By

Dr.H.Gusbakti,MD, MSC,PKK,AIFM
Professor of Physiology
University Islamic Of North Sumatera

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MUSCLE TISSUE
Muscles in human body
Specialised excitable tissues
~ 50 % body weight
Ability to contract
Contractions provide movements
Do work
Move body or limbs
Push, pull or hold an external load or object
Mix or move food through the gastrointestinal track
Pump blood out of the heart to the blood vessels
Contract uterus for birth of foetus
Micturition and defaecation

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MUSCLE OF TYPE

Three types of
muscle:
1.Skeletal muscle
2.Cardiac muscle
3.Smooth muscle

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Skeletal Muscle

Long cylindrical
cells
Many nuclei per
cell
Striated
Voluntary
Rapid
contractions
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Cardiac Muscle

Branching cells
One or two nuclei per cell
Striated
Involuntary
Medium speed contractions

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Smooth Muscle

Fusiform cells
One nucleus per cell
Nonstriated
Involuntary
Slow, wave-like contractions

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Basic Characteristics of
Muscle Tissues
Excitability
Response to stimuli
Conductivity
Able to conduct action potential
Contractibility
Able to shorten in length
Extensibility
Stretches when pulled
Elasticity
Tends to return to original shape & length after
contraction or extension
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Skeletal Muscle
Attached to bones & moves skeleton
Makes up 40% of BW in men and 32% of BW in women

Main functions of skeletal muscle:

Initiate movements
Perform work
Maintain posture
Stabilise joints
Generate heat

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Level of Organisationin Skeletal

Muscle
Skeletal Muscle(organ)
Fascicle
(bundle of muscle fibres)
Muscle Fibre(cell)
Myofibril
Sarcomere
Filaments(Thin actin)
(Thick -myosin)

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Membranes of Skeletal
Muscle
Muscle surrounded by epimysium
Bundles of fibres(fascicles) surrounded by perimysium
Muscle fibresurrounded by endomysium
These connective tissues extend beyond the ends of
muscle to form tendons that attach muscle to bones

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Skeletal Muscle Fibre

Large, elongated, shape like

Transverse tubules (T-tubules)
cylinder
internal conduction system
10 100 m in diameter, up to
Myofibrils for contraction
750,000 m (0.75 m) in length
Sarcomeresregular arrangement
(extend entire length of muscle) of thin (actin) & thick (myosin)
Multinucleated with abundant of filaments
mitochondria
Actinfilaments interdigitatewith
Sarcolemma(cell membrane)
myosin filaments
Sarcoplasm(muscle cell
Appears striated under
cytoplasm)
microscope
Sarcoplasmic reticulum (modified
ER)
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Structure of a Skeletal Muscle

Fibre

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Electron Micrograph
of Skeletal Muscle

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Sarcomere
The functional unit of skeletal muscle
Multi-protein complexes composed
different filament systems:
Thin filament system
Thick filament system

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Muscle Tissue
Skeletal Muscle
Cardiac Muscle
Smooth Muscle

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Microanatomy of
Skeletal Muscle

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Z line

Z line

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H Band

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Sarcomere Relaxed

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Sarcomere Partially
Contracted

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Sarcomere Completely
Contracted

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Binding Site

Tropomyosin

Troponin

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Myosin

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Sarcomere

sarcomere

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Sarcomere

Sarcomere

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Sarcomere

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Sarcomere
A band (dark band)
consists of a stacked set of thick filaments

I band (light band)

Consists of the array of thin filaments, and is the region where they do
not overlap the thick filaments

H zone
The lighter area in the centre of A band where the thin filaments do not
overlap with thick filaments

M line
Consists of supporting proteins that hold the thick filaments together
vertically within each stack

Z line
Consists of supporting proteins that hold the thin filaments together
vertically within each stack

Area between two Z lines is called a sarcomere

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Thin Filament

Actin
Spherical in shape, with a special binding site for attachment with
myosin cross bridge

Joined into two strands and twisted together to form the

backbone of a thin filament
Tropomyosin
Threadlike proteins that lie end-to-end alongside the
groove of the actin spiral
Covers active sites of actin
Troponin complex
binds to actin & holds tropomyosin in place
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Thin Filament

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Thin Filament
TroponinComplex

TnT binds to tropomyosin

TnC binds to Ca2+
TnI binds to actin
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Thick Filament
Each thick filament is composed of
several hundred myosin molecules
packed together
A single myosin protein looks like 2
golf clubs with shafts twisted about
one another
Myosin molecules have elongated
tails & globular heads
Heads form cross-bridges between
thick and thin filaments during
contraction
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Thick Filament
Cross Bridges
Each cross bridge has two
important sites:
An actin-binding site
A myosin ATPase site

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Organisationof Actinand MyosinCross bridges

Thin filaments are
arranged hexagonally
around thick filaments
Each thin filament is
surrounded by 3 thick
filaments
Cross bridges project
from each thick filament
in all 6 directions toward
the surrounding thin
filaments
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Contraction of Muscle Fibres

Done by sliding actin filaments

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Contraction of Muscle Fibres

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Contraction of Muscle Fibres

Sliding Filament Theory
Contraction occurs by actin filaments sliding into
myosin filaments
Actin filaments move, myosin filaments remain
stationary
Sarcomeres shortened
Cause whole muscle to contract

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Contraction of Muscle Fibres

Role of Calcium

Ca2+released from
sarcoplasmic reticulum
Ca2+binds to troponin C
Troponin turns, moves
tropomyosin & exposes actin
active site
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Contraction of Muscle Fibres

Role of Calcium
Myosin head binds to actin
active site, form cross-bridge, move
& produces powerful strokes
Actin slides in muscle fibre
contracts
Cross-bridge action continues
while Ca2+is present
When action potential stops,
Ca2+is pumped back to SR
Tropomyosin covers back actins
active site
Relaxation occurs

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Contraction of Muscle Fibres

Role of Calcium

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Contraction of Muscle Fibres

Role of ATP
ATP split by myosin ATPase ; ADP and
Pi remain attached to myosin; energy is
stored within the cross bridge
Mg2+must be attached to ATP before
ATPase can split the ATP
Ca2+ released on excitation, removes
inhibitory influence from actin
energised myosin cross bridge bind with
actin
Cross bridge bends and causes power
stroke
ADP and Piare released after power
stroke is completed
ATPase site is free for attachment of
another ATP
Attachment of new ATP permits
detachment of cross bridge
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Contraction of Muscle Fibres

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Contraction of Muscle Fibres

All the cross bridges power strokes are directed

toward the centre of the sarcomere
All 6 of the surrounding thin filaments on each end
of the sarcomere are pulled inward simultaneously
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Contraction of Muscle Fibres

Rigor Mortis

Stiffness of death a
generalised locking in place of
skeletal muscle that begins 3 to 4
hours after death
Following death, [Ca2+]ibegins
to rise
This Ca2+moves the regulatory
proteins aside, permitting actin
bind with the myosin cross bridges,
which were already charged with
ATP before death
No fresh ATP available after
death, actin and myosin remain
bound in rigor complex
Resulting in stiffness condition
of dead muscles
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Electrical Properties of Muscle Fibres

Resting membrane potential:-90mV

potential: +30mV

Membran potensial(mV)

When an adequate stimulus is given

action potential

Depolarisation is due to influx of Na+

Time taken: 1 2 msec
Absolute refractory period & relative
refractory period present
Action potential results in muscle
contraction

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Action Potential and Muscle Twitch

Latent period

Membran potensial(mV)

Tension

The delay between stimulation and the

onset of contraction (a few msec)

Contraction time
The time from the onset of contraction
until peak tension is developed (average ~
50 msec)

Relaxation time
The time from peak tension until
relaxation (~ 50 msec or more)

A single contraction/relaxation cycle

is called a muscle twitch
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Excitation-Contraction Coupling
Refers to the series of events linking muscle
excitation (electrical events) to muscle contraction
(mechanical events)
Electrical events presence of action potential
Mechanical events cross-bridge activity
Electrical events come first before mechanical
events
Ca2+ is the link between excitation and contraction
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Excitation-Contraction Coupling
Sarcoplasmic Reticulum (SR)
The surface membrane at each
junction of A band and I band
dips into muscle fiber to form a
T tubule
Action potential on the surface
membrane spreads down into the
T tubule
The presence of local action
potential in T tubule induces
permeability changes in the
sarcoplasmic reticulum
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Excitation-Contraction Coupling
Release of Ca2+ from SR
When action potential is
propagated down the T tubules,
local depolarisation activates the
voltage-gated dihydropyridine
receptors in T tubule
These activated receptors in
turn trigger the opening of
Ca2+-release channels (alias
ryanodine receptors) in adjacent
lateral sacs of SR
Ca2+ is released into the
surrounding sarcoplasm
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Relaxation of Muscle Fibres

When ACh is removed from the neuromuscular junction, the
muscle fibre action potential ceases
No longer a local potential in T tubules to trigger Ca2+
release
Released Ca2+ is pumped back into the lateral sacs by
Ca2+-ATPase pump
Removal of sarcoplasmic Ca2+allows the troponintropomyosin complex to slip back into its blocking position
Actin and myosin are no longer able to bind at the cross
bridges
Thin filaments are able to return passively to their resting
position
Relaxation occurs
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Excitation-Contraction Coupling

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Excitation-Contraction Coupling and Relaxation

Summary of Events
1.Ach released from the terminal of a motor neuron initiates an action potential in
the muscle fibres
2.Muscle action potential travels down T tubule
3.Causes SR to release Ca2+ into sarcoplasm
4.Ca2+ binds to troponin, exposing actins cross-bridge binding sites
5.Myosin head binds to active site, form cross-bride, moves and produces power
stroke
6.Actin slides in, muscle fibre contracts resulting in contraction of whole muscle
7.ADP and Piare released after the power stroke is complete
8.New ATP binds to myosin head; detachment of the cross bridge
9.Cross-bridge action continues while Ca2+ is present
10.When action potential stops, Ca2+ pumped back to SR
11.Tropomyosin covers back active sites
12.Relaxation occurs
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Neuromuscular Junction

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Acetylcholine Opens Na
Channel

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Muscle Contraction
Summary
Nerve impulse reaches myoneural
junction
Acetylcholine is released from motor
neuron
Ach binds with receptors in the muscle
membrane to allow sodium to enter
Sodium influx will generate an action
potential in the sarcolemma
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Muscle Contraction
Continued
Action potential travels down T tubule
Sarcoplamic reticulum releases
calcium
Calcium binds with troponin to move
the troponin, tropomyosin complex
Binding sites in the actin filament are
exposed

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Muscle Contraction
Continued
Myosin head attach to binding sites
and create a power stroke
ATP detaches myosin heads and
energizes them for another
contaction
When action potentials cease the
muscle stop contracting

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Motor Unit
All the muscle cells
controlled by one nerve cell

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Motor Unit Ratios

Back muscles
1:100

Finger muscles
1:10

Eye muscles
1:1

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ATP

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Creatine
Molecule capable of storing ATP
energy
Creatine + ATP

Creatine phosphate + ADP

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Creatine Phosphate
Molecule with stored ATP energy
Creatine phosphate + ADP

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Creatine + ATP

Muscle Fatique
Lack of oxygen causes ATP deficit
Lactic acid builds up from anaerobic
respiration

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Muscle Atrophy
Weakening and shrinking of a muscle
May be caused
Immobilization
Loss of neural stimulation

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Muscle Hypertrophy
Enlargement of a
muscle
More capillaries
More
mitochondria
Caused by
Strenuous exercise
Steroid hormones
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Steroid Hormones
Stimulate muscle growth and
hypertrophy

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Muscle Tonus
Tightness of a muscle
Some fibers always contracted

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Tetany
Sustained contraction of a muscle
Result of a rapid succession of nerve
impulses

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Tetanus

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Refractory Period
Brief period of time in which muscle
cells will not respond to a stimulus

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Refractory

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Refractory Periods

Skeletal Muscle

Cardiac Muscle

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Isometric Contraction
Produces no movement
Used in
Standing
Sitting
Posture

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Isotonic Contraction
Produces movement
Used in
Walking
Moving any part of the body

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