Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
13 Cards in this Set
- Front
- Back
|
What always precedes muscle contraction?
|
-1. Action Potential
-2. Rise in intracellular Ca+2 concentration -3. Contraction |
|
|
What is the sliding filament theory?
|
- that contraction occurs by the sliding of thin filaments past thick filaments
-there is a series of cyclic reactions between the myosin head and the actin filament that results in muscle shortening -contractile force is proportional to the number of myosin cross-bridge and actin interactions |
|
|
Describe cross-bridge cycling in the energized state
|
-cytosolic calcium is low
-myosin and actin are dissociated -myosin heads hold ADP and Pi -binding site on actin is blocked by tropomyosin/troponin complex |
|
|
How does myosin end up binding to actin?
|
-AP causes release of Ca+2 from the SR
-Ca+2 binds to troponin C -produces a conformational shift in the tropomyosin-troponin complex -exposure of myosin binding to actin site -myosin binds actin -Pi release initiates the powerstroke |
|
|
What is the powerstroke?
|
-the myosin head shifts causing the filaments to slide (10nm movement per cycle)
-ADP release -myosin remains bound to actin until new ATP binds |
|
|
What happens if no new ATP binds?
|
-The myosin remains bound and rigor mortis sets in
|
|
|
What does ATP binding cause to the myosin-actin complex?
|
- ATP hydrolyzed to ADP-Pi
-energy released is stored in conformational shift of myosin head back to the energized state -the next cross-bridge cycle can occur |
|
|
What are the overall steps in cross-bridge cycling?
|
- Pi is released and the myosin heads change conformation --> powerstroke and the filaments slide past eachother
-ADP is released from myosin -ATP binds to myosin head causing the dissociation of the actin-myosin complex -ATP is hydrolyzed to ADP-Pi causing the myosin heads to return to their resting conformation |
|
|
What does muscle relaxation depend on?
|
-calcium removal
|
|
|
What occurs in the cell when intracellular calcium concentrations are high?
|
-high Ca+2 in sarcoplasm triggers Ca+2 ATPase pump in SR (SERCA)
- causes decrease in intracellular Ca+2 so insufficient binding to troponin C -Ca+2 released and tropomyosin returns to resting position |
|
|
What is the Ca+2 binding protein in the SR?
|
-Calsequestrin
-allows the SR to store a large amount of Ca+2 and act as a calcium reservoir -keeps free Ca+2 concentration in the SR low -prevents Ca+2 leakage |
|
|
What is Malignant Hyperthermia?
|
- inherited syndrome that is sensitive to anesthetics
-linked to gene mutation in RyR and more recently Calsequestrin - due to Ca+2 channel of SR being more sensitive to anesthetics -release of Ca+2 uncoupled from sarcolemma AP causing skeletal muscles to forcefully contract without AP -generates tremendous heat -Treatment= dantrolene sodium; a muscle relaxant that abolishes E-C coupling by acting on the ryanodine receptor |
|
|
What is summation of muscle twitches?
|
-muscle twitch= response to a single threshold stimulus
-increased frequency of stimulation leads to successive contractions with increasing force -the high frequency stimulation keeps cytosolic Ca+2 levels high---> fused maximal contraction (tetanus) can occur |
