Professional Documents
Culture Documents
Muscle
Muscle
Muscle
Clinical Physiology
● 1. Myasthenia Gravis : An autoimmune disorder that is caused by immune system
antibodies that mask the nicotinic acetylcholine receptors and cause muscle
weakness.
● 2. Black widow spider venom involves a component , which is known as latrotoxin .
This toxin causes increased release of acetylcholine and stimulates severe and
painful muscle cramps.
● 3. Botulinum toxin prevents the release of acetylcholine from the end plate of the
motor nerve and thus causes muscle paralysis.
● The muscle fiber (cell) is composed of many myofibrils , which are made up of long
proteins , called myofilaments . There are two types of myofilaments :
● a- Thick myofilament ( Myosin) : The thick filament is composed of a protein called
myosin , which has a core tail , and a head , which is a projection from the tail .
● The head has two binding sites : one for actin molecule and other for ATP molecule
.It has a hinge ( neck) at the point , where it leaves the tail. The hinge of the myosin
head allows the head to swivel back and forth which causes muscle contraction.
● b- Thin myofilament ( Actin) : The thin filament is called actin . It is formed of three
proteins : Actin molecules ( G- Actin) is a spherical protein , which form two coils on
each other protein chains , Tropomyosin: molecules are thin proteins that wrap the G
Actin and cover the binding sites of myosin in the relaxing state of skeletal muscle ,
and Troponin molecules ( Troponin C , Troponin I and Troponin T) , which are small
proteins that are connected to each other and form troponin complex , which have
binding sites for calcium ions.
● The myofilaments in skeletal muscles are arranged in a specific pattern , called
Sarcomere . In Sarcomere a thick filament ( myosin) is surrounded by six thin
myofilaments ( actin) . But in a side view , each actin appears to be above and under
myosin. . In sarcomere the thin filaments extend to the end of the sarcomere , where
the adjacent thin filaments are connected by Z-line ( composed of different type
protein) , while the thick filaments remain in the center and not extend to the end of
sarcomere . This is the cause for the striated appearance of skeletal muscle under
the microscope , as the ends of sarcomere ( I bands ) appear lighter than the center (
A band ).
● The cell membrane of muscle cells ( also called sarcolemma ) is unique in that it has
transverse tubules ( T- tubules) which pass down the cell and open in the
endoplasmic reticulum of the muscle cell.
● Endoplasmic reticulum of the muscle cell ( known as sarcoplasmic reticulum) is
different in that it functions as a store for calcium ions , more than being involved in
protein synthesis .
● The membrane of the sarcoplasmic reticulum has many calcium pumps that pump
calcium inside the sarcoplasmic reticulum from the sarcoplasm ( cytoplasm of the
muscle cell ). Sarcoplasmic reticulum is abundant in the muscle cells , and is closely
associated with the myofibrils.
● T- Tubules of the sarcolemma are connected to sarcoplasmic reticulum by receptor
protein , known as DHP receptor , which is a voltage sensor. When the action
potential is conducted to the T- Tubule , it causes conformational change in the
mentioned receptor . This change activates a receptor , called ryanodine receptor ,
which will cause release of calcium from the sarcoplasm .
● Now, after we understood the structure of the skeletal muscle , we can explain how it
contracts:
● Muscle cells to contract have to receive a nerve impulse ( a voluntary muscle) .
When the nerve impulse reaches the plasmalemma and passes down the T-Tubules ,
it causes opening of the calcium pumps in the sarcoplasmic reticulum and releasing
of calcium within the myofilaments. Calcium ions then attach to the Troponin and
causes changes in shape and position of troponin , which will move the Tropomyosin
, which is attached to Troponin, this in turn will uncover the myosin binding site on
Actin molecule ( G actin) . This will enable the myosin head to connect to actin and
swivel , this will pull the actin forward.
● Here we have to notice that many myosin heads ( not only a single head ) swivel at
the same time , pulling the entire thin filament forward.
● ATP molecule bind to the myosin head at the end of swivel , breaking the bond
between the actin and myosin and the myosin swivel backward .This would break the
ATP into ADP and organic phosphate Pi, which causes the myosin to bind to a new
actin molecule and swivel forward again. The end result of this series of processes is
shortening of the sarcomere.
● When the nervous impulse stops , the muscle relaxes . Because in the absence of
nerve impulse , there is no release of calcium.
Clinical Physiology
Rigor mortis is a sign of death , which is presented as a muscle stiffness of the cadaver , due
to inability of muscles to relax , because of the lack of ATP , which production is stopped
after death , because the metabolism is terminated.
3- Extensibility : Muscles are able to stretch when they are pulled . The level of extensibility
depends on many factors within the muscle itself , including the connective tissue , the
muscle mass , and others.
4- Elasticity : Muscles are able to return to their original shape and length after contraction or
extension .
If a second stimulus affects the muscle on the top of the first one before relaxation is
complete , it will contract with more force . This is called wave summation .
If many stimuli (2-5/s) affect the muscle fiber before relaxation is complete , the muscle
contraction will increase with each stimulus . This is called staircase phenomena ( or
incomplete tetanus ) . If the stimuli are more than that ( 20/s ) the contraction will reach its
maximum and the staircase will fuse in a smooth curve ( complete tetanus).
A stronger contraction may occur if more motor-units are involved . Motor unit means : the
motor nerve and muscle fibers , innervated by it . Involving of more motor units to achieve
stronger contraction is called motor-units summation