MCAT Biology : Muscle Stimulation and Contraction

Study concepts, example questions & explanations for MCAT Biology

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Example Questions

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Example Question #1 : Muscle Stimulation And Contraction

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?

Possible Answers:

Mitochondria

Ribosomes

Golgi body

Sarcoplasmic reticulum

Nucleus

Correct answer:

Sarcoplasmic reticulum

Explanation:

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.

Example Question #2 : Muscle Stimulation And Contraction

Which of the following proteins directly interacts with the myosin-binding site on actin?

Possible Answers:

Calsequestrin

Tropomyosin

ATP hydrolase

Troponin

Correct answer:

Tropomyosin

Explanation:

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.

Example Question #3 : Muscle Stimulation And Contraction

What is the specialized organelle in muscle cells that serves to sequester calcium?

Possible Answers:

Sarcolemma

Sarcomere

Sarcoplasmic reticulum

T-tubule

Correct answer:

Sarcoplasmic reticulum

Explanation:

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.

Example Question #15 : Musculoskeletal System And Muscle Tissue

Which of the following changes will not take place in a muscle experiencing prolonged, powerful contractions?

Possible Answers:

Increased number of sarcomeres

Increased number of mitochondria

Enlargement of muscle cells

Division of muscle cells

Correct answer:

Division of muscle cells

Explanation:

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.

Example Question #4 : Muscle Stimulation And Contraction

What is the purpose of calcium in the muscles?

Possible Answers:

It allows tropomyosin to be pulled away from the actin filament

It releases the myosin head from the active site on actin

It pulls tropomyosin off of the myosin heads

It helps move the myosin head into a high-energy position

Correct answer:

It allows tropomyosin to be pulled away from the actin filament

Explanation:

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.

Example Question #5 : Muscle Stimulation And Contraction

Which of the following statements is true about the function of troponin during muscle contraction?

Possible Answers:

Troponin binds directly to actin to cover myosin binding sites

Troponin is ubiquinated and degraded once the sarcoplasmic reticulum releases calcium ions into the sarcomere

Troponin binds calcium ions and moves tropomyosin to expose myosin binding sites on actin

Troponin directly binds myosin in the presence of calcium ions

Correct answer:

Troponin binds calcium ions and moves tropomyosin to expose myosin binding sites on actin

Explanation:

Muscle contraction is very tightly regulated. Tropomyosin binds actin filaments and covers the myosin binding sites. Troponin interacts with tropomyosin. When stimulated by calcium, troponin undergoes a conformational change that moves the tropomyosin and exposes the myosin binding sites on the actin protein. When the binding sites are exposed myosin can bind actin and muscle contraction can occur. Troponin does not bind myosin or actin directly, and it does not get ubiquinated and degraded.

Example Question #6 : Muscle Stimulation And Contraction

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?

Possible Answers:

A mutated calcium-binding domain of troponin that increases the affinity for calcium ions

A mutated calcium-binding domain of tropomyosin that lowers the affinity for calcium

A mutated calcium-binding domain of tropomyosin that increases the affinity for calcium

A mutated calcium-binding domain of troponin that lowers the affinity for calcium ions

Correct answer:

A mutated calcium-binding domain of troponin that lowers the affinity for calcium ions

Explanation:

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.

Example Question #7 : Muscle Stimulation And Contraction

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?

Possible Answers:

Muscle microtears

Depleted sodium stores

Depleted calcium stores

Depleted ATP stores

Correct answer:

Depleted ATP stores

Explanation:

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.

Example Question #8 : Muscle Stimulation And Contraction

Which of the following is true of troponin and tropomyosin?

Possible Answers:

Tropomyosin binds to actin and prevents the myosin head from binding to actin

Troponin binds to myosin and tropomyosin binds to actin

Binding of ATP to troponin releases tropomyosin from the myosin head

Both are made up of fatty acids and play a big role in muscle contraction

Correct answer:

Tropomyosin binds to actin and prevents the myosin head from binding to actin

Explanation:

Troponin and tropomyosin are both proteins that play a big role in muscle contraction. Since they are proteins, troponin and tropomyosin are made up of amino acids. Recall that fatty acids make up lipids, not proteins. 

During a typical muscle contraction, tropomyosin is bound to actin. This blocks the binding of the myosin head to actin and prevents muscle contraction. When calcium ions are released from the sarcoplasmic reticulum, troponin interacts with actin and removes tropomyosin. Neither protein directly interacts with myosin. Tropomyosin is very important because it prevents prolonged muscle contraction which can lead to several muscle disorders.

ATP has a huge role in muscle contraction; however, it never interacts with tropomyosin. ATP is important to remove the myosin head from the active site on actin. Upon ATP binding, the myosin head detaches itself from actin, which allows tropomyosin to re-attach to the active site on actin. Without ATP, myosin heads can’t detach themselves from actin and prolonged muscle contraction occurs. After death a person stops producing ATP; therefore, contracted muscles can’t relax and rigor mortis ensues.

Example Question #9 : Muscle Stimulation And Contraction

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?

Possible Answers:

Troponin cannot remove tropomyosin from the active site on myosin

Tropomyosin cannot remove troponin from the active site on myosin

Tropomyosin cannot remove troponin from the active site on actin

Troponin cannot remove tropomyosin from the active site on actin

Correct answer:

Troponin cannot remove tropomyosin from the active site on actin

Explanation:

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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