Types of muscles
Muscle is a stimulating tissue, that is, a mechanically, chemically, or electrically stimulable action potential. The action potential is an electrical charge in the cell membrane due to a change in the conductivity of ions on the membrane. Nerve tissue is also excitable tissue. Muscle cells contain a contractile mechanism that is activated by an action potential. There are 630 muscles in the human body. The body is approx. 40% is skeletal muscle, add another 5-10% to heart and smooth muscle.
Contraction by a whole muscle
Isometric versus isotonic
Isotonic contractions are when muscle tension remains constant but the muscle shortens like a static amount of weight lifting. Isometric muscle contractions occur when the muscle is not shortened, such as when an object that can be moved like a wall is pushed. Isometric contraction differs from isotonic in that myofibrils do not slide on each other as force develops. Slippage occurs during isotonic contractions and external work is performed.
Engine unit concept
The motor nerve and all the fibers in which it is innervated are called motor units. The number of fibers depends on the need for fine control. Usually, small muscles that respond quickly to fine regulation have a nerve and only a few muscle fibers. Muscles that do not require fine control, such as the gastrocnemius (calf muscle), can have hundreds of muscle fibers per motor unit.
The contraction of each muscle fiber is completely or neutral. Therefore, each classified response should be the number of motor units stimulated simultaneously. The summation is the sum of the individual muscle twitches to the contraction of the whole muscle. This can be accomplished by increasing the number of simultaneously decreasing motor units (spatial summation) or by increasing the frequency of contractions of each muscle contraction (temporal summation).
These processes almost always take place simultaneously with normal muscle contraction. Each motor unit usually fires asynchronously.
Not all motor units are created equal. Therefore, a motor unit in one muscle can be up to 50 times stronger than another muscle. Small motor units are much easier to excite than larger ones because they are incorporated by smaller nerve fibers that naturally have a lower excitation threshold. In spatial summation, motor units are involved by increasing the strength of the stimulus, thereby increasing the strength of the contraction.
In time or wave summation, the contraction of each motor unit increases so rapidly that one contraction is not yet completely completed when the next stimulus arrives. So the force generated in the first is added to the force generated by the second, third, and so on. When a muscle is gradually stimulated at higher frequencies, the frequency at which successive contractions merge and are indistinguishable from each other is finally reached. The muscle then enters a long, continuous state of maximal contraction called tetany.
Prolonged strong contractions lead to muscle fatigue, which contractile and metabolic processes are unable to satisfy to maintain workload. The nerve continues to function properly and transmits action potential to muscle fibers, but the contractions are getting weaker and weaker due to a lack of ATP.
Muscle hypertrophy (increase in muscle mass) is caused by intense muscle function. The diameter of each fiber increases, nutrients and metabolism increase, mitochondria may increase, and the size and number of myofibrils increase. Muscle hypertrophy increases the ability of muscles to contract, and nutrient mechanisms that feed increased energy help.
The production of hypertrophy requires vigorous muscle activity in excess of 75% of the maximum value, so isometric exercise can have a significant effect on muscle mass even for a short time. However, prolonged light exercise increases endurance, increases oxidative enzymes, myoglobin, and even blood capillaries.
Muscle atrophy occurs when a muscle is not used for an extended period of time or is used only for weak contractions. For example, atrophy occurs when limbs are thrown. With only a month of inactivity, muscle size has halved to normal. Damage to the muscle nerve results in well atrophy. If the injury is repaired within the first 3-4 months, the muscle regains full function. After four months, the muscle fibers degenerate into fibrous and adipose tissue.
Muscle types and mechanism of contraction
The skeletal muscle makes up most of the muscles in the body and does not shrink without nerve stimulation. It is under voluntary control and anatomical cellular connections are missing between the fibers. The fibers (cells) are multinucleated and appear filamentous due to the arrangement of actin and myosin protein fibers.
Each fiber is unicellular, long, cylindrical, and surrounded by a cell membrane. Muscle fibers contain a number of myofibrils made from myofilaments. These myofilaments are made from contractile proteins. The most important proteins for muscle contraction are myosin, actin, tropomyosin, and troponin.
Skeletal muscle fibers have differences in metabolism and contractile properties. Type I fibers are mostly found in the muscles of the posture than in the long muscles of the back. These are also called red muscles because the fibers contain many mitochondria that give the muscle a more dark reddish tinge.
White muscles contain primarily type IIB fibers and specialize in rapid, subtle movements such as the muscles used to move the eyes or hand muscles. Differences in fiber type occur due to differences in the amino acid composition of backbone proteins without altering biological activity.
Different forms of proteins can be expressed, thereby determining the functional properties of muscles. Changes in muscle function can be caused by changes in activity (exercise), hormonal environment (steroids), or innervation. Skeletal muscle may have limited regeneration in the event of injury through satellite cells located at the edges of muscle fibers. These cells may also be active in muscle hypertrophy.
The skeletal muscle is made up of cells called fibers that specialize in shrinkage or shortening. Each fiber is made up of smaller subunits called myofibrils, which are made up of contractile proteins called myosin and actin, which are responsible for muscle contraction at the molecular level. These shrinking protein fibers are also called thick (myosin) and thin (actin) filaments. These fibers are interdigitated so that proteins can interact.
Myosin fibers are so-called junctions that exit the filament to interact with the actin fibers during contraction. Imagine a golf club set that is held by the axes and the heads radiate around the axes. This is a visual image of what the thick fibers look like. Because the clubs have axes of different lengths, the heads exit at different points in the cluster.
The myosin fibers thus look like a long filament at each end consisting of about 200 myosin protein molecules. This structure allows the myosin fiber to pull the actin fibers in both directions, thereby shortening the fiber.
Actin fibers are made up of two protein fibers that are woven together. The actin filaments are attached to the Z line, which defines the boundaries of the functional unit of muscle contraction known as sarcomometers. There are many sarcomas in muscle fibers, and the Z line is continuous between muscle fibers.
Muscle contraction occurs through a sliding filament mechanism in which the sarcorers are shortened (Z-lines get closer to each other) by actin filaments sliding through the myosin fibers.
Myosin fibers look a bit like a golf club, but they are not inflexible. In fact, muscle contraction would be impossible if the myosin molecules did not have a “hinge” along the axis that allows the head to be ratcheted. The force of muscle contraction is the ratchet movement of tiny myosin heads toward the center of their sarcomere. This ratchet movement often occurs during muscle contraction.
The thin fibers are not really just actin, which forms the backbone of the filament. Two other proteins are part of the thin fibers, tropomyosin and troponin. In addition to actin fibers, there are active sites where myosin contracts during contraction.
These active sites are covered with tropomyosin at rest so no contraction can occur. Troponin is a complex of three different affinity submissions. One has an affinity for actin, the other for tropomyosin, and the third for calcium. Troponin molecules are located along actin-tropomyosin filaments and act by placing tropomyosin filaments at active sites on actin filaments.
In the presence of calcium, it binds to troponin, which changes shape and tropomyosin moves away from active sites, allowing myosin and actin to interact and cause muscle contractions. When the active sites are explored, the myosin heads bind to the sites that initiate the movement of the head toward the center of the sarometer, thereby pulling the actin and shortening the saromore. Each of the myosin heads is believed to function independently of the others, and each fixes and pulls a continuous alternating ratchet cycle until the calcium is removed and the active sites are re-covered.
The utilization of sugars turns out to be increasingly significant as the force of activity increases.
The contraction of muscles requires a lot of energy. Energy is required to break the connection between the myosin head and the actin active sites and to remove calcium from the cytoplasm using a special pump in the sarcoplasmic reticulum.
When the myosin head is propelled forward, a site that binds to ATP (the main energy currency of the cell) is exposed after an electric shock. The decomposition of ATP as ADP releases the head from the actin fiber and picks it up for the next ratchet electric shock.
Muscles need the energy to contract. At rest and during light exercise, muscles use lipids as their source of energy. The utilization of sugars turns out to be increasingly significant as the force of activity increases.
The breakdown of glucose into water and carbon dioxide generates energy that is transferred to the regeneration of phosphoryl creatine and ATP. If the oxygen supply is inadequate, this process is short-circuited and a metabolite of one of the products (lactic acid) builds up in the muscle. This is called anaerobic metabolism (glycolysis) and is a normal process that can occur before the oxidative breakdown of glucose.
Lactate builds up in the muscles and changes the pH, which inhibits enzyme activity. After training, there is an oxygen content in which oxygen must be used to convert lactate to carbon dioxide and water and to replenish energy stores. Short, intense exercise uses anaerobic metabolic mechanisms rather than more sustained activities. For instance, in a 100 m hyphen, 85% of the energy is obtained from anaerobic methods, while in a mile run just 20% is delivered anaerobically.
Skeletal muscle contraction begins with action potential in muscle fiber. This causes the unfastening of calcium from the sarcoplasmic reticulum. The action potential of muscle fiber begins when it is excited to interact with highly isolated (myelinated) nerve fiber. The point of contact between a nerve and a muscle is called a neuromuscular node, which is usually located in the middle of the muscle fiber.
Therefore, the action potential initiated here extends toward the end of the fiber, allowing all sarometers to contract at the same time. The skeletal muscle has an adaptation that allows the action potential to spread deep in the fiber. T or transverse tubules are internal extensions of the sarcolemma that penetrate the fiber in such a way that the functional potential in the t-tubules causes calcium discharge from the nearby sarcoplasmic reticulum in the immediate region of the myofibrils.
The sarcoplasmic reticulum contains very high concentrations of calcium ions, which are released when excited by the adjacent T-tubule. Pumps within the wall of the sarcoplasmic reticulum return calcium within the cytoplasm below the level required to activate the contractile process.
The association of the motor nerve and muscle fibers occurs at the neuromuscular node. Here, the neuron terminates with a terminal button containing tiny vesicles with the neurotransmitter acetylcholine. When an action potential reaches the terminal button, the vesicles are released and acetylcholine diffuses in a narrow space and binds to receptors on the cell membrane of muscle fibers.
When acetylcholine binds to receptors, the local permeability of the muscle cell membrane changes so that the muscle cell action potential is initiated. This action potential then spreads across the muscle cell membrane and T-tubule system to initiate the contractile process. An enzyme called acetylcholinesterase is present in the neuromuscular node, which breaks down acetylcholine and removes contraction.
Smooth muscles are found in the dividers of veins, in cylindrical organs, for example, the stomach and uterus, in the iris, or in the hair follicles. It exists in the body in multiple units or in visceral smooth muscle. It is not voluntarily controlled, each cell has a nucleus and automatically shows in visceral form. In multi-unit smooth muscle, each cell exists as a discrete independent unit that is innervated by a single nerve end.
The visceral smooth muscle exists as a plate or bundle of bundles that are tightly connected by nodes that allow ions to flow freely and therefore act as syncytium. Therefore, when a portion of the visceral smooth muscle is stimulated, the action potential spreads to all other fibers.
Most of the same shrinking protein is present and active in smooth muscle contraction, but they are not arranged as parallel muscle fibers not visible microscopically as in a skeletal muscle. The shrinkage mechanism is very similar to skeletal muscle, with the difference that smooth muscle myosin interacts with actin only when it is phosphorylated. In smooth muscle, calcium binds to a protein called calmodulin, and then the complex interacts with an enzyme that adds a phosphate group to myosin, activating it.
There are no T-tubules in smooth muscles, the sarcoplasmic reticulum is poorly developed, and the calcium pump is present but acts more slowly. Due to these differences in contractile mechanism and structure, smooth muscle is approximately It takes 30 times as long to contract and relax as the skeletal muscle, and it does so with much less energy. There are no developed neuromuscular nodes in smooth muscle.
The neurotransmitter is often released only in the immediate vicinity of the muscle, so the neurotransmitter, which may be acetylcholine or norepinephrine, must diffuse into the muscle cells to interact with receptors on the cell membrane. These neurotransmitters may be excitatory or inhibitory, depending on the receptor in the particular smooth muscle cell.
Because smooth muscle has spontaneous activity, neuronal input is only used to modify activity, rather than trigger it, as in a skeletal muscle. Local tissue factors, hormones, and mechanical stretching can cause action potential and thus smooth muscle contraction. Smooth muscle is able to actively regenerate after injury.
The heart is made of special muscle tissue, showing some similarities to both smooth and skeletal muscles. It is involuntary and mononuclear, as is smooth muscle. The myocardium is stretched as a skeletal muscle, which means that microscopically visible myofilaments are arranged parallel to the sarcomere structure described above. These fibers contract with each other during contraction, just like in skeletal muscle.
Myocardial fibers branch and there is a single nucleus per cell. Another difference in the myocardium is the presence of intercalated discs, which are special connections between one myocardial cell and another. These tight connections allow the ions to move almost completely free so that the action potential can flow freely from one cell to another. This makes the myocardial tissue a functional syncity. When a cell is excited, the resulting action potential is distributed to each.
This important feature is that it allows the atrial or ventricular muscles to contract to pump strongly out of the blood. The functional potential of the heart muscle also specializes in maximizing the pumping function of the heart. They are 10 to 30 times as long as the skeletal muscle and cause a correspondingly expanded constriction period.
Myocardium has long been said to have no regenerative capacity in early childhood. Recently, however, evidence has been found to refute this claim. There is strong evidence that human myocardium regenerates to some extent after myocyte replication after cardiac injury.