speed of shortening=Vmax) : determined by
speed in which myosin ATPase split ATP
 slow and fast fibers


ATP-forming pathways
◦ Oxidative fibers : use aerobic pathways
◦ Glycolytic fibers : use anaerobic glycolysis

These two criteria define three categories :


1. Type I fibers (slow-oxidative or slow-twitch fibers)
2. Type IIx fibers (fast-glycolytic or fast-twitch fibers )
3. Type IIa fibers (fast oxidative-glycolytic fibers).
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Type I fibers (slow-oxidative or slow-twitch fibers)

High mitochondrial volume (large number of oxidative enzymes)

More capillaries, high myoglobin concentration

slow acting myosin ATPases
 high capacity for aerobic metabolism, & high resistance to fatigue, but

contract slowly


Type IIx fibers (fast-glycolytic or fast-twitch fibers )

Small number of mitochondrial

Rich in glycolytic enzymes

Higher myosin ATPase activity  highest Vmax
 limited capacity for aerobic metabolism, & less resistant to fatigue,

contract fastest


Type IIa fibers (fast oxidative-glycolytic fibers).

Mixture of both type I and IIx

Extremely adaptable : endurance training  increase oxidative capacity.
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Comparison

Characteristic Type I Type IIx Type IIa

Number of High Low High/ moderate


mitochondria
Resistance to High Low High/ moderate
fatigue
Predominant Aerobic Anaerobic Combination
energy system
ATPase activity Low Highest High

Vmax (speed of Low Highest Intermediate


shortening)
Efficiency High Low Moderate

Specific tension Moderate High High


Types of Contraction
Isotonic Contractions

 In isotonic contractions, the muscle


changes in length, and moves the load
 The two types of isotonic contractions
are concentric and eccentric

Concentric contractions : the muscle
shortens and does work

Eccentric contractions : the muscle
contracts as it lengthens
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Motor Unit:
The Nerve-Muscle Functional Unit

 A motor unit is a motor neuron and all


the muscle fibers it supplies
 The number of muscle fibers per motor unit can vary
from four to several hundred
 Muscles that control fine movements
(fingers, eyes) have small motor units
 Fine & complicated movement

1:1 nerve to fiber

Finger muscle
 Big muscles

1: 2000

Leg muscles
Receptors in muscle

 Chemoreceptors ; specialized free nerve ending, send


information to CNS about : changes in muscle pH,
extracellular K+ concentration, O2 & CO2 tension.

 Two types of mechanoreceptors monitor changes in muscle


length and tension :

Muscle spindles : monitor muscle length


The Golgi tendon organs: monitor muscle tone
Muscle Spindles

 Are composed of 3-10 intrafusal muscle fibers in the central


regions (noncontractile) and serve as receptive surfaces
 Muscle spindles are wrapped with two types of afferent
endings: primary sensory endings (type Ia fibers) and
secondary sensory endings (type II fibers)

Note :
 These regions are innervated by gamma () efferent fibers

 Contractile muscle fibers are extrafusal fibers and are

innervated by alpha () efferent fibers


Muscle Spindles

Figure 13.15
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Factors influence tension of contraction

1. The frequency & strength of


stimulation
2. The length of the fiber at the onset of
contraction
3. The extent of fatigue
4. The thickness of the fiber.
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The frequency of stimulation


1

repeated stimulation (before relaxation has


occurred) → additional activation of the
contractile elements → greater tension
developed
 Summation of contraction
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 Tetanic contraction ;
rapidly repeated stimulation, no relaxation has
occurred → continuous contraction.

Complete tetanus

Incomplete tetanus

 Staircase – increased contraction in response to multiple


stimuli of the same strength
Contractions increase because:
◦ There is increasing availability of Ca2+ in the sarcoplasm
◦ Muscle enzyme systems become more efficient because heat is
increased as muscle contracts
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Strength / INTENSITY of stimulus

 Threshold stimulus : the stimulus strength at


which the first observable muscle contraction
occurs

 Motor unit summation : as stimulus strength is


increase  more muscle fibers being
contracted  increase force/tension of
contraction
 This phenomenon, called recruitment (brings
more and more muscle fibers into play)
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Stimulus Intensity
and
Muscle Tension

Figure 9.15 (a, b)


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Length of the fiber


2

Maximum tension produce if length of the fiber at
the onset of contraction is normal (resting length)

If the muscle is stretched (longer) or shorter, the
active tension & total tension will reduced.

The velocity of muscle contraction is maximal at the
resting length, & declines if the muscle get shorter
or longer.
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Muscle Fatigue 3
 Muscle fatigue : the muscle is in a state of
physiological inability to contract

 Muscle fatigue occurs when:



ATP production fails to keep pace with ATP use

Lactic acid accumulates in the muscle

Ionic imbalances are present

 When muscle fiber are completely depleted of


ATP & Phosphorylcreatine, relaxation does not
occur → a state rigidity.
Kelelahan Otot
 Seberkas otot yang dirangsang berkali-kali untuk
berkontraksi, suatu saat akan memperlihatkan
penurunan kekuatan kontraksi.
 Penurunan kapasitas kerja yang bersifat sementara
akibat kerja disebut fatigue.
 Disebabkan oleh :

Kehabisan cadangan energi dalam otot

Penimbunan asam laktat

Perubahan konsentrasi ion

Perlambatan sintesis/ release neurotransmitter

Central fatigue (psikis)
Kontraktur dan Spasme
 Kontraktur fisiologis adalah kegagalan otot untuk kembali
ke panjang awal setelah proses kontraksi.
 Dengan demikian otot tetap berkontraksi meskipun tidak
ada potensial aksi baru.
 Hal ini terjadi pada kelelahan hebat yang mengakibatkan
tidak ada energi untuk relaksasi.

 Spasme otot terjadi akibat adanya stimulus nyeri yang hebat


disekitar otot yang mengalami spasme (misal : patah tulang,
peritonitis)
 Muscle cramps merupakan spasme otot yang diakibatkan
faktor iritan dan abnormalitas metabolik, seperti kedinginan,
overexercise dan penurunan aliran darah.
Hipertrofi Otot

Apabila sel otot distimulasi berulang (tegangan mendekati
maskimal), lebih sering & hingga menimbulkan kelelahan

- terbentuk lebih banyak mitokondria
- peningkatan enzim glikolitik
- penambahan cadangan glikogen
 terbentuk banyak miofibril (filamin tipis dan tebal
bertambah)
 setiap sel otot bertambah diameternya, meski jumlah sel
otot tidak bertambah
 pembesaran otot dan peningkatan tension/kontraksi.
Atrofi otot
 Yaitu : berkurangnya ukuran otot, tonus otot, dan tenaga yang
dihasilkan
 Terjadi pada otot yang jarang terstimulasi
 Terjadi pengurangan cadangan energi (ATP,fosfokreatin, & glikogen)
dan protein.

 Pada awalnya bersifat reversibel, tetapi jaringan otot yang telah mati
tidak dapat digantikan
 Pencegahan : terapi fisikal (fisioterapi) pada orang yang tidak dapat
bergerak normal untuk sementara waktu.
(stimulasi listrik & mekanis  saraf terstimulasi mencegah atrofi
otot).
Rigor Mortis
 Beberapa jam setelah kematian, seluruh otot tubuh
akan mengalami keadaan semacam kontraktur,
disebut rigor mortis.
 Kekakuan otot ini terjadi karena tidak tersedianya
ATP untuk perombakan ikatan silang antara aktin dan
miosin.
 Keadaan ini berlangsung sampai terjadi denaturasi
protein sebagai akibat autolisis oleh enzim yang
dihasilkan oleh lysosome.
 Autolisis terjadi 15-25 jam sesudah kematian, dan
dipercepat oleh peningkatan temperatur.
Myasthenia Gravis
 Suatu kondisi melemah/hilangnya kekuatan kontraksi
otot akibat gangguan hantaran listrik pada NMJ.
 Umumnya diawali gangguan pada otot-otot kecil
(kelopak mata), kemudian secara progresif
menyerang otot lain.
 Apabila menyerang otot pernapasan dapat
mengakibatkan kematian.

 Penatalaksanaan antara lain dengan anti-kolinesterase


(ACE-inhibitor : neostigmine)
Berbagai teori mengenai penyebab MG:
 Adanya antibodi (autoimun) yang mengakibatkan

kerusakan sel otot dan reseptor-reseptor


neurotransmitter pada NMJ.
 Berkurangnya jumlah asetilkolin pada ujung saraf.

 Meningkatnya jumlah asetilkolin-esterase pada

celah sinaps
 Terdapat zat yang bersifat seperti asetilkolin-

esterase (pseudoACE)
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