when calcium is released inside a muscle cell, what does it bind to?

Structure and Function of the Muscular System

The muscular arrangement controls numerous functions, which is possible with the significant differentiation of muscle tissue morphology and power.

Learning Objectives

Describe the three types of muscle tissue

Key Takeaways

Key Points

• The muscular organization is responsible for functions such every bit maintenance of posture, locomotion, and control of diverse circulatory systems.
• Muscle tissue can exist divided functionally (voluntarily or involuntarily controlled) and morphologically ( striated or not-striated).
• These classifications draw iii singled-out muscle types: skeletal, cardiac and polish. Skeletal muscle is voluntary and striated, cardiac musculus is involuntary and striated, and shine muscle is involuntary and non-striated.

Key Terms

• myofibril: A cobweb made up of several myofilaments that facilitates the generation of tension in a myocyte.
• myofilament: A filament equanimous of either multiple myosin or actin proteins that slide over each other to generate tension.
• myosin: A motor poly peptide which forms myofilaments that interact with actin filaments to generate tension.
• actin: A poly peptide which forms myofilaments that interact with myosin filaments to generate tension.
• striated: The striped appearance of certain musculus types in which myofibrils are aligned to produce a constant directional tension.
• voluntary: A muscle move under conscious control (due east.thousand. deciding to motion the forearm).
• involuntary: A muscle move non under witting control (east.one thousand. the beating of the heart).
• myocyte: A muscle cell.

The Musculoskeletal System

The muscular organization is fabricated upwards 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 motility. Both voluntary and involuntary muscular arrangement functions are controlled past the nervous system.

The muscular system: Skeletal muscle of the muscular system is closely associated with the skeletal organisation 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 strength. Muscle cells, or myocytes, comprise myofibrils comprised of actin and myosin myofilaments which slide past each other producing tension that changes the shape of the myocyte. Numerous myocytes make upward musculus tissue and the controlled production of tension in these cells tin can generate pregnant force.

Muscle tissue can be classified functionally every bit voluntary or involuntary and morphologically as striated or not-striated. Voluntary refers to whether the musculus is under conscious control, while striation refers to the presence of visible banding inside myocytes acquired by the organisation of myofibrils to produce constant tension.

Types of Muscle

The above classifications depict iii forms of muscle tissue that perform a broad range of diverse functions.

Skeletal Muscle

Skeletal muscle mainly attaches to the skeletal arrangement via tendons to maintain posture and control movement. For example, wrinkle of the biceps muscle, attached to the scapula and radius, volition raise the forearm. Some skeletal muscle can attach directly to other muscles or to the skin, equally seen in
the 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 Musculus Tissue

Cardiac muscle tissue is found only in the heart, where cardiac contractions pump blood throughout the body and maintain blood pressure level.

Every bit with skeletal musculus, 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 command the synchronized contraction of cardiac tissues. Cardiac myocytes are shorter than skeletal equivalents and contain only one or two centrally located nuclei.

Smooth Musculus Tissue

Polish muscle tissue is associated with numerous organs and tissue systems, such as the digestive system and respiratory system. Information technology plays an of import role in the regulation of flow in such systems, such as aiding the motility of nutrient through the digestive arrangement 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 trunk contains three types of muscle tissue: skeletal musculus, smooth muscle, and cardiac muscle, visualized hither using lite microscopy. Visible striations in skeletal and cardiac muscle are visible, differentiating them from the more than randomised appearance of smooth muscle.

Skeletal Muscle Fibers

Skeletal muscles are composed of striated subunits called sarcomeres, which are equanimous of the myofilaments actin and myosin.

Learning Objectives

Outline the structure of a skeletal muscle fiber

Key Takeaways

Fundamental Points

• Muscles are composed of long bundles of myocytes or muscle fibers.
• Myocytes contain thousands of myofibrils.
• Each myofibril is composed of numerous sarcomeres, the functional contracile region of a striated muscle. Sarcomeres are composed of myofilaments of myosin and actin, which collaborate using the sliding filament model and cross-bridge cycle to contract.

Key Terms

• sarcoplasm: The cytoplasm of a myocyte.
• sarcoplasmic reticulum: The equivalent of the smooth endoplasmic reticulum in a myocyte.
• sarcolemma: The cell membrane of a myocyte.
• sarcomere: The functional contractile unit of the myofibril of a striated musculus.

Skeletal Muscle Fiber Structure

Myocytes, sometimes called muscle fibers, class the bulk of musculus tissue. They are bound together by perimysium, a sheath of connective tissue, into bundles chosen fascicles, which are in turn bundled together to form muscle tissue. Myocytes contain numerous specialized cellular structures which facilitate their wrinkle and therefore that of the muscle equally a whole.

The highly specialized construction of myocytes has led to the cosmos of terminology which differentiates them from generic animal cells.

Generic cell > Myocyte

Cytoplasm > Sarcoplasm

Jail cell membrane > Sarcolemma

Smoothen endoplasmic reticulum > Sarcoplasmic reticulum

Myocyte Construction

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 of
myofilaments that facilitate muscle contraction.

The sarcolemma of myocytes contains numerous invaginations (pits) chosen transverse tubules which are usually perpendicular to the length of the myocyte. Transverse tubules play an important function in supplying the myocyte with Ca⁺ ions, which are key for musculus 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 so
as not to bear on myocyte contraction.

Myocyte: Skeletal muscle cell: A skeletal muscle prison cell is surrounded by a plasma membrane called the sarcolemma with a cytoplasm called the sarcoplasm. A musculus fiber is equanimous of many myofibrils, packaged into orderly units.

Myofibril Structure

Each myocyte tin can incorporate many thousands of myofibrils. Myofibrils run parallel to the myocyte and typically run for its entire length, attaching to the sarcolemma at either finish. 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.

Sarcomeres

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 up of thick and thin filaments.

Myofilaments (Thick and Thin Filaments)

Myofibrils are composed of smaller structures called myofilaments. There are ii 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 betwixt actin and myosin myofilaments is chosen the cantankerous-bridge wheel.

Sliding Filament Model of Wrinkle

In the sliding filament model, the thick and thin filaments pass each other, shortening the sarcomere.

Learning Objectives

Describe the sliding filament model of muscle contraction

Key Takeaways

Central Points

• The sarcomere is the region in which sliding filament contraction occurs.
• During wrinkle, myosin myofilaments ratchet over actin myofilaments contracting the sarcomere.
• Within the sarcomere, cardinal regions known as the I and H band shrink and expand to facilitate this movement.
• The myofilaments themselves practise not expand or contract.

Key Terms

• I-band: The expanse next to the Z-line, where actin myofilaments are not superimposed by myosin myofilaments.
• A-band: The length of a myosin myofilament inside a sarcomere.
• M-line: The line at the eye of a sarcomere to which myosin myofilaments demark.
• Z-line: Neighbouring, parallel lines that define a sarcomere.
• H-band: The area next to the One thousand-line, where myosin myofilaments are not superimposed past actin myofilaments.

Movement often requires the contraction of a skeletal musculus, as can be observed when the bicep musculus in the arm contracts, drawing the forearm upwardly towards the trunk. The sliding filament model describes the process used past 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.

Sarcomere Structure

To understand the sliding filament model requires an understanding of sarcomere construction. A sarcomere is divers as the segment between ii neighbouring, parallel Z-lines. Z lines are composed of a mixture of actin myofilaments and molecules of the highly rubberband protein titin crosslinked by blastoff-actinin. Actin myofilaments adhere straight to the Z-lines, whereas myosin myofilaments adhere via titin
molecules.

Surrounding the Z-line is the I-band, the region where actin myofilaments are not superimposed by myosin myofilaments. The I-ring 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-ring and contains the entire length of unmarried myosin myofilaments. Within the A-ring is a region known equally the H-band, which is the region non superimposed by actin myofilaments. Within the H-band is the Thousand-line, which is equanimous 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 musculus contraction. Titin molecules are thought to play a key office equally a molecular ruler maintaining parallel alignment within the sarcomere. Another poly peptide, nebulin, is thought to perform a similar role for actin myofilaments.

Model of Contraction

The molecular machinery whereby myosin and acting myofilaments slide over each other is termed the cantankerous-bridge cycle. During muscle contraction, the heads of myosin myofilaments quickly demark and release in a ratcheting manner, pulling themselves along the actin myofilament.

At the level of the sliding filament model, expansion and contraction merely occurs inside the I and H-bands. The myofilaments themselves practice not contract or expand and then the A-band remains constant.

The sarcomere and the sliding filament model of contraction: During wrinkle 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 abiding throughout as the length of the myosin myofilaments does not change.

The amount of force and move 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 corporeality of strength and motility generated is significant.

ATP and Muscle Contraction

ATP is critical for muscle contractions because it breaks the myosin-actin cantankerous-span, freeing the myosin for the adjacent contraction.

Learning Objectives

Discuss how free energy is consumed during motility

Key Takeaways

Key Points

• ATP prepares myosin for binding with actin by moving it to a higher- energy state and a "cocked" position.
• One time the myosin forms a cross-bridge with actin, the Pi disassociates and the myosin undergoes the power stroke, reaching a lower energy state when the sarcomere shortens.
• ATP must bind to myosin to break the cross-bridge and enable the myosin to rebind to actin at the side by side muscle contraction.

Fundamental Terms

• M-line: the disc in the middle of the sarcomere, within the H-zone
• troponin: a circuitous of three regulatory proteins that is integral to muscle contraction in skeletal and cardiac muscle, or whatever fellow member of this circuitous
• ATPase: a form of enzymes that catalyze the decomposition of ATP into ADP and a gratuitous phosphate ion, releasing energy that is oftentimes harnessed to drive other chemical reactions

ATP and Muscle Contraction

Muscles contract in a repeated pattern of binding and releasing betwixt the two thin and thick strands of the sarcomere. ATP is disquisitional to set myosin for bounden and to "recharge" the myosin.

The Cross-Bridge Muscle Contraction Bicycle

ATP beginning binds to myosin, moving it to a high-energy state. The ATP is hydrolyzed into ADP and inorganic phosphate (P_i) by the enzyme ATPase. The energy released during ATP hydrolysis changes the bending 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 loftier energy configuration.

Cantankerous-bridge muscle contraction bike: The cantankerous-bridge musculus contraction cycle, which is triggered past Ca2+ binding to the actin active site, is shown. With each contraction bicycle, actin moves relative to myosin.

The muscle contraction cycle is triggered by calcium ions binding to the protein circuitous troponin, exposing the active-binding sites on the actin. As presently as the actin-binding sites are uncovered, the high-energy myosin head bridges the gap, forming a cantankerous-bridge. Once myosin binds to the actin, the P_i is released, and the myosin undergoes a conformational change to a lower energy land. As myosin expends the free 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, only the cross-bridge formed is yet in identify. ATP then binds to myosin, moving the myosin to its high-free energy country, releasing the myosin head from the actin active site. ATP can then adhere to myosin, which allows the cantankerous-bridge bicycle to start again; farther muscle contraction tin occur. Therefore, without ATP, muscles would remain in their contracted state, rather than their relaxed land.

Regulatory Proteins

Tropomyosin and troponin preclude myosin from binding to actin while the muscle is in a resting state.

Learning Objectives

Draw how calcium, tropomyosin, and the troponin complex regulate the binding of actin by myosin

Key Takeaways

Key Points

• Tropomyosin covers the actin binding sites, preventing myosin from forming cross-bridges while in a resting country.
• When calcium binds to troponin, the troponin changes shape, removing tropomyosin from the bounden sites.
• The sarcoplasmic reticulum stores calcium ions, which information technology releases when a muscle prison cell is stimulated; the calcium ions then enable the cross-bridge muscle contraction bike.

Central Terms

• tropomyosin: any of a family of muscle proteins that regulate the interaction of actin and myosin
• acetylcholine: a neurotransmitter in humans and other animals, which is an ester of acetic acid and choline
• sarcoplasmic reticulum: southward polish endoplasmic reticulum found in smooth and striated muscle; information technology contains large stores of calcium, which information technology sequesters and then releases when the muscle jail cell is stimulated

Regulatory Proteins

The bounden of the myosin heads to the musculus actin is a highly-regulated process. When a musculus is in a resting state, actin and myosin are separated. To continue actin from binding to the agile site on myosin, regulatory proteins block the molecular binding sites. Tropomyosin blocks myosin binding sites on actin molecules, preventing cross-bridge germination, 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 musculus contraction, tropomyosin must change conformation and uncover the myosin-binding site on an actin molecule, thereby allowing cross-span formation. Troponin, which regulates the tropomyosin, is activated by calcium, which is kept at extremely depression concentrations in the sarcoplasm. If present, calcium ions bind to troponin, causing conformational changes in troponin that permit tropomyosin to move abroad from the myosin-bounden sites on actin. Once the tropomyosin is removed, a cross-bridge tin form between actin and myosin, triggering contraction. Cantankerous-bridge cycling continues until Ca²⁺ ions and ATP are no longer available; tropomyosin once again covers the bounden sites on actin.

Muscle wrinkle: Calcium remains in the sarcoplasmic reticulum until released past a stimulus. Calcium then binds to troponin, causing the troponin to change shape and remove the tropomyosin from the binding sites. Cantankerous-span 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 class of endoplasmic reticulum in the sarcoplasm. Musculus wrinkle ends when calcium ions are pumped back into the sarcoplasmic reticulum, assuasive the muscle cell to relax. During stimulation of the muscle cell, the motor neuron releases the neurotransmitter acetylcholine, which and so binds to a mail-synaptic nicotinic acetylcholine receptor.

A change in the receptor conformation causes an activeness potential, activating voltage-gated L-type calcium channels, which are present in the plasma membrane. The inwards catamenia 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 non understood whether the physical opening of the 50-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

Excitation–contraction coupling is the connectedness betwixt the electrical action potential and the mechanical muscle contraction.

Learning Objectives

Explain the process of excitation-contraction coupling and the role of neurotransmitters

Central Takeaways

Central Points

• A motor neuron connects to a musculus at the neuromuscular junction, where a synaptic concluding forms a synaptic cleft with a motor-terminate plate.
• The neurotransmitter acetylcholine diffuses across the synaptic cleft, causing the depolarization of the sarcolemma.
• The depolarization of the sarcolemma stimulates the sarcoplasmic reticulum to release Caⁱⁱ⁺, which causes the muscle to contract.

Central Terms

• motor-stop plate: postjunctional folds which increase the surface area of the membrane (and acetylcholine receptors) exposed to the synaptic cleft
• sarcolemma: a thin cell membrane that surrounds a striated muscle fiber
• acetylcholinesterase: an enzyme that catalyzes the hydrolysis of the neurotransmitter acetylcholine into choline and acetic acid

Excitation–Wrinkle Coupling

Excitation–contraction coupling is the physiological process of converting an electrical stimulus to a mechanical response. Information technology is the link (transduction) between the action potential generated in the sarcolemma and the outset of a musculus contraction.

Excitation-contraction coupling: This diagram shows excitation-wrinkle coupling in a skeletal muscle contraction. The sarcoplasmic reticulum is a specialized endoplasmic reticulum plant in musculus cells.

Communication between Fretfulness and Muscles

A neural signal is the electrical trigger for calcium release from the sarcoplasmic reticulum into the sarcoplasm. Each skeletal musculus cobweb is controlled past a motor neuron, which conducts signals from the brain or spinal cord to the muscle. Electrical signals called activity potentials travel forth 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; information technology does not actually contact the motor-stop plate. A small space chosen the synaptic crevice separates the synaptic terminal from the motor-end plate.

Because neuron axons do non directly contact the motor-end plate, communication occurs betwixt fretfulness and muscles through neurotransmitters. Neuron activeness potentials crusade the release of neurotransmitters from the synaptic terminal into the synaptic crevice, where they can and then lengthened across the synaptic crack and demark 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 demark to receptors. The receptors are sodium channels that open to permit 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 downwardly 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 motility to and demark with the presynaptic membrane (on the neuron) and release neurotransmitter from the vesicles into the synaptic cleft. In one case released past the synaptic terminal, ACh diffuses across the synaptic cleft to the motor stop plate, where information technology binds with ACh receptors.

Equally a neurotransmitter binds, these ion channels open up, 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. Every bit ACh binds at the motor end plate, this depolarization is called an end-plate potential. The depolarization so spreads along the sarcolemma and down the T tubules, creating an activity potential. The action potential triggers the sarcoplasmic reticulum to release of Ca²⁺, which activate troponin and stimulate muscle contraction.

ACh is broken down past the enzyme acetylcholinesterase (Ache) into acetyl and choline. Anguish resides in the synaptic crack, breaking down ACh so that it does not remain bound to ACh receptors, which would cause unwanted extended muscle contraction.

Control of Muscle Tension

Musculus tension is influenced by the number of cross-bridges that can be formed.

Learning Objectives

Describe the factors that command muscle tension

Central Takeaways

Key Points

• The more than cross-bridges that are formed, the more tension in the muscle.
• The corporeality of tension produced depends on the cross-sectional area of the muscle fiber and the frequency of neural stimulation.
• Maximal tension occurs when thick and sparse filaments overlap to the greatest degree inside a sarcomere; less tension is produced when the sarcomere is stretched.
• If more motor neurons are stimulated, more myofibers contract, and there is greater tension in the muscle.

Key Terms

• tension: status of being held in a state between two or more forces, which are acting in opposition to each other

Control of Muscle Tension

Neural control initiates the formation of actin – myosin cantankerous-bridges, leading to the sarcomere shortening involved in muscle contraction. These contractions extend from the muscle fiber through connective tissue to pull on basic, causing skeletal movement. The pull exerted past a muscle is called tension. The amount of force created past this tension can vary, which enables the same muscles to motility very light objects and very heavy objects. In individual musculus fibers, the corporeality of tension produced depends primarily on the amount of cantankerous-bridges formed, which is influenced by the cross-sectional area of the muscle cobweb and the frequency of neural stimulation.

Musculus tension: Muscle tension is produced when the maximum amount of cantankerous-bridges are formed, either within a muscle with a large bore or when the maximum number of musculus 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, assuasive myosin to bind to actin. If more cantankerous-bridges are formed, more myosin will pull on actin and more tension will be produced.

Maximal tension occurs when thick and sparse filaments overlap to the greatest degree inside a sarcomere. If a sarcomere at residue is stretched past an platonic resting length, thick and thin filaments practice not overlap to the greatest degree then fewer cantankerous-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 accomplish the H zone, which is composed of myosin tails. Because myosin heads grade cantankerous-bridges, actin will not bind to myosin in this zone, reducing the tension produced by the myofiber. If the sarcomere is shortened fifty-fifty more than, sparse filaments begin to overlap with each other, reducing cantankerous-span formation even further, and producing fifty-fifty 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 non unremarkably occur because accessory proteins, internal sensory fretfulness, and connective tissue oppose extreme stretching.

The primary variable determining force production is the number of myofibers (long muscle cells) inside the muscle that receive an action potential from the neuron that controls that cobweb. 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 simply 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 and then that every myofiber participates. This is shut to the maximum force the muscle can produce. As mentioned above, increasing the frequency of activeness potentials (the number of signals per 2nd) can increase the forcefulness a flake more than because the tropomyosin is flooded with calcium.

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Source: https://courses.lumenlearning.com/boundless-biology/chapter/muscle-contraction-and-locomotion/

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