Structure and Function of the Muscular System
The muscular system controls numerous functions, which is possible with the significant differentiation of muscle tissue morphology and ability.
The Musculoskeletal System
The muscular system is made up of muscle tissue and is responsible for functions such as maintenance of posture, locomotion and control of various circulatory systems. This includes the beating of the heart and the movement of food through the digestive system. The muscular system is closely associated with the skeletal system in facilitating movement. Both voluntary and involuntary muscular system functions are controlled by the nervous system.
The muscular system: Skeletal muscle of the muscular system is closely associated with the skeletal system and acts to maintain posture and control voluntary movement.
Muscle is a highly-specialized soft tissue that produces tension which results in the generation of force. Muscle cells, or myocytes, contain myofibrils comprised of actin and myosin myofilaments which slide past each other producing tension that changes the shape of the myocyte. Numerous myocytes make up muscle tissue and the controlled production of tension in these cells can generate significant force.
Muscle tissue can be classified functionally as voluntary or involuntary and morphologically as striated or non-striated. Voluntary refers to whether the muscle is under conscious control, while striation refers to the presence of visible banding within myocytes caused by the organization of myofibrils to produce constant tension.
Types of Muscle
The above classifications describe three forms of muscle tissue that perform a wide range of diverse functions.
Skeletal muscle mainly attaches to the skeletal system via tendons to maintain posture and control movement. For example, contraction of the biceps muscle, attached to the scapula and radius, will raise the forearm. Some skeletal muscle can attach directly to other muscles or to the skin, as seen inthe face where numerous muscles control facial expression.
Skeletal muscle is under voluntary control, although this can be subconscious when maintaining posture or balance. Morphologically skeletal myocytes are elongated and tubular and appear striated with multiple peripheral nuclei.
Cardiac Muscle Tissue
Cardiac muscle tissue is found only in the heart, where cardiac contractions pump blood throughout the body and maintain blood pressure.
As with skeletal muscle, cardiac muscle is striated; however it is not consciously controlled and so is classified as involuntary. Cardiac muscle can be further differentiated from skeletal muscle by the presence of intercalated discs that control the synchronized contraction of cardiac tissues. Cardiac myocytes are shorter than skeletal equivalents and contain only one or two centrally located nuclei.
Smooth Muscle Tissue
Smooth muscle tissue is associated with numerous organs and tissue systems, such as the digestive system and respiratory system. It plays an important role in the regulation of flow in such systems, such as aiding the movement of food through the digestive system via peristalsis.
Smooth muscle is non-striated and involuntary. Smooth muscle myocytes are spindle shaped with a single centrally located nucleus.
Types of muscle: The body contains three types of muscle tissue: skeletal muscle, smooth muscle, and cardiac muscle, visualized here using light microscopy. Visible striations in skeletal and cardiac muscle are visible, differentiating them from the more randomised appearance of smooth muscle.
Key Takeawayssarcoplasmsarcoplasmic reticulumsarcolemmasarcomere
Skeletal Muscle Fiber Structure
Myocytes, sometimes called muscle fibers, form the bulk of muscle tissue. They are bound together by perimysium, a sheath of connective tissue, into bundles called fascicles, which are in turn bundled together to form muscle tissue. Myocytes contain numerous specialized cellular structures which facilitate their contraction and therefore that of the muscle as a whole.
The highly specialized structure of myocytes has led to the creation of terminology which differentiates them from generic animal cells.
Generic cell > Myocyte
Cytoplasm > Sarcoplasm
Cell membrane > Sarcolemma
Smooth endoplasmic reticulum > Sarcoplasmic reticulum
Myocytes can be incredibly large, with diameters of up to 100 micrometers and lengths of up to 30 centimeters. The sarcoplasm is rich with glycogen and myoglobin, which store the glucose and oxygen required for energy generation, and is almost completely filled with myofibrils, the long fibers composed ofmyofilaments that facilitate muscle contraction.
The sarcolemma of myocytes contains numerous invaginations (pits) called transverse tubules which are usually perpendicular to the length of the myocyte. Transverse tubules play an important role in supplying the myocyte with Ca+ ions, which are key for muscle contraction.
Each myocyte contains multiple nuclei due to their derivation from multiple myoblasts, progenitor cells that give rise to myocytes. These myoblasts asre located to the periphery of the myocyte and flattened soas not to impact myocyte contraction.
Myocyte: Skeletal muscle cell: A skeletal muscle cell is surrounded by a plasma membrane called the sarcolemma with a cytoplasm called the sarcoplasm. A muscle fiber is composed of many myofibrils, packaged into orderly units.
Each myocyte can contain many thousands of myofibrils. Myofibrils run parallel to the myocyte and typically run for its entire length, attaching to the sarcolemma at either end. Each myofibril is surrounded by the sarcoplasmic reticulum, which is closely associated with the transverse tubules. The sarcoplasmic reticulum acts as a sink of Ca+ ions, which are released upon signalling from the transverse tubules.
Myofibrils are composed of long myofilaments of actin, myosin, and other associated proteins. These proteins are organized into regions termed sarcomeres, the functional contractile region of the myocyte. Within the sarcomere actin and myosin, myofilaments are interlaced with each other and slide over each other via the sliding filament model of contraction. The regular organization of these sarcomeres gives skeletal and cardiac muscle their distinctive striated appearance.
Sarcomere: The sarcomere is the functional contractile region of the myocyte, and defines the region of interaction between a set of thick and thin filaments.
Myofilaments (Thick and Thin Filaments)
Myofibrils are composed of smaller structures called myofilaments. There are two main types of myofilaments: thick filaments and thin filaments. Thick filaments are composed primarily of myosin proteins, the tails of which bind together leaving the heads exposed to the interlaced thin filaments. Thin filaments are composed of actin, tropomyosin, and troponin. The molecular model of contraction which describes the interaction between actin and myosin myofilaments is called the cross-bridge cycle.
Sliding Filament Model of Contraction
In the sliding filament model, the thick and thin filaments pass each other, shortening the sarcomere.
Movement often requires the contraction of a skeletal muscle, as can be observed when the bicep muscle in the arm contracts, drawing the forearm up towards the trunk. The sliding filament model describes the process used by muscles to contract. It is a cycle of repetitive events that causes actin and myosin myofilaments to slide over each other, contracting the sarcomere and generating tension in the muscle.
To understand the sliding filament model requires an understanding of sarcomere structure. A sarcomere is defined as the segment between two neighbouring, parallel Z-lines. Z lines are composed of a mixture of actin myofilaments and molecules of the highly elastic protein titin crosslinked by alpha-actinin. Actin myofilaments attach directly to the Z-lines, whereas myosin myofilaments attach via titinmolecules.
Surrounding the Z-line is the I-band, the region where actin myofilaments are not superimposed by myosin myofilaments. The I-band is spanned by the titin molecule connecting the Z-line with a myosin filament.
The region between two neighboring, parallel I-bands is known as the A-band and contains the entire length of single myosin myofilaments. Within the A-band is a region known as the H-band, which is the region not superimposed by actin myofilaments. Within the H-band is the M-line, which is composed of myosin myofilaments and titin molecules crosslinked by myomesin.
Titin molecules connect the Z-line with the M-line and provide a scaffold for myosin myofilaments. Their elasticity provides the underpinning of muscle contraction. Titin molecules are thought to play a key role as a molecular ruler maintaining parallel alignment within the sarcomere. Another protein, nebulin, is thought to perform a similar role for actin myofilaments.
Model of Contraction
The molecular mechanism whereby myosin and acting myofilaments slide over each other is termed the cross-bridge cycle. During muscle contraction, the heads of myosin myofilaments quickly bind and release in a ratcheting fashion, pulling themselves along the actin myofilament.
At the level of the sliding filament model, expansion and contraction only occurs within the I and H-bands. The myofilaments themselves do not contract or expand and so the A-band remains constant.
The sarcomere and the sliding filament model of contraction: During contraction myosin ratchets along actin myofilaments compressing the I and H bands. During stretching this tension is release and the I and H bands expand. The A-band remains constant throughout as the length of the myosin myofilaments does not change.
The amount of force and movement generated generated by an individual sarcomere is small. However, when multiplied by the number of sarcomeres in a myofibril, myofibrils in a myocyte and myocytes in a muscle, the amount of force and movement generated is significant.
ATP and Muscle Contraction
ATP is critical for muscle contractions because it breaks the myosin-actin cross-bridge, freeing the myosin for the next contraction.
ATP and Muscle Contraction
Muscles contract in a repeated pattern of binding and releasing between the two thin and thick strands of the sarcomere. ATP is critical to prepare myosin for binding and to “recharge” the myosin.
The Cross-Bridge Muscle Contraction Cycle
ATP first binds to myosin, moving it to a high-energy state. The ATP is hydrolyzed into ADP and inorganic phosphate (Pi) by the enzyme ATPase. The energy released during ATP hydrolysis changes the angle of the myosin head into a “cocked” position, ready to bind to actin if the sites are available. ADP and Pi remain attached; myosin is in its high energy configuration.
Cross-bridge muscle contraction cycle: The cross-bridge muscle contraction cycle, which is triggered by Ca2+ binding to the actin active site, is shown. With each contraction cycle, actin moves relative to myosin.
The muscle contraction cycle is triggered by calcium ions binding to the protein complex troponin, exposing the active-binding sites on the actin. As soon as the actin-binding sites are uncovered, the high-energy myosin head bridges the gap, forming a cross-bridge. Once myosin binds to the actin, the Pi is released, and the myosin undergoes a conformational change to a lower energy state. As myosin expends the energy, it moves through the “power stroke,” pulling the actin filament toward the M-line. When the actin is pulled approximately 10 nm toward the M-line, the sarcomere shortens and the muscle contracts. At the end of the power stroke, the myosin is in a low-energy position.
After the power stroke, ADP is released, but the cross-bridge formed is still in place. ATP then binds to myosin, moving the myosin to its high-energy state, releasing the myosin head from the actin active site. ATP can then attach to myosin, which allows the cross-bridge cycle to start again; further muscle contraction can occur. Therefore, without ATP, muscles would remain in their contracted state, rather than their relaxed state.
Tropomyosin and troponin prevent myosin from binding to actin while the muscle is in a resting state.
Describe how calcium, tropomyosin, and the troponin complex regulate the binding of actin by myosin
Key Takeawaystropomyosinacetylcholinesarcoplasmic reticulum
The binding of the myosin heads to the muscle actin is a highly-regulated process. When a muscle is in a resting state, actin and myosin are separated. To keep actin from binding to the active site on myosin, regulatory proteins block the molecular binding sites. Tropomyosin blocks myosin binding sites on actin molecules, preventing cross-bridge formation, which prevents contraction in a muscle without nervous input. The protein complex troponin binds to tropomyosin, helping to position it on the actin molecule.
Regulation of Troponin and Tropomyosin
To enable muscle contraction, tropomyosin must change conformation and uncover the myosin-binding site on an actin molecule, thereby allowing cross-bridge formation. Troponin, which regulates the tropomyosin, is activated by calcium, which is kept at extremely low concentrations in the sarcoplasm. If present, calcium ions bind to troponin, causing conformational changes in troponin that allow tropomyosin to move away from the myosin-binding sites on actin. Once the tropomyosin is removed, a cross-bridge can form between actin and myosin, triggering contraction. Cross-bridge cycling continues until Ca2+ ions and ATP are no longer available; tropomyosin again covers the binding sites on actin.
Muscle contraction: Calcium remains in the sarcoplasmic reticulum until released by a stimulus. Calcium then binds to troponin, causing the troponin to change shape and remove the tropomyosin from the binding sites. Cross-bridge cling continues until the calcium ions and ATP are no longer available.
Calcium-Induced Calcium Release
The concentration of calcium within muscle cells is controlled by the sarcoplasmic reticulum, a unique form of endoplasmic reticulum in the sarcoplasm. Muscle contraction ends when calcium ions are pumped back into the sarcoplasmic reticulum, allowing the muscle cell to relax. During stimulation of the muscle cell, the motor neuron releases the neurotransmitter acetylcholine, which then binds to a post-synaptic nicotinic acetylcholine receptor.
A change in the receptor conformation causes an action potential, activating voltage-gated L-type calcium channels, which are present in the plasma membrane. The inward flow of calcium from the L-type calcium channels activates ryanodine receptors to release calcium ions from the sarcoplasmic reticulum. This mechanism is called calcium-induced calcium release (CICR). It is not understood whether the physical opening of the L-type calcium channels or the presence of calcium causes the ryanodine receptors to open. The outflow of calcium allows the myosin heads access to the actin cross-bridge binding sites, permitting muscle contraction.
Excitation–contraction coupling is the connection between the electrical action potential and the mechanical muscle contraction.
Explain the process of excitation-contraction coupling and the role of neurotransmitters
Key Takeawaysmotor-end platesarcolemmaacetylcholinesterase
Excitation–contraction coupling is the physiological process of converting an electrical stimulus to a mechanical response. It is the link (transduction) between the action potential generated in the sarcolemma and the start of a muscle contraction.
Excitation-contraction coupling: This diagram shows excitation-contraction coupling in a skeletal muscle contraction. The sarcoplasmic reticulum is a specialized endoplasmic reticulum found in muscle cells.
Communication between Nerves and Muscles
A neural signal is the electrical trigger for calcium release from the sarcoplasmic reticulum into the sarcoplasm. Each skeletal muscle fiber is controlled by a motor neuron, which conducts signals from the brain or spinal cord to the muscle. Electrical signals called action potentials travel along the neuron’s axon, which branches through the muscle, connecting to individual muscle fibers at a neuromuscular junction. The area of the sarcolemma on the muscle fiber that interacts with the neuron is called the motor-end plate. The end of the neuron’s axon is called the synaptic terminal; it does not actually contact the motor-end plate. A small space called the synaptic cleft separates the synaptic terminal from the motor-end plate.
Because neuron axons do not directly contact the motor-end plate, communication occurs between nerves and muscles through neurotransmitters. Neuron action potentials cause the release of neurotransmitters from the synaptic terminal into the synaptic cleft, where they can then diffuse across the synaptic cleft and bind to a receptor molecule on the motor end plate. The motor end plate possesses junctional folds: folds in the sarcolemma that create a large surface area for the neurotransmitter to bind to receptors. The receptors are sodium channels that open to allow the passage of Na+ into the cell when they receive neurotransmitter signal.
Depolarization in the Sarcolemma
Acetylcholine (ACh) is a neurotransmitter released by motor neurons that binds to receptors in the motor end plate. Neurotransmitter release occurs when an action potential travels down the motor neuron’s axon, resulting in altered permeability of the synaptic terminal membrane and an influx of calcium. The Ca2+ ions allow synaptic vesicles to move to and bind with the presynaptic membrane (on the neuron) and release neurotransmitter from the vesicles into the synaptic cleft. Once released by the synaptic terminal, ACh diffuses across the synaptic cleft to the motor end plate, where it binds with ACh receptors.
As a neurotransmitter binds, these ion channels open, and Na+ ions cross the membrane into the muscle cell. This reduces the voltage difference between the inside and outside of the cell, which is called depolarization. As ACh binds at the motor end plate, this depolarization is called an end-plate potential. The depolarization then spreads along the sarcolemma and down the T tubules, creating an action potential. The action potential triggers the sarcoplasmic reticulum to release of Ca2+, which activate troponin and stimulate muscle contraction.
ACh is broken down by the enzyme acetylcholinesterase (AChE) into acetyl and choline. AChE resides in the synaptic cleft, breaking down ACh so that it does not remain bound to ACh receptors, which would cause unwanted extended muscle contraction.
Control of Muscle Tension
Muscle tension is influenced by the number of cross-bridges that can be formed.
Control of Muscle Tension
Neural control initiates the formation of actin – myosin cross-bridges, leading to the sarcomere shortening involved in muscle contraction. These contractions extend from the muscle fiber through connective tissue to pull on bones, causing skeletal movement. The pull exerted by a muscle is called tension. The amount of force created by this tension can vary, which enables the same muscles to move very light objects and very heavy objects. In individual muscle fibers, the amount of tension produced depends primarily on the amount of cross-bridges formed, which is influenced by the cross-sectional area of the muscle fiber and the frequency of neural stimulation.
Muscle tension: Muscle tension is produced when the maximum amount of cross-bridges are formed, either within a muscle with a large diameter or when the maximum number of muscle fibers are stimulated. Muscle tone is residual muscle tension that resists passive stretching during the resting phase.
Cross-bridges and Tension
The number of cross-bridges formed between actin and myosin determine the amount of tension that a muscle fiber can produce. Cross-bridges can only form where thick and thin filaments overlap, allowing myosin to bind to actin. If more cross-bridges are formed, more myosin will pull on actin and more tension will be produced.
Maximal tension occurs when thick and thin filaments overlap to the greatest degree within a sarcomere. If a sarcomere at rest is stretched past an ideal resting length, thick and thin filaments do not overlap to the greatest degree so fewer cross-bridges can form. This results in fewer myosin heads pulling on actin and less muscle tension. As a sarcomere shortens, the zone of overlap reduces as the thin filaments reach the H zone, which is composed of myosin tails. Because myosin heads form cross-bridges, actin will not bind to myosin in this zone, reducing the tension produced by the myofiber. If the sarcomere is shortened even more, thin filaments begin to overlap with each other, reducing cross-bridge formation even further, and producing even less tension. Conversely, if the sarcomere is stretched to the point at which thick and thin filaments do not overlap at all, no cross-bridges are formed and no tension is produced. This amount of stretching does not usually occur because accessory proteins, internal sensory nerves, and connective tissue oppose extreme stretching.
The primary variable determining force production is the number of myofibers (long muscle cells) within the muscle that receive an action potential from the neuron that controls that fiber. When using the biceps to pick up a pencil, for example, the motor cortex of the brain only signals a few neurons of the biceps so only a few myofibers respond. In vertebrates, each myofiber responds fully if stimulated. On the other hand, when picking up a piano, the motor cortex signals all of the neurons in the biceps so that every myofiber participates. This is close to the maximum force the muscle can produce. As mentioned above, increasing the frequency of action potentials (the number of signals per second) can increase the force a bit more because the tropomyosin is flooded with calcium.