MUSCLE CONTRACTION
Myofibrils
 1. thin filaments (Actin)
 2. thick filaments (Mysosin)
 3. elastic filaments (Titin)
 Thick and thin filaments overlap one another
to a greater or lesser extent. Pattern of
overlap causes cross striations in muscle
fibers.
MICROSCOPIC ANATOMY OF
SKELETAL MUSCLE TISSUE
Skeletal muscle contraction
 Myosin heads pull on the thin filaments
causing them to slide inward towards the Hzone.
 Thin filaments slide inward Z-discs come
toward each other.
 Sarcomere shortens, the lengths of thick and
thin filaments do not change.
Role of Ca2+ & Regulator proteins
 Muscle action potential starts Ca2+ channel
open in the SR membrane
 Increase Ca2+ in the sarcoplasm starts filament
sliding, decrease of Ca2+ turns off the process.
 Muscle fiber relaxed:- Ca2+ stored in SR
membrane.
 Ca2+ Combine with troponin causing it to
change shape
 Shape change moves the troponin-
tropomysin complex away from the myosin
binding sites on actin
 SR plays an active role by releasing Ca2+ and
actively absorbing them.
ATP in muscle contraction
 While muscle relaxed ATP attaches to ATP
binding sites on the mysosin heads.
 This transfers energy from ATP to the mysin
heads even before contraction begins.
 Mysoin cross bridges are in an activated state
 This produces the power stroke of contraction
during muscle contraction.
SMOOTH MUSCLE TISSUE
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Smooth muscle contraction
 Contraction starts slowly and last longer
(Ca2+ enters the sarcoplasm from extracellular fluid
and SR, it takes longer for Ca2+ to reach the actin
filaments, Moves slowly out of the muscle fiber)
 Smooth muscle cells can shorten & stretch to a
greater extent than other two types of muscles
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Contractile mechanism
1.
2.
3.
4.
5.
6.
7.
Sarcolemma depolarized, & Ca2+ enter into the
sarcoplasma
Ca2+binds to calmodulin protein
Ca2+ - calmodulin complex activates myosine
kinase enzyme
Myosine kinase enzyme phosphorylate myosin
Phosphorylate myosin & actin interact &
tension transmitted to intermediate filaments
Intermediate filaments pull on dense bodies
attached to sarcolemma
Contraction of muscle fibre
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Regulation of smooth muscle contraction
 Most fibres contracts in response to action
potentials from autonomic nervous system
(acetylcholine or noradrenalin
neurotransmitters). Involuntary
 Contracts & relax in response to stretching,
hormones, changes in pH, ions etc.
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Tutorial
 Compare & contrast the contraction process of
cardiac muscle with that of smooth muscle
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Cardiac muscle contraction
 Contractile mechanism of cardiac muscle is
similar to that of skeletal muscle
 But under normal conditions, cardiac muscle
tissue contracts & relaxes continuously &
rhythmically without stopping even the
person is at rest.
(compare with the skeletal muscle contraction)
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 Cardiac muscle tissue (in vertebrates) can
contract without nerve stimulation. Source of
stimulation – a conducting tissue of specialized
muscle tissue,
 nerve stimulation may cause the conducting
tissue to increase or decrease the rate of
discharge
(compare with the skeletal muscle)
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 Cardiac muscle depends mostly on aerobic
respiration to produce ATP (requires constant
supply of oxygen)
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 Cardiac muscle tissue remain contracted 10-15
times longer than skeletal muscle tissue
In cardiac muscle fibers, Ca2+ enters sarcoplasm
from


Sarcoplasmic Reticulum
extracellular fluid (ion channels open for a long
period)
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1.
Following the upstroke, cardiac muscle action
potential has a long plateau (longer
depolarization)
The long duration of action potential ensures that all
the cells of the ventricles are excited at the same
time, causing the ventricles to contract as a unit.
(essential for efficient pumping action of the heart)
Action potential of cardiac muscle differs from that of
nerve & skeletal muscle
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2. Each cardiac action potential follows a long
refractory period (several hundred milli
seconds)
This long period of refractoriness prevents
tetanic contractions.
Allows the muscle to relax and permit the
ventricles to fill with blood between action
potentials (No fatigue)
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