Muscle Stimulation and Contraction - MCAT Biological and Biochemical Foundations of Living Systems
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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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What is the purpose of calcium in the muscles?
What is the purpose of calcium in the muscles?
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The proteins troponin and tropomyosin are attached to the actin filaments in sarcomeres. These proteins function to block the myosin-binding site on the actin protein, preventing unnecessary contraction. When calcium is released from the sarcoplasmic reticulum, it will attach to troponin. The troponin will then pull tropomyosin away from the actin filament, which allows myosin heads to attach and cause a contraction.
ATP binds myosin to release it from the actin binding site and is converted to ADP in order to adjust the myosin head to a high-energy position.
The proteins troponin and tropomyosin are attached to the actin filaments in sarcomeres. These proteins function to block the myosin-binding site on the actin protein, preventing unnecessary contraction. When calcium is released from the sarcoplasmic reticulum, it will attach to troponin. The troponin will then pull tropomyosin away from the actin filament, which allows myosin heads to attach and cause a contraction.
ATP binds myosin to release it from the actin binding site and is converted to ADP in order to adjust the myosin head to a high-energy position.
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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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What is the purpose of calcium in the muscles?
What is the purpose of calcium in the muscles?
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The proteins troponin and tropomyosin are attached to the actin filaments in sarcomeres. These proteins function to block the myosin-binding site on the actin protein, preventing unnecessary contraction. When calcium is released from the sarcoplasmic reticulum, it will attach to troponin. The troponin will then pull tropomyosin away from the actin filament, which allows myosin heads to attach and cause a contraction.
ATP binds myosin to release it from the actin binding site and is converted to ADP in order to adjust the myosin head to a high-energy position.
The proteins troponin and tropomyosin are attached to the actin filaments in sarcomeres. These proteins function to block the myosin-binding site on the actin protein, preventing unnecessary contraction. When calcium is released from the sarcoplasmic reticulum, it will attach to troponin. The troponin will then pull tropomyosin away from the actin filament, which allows myosin heads to attach and cause a contraction.
ATP binds myosin to release it from the actin binding site and is converted to ADP in order to adjust the myosin head to a high-energy position.
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The sarcoplasmic reticulum has the ability to aid in muscle contraction by storing large amounts of which ion?
The sarcoplasmic reticulum has the ability to aid in muscle contraction by storing large amounts of which ion?
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Calcium plays a huge role in the regulation of muscle contraction. Without the presence of calcium, the myosin binding sites on the actin filaments are blocked by tropomyosin and muscle contraction cannot occur. Stimulation from the nervous system causes a chain reaction that releases large stores of calcium from the sarcoplasmic reticulum to regulate muscle contraction.
Sodium ions play an essential role in initiating the chain reaction that eventually leads to calcium release, but is not stored in the sarcoplasmic reticulum. Potassium plays a role in regulating membrane potential, but also is not stored in the sarcoplasmic reticulum. Protons are essential to mitochondrial function and play a crucial role in myocyte metabolism, but are not linked to the sarcoplasmic reticulum or contractile function.
Calcium plays a huge role in the regulation of muscle contraction. Without the presence of calcium, the myosin binding sites on the actin filaments are blocked by tropomyosin and muscle contraction cannot occur. Stimulation from the nervous system causes a chain reaction that releases large stores of calcium from the sarcoplasmic reticulum to regulate muscle contraction.
Sodium ions play an essential role in initiating the chain reaction that eventually leads to calcium release, but is not stored in the sarcoplasmic reticulum. Potassium plays a role in regulating membrane potential, but also is not stored in the sarcoplasmic reticulum. Protons are essential to mitochondrial function and play a crucial role in myocyte metabolism, but are not linked to the sarcoplasmic reticulum or contractile function.
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A researcher discovers a mutant strain of contractile cells that will not contract under physiological conditions; however, when presented with supraphysiological concentrations of calcium, the cells contract. Which of the following mutations might be the cause of this phenotype?
A researcher discovers a mutant strain of contractile cells that will not contract under physiological conditions; however, when presented with supraphysiological concentrations of calcium, the cells contract. Which of the following mutations might be the cause of this phenotype?
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Muscle contraction is regulated by blocking the myosin binding sites of actin and selectively exposing them when contraction is supposed to occur. Tropomyosin binds actin fibers and recruits troponin to perform this blocking function. Troponin will bind calcium ions, change conformation, and move tropomyosin out of the way of the myosin binding sites to allow contraction to occur. The most likely mutation described in the question is one that causes troponin to have a decreased affinity for calcium, thus never allowing the myosin binding sites to be exposed under normal physiological concentrations.
Muscle contraction is regulated by blocking the myosin binding sites of actin and selectively exposing them when contraction is supposed to occur. Tropomyosin binds actin fibers and recruits troponin to perform this blocking function. Troponin will bind calcium ions, change conformation, and move tropomyosin out of the way of the myosin binding sites to allow contraction to occur. The most likely mutation described in the question is one that causes troponin to have a decreased affinity for calcium, thus never allowing the myosin binding sites to be exposed under normal physiological concentrations.
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Tests reveal that a certain patient has depleted calcium stores in his sarcoplasmic reticulum. Which of the following is a direct consequence of this abnormality?
Tests reveal that a certain patient has depleted calcium stores in his sarcoplasmic reticulum. Which of the following is a direct consequence of this abnormality?
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In a typical muscle cell, tropomyosin is bound to an active site on actin. This prevents muscle contraction because the myosin head cannot bind to actin active site. Muscle contraction is initiated when the sarcoplasmic reticulum releases calcium ions into the cytoplasm of the muscle cell. Calcium ions bind to and activate troponin. Activated troponin molecules subsequently remove tropomyosin from the active site on actin. This allows muscle contraction to occur because the myosin head can now bind to the active site on actin and initiate a power stroke to shorten the sarcomere.
An individual with depleted calcium ions in his sarcoplasmic reticulum will not activate troponin and, therefore, will have reduced muscle tone and strength.
In a typical muscle cell, tropomyosin is bound to an active site on actin. This prevents muscle contraction because the myosin head cannot bind to actin active site. Muscle contraction is initiated when the sarcoplasmic reticulum releases calcium ions into the cytoplasm of the muscle cell. Calcium ions bind to and activate troponin. Activated troponin molecules subsequently remove tropomyosin from the active site on actin. This allows muscle contraction to occur because the myosin head can now bind to the active site on actin and initiate a power stroke to shorten the sarcomere.
An individual with depleted calcium ions in his sarcoplasmic reticulum will not activate troponin and, therefore, will have reduced muscle tone and strength.
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Muscle cramps are caused because of prolonged muscle contraction. Prolonged periods of muscle contraction occur because the myosin heads can’t detach themselves from the actin filaments. What is the most likely cause of muscle cramps?
Muscle cramps are caused because of prolonged muscle contraction. Prolonged periods of muscle contraction occur because the myosin heads can’t detach themselves from the actin filaments. What is the most likely cause of muscle cramps?
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The question states that muscle cramps occur because myosin heads remain attached to the active site on actin; therefore, you are looking for a molecule that is responsible for the detachment of the myosin head from actin. Recall that binding of ATP to the myosin head releases the myosin head from the actin binding site. This allows tropomyosin to re-attach to actin and causes the muscle to relax. The ATP that is bound to the myosin head dissociates into ADP and inorganic phosphate, allowing the myosin head to enter its high-energy state and prepare for another contractile stroke. Once tropomyosin is released again from the actin filament, the ADP and inorganic phosphate on the myosin head are released, the myosin head attaches to actin, and the cycle continues.
Calcium is essential for muscle contraction because it allows for the removal of tropomyosin from the actin binding sites. Depletion of calcium, however, would cause the actin sites to be blocked, preventing contraction from occurring (as opposed to the sustained contraction of a muscle cramp). Depleted sodium may result in fewer action potentials at the neuromuscular junction. This would also inhibit muscle contraction, rather than sustain it. Muscular microtears can occur during exercise, but are unrelated to muscle cramps.
The question states that muscle cramps occur because myosin heads remain attached to the active site on actin; therefore, you are looking for a molecule that is responsible for the detachment of the myosin head from actin. Recall that binding of ATP to the myosin head releases the myosin head from the actin binding site. This allows tropomyosin to re-attach to actin and causes the muscle to relax. The ATP that is bound to the myosin head dissociates into ADP and inorganic phosphate, allowing the myosin head to enter its high-energy state and prepare for another contractile stroke. Once tropomyosin is released again from the actin filament, the ADP and inorganic phosphate on the myosin head are released, the myosin head attaches to actin, and the cycle continues.
Calcium is essential for muscle contraction because it allows for the removal of tropomyosin from the actin binding sites. Depletion of calcium, however, would cause the actin sites to be blocked, preventing contraction from occurring (as opposed to the sustained contraction of a muscle cramp). Depleted sodium may result in fewer action potentials at the neuromuscular junction. This would also inhibit muscle contraction, rather than sustain it. Muscular microtears can occur during exercise, but are unrelated to muscle cramps.
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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 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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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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