Elevated levels of Pi in the sarcoplasm of skeletal muscle fibers would decrease the release of Pi from myosin. What direct impact would this have on the cross bridge cycle? troponin wouldn't be able to bind myosin if Pi isn't released myosin wouldn't be able to initiate the power stroke if Pi isn't released the muscle wouldn't be able to relax if Pi isn't released myosin wouldn't be able to bind to actin if Pi isn't released
Elevated levels of Pi in the sarcoplasm of skeletal muscle fibers would decrease the release of Pi from myosin. What direct impact would this have on the cross bridge cycle? troponin wouldn't be able to bind myosin if Pi isn't released myosin wouldn't be able to initiate the power stroke if Pi isn't released the muscle wouldn't be able to relax if Pi isn't released myosin wouldn't be able to bind to actin if Pi isn't released
Human Anatomy & Physiology (11th Edition)
11th Edition
ISBN:9780134580999
Author:Elaine N. Marieb, Katja N. Hoehn
Publisher:Elaine N. Marieb, Katja N. Hoehn
Chapter1: The Human Body: An Orientation
Section: Chapter Questions
Problem 1RQ: The correct sequence of levels forming the structural hierarchy is A. (a) organ, organ system,...
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![**Question:**
Elevated levels of Pi in the sarcoplasm of skeletal muscle fibers would decrease the release of Pi from myosin. What direct impact would this have on the cross bridge cycle?
**Options:**
- [Selected] *Troponin wouldn’t be able to bind myosin if Pi isn’t released*
- Myosin wouldn’t be able to initiate the power stroke if Pi isn’t released
- The muscle wouldn’t be able to relax if Pi isn’t released
- Myosin wouldn’t be able to bind to actin if Pi isn’t released
**Explanation:**
In this multiple-choice question, the focus is on the biochemical and physiological process involving Pi (inorganic phosphate) within the cross bridge cycle of muscle contraction. Elevated levels of Pi in the sarcoplasm can affect various steps within this cycle.
The selected answer suggests that "troponin wouldn’t be able to bind myosin if Pi isn’t released," which might be misunderstood as troponin interacting directly with the myosin (which it does not). However, this selection reflects upon the broader implication of impaired Pi release affecting the regulatory mechanisms of muscular contraction and relaxation.
It's important to note that for muscular contraction to proceed, myosin must release Pi to transition from the weak binding state to the strong binding state with actin, therefore initiating the power stroke. Increased levels of Pi potentially impede this release, affecting the efficiency of the power stroke and muscle contraction.](/v2/_next/image?url=https%3A%2F%2Fcontent.bartleby.com%2Fqna-images%2Fquestion%2F99652214-81b8-42bc-94d3-33a40a2ac31e%2Fe35490d2-e6dd-41fb-96f0-e0067fdacfa6%2Fdqbmwfr_processed.png&w=3840&q=75)
Transcribed Image Text:**Question:**
Elevated levels of Pi in the sarcoplasm of skeletal muscle fibers would decrease the release of Pi from myosin. What direct impact would this have on the cross bridge cycle?
**Options:**
- [Selected] *Troponin wouldn’t be able to bind myosin if Pi isn’t released*
- Myosin wouldn’t be able to initiate the power stroke if Pi isn’t released
- The muscle wouldn’t be able to relax if Pi isn’t released
- Myosin wouldn’t be able to bind to actin if Pi isn’t released
**Explanation:**
In this multiple-choice question, the focus is on the biochemical and physiological process involving Pi (inorganic phosphate) within the cross bridge cycle of muscle contraction. Elevated levels of Pi in the sarcoplasm can affect various steps within this cycle.
The selected answer suggests that "troponin wouldn’t be able to bind myosin if Pi isn’t released," which might be misunderstood as troponin interacting directly with the myosin (which it does not). However, this selection reflects upon the broader implication of impaired Pi release affecting the regulatory mechanisms of muscular contraction and relaxation.
It's important to note that for muscular contraction to proceed, myosin must release Pi to transition from the weak binding state to the strong binding state with actin, therefore initiating the power stroke. Increased levels of Pi potentially impede this release, affecting the efficiency of the power stroke and muscle contraction.
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