Skeletal Muscle Quiz

Before the depolarization of the T tubules in the mechanism of excitation-contraction coupling in skeletal muscle, the sarcolemmal membrane must depolarize. This depolarization triggers the opening of Ca2+ release channels on the sarcoplasmic reticulum, allowing the release of Ca2+ into the cytoplasm. This Ca2+ then binds to troponin C, which causes a conformational change in the troponin-tropomyosin complex, allowing actin and myosin to bind and initiate muscle contraction. The depolarization of the sarcolemmal membrane is the initial event that sets off the cascade of events leading to muscle contraction.

Excitation-contraction coupling in skeletal muscle begins with an action potential in the muscle membrane, which then leads to depolarization of the T tubules. This depolarization triggers the release of Ca2+ from the sarcoplasmic reticulum (SR). Therefore, the correct temporal sequence is: Action potential in the muscle membrane; depolarization of the T tubules; release of Ca2+ from the SR.

Decreasing the interval between contractions can increase the amount of force produced by a skeletal muscle. This is because decreasing the interval between contractions allows for more frequent muscle contractions, leading to a higher overall force output. By reducing the time between contractions, the muscle has less time to relax and can generate more force over a shorter period of time. This increased frequency of contractions can result in a stronger muscle contraction and greater force production.

Tropomyosin is the protein that directly prevents myosin cross-bridges from binding to actin molecules when skeletal muscle is in its resting state.

Repeated stimulation of skeletal muscle fiber causes a sustained contraction called tetanus. This is due to the accumulation of calcium ions (Ca2+) in the intracellular fluid. Calcium ions play a crucial role in muscle contraction by binding to troponin, which allows the interaction between actin and myosin filaments. The binding of calcium ions to troponin triggers a series of events that lead to muscle contraction. Therefore, the accumulation of calcium ions in the intracellular fluid is responsible for tetanus.

Increasing the [K+] in the extracellular solution is not a way of increasing the tension of a given muscle contraction. This is because an increase in extracellular potassium concentration would actually have the opposite effect and decrease muscle contraction. Potassium ions play a role in repolarizing the muscle cell membrane after an action potential, so an increase in extracellular potassium would interfere with this process and impair muscle function.

When there is a decrease in ATP level in skeletal muscle, it leads to rigor. ATP is required for muscle relaxation as it provides energy for the detachment of myosin heads from actin filaments. When ATP levels decrease, the myosin heads remain attached to actin, causing the muscles to become stiff and rigid. This condition is known as rigor.

Before depolarization of the T tubules, the sarcolemmal membrane must first depolarize. This depolarization triggers the opening of Ca2+ release channels on the sarcoplasmic reticulum (SR), allowing Ca2+ to be released into the cytoplasm. This Ca2+ release then leads to the binding of Ca2+ to troponin C, which allows for the binding of actin and myosin and initiates the process of muscle contraction. Therefore, depolarization of the sarcolemmal membrane is the initial event in the mechanism of excitation-contraction coupling in skeletal muscle.

During muscle contraction, myosin and actin interact to generate force and movement. Myosin is a motor protein that binds to actin and uses ATP as an energy source to perform its function. In this experiment, radiolabeled ATP is injected into the muscle fiber, and during contraction, the radiolabeled ATP will bind to myosin as it carries out its role in muscle contraction. Therefore, an autoradiogram from a biopsy taken during this contraction will show radiolabeled ATP bound to myosin.

During the process of excitation-contraction coupling in skeletal muscle, calcium is released from the sarcoplasmic reticulum by membrane depolarization. Membrane depolarization occurs when there is a change in the electrical potential across the muscle cell membrane, causing it to become less negative. This change in membrane potential triggers the opening of voltage-gated calcium channels in the sarcoplasmic reticulum, allowing calcium to flow into the cytoplasm. This calcium release is essential for the contraction of skeletal muscle fibers.

Decreasing the interval between contractions can increase the amount of force produced by a skeletal muscle. This is because a shorter interval allows for more frequent contractions, leading to a higher overall force output. When the interval between contractions is decreased, the muscle has less time to relax and recover, resulting in a sustained contraction and increased force generation. This is known as summation of contractions, where the force of each contraction adds up to produce a greater overall force.

During an isotonic twitch, the muscle fiber is shortening, which means that action potentials propagate more slowly. This slower propagation requires extra time to activate the entire fiber. Additionally, it takes time for enough cross-bridges to attach and generate tension greater than the load. This delay in cross-bridge attachment contributes to the longer latent period during an isotonic twitch compared to an isometric twitch.

A "fast-oxidative" type of skeletal muscle fiber is characterized by high myoglobin content and intermediate glycolytic enzyme activity. Myoglobin is a protein that stores oxygen in muscle cells, allowing for efficient oxygen delivery during exercise. Intermediate glycolytic enzyme activity suggests that these fibers can utilize both aerobic and anaerobic energy pathways. This combination of high myoglobin content and intermediate glycolytic enzyme activity allows for sustained, moderate-intensity exercise.

During normal voluntary movement, weak muscle fibers are recruited before strong muscle fibers. This is because the body follows the principle of "size principle" in muscle fiber recruitment. According to this principle, motor units consisting of smaller, weaker muscle fibers are recruited first, followed by larger, stronger muscle fibers as the intensity of the movement increases. This allows for finer control and precision in movements, as well as conserving energy by only recruiting the necessary muscle fibers for the task at hand.

Repetitive stimulation of a skeletal muscle fiber causes an increase in contractile strength because it leads to an increase in the duration of cross-bridge cycling. Cross-bridge cycling refers to the process by which myosin heads bind to actin filaments and generate force during muscle contraction. When a muscle fiber is stimulated repeatedly, the cross-bridge cycling continues for a longer duration, allowing for more force generation and ultimately increasing the contractile strength of the muscle.