Help with Muscle Proteins and Signals - Anatomy
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What protein must undergo a conformational change so that myosin can be attached to actin?
What protein must undergo a conformational change so that myosin can be attached to actin?
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Actin houses binding sites for myosin that must be covered when a muscle is not contracting; otherwise myosin would constantly attach to actin, initiating unstimulated contraction. When calcium is released from the sarcoplasmic reticulum, it attaches to troponin. The troponin then causes a conformational change in tropomyosin. This change alters the orientation of tropomyosin away from the binding site on action. With the binding site revealed, myosin can adhere to the actin filament and contract the sarcomere.
Titin spans the length of the sarcomere and plays a key role in maintaining muscle elasticity. Collagen provides tensile strength around the muscles, and is mostly found in the extracellular matrix. ATP is not a protein, and is used to provide energy for the contraction process.
Actin houses binding sites for myosin that must be covered when a muscle is not contracting; otherwise myosin would constantly attach to actin, initiating unstimulated contraction. When calcium is released from the sarcoplasmic reticulum, it attaches to troponin. The troponin then causes a conformational change in tropomyosin. This change alters the orientation of tropomyosin away from the binding site on action. With the binding site revealed, myosin can adhere to the actin filament and contract the sarcomere.
Titin spans the length of the sarcomere and plays a key role in maintaining muscle elasticity. Collagen provides tensile strength around the muscles, and is mostly found in the extracellular matrix. ATP is not a protein, and is used to provide energy for the contraction process.
In malignant hyperthermia, general anesthesia triggers an uncontrolled increase in skeletal muscle metabolism, which causes the body to generate heat faster than it can cool down and use up the body’s store of oxygen. Dantrolene is the medication used to treat this condition, as it will block increases in intracellular calcium. What is the role of calcium in muscle contraction?
In malignant hyperthermia, general anesthesia triggers an uncontrolled increase in skeletal muscle metabolism, which causes the body to generate heat faster than it can cool down and use up the body’s store of oxygen. Dantrolene is the medication used to treat this condition, as it will block increases in intracellular calcium. What is the role of calcium in muscle contraction?
Tap to see back →
For skeletal muscle contraction, calcium binds to troponin to uncover actin binding sites.
In order for skeletal muscle contraction to occur, the protein myosin needs to bind to the protein actin and slide it to decrease the length of the sarcomere, which is the contractile unit of a muscle. At rest, the sites on actin that myosin needs to bind to are covered up by the protein tropomyosin. Troponin is a protein that is attached to tropomyosin, to which calcium can bind.
When an action potential reaches a muscle cell, it travels down T-tubules to reach the sarcoplasmic reticulum. The sarcoplasmic reticulum releases stores of calcium, which bind to troponin. This binding causes a conformational change in troponin that causes it to shift the position of the attached tropomyosin to uncover binding sites on actin. Myosin is then able to bind and contraction can occur.
Myosin binds to actin and slides it to shorten the sarcomere. Secretory vesicles release acetylcholine into the synaptic cleft upon stimulation of the presynaptic neuron. This stimulation causes an influx of calcium at the axon terminal, but is not directly linked to increases in intracellular calcium of the muscle cell. Dystrophin is the protein that stabilizes the cell membrane of skeletal muscles. Myelination of axons speeds up conduction of action potentials.
For skeletal muscle contraction, calcium binds to troponin to uncover actin binding sites.
In order for skeletal muscle contraction to occur, the protein myosin needs to bind to the protein actin and slide it to decrease the length of the sarcomere, which is the contractile unit of a muscle. At rest, the sites on actin that myosin needs to bind to are covered up by the protein tropomyosin. Troponin is a protein that is attached to tropomyosin, to which calcium can bind.
When an action potential reaches a muscle cell, it travels down T-tubules to reach the sarcoplasmic reticulum. The sarcoplasmic reticulum releases stores of calcium, which bind to troponin. This binding causes a conformational change in troponin that causes it to shift the position of the attached tropomyosin to uncover binding sites on actin. Myosin is then able to bind and contraction can occur.
Myosin binds to actin and slides it to shorten the sarcomere. Secretory vesicles release acetylcholine into the synaptic cleft upon stimulation of the presynaptic neuron. This stimulation causes an influx of calcium at the axon terminal, but is not directly linked to increases in intracellular calcium of the muscle cell. Dystrophin is the protein that stabilizes the cell membrane of skeletal muscles. Myelination of axons speeds up conduction of action potentials.
After the New Year, you decide to make a resolution to exercise more and you enthusiastically wake up early in the cold morning to go for a run. You feel great initially, but ten minutes into your run, you feel a disabling pain in your right calf that forces you to stop and sit on the curb. You feel your calf spasming and note that your toes are pointed downward. You are unable to change this position and think that you have a muscle cramp. A few minutes later the pain subsides and you are able to move your foot again. What molecular deficiency is responsible for this condition?
After the New Year, you decide to make a resolution to exercise more and you enthusiastically wake up early in the cold morning to go for a run. You feel great initially, but ten minutes into your run, you feel a disabling pain in your right calf that forces you to stop and sit on the curb. You feel your calf spasming and note that your toes are pointed downward. You are unable to change this position and think that you have a muscle cramp. A few minutes later the pain subsides and you are able to move your foot again. What molecular deficiency is responsible for this condition?
Tap to see back →
A deficiency of ATP is the main cause of skeletal muscle cramps.
During the anaerobic phase of exercise, ATP is quickly used up before cellular respiration can kick in. Muscle contraction requires myosin to bind to actin and slide it for sarcomere shortening. Attachment of ADP and inorganic phosphate to the myosin head causes it to bind to actin. Release of ADP and inorganic phosphate causes the myosin head to bend and pull on actin. Binding of ATP to myosin is needed for myosin to release its hold on actin. Hydrolysis of ATP to ADP and inorganic phosphate causes myosin to bind to actin again.
When ATP stores are depleted, myosin is unable to detach from actin so that skeletal muscle is "stuck" in its position. During this cramping period, the affected muscle cannot move and attempting to forcefully do so may tear it. As you rest and replete your ATP stores, myosin will be able to release from actin and the muscle can shorten or lengthen again.
While electrolyte deficiencies can also cause muscular weakness and cramping, this only happens when they are depleted during excessive sweating and rehydration with plain water. Sweating causes loss of electrolytes and intake of water will dilute the concentration of existing electrolytes. Hyponatremia and hypocalcemia are the main causes of electrolyte-deficiency cramps. Deficiency of acetylcholine can cause muscular weakness as seen in myasthenia gravis or botulism.
A deficiency of ATP is the main cause of skeletal muscle cramps.
During the anaerobic phase of exercise, ATP is quickly used up before cellular respiration can kick in. Muscle contraction requires myosin to bind to actin and slide it for sarcomere shortening. Attachment of ADP and inorganic phosphate to the myosin head causes it to bind to actin. Release of ADP and inorganic phosphate causes the myosin head to bend and pull on actin. Binding of ATP to myosin is needed for myosin to release its hold on actin. Hydrolysis of ATP to ADP and inorganic phosphate causes myosin to bind to actin again.
When ATP stores are depleted, myosin is unable to detach from actin so that skeletal muscle is "stuck" in its position. During this cramping period, the affected muscle cannot move and attempting to forcefully do so may tear it. As you rest and replete your ATP stores, myosin will be able to release from actin and the muscle can shorten or lengthen again.
While electrolyte deficiencies can also cause muscular weakness and cramping, this only happens when they are depleted during excessive sweating and rehydration with plain water. Sweating causes loss of electrolytes and intake of water will dilute the concentration of existing electrolytes. Hyponatremia and hypocalcemia are the main causes of electrolyte-deficiency cramps. Deficiency of acetylcholine can cause muscular weakness as seen in myasthenia gravis or botulism.
Where within the sarcomere is the 
ATPase?
Where within the sarcomere is the
Tap to see back →
The sarcoplasmic reticulum within a muscle cells is where many calcium ions are stored and released. The release of calcium is a required step in muscle contraction. The ryanodine receptor pumps calcium ions from the intracellular fluid into the interior of the sarcoplasmic reticulum, this process keeps the intracellular calcium ions low, provides a quick store of calcium, and creates a concentration gradient. The sarcoplasmic reticulum membrane contains calcium ion/ATPase 
pumps. This pump transports intracellular calcium ions into the sarcoplasmic reticulum.
The sarcoplasmic reticulum within a muscle cells is where many calcium ions are stored and released. The release of calcium is a required step in muscle contraction. The ryanodine receptor pumps calcium ions from the intracellular fluid into the interior of the sarcoplasmic reticulum, this process keeps the intracellular calcium ions low, provides a quick store of calcium, and creates a concentration gradient. The sarcoplasmic reticulum membrane contains calcium ion/ATPase
Tetanic contraction of a muscle fiber results in a substantial increase in the intracellular concentration of which of the following?
Tetanic contraction of a muscle fiber results in a substantial increase in the intracellular concentration of which of the following?
Tap to see back →
Muscle contraction relies on elevations in the intracellular concentration of calcium. In order to sustain maximal contraction of a muscle fiber, intracellular calcium levels must remain higher than normal. Intracellular concentrations of sodium, potassium, and magnesium do not affect muscle contraction.
Muscle contraction relies on elevations in the intracellular concentration of calcium. In order to sustain maximal contraction of a muscle fiber, intracellular calcium levels must remain higher than normal. Intracellular concentrations of sodium, potassium, and magnesium do not affect muscle contraction.
What is the role of creatine phosphokinase (CPK) in skeletal muscle?
What is the role of creatine phosphokinase (CPK) in skeletal muscle?
Tap to see back →
When ATP is used during the muscle contraction process, it is regenerated through the transfer of phosphate from PCr (phosphocreatine) to ADP (adenosine diphosphate). This reaction is catalyzed by the enzyme CPK (creatine phosphokinase).
The net reaction that is catalyzed by CPK is: PCr + ADP -> ATP + Cr
When ATP is used during the muscle contraction process, it is regenerated through the transfer of phosphate from PCr (phosphocreatine) to ADP (adenosine diphosphate). This reaction is catalyzed by the enzyme CPK (creatine phosphokinase).
The net reaction that is catalyzed by CPK is: PCr + ADP -> ATP + Cr
What is the role of parvalbumin during a muscle contraction?
What is the role of parvalbumin during a muscle contraction?
Tap to see back →
Parvalbumin is a protein related to albumin, which is found in the blood. Parvalbumin plays a different role though, and is found in the muscle. Parvalbumin exists in muscle cytoplasm, and binds reversibly with calcium that is released from the sarcoplasmic reticulum during the muscle contraction process. Parvalbumin binding calcium is exothermic and produces labile heat. Parvalbumin then slowly releases calcium back into the cytoplasm. This makes parvalbumin a slow-releasing calcium buffer.
Parvalbumin is a protein related to albumin, which is found in the blood. Parvalbumin plays a different role though, and is found in the muscle. Parvalbumin exists in muscle cytoplasm, and binds reversibly with calcium that is released from the sarcoplasmic reticulum during the muscle contraction process. Parvalbumin binding calcium is exothermic and produces labile heat. Parvalbumin then slowly releases calcium back into the cytoplasm. This makes parvalbumin a slow-releasing calcium buffer.
What is the role of phosphocreatine (PCr) in maintaining ATP concentrations during muscle contraction?
What is the role of phosphocreatine (PCr) in maintaining ATP concentrations during muscle contraction?
Tap to see back →
PCr or phosphocreatine works to maintain ATP concentrations during muscle contraction and use. It does so by transferring its phosphate group to ADP, which is the product of ATP breakdown. When ATP is broken down to ADP, PCr donates a phosphate to ADP to recreate an ATP. This reaction, PCr + ADP -> ATP + Cr, is catalyzed by the enzyme CPK.
PCr or phosphocreatine works to maintain ATP concentrations during muscle contraction and use. It does so by transferring its phosphate group to ADP, which is the product of ATP breakdown. When ATP is broken down to ADP, PCr donates a phosphate to ADP to recreate an ATP. This reaction, PCr + ADP -> ATP + Cr, is catalyzed by the enzyme CPK.
What protein must undergo a conformational change so that myosin can be attached to actin?
What protein must undergo a conformational change so that myosin can be attached to actin?
Tap to see back →
Actin houses binding sites for myosin that must be covered when a muscle is not contracting; otherwise myosin would constantly attach to actin, initiating unstimulated contraction. When calcium is released from the sarcoplasmic reticulum, it attaches to troponin. The troponin then causes a conformational change in tropomyosin. This change alters the orientation of tropomyosin away from the binding site on action. With the binding site revealed, myosin can adhere to the actin filament and contract the sarcomere.
Titin spans the length of the sarcomere and plays a key role in maintaining muscle elasticity. Collagen provides tensile strength around the muscles, and is mostly found in the extracellular matrix. ATP is not a protein, and is used to provide energy for the contraction process.
Actin houses binding sites for myosin that must be covered when a muscle is not contracting; otherwise myosin would constantly attach to actin, initiating unstimulated contraction. When calcium is released from the sarcoplasmic reticulum, it attaches to troponin. The troponin then causes a conformational change in tropomyosin. This change alters the orientation of tropomyosin away from the binding site on action. With the binding site revealed, myosin can adhere to the actin filament and contract the sarcomere.
Titin spans the length of the sarcomere and plays a key role in maintaining muscle elasticity. Collagen provides tensile strength around the muscles, and is mostly found in the extracellular matrix. ATP is not a protein, and is used to provide energy for the contraction process.
In malignant hyperthermia, general anesthesia triggers an uncontrolled increase in skeletal muscle metabolism, which causes the body to generate heat faster than it can cool down and use up the body’s store of oxygen. Dantrolene is the medication used to treat this condition, as it will block increases in intracellular calcium. What is the role of calcium in muscle contraction?
In malignant hyperthermia, general anesthesia triggers an uncontrolled increase in skeletal muscle metabolism, which causes the body to generate heat faster than it can cool down and use up the body’s store of oxygen. Dantrolene is the medication used to treat this condition, as it will block increases in intracellular calcium. What is the role of calcium in muscle contraction?
Tap to see back →
For skeletal muscle contraction, calcium binds to troponin to uncover actin binding sites.
In order for skeletal muscle contraction to occur, the protein myosin needs to bind to the protein actin and slide it to decrease the length of the sarcomere, which is the contractile unit of a muscle. At rest, the sites on actin that myosin needs to bind to are covered up by the protein tropomyosin. Troponin is a protein that is attached to tropomyosin, to which calcium can bind.
When an action potential reaches a muscle cell, it travels down T-tubules to reach the sarcoplasmic reticulum. The sarcoplasmic reticulum releases stores of calcium, which bind to troponin. This binding causes a conformational change in troponin that causes it to shift the position of the attached tropomyosin to uncover binding sites on actin. Myosin is then able to bind and contraction can occur.
Myosin binds to actin and slides it to shorten the sarcomere. Secretory vesicles release acetylcholine into the synaptic cleft upon stimulation of the presynaptic neuron. This stimulation causes an influx of calcium at the axon terminal, but is not directly linked to increases in intracellular calcium of the muscle cell. Dystrophin is the protein that stabilizes the cell membrane of skeletal muscles. Myelination of axons speeds up conduction of action potentials.
For skeletal muscle contraction, calcium binds to troponin to uncover actin binding sites.
In order for skeletal muscle contraction to occur, the protein myosin needs to bind to the protein actin and slide it to decrease the length of the sarcomere, which is the contractile unit of a muscle. At rest, the sites on actin that myosin needs to bind to are covered up by the protein tropomyosin. Troponin is a protein that is attached to tropomyosin, to which calcium can bind.
When an action potential reaches a muscle cell, it travels down T-tubules to reach the sarcoplasmic reticulum. The sarcoplasmic reticulum releases stores of calcium, which bind to troponin. This binding causes a conformational change in troponin that causes it to shift the position of the attached tropomyosin to uncover binding sites on actin. Myosin is then able to bind and contraction can occur.
Myosin binds to actin and slides it to shorten the sarcomere. Secretory vesicles release acetylcholine into the synaptic cleft upon stimulation of the presynaptic neuron. This stimulation causes an influx of calcium at the axon terminal, but is not directly linked to increases in intracellular calcium of the muscle cell. Dystrophin is the protein that stabilizes the cell membrane of skeletal muscles. Myelination of axons speeds up conduction of action potentials.
After the New Year, you decide to make a resolution to exercise more and you enthusiastically wake up early in the cold morning to go for a run. You feel great initially, but ten minutes into your run, you feel a disabling pain in your right calf that forces you to stop and sit on the curb. You feel your calf spasming and note that your toes are pointed downward. You are unable to change this position and think that you have a muscle cramp. A few minutes later the pain subsides and you are able to move your foot again. What molecular deficiency is responsible for this condition?
After the New Year, you decide to make a resolution to exercise more and you enthusiastically wake up early in the cold morning to go for a run. You feel great initially, but ten minutes into your run, you feel a disabling pain in your right calf that forces you to stop and sit on the curb. You feel your calf spasming and note that your toes are pointed downward. You are unable to change this position and think that you have a muscle cramp. A few minutes later the pain subsides and you are able to move your foot again. What molecular deficiency is responsible for this condition?
Tap to see back →
A deficiency of ATP is the main cause of skeletal muscle cramps.
During the anaerobic phase of exercise, ATP is quickly used up before cellular respiration can kick in. Muscle contraction requires myosin to bind to actin and slide it for sarcomere shortening. Attachment of ADP and inorganic phosphate to the myosin head causes it to bind to actin. Release of ADP and inorganic phosphate causes the myosin head to bend and pull on actin. Binding of ATP to myosin is needed for myosin to release its hold on actin. Hydrolysis of ATP to ADP and inorganic phosphate causes myosin to bind to actin again.
When ATP stores are depleted, myosin is unable to detach from actin so that skeletal muscle is "stuck" in its position. During this cramping period, the affected muscle cannot move and attempting to forcefully do so may tear it. As you rest and replete your ATP stores, myosin will be able to release from actin and the muscle can shorten or lengthen again.
While electrolyte deficiencies can also cause muscular weakness and cramping, this only happens when they are depleted during excessive sweating and rehydration with plain water. Sweating causes loss of electrolytes and intake of water will dilute the concentration of existing electrolytes. Hyponatremia and hypocalcemia are the main causes of electrolyte-deficiency cramps. Deficiency of acetylcholine can cause muscular weakness as seen in myasthenia gravis or botulism.
A deficiency of ATP is the main cause of skeletal muscle cramps.
During the anaerobic phase of exercise, ATP is quickly used up before cellular respiration can kick in. Muscle contraction requires myosin to bind to actin and slide it for sarcomere shortening. Attachment of ADP and inorganic phosphate to the myosin head causes it to bind to actin. Release of ADP and inorganic phosphate causes the myosin head to bend and pull on actin. Binding of ATP to myosin is needed for myosin to release its hold on actin. Hydrolysis of ATP to ADP and inorganic phosphate causes myosin to bind to actin again.
When ATP stores are depleted, myosin is unable to detach from actin so that skeletal muscle is "stuck" in its position. During this cramping period, the affected muscle cannot move and attempting to forcefully do so may tear it. As you rest and replete your ATP stores, myosin will be able to release from actin and the muscle can shorten or lengthen again.
While electrolyte deficiencies can also cause muscular weakness and cramping, this only happens when they are depleted during excessive sweating and rehydration with plain water. Sweating causes loss of electrolytes and intake of water will dilute the concentration of existing electrolytes. Hyponatremia and hypocalcemia are the main causes of electrolyte-deficiency cramps. Deficiency of acetylcholine can cause muscular weakness as seen in myasthenia gravis or botulism.
Where within the sarcomere is the ATPase?
Where within the sarcomere is the
Tap to see back →
The sarcoplasmic reticulum within a muscle cells is where many calcium ions are stored and released. The release of calcium is a required step in muscle contraction. The ryanodine receptor pumps calcium ions from the intracellular fluid into the interior of the sarcoplasmic reticulum, this process keeps the intracellular calcium ions low, provides a quick store of calcium, and creates a concentration gradient. The sarcoplasmic reticulum membrane contains calcium ion/ATPase pumps. This pump transports intracellular calcium ions into the sarcoplasmic reticulum.
The sarcoplasmic reticulum within a muscle cells is where many calcium ions are stored and released. The release of calcium is a required step in muscle contraction. The ryanodine receptor pumps calcium ions from the intracellular fluid into the interior of the sarcoplasmic reticulum, this process keeps the intracellular calcium ions low, provides a quick store of calcium, and creates a concentration gradient. The sarcoplasmic reticulum membrane contains calcium ion/ATPase
Tetanic contraction of a muscle fiber results in a substantial increase in the intracellular concentration of which of the following?
Tetanic contraction of a muscle fiber results in a substantial increase in the intracellular concentration of which of the following?
Tap to see back →
Muscle contraction relies on elevations in the intracellular concentration of calcium. In order to sustain maximal contraction of a muscle fiber, intracellular calcium levels must remain higher than normal. Intracellular concentrations of sodium, potassium, and magnesium do not affect muscle contraction.
Muscle contraction relies on elevations in the intracellular concentration of calcium. In order to sustain maximal contraction of a muscle fiber, intracellular calcium levels must remain higher than normal. Intracellular concentrations of sodium, potassium, and magnesium do not affect muscle contraction.
What is the role of creatine phosphokinase (CPK) in skeletal muscle?
What is the role of creatine phosphokinase (CPK) in skeletal muscle?
Tap to see back →
When ATP is used during the muscle contraction process, it is regenerated through the transfer of phosphate from PCr (phosphocreatine) to ADP (adenosine diphosphate). This reaction is catalyzed by the enzyme CPK (creatine phosphokinase).
The net reaction that is catalyzed by CPK is: PCr + ADP -> ATP + Cr
When ATP is used during the muscle contraction process, it is regenerated through the transfer of phosphate from PCr (phosphocreatine) to ADP (adenosine diphosphate). This reaction is catalyzed by the enzyme CPK (creatine phosphokinase).
The net reaction that is catalyzed by CPK is: PCr + ADP -> ATP + Cr
What is the role of parvalbumin during a muscle contraction?
What is the role of parvalbumin during a muscle contraction?
Tap to see back →
Parvalbumin is a protein related to albumin, which is found in the blood. Parvalbumin plays a different role though, and is found in the muscle. Parvalbumin exists in muscle cytoplasm, and binds reversibly with calcium that is released from the sarcoplasmic reticulum during the muscle contraction process. Parvalbumin binding calcium is exothermic and produces labile heat. Parvalbumin then slowly releases calcium back into the cytoplasm. This makes parvalbumin a slow-releasing calcium buffer.
Parvalbumin is a protein related to albumin, which is found in the blood. Parvalbumin plays a different role though, and is found in the muscle. Parvalbumin exists in muscle cytoplasm, and binds reversibly with calcium that is released from the sarcoplasmic reticulum during the muscle contraction process. Parvalbumin binding calcium is exothermic and produces labile heat. Parvalbumin then slowly releases calcium back into the cytoplasm. This makes parvalbumin a slow-releasing calcium buffer.
What is the role of phosphocreatine (PCr) in maintaining ATP concentrations during muscle contraction?
What is the role of phosphocreatine (PCr) in maintaining ATP concentrations during muscle contraction?
Tap to see back →
PCr or phosphocreatine works to maintain ATP concentrations during muscle contraction and use. It does so by transferring its phosphate group to ADP, which is the product of ATP breakdown. When ATP is broken down to ADP, PCr donates a phosphate to ADP to recreate an ATP. This reaction, PCr + ADP -> ATP + Cr, is catalyzed by the enzyme CPK.
PCr or phosphocreatine works to maintain ATP concentrations during muscle contraction and use. It does so by transferring its phosphate group to ADP, which is the product of ATP breakdown. When ATP is broken down to ADP, PCr donates a phosphate to ADP to recreate an ATP. This reaction, PCr + ADP -> ATP + Cr, is catalyzed by the enzyme CPK.
What protein must undergo a conformational change so that myosin can be attached to actin?
What protein must undergo a conformational change so that myosin can be attached to actin?
Tap to see back →
Actin houses binding sites for myosin that must be covered when a muscle is not contracting; otherwise myosin would constantly attach to actin, initiating unstimulated contraction. When calcium is released from the sarcoplasmic reticulum, it attaches to troponin. The troponin then causes a conformational change in tropomyosin. This change alters the orientation of tropomyosin away from the binding site on action. With the binding site revealed, myosin can adhere to the actin filament and contract the sarcomere.
Titin spans the length of the sarcomere and plays a key role in maintaining muscle elasticity. Collagen provides tensile strength around the muscles, and is mostly found in the extracellular matrix. ATP is not a protein, and is used to provide energy for the contraction process.
Actin houses binding sites for myosin that must be covered when a muscle is not contracting; otherwise myosin would constantly attach to actin, initiating unstimulated contraction. When calcium is released from the sarcoplasmic reticulum, it attaches to troponin. The troponin then causes a conformational change in tropomyosin. This change alters the orientation of tropomyosin away from the binding site on action. With the binding site revealed, myosin can adhere to the actin filament and contract the sarcomere.
Titin spans the length of the sarcomere and plays a key role in maintaining muscle elasticity. Collagen provides tensile strength around the muscles, and is mostly found in the extracellular matrix. ATP is not a protein, and is used to provide energy for the contraction process.
In malignant hyperthermia, general anesthesia triggers an uncontrolled increase in skeletal muscle metabolism, which causes the body to generate heat faster than it can cool down and use up the body’s store of oxygen. Dantrolene is the medication used to treat this condition, as it will block increases in intracellular calcium. What is the role of calcium in muscle contraction?
In malignant hyperthermia, general anesthesia triggers an uncontrolled increase in skeletal muscle metabolism, which causes the body to generate heat faster than it can cool down and use up the body’s store of oxygen. Dantrolene is the medication used to treat this condition, as it will block increases in intracellular calcium. What is the role of calcium in muscle contraction?
Tap to see back →
For skeletal muscle contraction, calcium binds to troponin to uncover actin binding sites.
In order for skeletal muscle contraction to occur, the protein myosin needs to bind to the protein actin and slide it to decrease the length of the sarcomere, which is the contractile unit of a muscle. At rest, the sites on actin that myosin needs to bind to are covered up by the protein tropomyosin. Troponin is a protein that is attached to tropomyosin, to which calcium can bind.
When an action potential reaches a muscle cell, it travels down T-tubules to reach the sarcoplasmic reticulum. The sarcoplasmic reticulum releases stores of calcium, which bind to troponin. This binding causes a conformational change in troponin that causes it to shift the position of the attached tropomyosin to uncover binding sites on actin. Myosin is then able to bind and contraction can occur.
Myosin binds to actin and slides it to shorten the sarcomere. Secretory vesicles release acetylcholine into the synaptic cleft upon stimulation of the presynaptic neuron. This stimulation causes an influx of calcium at the axon terminal, but is not directly linked to increases in intracellular calcium of the muscle cell. Dystrophin is the protein that stabilizes the cell membrane of skeletal muscles. Myelination of axons speeds up conduction of action potentials.
For skeletal muscle contraction, calcium binds to troponin to uncover actin binding sites.
In order for skeletal muscle contraction to occur, the protein myosin needs to bind to the protein actin and slide it to decrease the length of the sarcomere, which is the contractile unit of a muscle. At rest, the sites on actin that myosin needs to bind to are covered up by the protein tropomyosin. Troponin is a protein that is attached to tropomyosin, to which calcium can bind.
When an action potential reaches a muscle cell, it travels down T-tubules to reach the sarcoplasmic reticulum. The sarcoplasmic reticulum releases stores of calcium, which bind to troponin. This binding causes a conformational change in troponin that causes it to shift the position of the attached tropomyosin to uncover binding sites on actin. Myosin is then able to bind and contraction can occur.
Myosin binds to actin and slides it to shorten the sarcomere. Secretory vesicles release acetylcholine into the synaptic cleft upon stimulation of the presynaptic neuron. This stimulation causes an influx of calcium at the axon terminal, but is not directly linked to increases in intracellular calcium of the muscle cell. Dystrophin is the protein that stabilizes the cell membrane of skeletal muscles. Myelination of axons speeds up conduction of action potentials.
After the New Year, you decide to make a resolution to exercise more and you enthusiastically wake up early in the cold morning to go for a run. You feel great initially, but ten minutes into your run, you feel a disabling pain in your right calf that forces you to stop and sit on the curb. You feel your calf spasming and note that your toes are pointed downward. You are unable to change this position and think that you have a muscle cramp. A few minutes later the pain subsides and you are able to move your foot again. What molecular deficiency is responsible for this condition?
After the New Year, you decide to make a resolution to exercise more and you enthusiastically wake up early in the cold morning to go for a run. You feel great initially, but ten minutes into your run, you feel a disabling pain in your right calf that forces you to stop and sit on the curb. You feel your calf spasming and note that your toes are pointed downward. You are unable to change this position and think that you have a muscle cramp. A few minutes later the pain subsides and you are able to move your foot again. What molecular deficiency is responsible for this condition?
Tap to see back →
A deficiency of ATP is the main cause of skeletal muscle cramps.
During the anaerobic phase of exercise, ATP is quickly used up before cellular respiration can kick in. Muscle contraction requires myosin to bind to actin and slide it for sarcomere shortening. Attachment of ADP and inorganic phosphate to the myosin head causes it to bind to actin. Release of ADP and inorganic phosphate causes the myosin head to bend and pull on actin. Binding of ATP to myosin is needed for myosin to release its hold on actin. Hydrolysis of ATP to ADP and inorganic phosphate causes myosin to bind to actin again.
When ATP stores are depleted, myosin is unable to detach from actin so that skeletal muscle is "stuck" in its position. During this cramping period, the affected muscle cannot move and attempting to forcefully do so may tear it. As you rest and replete your ATP stores, myosin will be able to release from actin and the muscle can shorten or lengthen again.
While electrolyte deficiencies can also cause muscular weakness and cramping, this only happens when they are depleted during excessive sweating and rehydration with plain water. Sweating causes loss of electrolytes and intake of water will dilute the concentration of existing electrolytes. Hyponatremia and hypocalcemia are the main causes of electrolyte-deficiency cramps. Deficiency of acetylcholine can cause muscular weakness as seen in myasthenia gravis or botulism.
A deficiency of ATP is the main cause of skeletal muscle cramps.
During the anaerobic phase of exercise, ATP is quickly used up before cellular respiration can kick in. Muscle contraction requires myosin to bind to actin and slide it for sarcomere shortening. Attachment of ADP and inorganic phosphate to the myosin head causes it to bind to actin. Release of ADP and inorganic phosphate causes the myosin head to bend and pull on actin. Binding of ATP to myosin is needed for myosin to release its hold on actin. Hydrolysis of ATP to ADP and inorganic phosphate causes myosin to bind to actin again.
When ATP stores are depleted, myosin is unable to detach from actin so that skeletal muscle is "stuck" in its position. During this cramping period, the affected muscle cannot move and attempting to forcefully do so may tear it. As you rest and replete your ATP stores, myosin will be able to release from actin and the muscle can shorten or lengthen again.
While electrolyte deficiencies can also cause muscular weakness and cramping, this only happens when they are depleted during excessive sweating and rehydration with plain water. Sweating causes loss of electrolytes and intake of water will dilute the concentration of existing electrolytes. Hyponatremia and hypocalcemia are the main causes of electrolyte-deficiency cramps. Deficiency of acetylcholine can cause muscular weakness as seen in myasthenia gravis or botulism.
Where within the sarcomere is the ATPase?
Where within the sarcomere is the
Tap to see back →
The sarcoplasmic reticulum within a muscle cells is where many calcium ions are stored and released. The release of calcium is a required step in muscle contraction. The ryanodine receptor pumps calcium ions from the intracellular fluid into the interior of the sarcoplasmic reticulum, this process keeps the intracellular calcium ions low, provides a quick store of calcium, and creates a concentration gradient. The sarcoplasmic reticulum membrane contains calcium ion/ATPase pumps. This pump transports intracellular calcium ions into the sarcoplasmic reticulum.
The sarcoplasmic reticulum within a muscle cells is where many calcium ions are stored and released. The release of calcium is a required step in muscle contraction. The ryanodine receptor pumps calcium ions from the intracellular fluid into the interior of the sarcoplasmic reticulum, this process keeps the intracellular calcium ions low, provides a quick store of calcium, and creates a concentration gradient. The sarcoplasmic reticulum membrane contains calcium ion/ATPase