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Muscle System Function

Author: Sophia
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what's covered
In this lesson, you will learn how muscles work. First, you will learn about how skeletal muscles contract, which is described by the sliding filament model. You will learn how impulses arrive at a neuromuscular junction, triggering a muscle to contract. After reviewing a summary of the steps of skeletal muscle contraction, you will learn about terms related to larger scale muscle movement. Specifically, this lesson will cover:

Table of Contents

1. Skeletal Muscle Contraction

You have learned about three major types of muscles, which are summarized in the table below. In this lesson, we will focus on skeletal muscle contraction. Keep in mind that there are important differences in structure and function, including mechanisms of contraction, in each muscle type.

Comparison of Structure and Properties of Muscle Tissue Types
Tissue Histology Function Location
Skeletal Long cylindrical fiber, striated, many peripherally located nuclei Voluntary movement, produces heat, protects organs Attached to bones and around entrance points to body (e.g., mouth, anus)
Cardiac Short, branched, striated, single central nucleus Contracts to pump blood Heart
Smooth Short, spindle-shaped, no evident striation, single nucleus in each fiber Involuntary movement, moves food, involuntary control of respiration, moves secretions, regulates flow of blood in arteries by contraction Walls of major organs and passageways

The image below shows the three types of muscle tissue for you to compare. Note the striated appearance of the skeletal muscle shown on top, the lack of striations in the smooth muscle shown in the middle, and the branched appearance of the cardiac muscle on the bottom.

All three muscle tissues have some properties in common; they all exhibit a quality called excitability as their plasma membranes can change their electrical states (from polarized to depolarized) and send an electrical wave called an action potential along the membrane. Note that cells have a resting membrane potential representing a difference in charge across the membrane; during an action potential, charged species (ions) cross the membrane to reverse this charge from negative to positive.

While the nervous system can influence the excitability of cardiac and smooth muscle to some degree, skeletal muscle completely depends on signaling from the nervous system to work properly. On the other hand, both cardiac muscle and smooth muscle can respond to other stimuli, such as hormones and local stimuli.

The muscles all begin the actual process of contracting (shortening) when a protein called actin is pulled by a protein called myosin. This occurs in striated muscle (skeletal and cardiac) after specific binding sites on the actin have been exposed in response to the interaction between calcium ions open parentheses Ca to the power of 2 plus end exponent close parentheses and proteins (troponin and tropomyosin) that “shield” the actin-binding sites. Ca to the power of 2 plus end exponent also is required for the contraction of smooth muscle, although its role is different: here Ca to the power of 2 plus end exponent activates enzymes, which in turn activate myosin heads. All muscles require adenosine triphosphate (ATP), which is used to store energy that can power biological activities, to continue the process of contracting, and they all relax when the Ca to the power of 2 plus end exponent is removed and the actin-binding sites are re-shielded.

A muscle can return to its original length when relaxed due to a quality of muscle tissue called elasticity. It can recoil back to its original length due to elastic fibers. Muscle tissue also has the quality of extensibility; it can stretch or extend. Contractility allows muscle tissue to pull on its attachment points and shorten with force.

Remember that differences among the three muscle types include the microscopic organization of their contractile proteins—actin and myosin. The actin and myosin proteins are arranged very regularly in the cytoplasm of individual muscle cells (fibers) in both skeletal muscle and cardiac muscle, which creates a pattern, or stripes, called striations. The striations are visible with a light microscope under high magnification. Skeletal muscle fibers are multinucleated structures that compose the skeletal muscle. Cardiac muscle fibers each have one to two nuclei and are physically and electrically connected to each other so that the entire heart contracts as one unit (called a syncytium).

1a. The Neuromuscular Junction

Now that you know the basics of muscle contraction, it’s time to explore the process in more detail.

A neuromuscular junction is the place where a neuron meets a muscle cell. When an action potential reaches the neuromuscular junction, a neurotransmitter called acetylcholine (ACh) is released.

The figure below shows a neuromuscular junction. The axon is the part of the neuron that carries information to the nerve terminal, where synaptic vesicles are triggered to release their contents (ACh) into the small gap between the neuron and the muscle cell (called a synapse). ACh binds to receptors on the nearby muscle cell.

The sequence of events that result in the contraction of an individual muscle fiber begins with this signal, the release of ACh from a motor neuron (a neuron that sends a signal from the brain, as opposed to a sensory neuron that carries information to the brain). The local membrane of the muscle fiber will depolarize as positively charged sodium ions open parentheses Na to the power of plus close parentheses enter, triggering an action potential that spreads to the rest of the membrane, which will depolarize, including the T-tubules. T-tubules are tubular folds of membrane that penetrate into the cell to rapidly spread the depolarization.

Depolarization triggers the release of calcium ions open parentheses Ca to the power of 2 plus end exponent close parentheses from storage in a membranous structure called the sarcoplasmic reticulum (SR), which is a specialized form of an organelle called the endoplasmic reticulum. The Ca to the power of 2 plus end exponent then binds to troponin, causing the troponin complex to move tropomyosin, exposing a myosin-binding site on actin. A part of myosin called the myosin head binds, and this initiates contraction, which is sustained by ATP. As long as Ca to the power of 2 plus end exponent ions remain in the sarcoplasm to bind to troponin, which keeps the actin-binding sites “unshielded,” and as long as ATP is available to drive the cross-bridge cycling and the pulling of actin strands by myosin, the muscle fiber will continue to shorten to an anatomical limit. You will learn more about this process in the next section.

The top panel in this figure shows the interaction of a motor neuron with a muscle fiber and how the release of acetylcholine into the muscle cells leads to the release of calcium. The middle panel shows how calcium release activates troponin and leads to muscle contraction through interactions of the thick and thin filaments. The bottom panel shows an image of a muscle fiber being shortened and producing tension.

Muscle contraction usually stops when signaling from the motor neuron ends, which repolarizes the sarcolemma (muscle cell membrane) and T-tubules, and closes the channels in the SR that allow calcium to leave. Ca to the power of 2 plus end exponent ions are then pumped back into the SR, which causes the tropomyosin to reshield (or re-cover) the myosin binding sites on the actin strands. A muscle can also stop contracting when it runs out of ATP and becomes fatigued.

The interaction of a motor neuron with a muscle fiber showing how calcium is resorbed into the muscle fiber. This results in the relaxation of the thin and thick filament.

The contraction of a striated muscle fiber occurs as the sarcomeres shorten as myosin heads pull on the actin filaments.

The region where thick and thin filaments overlap has a dense appearance, as there is little space between the filaments. This zone, where thin and thick filaments overlap, is very important to muscle contraction, as it is the site where filament movement starts. Thin filaments, anchored at their ends by the Z-discs, do not extend completely into the central region that only contains thick filaments, anchored at their bases at a spot called the M-line. A myofibril is composed of many sarcomeres running along its length; thus, myofibrils and muscle cells contract as the sarcomeres contract.

try it
What protein binds to calcium to trigger the movement of another protein, tropomyosin, allowing myosin to bind to actin?
Troponin

did you know
When someone is suspected of having a myocardial infarction (heart attack), prompt diagnosis is critical. This allows them the best chance of surviving with as little heart muscle damage as possible.

IN CONTEXT

Medical societies periodically issue clinical practice guidelines with recommendations for managing particular medical conditions. In 2021, a major clinical guideline was released by the American College of Cardiology, American Heart Association (AHA), and other organizations. This guideline provided recommendations for how clinicians should treat patients who present with chest pain. One of the major recommendations is that patients suspected of having a myocardial infarction should have blood work to test cardiac troponin levels. Specifically, high sensitivity cardiac troponin (cTn) levels should be measured (Gulati et al., 2021).

There are three troponin subunits. Troponin C binds to calcium to initiate contraction. Cardiac troponins I and T are the most useful for cardiac diagnostic testing (Gulati et al., 2021).

These troponin levels are valuable because they are normally not present in the blood, but are released by damaged heart muscle. Detection of these biomarkers suggests that further testing is needed to find out what sort of damage is present.

It takes time for troponin levels to rise after heart muscle damage occurs. Therefore, serial measurements are often used to detect rising troponin levels in case a patient has presented too soon after heart muscle injury for elevated troponin to show on blood work.

1b. The Sliding Filament Model

When signaled by a motor neuron, a skeletal muscle fiber contracts as the thin filaments are pulled and then slide past the thick filaments within the fiber’s sarcomeres. This process is known as the sliding filament model of muscle contraction. The sliding can only occur when myosin-binding sites on the actin filaments are exposed by a series of steps that begin with Ca to the power of 2 plus end exponent entry into the sarcoplasm.

An illustration of the sliding filament theory of muscle contraction is shown with each structure labeled. The thick filaments, myosin, are depicted as thick purple rods with small protruding oval heads, arranged horizontally in the middle of the sarcomere. The thin filaments, actin, are depicted as horizontal rows of green strands with yellow and orange dots, extending inward from both ends of the sarcomere toward the center but stopping short of full overlap with the thick filaments. There are wavy vertical green lines composed of small overlapping circles at both ends of the sarcomere, labeled ‘Z’ for Z-lines. Three thin vertical purple lines are in the center of the sarcomere. A horizontal bracket around these lines is labeled ‘H’. A light gray rectangle overlays the three thin vertical purple lines and is labeled ‘M-Line’. There is a horizontal bracket at the bottom of the sarcomere that extends from the center on either side out to the edges of the myosin heads and is labeled ‘Darker A Band’. On each side of this horizontal bracket is another horizontal bracket that starts at the ending edge of the myosin heads and extends to each opposing side of the screen, where each bracket is labeled ‘Lighter I-band’. The thin actin filaments as the green strand structures start to move gradually inward toward the center. A black inward-pointing arrow appears at the second green actin filament at each side to depict sliding inward. The myosin heads, as the small protruding oval heads on the thick purple rods, begin to extend out with each one attaching to the green actin filaments, as the green strands increase their overlap with the purple filaments. The Z-lines move closer together, the I-bands shorten, and the H-band gradually narrows, as the A band remains constant in length and the M line remains centered. The animation pauses briefly as the black arrows fade, and then the animation reverses, depicting the myosin heads detaching from the actin filaments, the overlap between the green and purple filaments increasing, and everything returning to the depiction described at the beginning.

Tropomyosin is a protein that winds around the chains of the actin filament and covers the myosin-binding sites to prevent actin from binding to myosin. Tropomyosin binds to troponin to form a troponin-tropomyosin complex. The troponin-tropomyosin complex prevents the myosin “heads” from binding to the active sites on the actin microfilaments. Troponin also has a binding site for Ca to the power of 2 plus end exponent ions.

To initiate muscle contraction, tropomyosin has to expose the myosin-binding site on an actin filament to allow cross-bridge formation between the actin and myosin microfilaments. The first step in the process of contraction is for Ca to the power of 2 plus end exponent to bind to troponin so that tropomyosin can slide away from the binding sites on the actin strands. This allows the myosin heads to bind to these exposed binding sites and form cross-bridges. The thin filaments are then pulled by the myosin heads to slide past the thick filaments toward the center of the sarcomere. But each head can only pull a very short distance before it has reached its limit and must be “re-cocked” before it can pull again, a step that requires ATP.

For thin filaments to continue to slide past thick filaments during muscle contraction, myosin heads must pull the actin at the binding sites, detach, re-cock, attach to more binding sites, pull, detach, re-cock, etc. This repeated movement is known as the cross-bridge cycle. This motion of the myosin heads is similar to the oars when an individual rows a boat: The paddle of the oars (the myosin heads) pulls are lifted from the water (detach), repositioned (re-cocked), and then immersed again to pull. Each cycle requires energy, which is provided by ATP.

Cross-bridge formation occurs when the myosin head attaches to the actin while adenosine diphosphate (ADP) and inorganic phosphate open parentheses straight P subscript straight i close parentheses are still bound to myosin. straight P subscript straight i is then released, causing myosin to form a stronger attachment to the actin, after which the myosin head moves toward the M-line, pulling the actin along with it. As actin is pulled, the filaments move approximately 10nm toward the M-line. This movement is called the power stroke, as movement of the thin filament occurs at this step. In the absence of ATP, the myosin head will not detach from actin.

One part of the myosin head attaches to the binding site on the actin, but the head has another binding site for ATP. ATP binding causes the myosin head to detach from the actin. After this occurs, ATP is converted to ADP and straight P subscript straight i by the intrinsic ATPase activity of myosin. The energy released during ATP hydrolysis changes the angle of the myosin head into a cocked position. The myosin head is now in position for further movement.

When the myosin head is cocked, myosin is in a high-energy configuration. This energy is expended as the myosin head moves through the power stroke, and at the end of the power stroke, the myosin head is in a low-energy position. After the power stroke, ADP is released; however, the formed cross-bridge is still in place, and actin and myosin are bound together. As long as ATP is available, it readily attaches to myosin, the cross-bridge cycle can recur, and muscle contraction can continue.

Considerable amounts of ATP are required for contraction, and the loss of ATP that results in the rigor mortis is observed soon after someone dies. With no further ATP production possible, there is no ATP available for myosin heads to detach from the actin-binding sites, so the cross-bridges stay in place, causing the rigidity in the skeletal muscles.

Relaxing skeletal muscle fibers begins with the motor neuron, which stops releasing its chemical signal, ACh, into the synapse at the neuromuscular junction. The muscle fiber repolarizes, which closes the gates in the SR where Ca to the power of 2 plus end exponent was being released. ATP-driven pumps move Ca to the power of 2 plus end exponent out of the sarcoplasm back into the SR. This results in the “reshielding” of the actin-binding sites on the thin filaments. Without the ability to form cross-bridges, the muscle fiber loses its tension and relaxes.

The number of skeletal muscle fibers in a given muscle is genetically determined and does not change. Muscle strength is related to the number of myofibrils and sarcomeres within each fiber. Factors, such as hormones and stress, can increase the production of sarcomeres and myofibrils within the muscle fibers, a change called hypertrophy, which results in the increased mass and bulk in a skeletal muscle. Likewise, decreased use of a skeletal muscle results in atrophy, where the number of sarcomeres and myofibrils disappear (but not the number of muscle fibers).

1c. Summary of Contraction

The basic steps of skeletal muscle contraction are as follows.

  1. An action potential reaches a neuromuscular junction where the neuron meets a muscle cell.
  2. Acetylcholine is released into the neuromuscular cleft, a small space between the neuron and the muscle cell.
  3. Acetylcholine binds to receptors on the muscle cell.
  4. Binding of acetylcholine triggers depolarization of the muscle cell, which spreads rapidly through T-tubules (membranous structures that extend deep into the cell).
  5. Depolarization triggers the release of calcium ions from the sarcoplasmic reticulum, a specialized form of smooth endoplasmic reticulum found in muscle cells.
  6. Calcium binds to troponin, causing a conformational change that moves tropomyosin and exposes myosin binding sites on actin.
  7. The myosin head binds to actin.
  8. A power stroke occurs, causing the filaments to slide against each other.
  9. ATP binds, and the myosin head separates from actin.
  10. ATP hydrolysis provides the energy to move the myosin head back to a cocked configuration, ready to repeat the process.
A illustration of a portion of a muscle is displayed on the left side of the screen with red striations, with a neuron extending toward the muscle cell. A thin black rectangle is around the end of the neuron to highlight the neuromuscular junction, and a zoomed-in view of the neuromuscular junction is on the right side of the screen within a thin black rectangular frame. The zoomed-in view shows a closeup of the neuromuscular junction with the neuron’s branches as yellow, and the muscle cell as a bundled cylindrical shape. Text above the zoomed-in view reads ‘Action potential arrives’. The zoomed-in view on the right shifts to the left of the screen, with a thin black rectangle selecting a single branch of the neuron in the neuromuscular junction. The right side of the screen shows an even further zoomed-in view that depicts a single end plate of the yellow neuron in contact with the muscle. The muscle itself has small blue receptors that are H-shaped and are releasing even smaller purple circles to represent acetylcholine. Text above this view reads ‘Acetylcholine is released and binds to receptors’. The view of the single end plate of the yellow neuron in contact with the muscle zooms in to fill the entire screen as the blue H-shaped receptors continue to release the acetylcholine depicted as the small purple circles. A black arrow extends out from each side of the neuromuscular junction to run horizontally away from the neuron and then down a path in the muscle depicted as a slightly darker red thick line, as the text ‘Muscle cell depolarizes’ appears. The perspective of the image zooms out slightly further to show the two black arrows continuing to extend downward, with the paths taking them through a thick horizontal porous orange structure that is overlaid atop the muscle. Text on screen appears, labeling the orange structure as ‘Sarcoplasmic Reticulum’. Small blue circles begin to float around the sarcoplasmic reticulum, as text appears at the top of the screen reading ‘Calcium ions released’. The view then zooms in further to the sarcoplasmic reticulum, where the orange structure fades out to reveal a sarcomere, labeled ‘Sarcomere’ at top. Thick filaments, myosin, are depicted as thick purple rods with small protruding oval heads, arranged horizontally in the middle of the sarcomere. The thin filaments, actin, are depicted as horizontal rows of green strands with yellow and orange dots, extending inward from both ends of the sarcomere toward the center but stopping short of full overlap with the thick filaments. The view zooms in to a single filament of actin and a single filament of myosin in a horizontal row parallel to each other. There is a beige circle on each portion of the green actin filament where it twists, which is labeled ‘Troponin’ with text on screen. Small gray circles begin to float down from the top of the screen, with text appearing ‘Calcium binds to troponin’. Some of the protruding oval heads on the purple rod of the myosin begin to extend out and change angle slightly, cocking to attach to sites on the green actin filament, as text appears ‘Myosin binds to actin’. A label appears with text ‘Myosin head’ pointing to the protruding purple oval heads, and a label ‘Actin’ points to the green twisted filament. The text ‘Power Stroke’ appears on screen as the myosin heads that are attached to the actin begin to pull the filament horizontally. From the top of the screen, small orange ovals float in that are labeled ‘ATP’. Text on screen changes to ‘ATP binds to myosin’, as the ATP ovals each respectively bind to an attached myosin head, with a yellow star appearing to depict binding, and the text on screen changing to ‘ATP hydrolysis’. The myosin heads return to their cocked position and detach from the green filament.

2. Muscle Movements

There are many important terms that describe the ways that muscles move body parts. You have already encountered some of these. The table below provides an overview of important terms.

Action Description
Flexion (FLĔK-shŏn) Movement that decreases the angle between two bones, such as bending the arm at the elbow.
Extension (ĕk-STĔN-shŏn) Movement that increases the angle between two bones, such as straightening the arm at the elbow.
Abduction (ăb-DŬK-shŏn) Movement of a limb away from the midline of the body.
Adduction (ă-DŬK-shŏn) Movement of a limb toward the midline of the body.
Rotation (rō-TĀ-shŏn) Circular movement around a central point. Internal rotation is toward the center of the body, and external rotation is away from the center of the body.
Dorsiflexion (dôr-sĭ-FLĔK-shŏn) Decreasing the angle of the foot and the leg (i.e., the foot moves upward toward the knee). This movement is the opposite of plantar flexion.
Plantar Flexion (PLĂN-tăr FLĔK-shŏn) Increasing the angle of the foot and leg (i.e., the foot moves downward toward the ground, such as when pressing down on a gas pedal in a car).
Supination (sū-pi- NĀ- shŭn) Movement of the hand or foot turning upward. When applied to the hand, it is the act of turning the palm upwards. When applied to the foot, it is the outward roll of the foot/ankle during normal movement.
Pronation (prō-NĀ-shŭn) Movement of the hand or foot turning downward. When applied to the hand, it is the act of turning the palm downward. When applied to the foot, it is the inward roll of the foot/ankle during normal movement.
Eversion (ē-VĔR-zhŭn) Excessive movement involving turning outward the sole of the foot away from the body’s midline, a common cause of an ankle sprain.
Inversion (in-VĔR-zhŭn) Excessive movement involving turning inward the sole of the foot towards the median plane, a common cause of an ankle sprain.

The figure below illustrates some of the most important movement terms to know. Make sure that you can distinguish these.

An illustration of a female human figure is shown on the left side of the screen, standing and facing forward with feet slightly apart and arms straight at sides. The figure’s arm and leg on the same side move away from the body, and the text ‘Abduction’ is shown to the left of the figure. The same figure appears on the right side of the screen, standing and facing forward with feet slightly apart and arms straight at sides. The figure’s arm and leg on the same side move toward the midline of the body, crossing the midline so the arm is in front of the body and the leg slightly crosses over the other leg, while the text ‘Adduction’ is shown to the right of the figure. This view moves upward to disappear off screen and a new view appears coming up from the bottom. The same female figure is shown facing forward, with one arm out to the side that moves in a complete circle at the shoulder joint. A thin gray line with an arrow is shown following the circle to depict rotation, while the text ‘Rotation’ is shown on the right side of the screen. This view moves upward to disappear off screen and a new view appears coming up from the bottom. The same female figure is shown facing forward and then the perspective zooms in further to show only her torso and arms. The female’s hands turn to face palms forward, and the text ‘Supination’ is shown to the left of the figure. The female’s hands turn to face palms facing away, with backs of hands visible, and the text ‘Pronation’ is shown to the right of the figure. This view moves upward to disappear off screen and a new view appears coming up from the bottom, which is a view of only the ankles and feet. The feet move where the sole of the foot turns outward away from the midline of the body through movement at the ankle joint, and the text ‘Eversion’ is shown on the left. The feet move where the sole of the foot turns inward toward the midline of the body through movement at the ankle joint and the text ‘Inversion’ is shown on the right. This view moves upward to disappear off screen and a new view appears coming up from the bottom, which is a side view of a single foot from the ankle downward. The toes point away from the body with a blue arrow pointing downward, with the text ‘Plantar Flexion’ shown on the left. The toes then pull up toward the body with a blue arrow pointing up, with the text ‘Dorsiflexion’ shown on the right. This view moves upward to disappear off screen and a new view appears coming up from the bottom, which is a side view of the entire female illustrated figure on the left side of the screen. A blue line with a fulcrum at the joint is overlaid on top of the arm, with the fulcrum at the elbow, and on top of the leg, with the fulcrum at the knee. The figure bends the elbow and the knee simultaneously where the angles of the fulcrum move closer to each other, and the text ‘Flexion’ is shown. This view is retained on screen and the same female figure is duplicated on the left side of the screen. The figure extends the elbow and the knee simultaneously where the angles of the fulcrum increase, and the text ‘Extension’ is shown.

try it
You bend your arm at the elbow. Is this extension or flexion?
Flexion
You are standing with your arms hanging down vertically along your sides. You lift your right arm until it extends horizontally away from your body. Is this abduction or adduction?
Abduction

The figure below provides details about movements of the hands, feet, jaw, and fingers.

Illustration showing Pronation, Supination, Dorsiflexion, Plantar Flexion, Inversion, Eversion, Protraction, Retraction, Elevation, Depression, and Opposition body movements.

try it
You are standing in the anatomical position with your feet parallel and toes pointing forward. You keep your heels together and move the toes of your right foot away from the midline. Is this inversion or eversion?
Eversion
You push your lower jaw forward and outward. Is this protraction or retraction?
Protraction

summary
In this lesson, you learned about muscle contraction, focusing on skeletal muscle contraction. You learned about the role of the neuromuscular junction in transmitting an impulse from the nervous system to a muscle, then learned about the sliding filament model used to describe how the sarcomeres of skeletal muscle tissue contract. After reviewing a summary of contraction, you learned about terms used to describe muscle movement. These terms will help you describe symptoms associated with muscular disorders and responses to treatment for these disorders.

SOURCE: THIS TUTORIAL HAS BEEN ADAPTED FROM (1) “OPEN RN | MEDICAL TERMINOLOGY – 2E” BY ERNSTMEYER & CHRISTMAN AT OPEN RESOURCES FOR NURSING (OPEN RN). (2) "ANATOMY AND PHYSIOLOGY 2E" AT OPENSTAX. ACCESS FOR FREE AT WTCS.PRESSBOOKS.PUB/MEDTERM/ AND OPENSTAX.ORG/DETAILS/BOOKS/ANATOMY-AND-PHYSIOLOGY-2E. LICENSING: CREATIVE COMMONS ATTRIBUTION 4.0 INTERNATIONAL.

REFERENCES

Gulati, M., Levy, P. D., Mukherjee, D., Amsterdam, E., Bhatt, D. L., Birtcher, K. K., Blankstein, R., Boyd, J., Bullock-Palmer, R. P., Conejo, T., Diercks, D. B., Gentile, F., Greenwood, J. P., Hess, E. P., Hollenberg, S. M., Jaber, W. A., Jneid, H., Joglar, J. A., Morrow, D. A., O'Connor, R. E., … Shaw, L. J. (2021). 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation, 144(22), e368–e454. doi.org/10.1161/CIR.0000000000001029

Terms to Know
ATPase

An enzyme that hydrolyzes ATP to ADP and inorganic phosphate.

Acetylcholine (ACh)

A neurotransmitter that is released at neuromuscular junctions, among other places.

Action Potential

An electrical signal caused by depolarization of a cell, allowing the signal to travel rapidly.

Adenosine Triphosphate (ATP)

A molecule used to store energy to power cellular activities.

Contractility

The ability to contract.

Depolarized

The condition in which the membrane potential of a cell changes from negative to positive (e.g., when an action potential is triggered).

Elasticity

Being elastic; having the ability to return to an initial state after stretching.

Excitability

The ability to respond to signals (e.g., a cell that can produce an action potential in response to a stimulus).

Extensibility

The ability to stretch or extend.

Motor Neuron

A neuron that carries information away from the central nervous system, such as a neuron that stimulates a muscle cell to contract.

Neuromuscular Junction

The place that a nerve cell contacts a muscle cell, allowing the nerve cell to send signals to the muscle cell.

Neurotransmitter

A chemical messenger that sends signals from a neuron to another cell.

Power Stroke

The movement of myosin that pulls actin during muscle contraction.

Sensory Neuron

A neuron that carries information to the central nervous system.

Sliding Filament Model

A model that describes how sarcomeres contract by the sliding of actin and myosin filaments.

T-tubule

A membranous tubule that helps rapidly carry depolarization deep into a muscle cell so contraction can occur.

Tropomyosin

A protein that moves to reveal the myosin head binding site on actin.

Troponin

A protein complex that binds to a calcium ion to allow a sarcomere to contract.

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