Chapter 3 (6%)
Support and movement system
Movements:
The act of changing position or place by
the entire body of an organism or by one or more of its parts is called
movement.
1.
Brownian
movement: Zig-zag motion of molecules in the
cytosol.(molecular level)
2.
Cyclosis:
Streaming movement of cytoplasm. It ensures uniform distribution of materials
within the cell.(cellular level)
3.
Amoeboid
movement: Movement produced by temporary protoplasmic
outgrowth, called Pseudopodia.
4.
Ciliary
movement: movement triggered by very fine hair like
structures called ‘Cilia’.
5. Flagellar movement:
Movement by using flagellum, a whip like structure found in some sponges and
coelenterates.
Cyclosis, Amoeboid movement, ciliary movement and flagellar
movement are examples of nonmuscular
movements.
Muscular
Movement: Movement produced by Muscles, responsible for
locomotion as well as movement of body parts. Organisms with the ability to
move are called Motile. Locomotion
is the movement of an organism as a whole resulting in displacement.
Muscle:Muscles
are formed of specialised elongated cells called Muscle fibres. The
properties of muscle fibres are electric
excitability, contractility and elasticity.
There are three types of Muscles:
1.
Voluntary/
skeletal/striated muscles: These muscles exhibit striations,
found attached with the skeleton by tendon. When
examined under microscope, fibres of this muscle show prominent transverse
striations (striated muscles) and they work under the will or conscious control
of nervous system, hence are also called voluntary muscles.
2.
Involuntary/
smooth/ non-striated/visceral muscles: No
striations and are smooth in appearance. They are not under the voluntary
control of our nervous system. These muscles are found in the hollow internal
organs like digestive tracts, blood vessels etc. hence called as visceral
muscles.
3.
Cardiac
muscles: these are the striated muscles of the wall
of Heart. They are involuntary in action and work tirelessly till the end. They have
inherent rhythmic contractility.
Structure of Striated (skeletal) Muscles:
The
striated muscles form the body flesh and about 80% of the soft body tissue. Human
body has around 650 skeletal muscles.Each muscle is enclosed in a dense
connective tissue sheath called epimysium.
It encloses numerous small muscle bundles called Muscle Fasciculi, each with a connective tissue covering called Perimysium. Each muscle fascicle is in
turn formed of several Muscle fibres. Each Muscle fibre is covered with endomysium formed of loose connective
tissue. At the junction of a muscle with a tendon, the endomysium, perimysium
and epimysium are continuous with the fibres of the tendon.
Structure of a muscle fibre (myocyte):
Muscle fibres are the structural and
functional unit of Muscle. Each muscle fibre is a long, unbranched and
cylindrical fibre. It is covered with a thin elastic membrane called sarcolemma which encloses a
multinucleated (syncytial) cytoplasm called sarcoplasm. In the sarcoplasm, numerous myofibrils are embedded. These are tightly packed in parallel
bundles, separated by thin sheet of cytoplasm.
Myofibrils
form the contractile apparatus of a muscle fibre. It has transverse striations
in the form of alternate dark and light
cross bands. Because of these
striations, these muscles are called
striated or striped muscles.
Light
bands (I-band) are formed of thin actin filaments.
Actin filaments are firmly attached to Z
disc. The part of myofibril between two adjacent Z discs is known as Sarcomere.
Dark bands
(A band) are formed of thick Myosin filaments.
They are free at both ends and are thicker than I-bands. A band is also
bisected at the mid-point by a thin paler line which is known as H zone.
A narrow dark line passes through H- band. It is called M-line.
Myosin and Actin myofilaments are called as Primary and secondary myofilaments
respectively.
Different types of proteins present in
muscles:
1.
Contractile proteins: Actin and
Myosin.
2.
Regulatory proteins: Tropomyosin
and troponin. They regulate the interaction between myosin and actin.
Tropomyosins are
long filaments that lay in the groove between two chains of actin molecules.
With troponin molecules it covers the binding site on actin where myosin head
aligns.
Troponins are small
globular proteins molecule. Binding of Troponin to tropomyosin prevents the
myosin heads from contacting actin and prevent contraction.
Mechanism of muscle contraction (Sliding filament theory):
Sarcomere is the unit of muscle contraction.
At rest, when muscle is relaxed, the actin and myosin filaments lie
parallel to each other and actin partially overlapping at the two ends of
myosin filament. The H zones remain wide.
During muscle contraction, the thin actin filaments slides over myosin
filaments towards H zone till the H zone disappears. Hence the sarcomere
shortens in size and also the whole muscle filament. This mechanism of muscle
contraction was given by A.F.Huxley, H.E. Huxley and Jean
Hanson and was called Sliding filament theory .
Here is what happens in detail.
1.
A nervous impulse arrives at the neuromuscular junction, which
causes release of a chemical called Acetylcholine. The presence of
Acetylcholine causes the depolarisation of the motor end plate which travels
throughout the muscle by the transverse tubules, causing Calcium (Ca+) to be
released from the sarcoplasmic reticulum.
2.
In the presence of high concentrations of Ca+, the
Ca+ binds to Troponin, changing its shape and so moving Tropomyosin from the
active site of the Actin. The Myosin filaments can now attach to the Actin,
forming a cross-bridge.
3.
The breakdown of ATP releases energy which
enables the Myosin to pull the Actin filaments inwards and so shortening the
muscle. This occurs along the entire length of every myofibril in the muscle
cell.
4.
The Myosin detaches from the Actin and the
cross-bridge is broken when an ATP molecule binds to the Myosin head. When the
ATP is then broken down, the Myosin head can again attach to an Actin binding
site further along the Actin filament and repeat the 'power stroke'.
5.
This process of muscular contraction can last for as
long as there is adequate ATP and Ca+ stores. Once the impulse stops the Ca+ is
pumped back to the Sarcoplasmic Reticulum and the Actin returns to its resting
position causing the muscle to lengthen and relax.
Prerequisites for muscle contraction:
1. Nervous stimulus for
contraction.
2. ATP as a source of energy
3. Ca++ ions to expose binding
site of actin molecules and initiate ATPase
activity of myosin head.
Electrical and biochemical events during muscle contraction:
a.
Depolarisation of Sarcolemma to set up
action potential.
b.
Action potential transferred to
sarcoplasmic reticulum cause release of calcium ions.
c.
Calcium ions bind to troponin and
tropomyosin and thus changes the 3D shape of troponin-tropomyosin-actin complex that makes the active site on
actin filaments exposed.
d.
Calcium ions also act on myosin heads,
activating them to release energy.
e.
Formation of actin-myosin complex:
myosin heads bind to the active sites of actin filament forming cross-bridges.
f.
Sliding of actin filaments over myosin
filaments and contraction of muscle.
g.
Repolarisation of sarcolemma and
relaxation of muscles.
Energy for muscle contraction:
·
Energy for contraction is provided by
hydrolysis of ATP by the enzyme myosin
ATPase.
·
Creatine- phosphate ADP change to
ATP
·
When ATP consumption is more muscle
fibres respire anaerobically (glycolysis) to replenish ATP. This produce Lactic
acid as a by-product.
·
1/5th of lactic acid is
oxidised to CO2 and water.
·
4/5th of it is changed into
glycogen in the liver. (refer fig.3.7)
Cori Cycle
Lactic acid formed during anaerobic
respiration in voluntary muscles is carried by blood to liver, where it is
converted to glycogen. Glycogen releases glucose in to the blood which is again
converted into glycogen in the muscles. This lactic acid-glycogen-glucose-glycogen
cycle is called Cori’s cycle.
Motor unit:
The set of muscle fibres innervated by all the axonal branches of
a motor neuron constitutes a motor unit.
The area of contact between a nerve and muscle fibre is known as Motor end plate or neuro-muscular junction. (fig. 3.10)
Threshold
stimulus: for being stimulated to contract, the muscle fibre
always requires a specific minimum intensity of the nerve impulse. Below this
intensity, the stimulus fails to evoke contraction. This is called threshold
stimulus.
Summation:
When a muscle is stimulated by a single inadequate stimulus, no
contraction occurs. But if two or more such below threshold stimuli are given
in rapid succession, contraction is evoked. This addictive effect is called
Summation.
All or
none law: A muscle fibre fails to contract if the
strength of stimulus is below threshold. But if the strength of stimulus is
equal to or higher than the threshold stimulus, the muscle fibre will contract
with maximum force irrespective of strength of stimulus. This is known as ‘All
or none law’.
Muscle
Twitch and Tetanus: A muscle fibre contracts only once on
stimulated by a single nerve impulse or by single electric shock. This single
isolated contraction of muscle fibre is called single muscle twitch. Immediately after a twitch, the muscle fibre
relaxes.
But, if a muscle fibre is stimulated by a
rapid succession, due to repeated brief stimuli, the muscle remains in a state
of long contraction phase. Such a sustained contraction is called Tetanus. Almost all our daily
activities are carried out by tetanic contraction.
Muscle
Fatigue: Reduction in the
force of contraction of muscle fibres after their prolonged contraction is
called muscle fatigue. It may develop due to lactic acid accumulation, fall of
pH, exhaustion of glycogen or exhaustion of ATP.
Refractory
period: It is the time
between two successive stimuli during which a muscle fibre fails in responding
to the second stimulus after the first excitation.
Rigor
Mortis: ATP is essential during muscle contraction for
dissociation of actin and myosin association. After death, cells cannot
synthesise ATP. Hence the actomyosin-ADP bonds fail to separate and muscle
remains in a contracted state. This is called Death rigor or Rigor Mortis.
Antagonistic
muscles: The set of muscles which contract to produce
opposite movements at the same joint are called Antagonistic muscle. Eg: Biceps
and Triceps.
Types of
muscles on the basis of their function:
1. Abductors and Adductors: Abductor
muscles move the bone away from the middle line, while Adductor muscles moves
the bone towards the middle line.
2. Rotators: Rotators
cause a part to rotate on its axis.
3. Supinators and pronators: Contraction
of supinators rotates the forarm and turns the palm upward, while pronators
turn the hand or palm downward.
4. Flexors and Extensors: contraction of Flexor
muscle brings two bones closer while extensors increase the angle of a joint.
5. Levators and depressors: levators
raise the part while depressors lower the part.
6. Invertors and evertors: Invertor
muscle turn the sole inward and evertor muscle turn the sole outwards.
7.
Sphinctors:
These muscles are arranged like a ring around the apertures. They
open or close those apertures.
8.
Tensors:
these muscles make a part tense or more rigid.
The skeletal muscles are attached with the
bones by tendons. All the skeletal
muscles have their origin on one
bone and their insertion on the
other bone. The broad end of muscle attached to the relatively fixed bone is
called Origin. The opposite end of
muscle which is attached to the movable bone is called Insertion. The thick part of muscle between the two ends is called belly. (Fig.3.12)
Red and white muscle fibres:
Red muscle fibre
|
White muscle fibre
|
Red muscle fibres are thin and smaller in size
|
White muscle fibre are thick and larger in size
|
They are red in colour as they contain large amounts of
myoglobin
|
They
are white in colour as they contain small amounts of myoglobin
|
They contain numerous mitochondria
|
They contain less number of mitochondria
|
They carry out slow and sustained contractions for a long period
|
They
carry out fast work for short duration
|
1 Comments
thank you very much for this note la. I t is very helpful la.
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