Muscles contract as a result of direct interaction between two proteins--actin and myosin. Other proteins and substances such as calcium, sodium, neurotransmitter, and ATP play important supportive and regulatory roles.







Myosin is a a motor protein with a double globular head and a double intertwined coiled tail region


The globular head has a region bound with ATPase and an actin binding site.


Actin is a protein that appears as a twisted strand of pearls.


There are two other proteins associated with actin.


Tropomyosin surrounds the actin and serves to stiffen the molecule. It also plays a major regulatory role by covering active sites. Myosin has a significant chemical affinity to the active sites.


Troponin binds to tropomyosin and actin and under specific conditions, can change the shape of the tropomyosin.





Functional muscle contraction is dependent upon an intact nervous system.







The basic structure of the nervous system is the neuron. Neurons are specialized to receive chemical signals, transmit the signal down the neuron, and then release a chemical (neurotransmitter) onto another structure (neuron, muscle fiber, gland, etc) to influence or control its function.







Muscle fiber contraction is a depolarizing event.







Though the neuron controls the contractile function of a muscle cell. The neuron and muscle cell do not touch each other.





The secretory region of the neuron is called the terminal buton.


The space between the neuron and muscle is called the synaptic cleft.


On average, the space is 20 nanometers.


The terminal buton contains acetylcholine (ACh) vesicles. ACh is a chemical known as a neurotransmitter.


Because of the synaptic cleft, the neuron must release a chemical that crosses over the synapse and binds to the sarcolemma.






When the neuron signal reaches the terminal buton, it causes a change in the permeability in calcium.


At rest the terminal buton is impermeable to calcium.


There is a higher concentration of calcium outside of the cell as compared to inside.


When protein calcium channels open, calcium enters the terminal buton.


The presence of calcium in the terminal buton cause the ACh vesicles to bind to the neuronal plasma membrane and release ACh onto the sarcolemma.


The area where the terminal buton and muscle fiber is called the neuromuscular junction.


The sarcolemma in the in the neuromuscular junction is called the motor endplate.


The motor endplate presents with extra folding known as junctional folds that greatly increase the sarcolemma surface area.


The motor endplate also includes many ACh receptors situated on protein sodium channels.


When ACh binds to these receptors, the configuration of the proteins is changed and the sodium channels open.


Given the concentration gradient. Sodium rushes into the cell at the motor endplate.


The motor endplate begins to depolarize.













As sodium ions continue to diffuse into the cell at the motor endplate, the membrane potential continues to decrease.

At a membrane potential of -55 mV, sodium channels open all along the sarcolemma.

-55 mV is referred to as threshold potential.

Action potential is when the sodium ions channel open all along the sarcolemma.

Once threshold is reached and action potential initiated, the muscle fiber will contract.





When the influxing sodium enters the transverse tubules it facilitates the release of intracellular calcium from the terminal cisterns.

The released calcium binds to troponin, changing the configuration of the tropomyosin thereby exposing the active sites on the actin molecule.

With the actin active sites exposed, the myosin heads form the myosin-actin cross bridge and pulls the actin that in turn pulls the Z disc, shortening the length of the sarcomere. Hence, the muscle fiber contracts.


This is called the sliding filament mechanism.

ATP plays a critical role in breaking the cross-bridge so that the myosin-actin interaction can be repeated.