Muscles and Myocytes - MCAT Biological and Biochemical Foundations of Living Systems
Card 1 of 696
Which of the following proteins binds to calcium released from the sarcoplasmic reticulum?
Which of the following proteins binds to calcium released from the sarcoplasmic reticulum?
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Troponin binds free calcium once it is released from the sarcoplasmic reticulum, causing a conformational change in tropomyosin. This change exposes the myosin binding site on actin, allowing for cross-bridge formation and contraction.
Troponin binds free calcium once it is released from the sarcoplasmic reticulum, causing a conformational change in tropomyosin. This change exposes the myosin binding site on actin, allowing for cross-bridge formation and contraction.
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Which of the following proteins directly interacts with the myosin-binding site on actin?
Which of the following proteins directly interacts with the myosin-binding site on actin?
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Tropomyosin is interwoven with actin and serves to cover the myosin-binding site in the absence of calcium. Once calcium enters the cell it interacts with troponin, which in turn causes a conformational change in tropomyosin leading to the interaction of myosin with actin and a resulting muscle contraction. Without tropomyosin in place spontaneous cross-bridges could form, leading to inappropriate muscle contraction in the absence of action potentials.
Tropomyosin is interwoven with actin and serves to cover the myosin-binding site in the absence of calcium. Once calcium enters the cell it interacts with troponin, which in turn causes a conformational change in tropomyosin leading to the interaction of myosin with actin and a resulting muscle contraction. Without tropomyosin in place spontaneous cross-bridges could form, leading to inappropriate muscle contraction in the absence of action potentials.
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Which neurotransmitter is released at the neuromuscular junctions of skeletal muscle?
Which neurotransmitter is released at the neuromuscular junctions of skeletal muscle?
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Acetylcholine (ACh) is released from neurons at the neuromuscular junction. Once ACh binds to its receptor in the muscle T-tubule, the sarcolemma is depolarized and calcium can be released from the sarcoplasmic reticulum, triggering muscle contraction.
Acetylcholine (ACh) is released from neurons at the neuromuscular junction. Once ACh binds to its receptor in the muscle T-tubule, the sarcolemma is depolarized and calcium can be released from the sarcoplasmic reticulum, triggering muscle contraction.
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Duchenne Muscular Dystrophy is an X-linked recessive genetic disorder, resulting in the loss of the dystrophin protein. In healthy muscle, dystrophin localizes to the sarcolemma and helps anchor the muscle fiber to the basal lamina. The loss of this protein results in progressive muscle weakness, and eventually death.
In the muscle fibers, the effects of the disease can be exacerbated by auto-immune interference. Weakness of the sarcolemma leads to damage and tears in the membrane. The body’s immune system recognizes the damage and attempts to repair it. However, since the damage exists as a chronic condition, leukocytes begin to present the damaged protein fragments as antigens, stimulating a targeted attack on the damaged parts of the muscle fiber. The attack causes inflammation, fibrosis, and necrosis, further weakening the muscle.
Studies have shown that despite the severe pathology of the muscle fibers, the innervation of the muscle is unaffected.
When a healthy muscle fiber is activated, Ca2+ ions will .
Duchenne Muscular Dystrophy is an X-linked recessive genetic disorder, resulting in the loss of the dystrophin protein. In healthy muscle, dystrophin localizes to the sarcolemma and helps anchor the muscle fiber to the basal lamina. The loss of this protein results in progressive muscle weakness, and eventually death.
In the muscle fibers, the effects of the disease can be exacerbated by auto-immune interference. Weakness of the sarcolemma leads to damage and tears in the membrane. The body’s immune system recognizes the damage and attempts to repair it. However, since the damage exists as a chronic condition, leukocytes begin to present the damaged protein fragments as antigens, stimulating a targeted attack on the damaged parts of the muscle fiber. The attack causes inflammation, fibrosis, and necrosis, further weakening the muscle.
Studies have shown that despite the severe pathology of the muscle fibers, the innervation of the muscle is unaffected.
When a healthy muscle fiber is activated, Ca2+ ions will .
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The troponin-tropomyosin complex wraps around actin when the muscle fiber is inactive, blocking all myosin-binding sites. When Ca2+ is released it binds to troponin, inducing a change in tropomyosin, which shifts its position to expose the myosin-binding sites on the actin filament.
Calcium does not bind any of the other listed answer choices.
The troponin-tropomyosin complex wraps around actin when the muscle fiber is inactive, blocking all myosin-binding sites. When Ca2+ is released it binds to troponin, inducing a change in tropomyosin, which shifts its position to expose the myosin-binding sites on the actin filament.
Calcium does not bind any of the other listed answer choices.
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Duchenne Muscular Dystrophy is an X-linked recessive genetic disorder, resulting in the loss of the dystrophin protein. In healthy muscle, dystrophin localizes to the sarcolemma and helps anchor the muscle fiber to the basal lamina. The loss of this protein results in progressive muscle weakness, and eventually death.
In the muscle fibers, the effects of the disease can be exacerbated by auto-immune interference. Weakness of the sarcolemma leads to damage and tears in the membrane. The body’s immune system recognizes the damage and attempts to repair it. However, since the damage exists as a chronic condition, leukocytes begin to present the damaged protein fragments as antigens, stimulating a targeted attack on the damaged parts of the muscle fiber. The attack causes inflammation, fibrosis, and necrosis, further weakening the muscle.
Studies have shown that despite the severe pathology of the muscle fibers, the innervation of the muscle is unaffected.
ATP is required for muscle contraction. Identify which of the following are true
I. ATP binding causes myosin to release actin
II. Actin carries an inactive ADP when myosin binds
III. The myosin head movement to contract the muscle converts ATP to ADP
Duchenne Muscular Dystrophy is an X-linked recessive genetic disorder, resulting in the loss of the dystrophin protein. In healthy muscle, dystrophin localizes to the sarcolemma and helps anchor the muscle fiber to the basal lamina. The loss of this protein results in progressive muscle weakness, and eventually death.
In the muscle fibers, the effects of the disease can be exacerbated by auto-immune interference. Weakness of the sarcolemma leads to damage and tears in the membrane. The body’s immune system recognizes the damage and attempts to repair it. However, since the damage exists as a chronic condition, leukocytes begin to present the damaged protein fragments as antigens, stimulating a targeted attack on the damaged parts of the muscle fiber. The attack causes inflammation, fibrosis, and necrosis, further weakening the muscle.
Studies have shown that despite the severe pathology of the muscle fibers, the innervation of the muscle is unaffected.
ATP is required for muscle contraction. Identify which of the following are true
I. ATP binding causes myosin to release actin
II. Actin carries an inactive ADP when myosin binds
III. The myosin head movement to contract the muscle converts ATP to ADP
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This question requires us to know the ATP binding cycle associated with muscle contraction. I is true; binding of ATP causes myosin to release actin. When there is no ATP present, the myosin remains bound and the muscle becomes stiff (rigor mortis). II is false; actin does not bind ATP. III is also false; ATP is converted to ADP when the myosin head goes from the contracted position to the relaxed position, not the other way around.
This question requires us to know the ATP binding cycle associated with muscle contraction. I is true; binding of ATP causes myosin to release actin. When there is no ATP present, the myosin remains bound and the muscle becomes stiff (rigor mortis). II is false; actin does not bind ATP. III is also false; ATP is converted to ADP when the myosin head goes from the contracted position to the relaxed position, not the other way around.
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The area where the motor neuron intersects the muscle is known as the .
The area where the motor neuron intersects the muscle is known as the .
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The neuromuscular junction is where the nerve fibers directly connect to the muscle to deliver signals from the brain to the muscle tissue. "Cross bridge" refers to the linkage of actin and myosin filaments. The other answers sound similar, but are incorrect.
The neuromuscular junction is where the nerve fibers directly connect to the muscle to deliver signals from the brain to the muscle tissue. "Cross bridge" refers to the linkage of actin and myosin filaments. The other answers sound similar, but are incorrect.
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Muscle contraction is mainly powered by which chemical?
Muscle contraction is mainly powered by which chemical?
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ATP (adenosine triphosphate) is the primary chemical that provides the power for muscle contraction. ADP (adenosine diphosphate) is the resulting chemical when ATP is expended. ATP is required for the cross-bridge cycle. Acetylcholine is a neurotransmitter used in muscle contraction, but does not provide a power source. Lactic acid results from anaerobic production of ATP.
ATP (adenosine triphosphate) is the primary chemical that provides the power for muscle contraction. ADP (adenosine diphosphate) is the resulting chemical when ATP is expended. ATP is required for the cross-bridge cycle. Acetylcholine is a neurotransmitter used in muscle contraction, but does not provide a power source. Lactic acid results from anaerobic production of ATP.
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A sarcoplasmic reticulum is found within a muscle cell. The sarcoplasmic reticulum is a modified version of the endoplasmic reticulum.
What is the modified characteristic of a sarcoplasmic reticulum?
A sarcoplasmic reticulum is found within a muscle cell. The sarcoplasmic reticulum is a modified version of the endoplasmic reticulum.
What is the modified characteristic of a sarcoplasmic reticulum?
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The sarcoplasmic reticulum contains a large amount of Ca2+ ions. This calcium is released from the sarcoplasmic reticulum when an electrical signal is sent to the cell. This release of calcium allows for contraction.
The sarcoplasmic reticulum contains a large amount of Ca2+ ions. This calcium is released from the sarcoplasmic reticulum when an electrical signal is sent to the cell. This release of calcium allows for contraction.
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A muscle will not have all of its fibers contract at once. Instead, the muscle is divided into multiple bundles of muscle fibers, with a neuron innervating all of the fibers in a given bundle. Each collection of fibers controlled by a single neuron is referred to as a motor unit.
Which of the following statements is false when discussing motor units?
A muscle will not have all of its fibers contract at once. Instead, the muscle is divided into multiple bundles of muscle fibers, with a neuron innervating all of the fibers in a given bundle. Each collection of fibers controlled by a single neuron is referred to as a motor unit.
Which of the following statements is false when discussing motor units?
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Smaller motor units are activated first during muscular contraction. If more force is needed, larger motor units will be recruited in order to provide the necessary force.
Smaller motor units are activated first during muscular contraction. If more force is needed, larger motor units will be recruited in order to provide the necessary force.
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A toxin prevents calcium from being actively pumped back into the sarcoplasmic reticulum. What would you expect to be a consequence of this toxin's presence in the body?
A toxin prevents calcium from being actively pumped back into the sarcoplasmic reticulum. What would you expect to be a consequence of this toxin's presence in the body?
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Before a contraction, calcium is released from the sarcoplasmic reticulum and attaches to troponin. Troponin will then remove tropomyosin from the active site on actin where myosin is able to attach.
If calcium is never pumped back into the sarcoplasmic reticulum, the active site on actin will stay exposed, which allows myosin to attach at all times.
Note that calcium is also responsible for initiating acetylcholine release from the neuron at the neuromuscular junction; however, this process involves extracellular calcium ions and is not linked to the sarcoplasmic reticulum.
Before a contraction, calcium is released from the sarcoplasmic reticulum and attaches to troponin. Troponin will then remove tropomyosin from the active site on actin where myosin is able to attach.
If calcium is never pumped back into the sarcoplasmic reticulum, the active site on actin will stay exposed, which allows myosin to attach at all times.
Note that calcium is also responsible for initiating acetylcholine release from the neuron at the neuromuscular junction; however, this process involves extracellular calcium ions and is not linked to the sarcoplasmic reticulum.
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What role does calcium play during muscle contraction?
What role does calcium play during muscle contraction?
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Calcium is released from the sarcoplasmic reticulum and binds to troponin. At rest, troponin interacts with tropomyosin to block the active sites on actin, preventing myosin from binding. When calcium binds troponin, it causes a conformational change in tropomyosin. This allows the myosin heads to bind to the actin active sites, initiating the contraction process. ATP is used to cause the dissociation of the myosin head from the actin filament, and is not involved in initiating actin-myosin interaction.
Calcium is released from the sarcoplasmic reticulum and binds to troponin. At rest, troponin interacts with tropomyosin to block the active sites on actin, preventing myosin from binding. When calcium binds troponin, it causes a conformational change in tropomyosin. This allows the myosin heads to bind to the actin active sites, initiating the contraction process. ATP is used to cause the dissociation of the myosin head from the actin filament, and is not involved in initiating actin-myosin interaction.
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Rigor mortis, a recognizable sign of death, is the stiffness observed in the muscle of an individual who has just passed away. On a molecular level, what causes rigor mortis?
Rigor mortis, a recognizable sign of death, is the stiffness observed in the muscle of an individual who has just passed away. On a molecular level, what causes rigor mortis?
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After the myosin head has attached to the actin filament, a power stroke occurs, which causes the "sliding filament theory" (contraction).This process occurs in a cycle as long as two conditions are present: calcium must be available to bind to troponin, revealing the binding sites on actin, and ATP must be available for the movement of the myosin head. When an individual is no longer alive, calcium is no longer sequestered and remains available to bind to troponin, revealing the binding sites. This would allow continued normal contraction, but is not the cause of sustained contraction seen in rigor mortis. After death, cellular metabolism no longer produces ATP, and stores of ATP are quickly depleted. This results in a break in the contraction cycle. ATP is necessary to detach the myosin head from the actin filament. Without ATP present, the myosin head remains bound and the contraction is sustained. The depletion of ATP is thus the cause of rigor mortis, causing stiffness due to myosin's inability to detach from actin.
After the myosin head has attached to the actin filament, a power stroke occurs, which causes the "sliding filament theory" (contraction).This process occurs in a cycle as long as two conditions are present: calcium must be available to bind to troponin, revealing the binding sites on actin, and ATP must be available for the movement of the myosin head. When an individual is no longer alive, calcium is no longer sequestered and remains available to bind to troponin, revealing the binding sites. This would allow continued normal contraction, but is not the cause of sustained contraction seen in rigor mortis. After death, cellular metabolism no longer produces ATP, and stores of ATP are quickly depleted. This results in a break in the contraction cycle. ATP is necessary to detach the myosin head from the actin filament. Without ATP present, the myosin head remains bound and the contraction is sustained. The depletion of ATP is thus the cause of rigor mortis, causing stiffness due to myosin's inability to detach from actin.
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In the muscle unit, the action potential travels down what specialized structure to eventually allow for muscle contraction?
In the muscle unit, the action potential travels down what specialized structure to eventually allow for muscle contraction?
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The T-tubules are responsible for propagating action potentials deep down into muscle fibers, allowing for a uniform and coordinated contraction. The T-tubules are invaginations of the sarcolemma, the specialized cell membrane of muscle cells. T-tubules run adjacent to the sarcoplasmic reticulum, triggering calcium release as the tubule is depolarized. The sarcoplasmic reticulum stores calcium, while the extracellular matrix provides structural support for cells.
The T-tubules are responsible for propagating action potentials deep down into muscle fibers, allowing for a uniform and coordinated contraction. The T-tubules are invaginations of the sarcolemma, the specialized cell membrane of muscle cells. T-tubules run adjacent to the sarcoplasmic reticulum, triggering calcium release as the tubule is depolarized. The sarcoplasmic reticulum stores calcium, while the extracellular matrix provides structural support for cells.
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An individual has muscle cells that have an abnormally high level of intracellular calcium. The physician suspects that he may have a genetic defect affecting one of his organelles. Which organelle is likely to be the cause of this condition?
An individual has muscle cells that have an abnormally high level of intracellular calcium. The physician suspects that he may have a genetic defect affecting one of his organelles. Which organelle is likely to be the cause of this condition?
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The sarcoplasmic reticulum, an organelle unique to muscle cells, sequesters calcium when the muscle is at rest. This calcium is released into the cytosol during stimulation, and is an integral part of contraction. The affected individual probably has a leaky sarcoplasmic reticulum, allowing the release of calcium into the cytosol and resulting in abnormally high levels of intracellular ion.
Ribosomes are used during protein synthesis and not related to muscle contraction. The nucleus also is not involved in muscle contraction. The Golgi body is involved in modification and packaging of proteins, and also not involved in muscle contraction. Mitochondria are responsible for producing ATP. While ATP is an important part of the contraction process, and mitochondria are abundant in muscle cells, a defect in the mitochondria would not directly cause an increase in intracellular calcium.
The sarcoplasmic reticulum, an organelle unique to muscle cells, sequesters calcium when the muscle is at rest. This calcium is released into the cytosol during stimulation, and is an integral part of contraction. The affected individual probably has a leaky sarcoplasmic reticulum, allowing the release of calcium into the cytosol and resulting in abnormally high levels of intracellular ion.
Ribosomes are used during protein synthesis and not related to muscle contraction. The nucleus also is not involved in muscle contraction. The Golgi body is involved in modification and packaging of proteins, and also not involved in muscle contraction. Mitochondria are responsible for producing ATP. While ATP is an important part of the contraction process, and mitochondria are abundant in muscle cells, a defect in the mitochondria would not directly cause an increase in intracellular calcium.
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Which of the following is NOT a function of the muscular system?
Which of the following is NOT a function of the muscular system?
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The muscular system has a variety of functions. It helps regulate the temperature of the body by generating heat through contraction; this is why we shiver when we are cold. It helps push blood and lymph throughout the blood vessels via the action of smooth muscle, as well as cardiac muscle. Skeletal muscle also maintains body stability and aids in body movement. Calcium storage is not a main function of the skeletal system, although calcium is an important ion for muscular function.
The muscular system has a variety of functions. It helps regulate the temperature of the body by generating heat through contraction; this is why we shiver when we are cold. It helps push blood and lymph throughout the blood vessels via the action of smooth muscle, as well as cardiac muscle. Skeletal muscle also maintains body stability and aids in body movement. Calcium storage is not a main function of the skeletal system, although calcium is an important ion for muscular function.
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Skeletal muscle fibers are not all contracted at once by the same action potential. Instead, muscle fibers are divided into clusters that can range from two to two thousand cells. All of these muscle fibers are innervated by the same neuron; the muscle fibers and the neuron that innervates them are collectively referred to as a motor unit.
Which of the following statements is true concerning motor units?
Skeletal muscle fibers are not all contracted at once by the same action potential. Instead, muscle fibers are divided into clusters that can range from two to two thousand cells. All of these muscle fibers are innervated by the same neuron; the muscle fibers and the neuron that innervates them are collectively referred to as a motor unit.
Which of the following statements is true concerning motor units?
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During a contraction, smaller motor units are typically fired first, followed by larger units in order to have a smooth, controlled movement. Movements that require fine, controlled motion, such as the muscles of the fingers, will be composed of smaller motor units.
The neurotransmitter associated with skeletal muscle is acetylcholine, not epinephrine. A single action potential may initiate contraction of a motor unit, but the neuron must continue to fire in order to sustain the contraction.
During a contraction, smaller motor units are typically fired first, followed by larger units in order to have a smooth, controlled movement. Movements that require fine, controlled motion, such as the muscles of the fingers, will be composed of smaller motor units.
The neurotransmitter associated with skeletal muscle is acetylcholine, not epinephrine. A single action potential may initiate contraction of a motor unit, but the neuron must continue to fire in order to sustain the contraction.
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Skeletal muscle fibers are not all contracted at once by the same action potential. Instead, muscle fibers are divided into clusters that can range from two to two thousand cells. All of these muscle fibers are innervated by the same neuron; the muscle fibers and the neuron that innervates them are collectively referred to as a motor unit.
When the neurotransmitter attaches to the sarcolemma of the muscle fibers, it stimulates the release of calcium. What is the primary role of calcium in skeletal muscle?
Skeletal muscle fibers are not all contracted at once by the same action potential. Instead, muscle fibers are divided into clusters that can range from two to two thousand cells. All of these muscle fibers are innervated by the same neuron; the muscle fibers and the neuron that innervates them are collectively referred to as a motor unit.
When the neurotransmitter attaches to the sarcolemma of the muscle fibers, it stimulates the release of calcium. What is the primary role of calcium in skeletal muscle?
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Acetylcholine will stimulate sodium channels on the sarcolemma, which will consequently trigger the release of calcium ions from the sarcoplasmic reticulum. The calcium will then attach to troponin, which pulls tropomyosin away from the active site on actin. With the active site available, myosin heads are able to attach to the actin filament.
Acetylcholine will stimulate sodium channels on the sarcolemma, which will consequently trigger the release of calcium ions from the sarcoplasmic reticulum. The calcium will then attach to troponin, which pulls tropomyosin away from the active site on actin. With the active site available, myosin heads are able to attach to the actin filament.
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Which of the following changes will not take place in a muscle experiencing prolonged, powerful contractions?
Which of the following changes will not take place in a muscle experiencing prolonged, powerful contractions?
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Keep in mind that muscle cells do not undergo mitosis. Instead, the increase in muscle size is due to increased muscle fiber diameter. The number of sarcomeres and mitochondria in each muscle fiber will also increase over time. This increase in size, but not cell number, is called hypertrophy.
Keep in mind that muscle cells do not undergo mitosis. Instead, the increase in muscle size is due to increased muscle fiber diameter. The number of sarcomeres and mitochondria in each muscle fiber will also increase over time. This increase in size, but not cell number, is called hypertrophy.
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What is the specialized organelle in muscle cells that serves to sequester calcium?
What is the specialized organelle in muscle cells that serves to sequester calcium?
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The sarcoplasmic reticulum is the specialized organelle of the muscle cells that allows for calcium to be sequestered. Once calcium is released into the cytoplasm it interacts with troponin and tropomyosin, allowing myosin and actin to bind and cause contraction. Calcium must be sequestrated to allow for the myosin-actin bridges to be broken and reset for future contraction.
The sarcolemma is the muscle cell membrane. The T-tubules permeate the muscle cell to allow for propagation of the stimulating action potential to all parts to the cell. The sarcomeres are the contractile units of the muscle cell.
The sarcoplasmic reticulum is the specialized organelle of the muscle cells that allows for calcium to be sequestered. Once calcium is released into the cytoplasm it interacts with troponin and tropomyosin, allowing myosin and actin to bind and cause contraction. Calcium must be sequestrated to allow for the myosin-actin bridges to be broken and reset for future contraction.
The sarcolemma is the muscle cell membrane. The T-tubules permeate the muscle cell to allow for propagation of the stimulating action potential to all parts to the cell. The sarcomeres are the contractile units of the muscle cell.
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The force of a muscle contraction is not proportional to which of the following?
The force of a muscle contraction is not proportional to which of the following?
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The force of a muscle contraction can be manipulated in several ways. When a muscle is stimulated by an action potential, all fibers within a given motor unit are activated together. Increasing the number of motor units will increase the percentage of the muscle mass that is contracting, increasing the force. Increasing the size of the motor units will have the same effect. Increasing the number of action potentials will allow for sustained contraction.
Action potentials themselves are all-or-nothing; they either happen or they do not. There is no such thing as a large or small action potential. Several action potentials can arrive simultaneously, causing a summation effect, but the size of an action potential on its own cannot affect the force of a muscle contraction.
The force of a muscle contraction can be manipulated in several ways. When a muscle is stimulated by an action potential, all fibers within a given motor unit are activated together. Increasing the number of motor units will increase the percentage of the muscle mass that is contracting, increasing the force. Increasing the size of the motor units will have the same effect. Increasing the number of action potentials will allow for sustained contraction.
Action potentials themselves are all-or-nothing; they either happen or they do not. There is no such thing as a large or small action potential. Several action potentials can arrive simultaneously, causing a summation effect, but the size of an action potential on its own cannot affect the force of a muscle contraction.
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