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Page1
dr:
Ayub
abdulkadir
abdi
Skeletal muscle contraction follow a term known as excitation – contraction coupling
First coined by Alexander Sandow in 1952, the term excitation–contraction coupling (ECC)
describes the rapid communication between electrical events occurring in the plasma membrane
of skeletal muscle fibres and Ca2+
release from the Sarcoplasmic Reticulum, which leads
to contraction.
Steps Involving in muscle contraction:
A) Events at the nerve terminal:
1- Propagation of action potential at the axonal terminal of the motor neuron.
2- Activation and opening of voltage gated calcium channels.
3- Calcium enters the nerve and bind with a protein called calmodulin.
4- Formation of calcium calmodulin complex which in turn activates a protein kinase
(PK).
5- Protein kinase activates a SNAREs protein on a vesicle that contains a
neurotransmitter known as ACETYLCHOLINE.
6- Now the vesicle come close to the membrane of axon terminal.
7- Fusion of the vesicle membrane and the axon terminal membrane.
8- Release of acetylcholine from the vesicle.
Mechanism of skeletal muscle contraction:
Page2
dr:
Ayub
abdulkadir
abdi
B) Events at the neuromuscular junction “space b/w nerve and the
muscle”:
9- The acetylcholine binds to the ligand gated sodium channels on the muscle cell, the
receptors are called Cholinergic (muscarinic M) receptors.
10- Activation of these receptors and opening, before this step the inside muscle cell are
negative ~ (-90 mV).
11- Extracellular sodium enters the muscle cell and creates a local potential across the
cell membrane ~ (- 70 mV)
12- These local potential activates another channels on the muscle cell called ‘voltage
gated sodium channels’.
13- Opening these channels and causes more sodium to enter the cell and leads to
generation of action potential; now inside the cell will become more positive ~ (+ 55
mV).
Page3
dr:
Ayub
abdulkadir
abdi
C) Events at the muscle cell:
14- Action potential travels across the T – tube of the muscle cell.
15- This action potential causes a conformational changes on a protein called voltage-
sensing DIHYDROPYRIDINE (DHP) RECEPTORS.
16- Activated DHP receptors in turn trigger the opening of Ca2+-release channels located
on the terminal cisterns called RYANODINE RECEPTOR (RYR).
17- Release of calcium ions into the sarcoplasm and concentration of Ca2+
in the ICF is
increased creates a calcium signals or spark.
18- Calcium binds to troponin (TnC) complex and causes alteration in on their shape
which causes the tropomyosin molecule to move laterally, uncovering the binding
sites on the actin molecules.
19- The head of myosin molecule binds with ATP so the head is energized and extends
perpendicularly (at 90° conformation) towards the actin filament and gets attached to
the actin filament, so the head of myosin bind
20- Formation of actin – myosin complex [cross bridge] causes a power stroke.
21- Another ATP will bind to myosin head to detach from actin binding site.
22- Steps 19- 21 are continues until the close of actin binding site by tropomysin.
Page4
dr:
Ayub
abdulkadir
abdi
Is a state in which the muscle return to its normal position and length.
Steps involving in muscle relaxation:
1- Relaxation of the muscle occurs when calcium ions are pumped back into the L tubules.
2- Calcium content in sarcoplasm decreases leading to the release of calcium ions from the
troponin.
3- So calcium will enter the sarcoplasmic reticulum by using an ATP and bind to a protein
in the SR known as CALSEQUESTRIN ‘is protein that can bind up to 40 times more
calcium’
4- Binding of ATP to myosin head causes detachment of actin and myosin head.
5- Relaxation of muscle fiber.
6- Na/ K Pump is used pumping 3 Na outside the muscle cell and pumping 2 K inside the
muscle cell.
7- Release of Acetylcholine from cholinergic receptors.
8- Breakdown of acetylcholine by an enzyme called ACETYLCHOLINESTRASE and
reuptake by nerve axonal terminal.
Mechanism of skeletal muscle relaxation:

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A summary of skeletal muscle contraction and relaxation

  • 1. Page1 dr: Ayub abdulkadir abdi Skeletal muscle contraction follow a term known as excitation – contraction coupling First coined by Alexander Sandow in 1952, the term excitation–contraction coupling (ECC) describes the rapid communication between electrical events occurring in the plasma membrane of skeletal muscle fibres and Ca2+ release from the Sarcoplasmic Reticulum, which leads to contraction. Steps Involving in muscle contraction: A) Events at the nerve terminal: 1- Propagation of action potential at the axonal terminal of the motor neuron. 2- Activation and opening of voltage gated calcium channels. 3- Calcium enters the nerve and bind with a protein called calmodulin. 4- Formation of calcium calmodulin complex which in turn activates a protein kinase (PK). 5- Protein kinase activates a SNAREs protein on a vesicle that contains a neurotransmitter known as ACETYLCHOLINE. 6- Now the vesicle come close to the membrane of axon terminal. 7- Fusion of the vesicle membrane and the axon terminal membrane. 8- Release of acetylcholine from the vesicle. Mechanism of skeletal muscle contraction:
  • 2. Page2 dr: Ayub abdulkadir abdi B) Events at the neuromuscular junction “space b/w nerve and the muscle”: 9- The acetylcholine binds to the ligand gated sodium channels on the muscle cell, the receptors are called Cholinergic (muscarinic M) receptors. 10- Activation of these receptors and opening, before this step the inside muscle cell are negative ~ (-90 mV). 11- Extracellular sodium enters the muscle cell and creates a local potential across the cell membrane ~ (- 70 mV) 12- These local potential activates another channels on the muscle cell called ‘voltage gated sodium channels’. 13- Opening these channels and causes more sodium to enter the cell and leads to generation of action potential; now inside the cell will become more positive ~ (+ 55 mV).
  • 3. Page3 dr: Ayub abdulkadir abdi C) Events at the muscle cell: 14- Action potential travels across the T – tube of the muscle cell. 15- This action potential causes a conformational changes on a protein called voltage- sensing DIHYDROPYRIDINE (DHP) RECEPTORS. 16- Activated DHP receptors in turn trigger the opening of Ca2+-release channels located on the terminal cisterns called RYANODINE RECEPTOR (RYR). 17- Release of calcium ions into the sarcoplasm and concentration of Ca2+ in the ICF is increased creates a calcium signals or spark. 18- Calcium binds to troponin (TnC) complex and causes alteration in on their shape which causes the tropomyosin molecule to move laterally, uncovering the binding sites on the actin molecules. 19- The head of myosin molecule binds with ATP so the head is energized and extends perpendicularly (at 90° conformation) towards the actin filament and gets attached to the actin filament, so the head of myosin bind 20- Formation of actin – myosin complex [cross bridge] causes a power stroke. 21- Another ATP will bind to myosin head to detach from actin binding site. 22- Steps 19- 21 are continues until the close of actin binding site by tropomysin.
  • 4. Page4 dr: Ayub abdulkadir abdi Is a state in which the muscle return to its normal position and length. Steps involving in muscle relaxation: 1- Relaxation of the muscle occurs when calcium ions are pumped back into the L tubules. 2- Calcium content in sarcoplasm decreases leading to the release of calcium ions from the troponin. 3- So calcium will enter the sarcoplasmic reticulum by using an ATP and bind to a protein in the SR known as CALSEQUESTRIN ‘is protein that can bind up to 40 times more calcium’ 4- Binding of ATP to myosin head causes detachment of actin and myosin head. 5- Relaxation of muscle fiber. 6- Na/ K Pump is used pumping 3 Na outside the muscle cell and pumping 2 K inside the muscle cell. 7- Release of Acetylcholine from cholinergic receptors. 8- Breakdown of acetylcholine by an enzyme called ACETYLCHOLINESTRASE and reuptake by nerve axonal terminal. Mechanism of skeletal muscle relaxation: