The contraction of a muscle is the physiological process by which the muscle fibers develop tension. This tension is produced by actin and myosin interaction in the filaments of muscle fibers and is activated by a nerve impulse from the Central Nervous System.
The opposite process, muscle relaxation, is the return of the fibers to a state of low tension and occurs in the absence of nervous stimulation.
skeletal muscle contraction
As in all vertebrate animals, skeletal muscle contraction is triggered by a nerve stimulation generated in the Central Nervous System and transmitted to the muscle through neurons. These neurons that innervate skeletal muscles are known as motor neurons.
Skeletal muscle contraction is, in general, a voluntary action whose signal is produced in the brain. Only in the case of simple reflexes does the signal originate in the spinal cord and they are not voluntary actions, although they continue to originate in the Central Nervous System.
The synapse between the motor neuron and muscle fibers forms the motor plate. Through this synapse, the electrical impulse is transmitted from the neuron, generating the depolarization of the muscle fiber membrane. This depolarization triggers the contraction of protein filaments in muscle fibers and thus muscle contraction.
To fully understand the process, it is necessary to know the structure of muscle fibers and myofilaments. Let's see each step.
motor end plate structure
In humans, and in all mammals, skeletal muscle fibers are unifocal. This means that a muscle fiber is innervated and controlled by a single motor neuron. However, a motor neuron, through the multiple axons it has, can innervate several muscle fibers at the same time causing them to contract as a group.
The motor neuron and all the muscle fibers it innervates form what is known as the motor unit. Within the motor unit, the synapse between the termination of each axon and the muscle fiber it innervates forms the motor end plate or neuromuscular junction.
The general structure of the end plate is similar to the synapse between two neurons. On the one hand there is the presynaptic neuron, which in this case is the motor neuron, followed by the synaptic cleft and then there is the postsynaptic element, which in the motor plate is the membrane of the muscle fiber, the sarcolemma.
In the cytoplasm of the presynaptic axon there are many acetylcholine vesicles, the neurotransmitter responsible for transmitting the action potential of the motor neuron to the muscle fiber. located in the muscle fiber membrane nicotinic-like cholinergic receptors that are activated by acetylcholine. In the synaptic cleft there acetylcholinesterasesenzymes responsible for degrading acetylcholine.
In the area of the motor plate, the sarcolemma presents folds called synaptic folds. Cholinergic receptors are located at the crests of these folds. In each end plate there are between 107 and 108 cholinergic receptors and are very scarce in the rest of the sarcolemma. The half-life of each receptor is approximately 10 days.
neuromuscular transmission
When the action potential of a motor neuron reaches the axon terminal of the motor end plate, acetylcholine is released which binds to cholinergic receptors on the muscle fiber and transmits the nerve impulse to the muscle. The process can be outlined in these steps:
- The action potential in the axon activates voltage-gated calcium channels. When these channels open, Ca enters2+ into the cytoplasm of the axon and exocytosis of acetylcholine vesicles.
- The acetylcholine diffuses across the synaptic cleft binds to cholinergic receptors of the muscle fiber.
- Binding of acetylcholine to its receptors causes a conformational change in the Na+ and K+ channels and opens them allowing the passage of these ions into the muscle fiber in favor of the electrochemical gradient.
- Approximately 60% of acetylcholine is degraded in the synaptic cleft before reaching receptors. the rest binds to the receptors and in just a few milliseconds it detaches and is also degraded. Acetylcholinestera splits acetylcholine into acetate and choline; choline is reuptaken by the presynaptic axon and acetate diffuses through the extracellular space.
- The flow of ions into the muscle fiber is predominantly Na+ due to its greater driving force. The entry of these ions causes a local membrane depolarization that is transmitted to adjacent areas generating the depolarization of the membrane of the entire muscle fiber. The nerve impulse has been transmitted to the muscle.
- The depolarization of the membrane activates the sarcoplasmic reticulum, already inside the muscle cell, and causes the contraction of proteins that form myofilaments.
structure of muscle fibers
Each muscle fiber of a skeletal muscle is a highly specialized cell with an elongated, cylindrical, multinucleated shape. In its membrane, called sarcolemmais where the motor plate is located.
The cytoplasm, called sarcoplasmis occupied almost entirely by fibrillar structures called myofibrils. Each myofibril is composed of protein microfilaments known as myofilaments.
The sarcolemma has numerous invaginations that form a tubular network, known as T tubules. This network allows the transmission of the impulse even to deep myofibrils.
Observing a myofibril under a microscope shows alternating dark and light bands, which is why skeletal muscle is also called striated muscle. The dark bands are called A-bands and the light bands are called I-bands.
In the center of each I band is a line, known as line or disk Z. From one line Z to the next one finds the sarcomere, the fundamental functional unit of muscle. Each myofibril is composed of a succession of sarcomeres with the same repeating structure.
Within each sarcomere, from the Z line at one end to the Z line at the other end, are the myofilaments. There are Two types of myofilaments, thick and thin, arranged alternately and cause the appearance of the A bands, made up of thick filaments, and the I bands, made up of thin filaments.
Since the Z line is located in the center of the I band, in the center of each sarcomere is a full A-band and on each side half band I.
On the sides of band A thick and thin filaments overlap but not in the central zone. For this reason, the central area of the A band appears lighter and forms the H band.
Each sarcomere is surrounded by the sarcoplasmic reticulum, a type of endoplasmic reticulum that does not have ribosomes, and by T tubules from the sarcolemma. The terminal vesicles of the sarcoplasmic reticulum of two neighboring sarcomeres are located on the sides of the same T tubule, forming what is known as the triad.
It is right here, in the triad, where electrical depolarization originating from the motor endplate reaches the sarcoplasmic reticulum and is transmitted to the myofilaments causing its contraction and with it muscle contraction.
contraction of myofilaments
Thin myofilaments are made up of actin microfilaments. On the outside of each actin microfilament there is tropomycin and troponin forming protein complexes, each with three subunits:
- Troponin C: can bind Ca ions2+.
- Troponin T: binds to tropomyosin and this to the actin microfilament.
- Toponin I: blocks actin.
For their part, thick myofilaments are made up of myosin microfilaments.
When an action potential arrives at the motor end plate and causes depolarization of the sarcolemma, the electrical impulse is transmitted through the T tubules until it reaches the sarcoplasmic reticulum in the triads. This causes Ca to be released2+ from the endoplasmic reticulum to the sarcoplasm.
These Ca ions2+ binds to troponin C and causes muscle contraction. When the stimulus ceases, the Ca ATPase2+ of the sarcoplasmic reticulum (SERCA) introduce the Ca2+ back into the sarcoplasmic reticulum. The decline in Ca concentration2+ in the sarcoplasm it makes possible the muscular relationship and the return to rest in the absence of nervous stimulation.
Filament sliding theory
One of the most widely accepted theories of muscle contraction holds that shortening and lengthening of muscle fibers is produced by interdigitate sliding of thin myofilaments on thick myofilaments. This sliding would cause the change in length of the sarcomere and thus muscle contraction:
Myosin microfilaments are rod-shaped. Each filament is arranged head out and the tail towards the center. In this way, the tails form the central axis of the thick myofilaments and the heads face out. The head is made up of heavy or globular meromyosin (with two subunits, the head or S1 and the neck or S2) and the tail is made up of light meromyosin (subunit S3).
The sliding of the thin filaments over the thick filaments is believed to be caused by the union of the meromyosin heads of the thick filaments with complementary areas of actin on the thin filaments.
The displacement process between the myofilaments would follow these phases:
- The ca2+ released by the sarcoplasmic reticulum binds to troponin C in the thin filaments and causes a conformational change in tropomyosin that leaves actin free to bind to myosin.
- In the resting state, the myosin heads are bound to ADP+Pi, when actin binds to the myosin heads, ADP is released.
- For actin and myosin to separate, ATP binding to the myosin head and its hydrolysis.
- This cycle can be repeated indefinitely as long as ATP is not exhausted and the maximum shortening of the sarcomere is not reached.
- each cycle displaces thin filaments about 10 nm on the thick filaments.
- The force generated by each cycle is approximately 5 10-12 N.
- The synergy of millions of cycles in millions of fibers generates the total strength and shortening of the muscle as a whole.
Length, tension and types of contraction
If we remember the physiological definition of muscle contraction, reference is made to the development of tension but not to the length of the muscle fibers. Y the development of tension does not necessarily mean that the muscle shortens. Tension can be developed without changes in the length of the muscle fibers, even if they are lengthened.
For example, if we hold something heavy in our hands for a while, the fibers that support it generate tension against gravity but do not change in length.
So, to describe muscle contraction, two components are needed, length and tension. Combining both, the different types of muscle contraction can be classified:
- isometric contraction: tension is created but the length of the muscle remains constant.
- heterometric contraction: the length of the muscle does not remain constant. If the fibers shorten, the contraction is concentric. If the fibers lengthen, the contraction is eccentric. Heterometric contraction is also often called isotonic contraction but this name is not appropriate since isotonia does not occur in this type of contraction.
- auxotonic contraction: isometric and heterometric contraction is combined. It is very common in skeletal movements. For example, if we contract a muscle first there is a concentric heterometric contraction, we can keep it there for a few moments with isometric contraction and then return to the initial position with eccentric heterometric contraction.