Saturday, October 13, 2012

Smooth Muscles and other Muscle Questions

Hello All,

First off I would like to share a resource that one of your fellow classmates found for you.  It is an animation that helps explain the cross-bridge cycle:
http://highered.mcgraw-hill.com/sites/0072495855/student_view0/chapter10/animation__breakdown_of_atp_and_cross-bridge_movement_during_muscle_contraction.html

Secondly a correction.  NOTE:  On Slide 19 (and others) the Ca2+ ATPase on the membrane of the sarcoplasmic reticulum shows that it is pumping Ca2+ out of the sarcoplasmic reticulum.  However, this arrow is an error and should be going in the other direction causing Ca2+ to be pumped INTO the sarcoplasmic reticulum.

Here are some more questions remaining about Muscle Physiology:


1.  I'm a little bit confused about a question that appears to have two possible correct answers:
When comparing the contractile responses in smooth and skeletal muscle, which of the following is most different?
Correct->The role of calcium in initiating contraction
The source of energy used during contraction
The mechanism of force generation
Also possibly correct?->The source of activator calcium
The nature of the contractile proteins

In skeletal muscle the source of activating calcium is the SR.
In smooth muscle, it is both the SR and the ECM.
Am I correct in my assessment?


Your assessment regarding where the Ca2+ comes from is definitely correct.  Obviously the question above has an amount of 'judgement' associated with it in that it asks what is the 'most different'.  Therefore, the correct answer must also have some judgement associated with it.  Therefore, you would have an argument for that also being correct.  Overall, however, it is important that you can differentiate where the Ca2+ comes from to initiate contraction in both muscle types.

2.  Synaptotagmin is the calcium-binding regulatory protein.  When intracellular calcium levels rise, it binds to the regulatory protein, synaptotagmin (picture 3 in the sequence). I'm having trouble understanding the sentences above in purple. If synaptotagmin is the calcium binding reg protein when intracellular calcium levels rise, it binds to itself or another regulatory protein?
 
Calcium comes into the intracellular space of the presynaptic cell and binds to synaptotagmin.  Calcium is the 'it' that binds to the regulatory protein which is called synaptotagmin.
 
3.  Here was an exchange on your blog:

[6. Regarding #13 on the study quiz:  I understand why E is correct, but would A be correct if the world myoplasm was replaced with the word sarcoplasm?
 
13.  Repetitive stimulation of a skeletal muscle fiber will cause an increase in contractile strength because repetitive stimulation causes an increase in what?
  A.  The total duration of cross-bridge cycling
  B.  The concentration of calcium in the myoplasm
  C.  The magnitude of the end-plate potential
  D.  The number of muscle myofibrils generating tension
  E.  The velocity of muscle contraction
 
Yes, exactly! ]


--Of the above choices, the powerpoint showed that (B) is correct...the online version of the study quiz showed that (A) is correct...and in this blog exchange you indicate that (E) is correct...What is correct?? Clearly the pasted question's answer choices are different than what the student specifically asked you about.

I think (A) is correct and (B) would basically mean the same thing as (A)
if myoplasm was replaced with sarcoplasm, since an increased duration of cross-bridge cycling would be caused by increased Ca++ in the sarcoplasm...but I want to make sure with you because its appearance on the blog was very confusing.
 
I sincerely apologize for that misleading exchange.  I was saying yes exactly that B would be correct if it said sarcoplasm rather than myoplasm, but E is not correct.  The correct, correct, answer of the question is A.  Repetitive stimulation would lead to an increase in intracellular Ca2+ and that would lead to a continued duration of cross-bridge cycling.  Again, I apologize for not completely answering and addressing the confusion in the question, it appears that by the time you get to question #13 late in the evening my mind is not working at its peak.
 
4.  One more question, will you point out any flaws in my understanding of fatigue?
1. T-tubule conduction failure= lack of AP propagation inhibits SR Ca++ release by DHP-RyR activation
2. Cross-bridge cycle inhibition= high ADP & Pi conc. reduces/inhibits powerstroke since myosin will be less likely to release its ADP & Pi
3. Increased lactic acid & glycogen depletion= Do the acidity and loss of glucose stores result in reduced ATP production, therefore inhibiting myosin heads from releasing actin (a rigor mortis-like effect)?
 
Mainly the high acidity messes with everything that is happening within the cell including the production of ATP, the hydrolysis of ATP by myosin head groups, and the movement of the myosin molecules.  pH is an important component that is tightly regulated typically because changes in it cause proteins themselves to not work properly, therefore it is mainly the change in acidity within the cell that causes muscle fatigue. 

5. Can I use Chapter 7: Muscle / Cellular Physiology / Landowne, as a reading material for this lecture? (This might be an obvious questions, but I am asking since it is not pointed out in the ppt)
 
You may ABSOLUTELY use that chapter as supplemental reading material.  I simply provided some reading recommendations that I thought are helpful, but if you find the information in Landowne helpful to your understanding of muscle physiology, then by all means utilize that as one of your resources.
 
Know that your knowledge building is your own responsibility always in addition to our help as your educators.  Therefore if you ever find a helpful resource that helps you understand what it is that we are teaching you should use your own knowledge to determine if it is a valid resource and if it supplements your knowledge.
 
6. In slide 54, it is stated that "reflex allows stretched muscle to contract"; does that means that the only response of a muscle is contraction when there is a reflex from the spindle? or could it be that also the muscle relaxes? Is this response autonomous in the muscle? or is it integrated in the CNS?
 
In the event that the muscle spindle is activated, a reflex arc will cause the muscle to contract involuntarily.  Typically, however, skeletal muscle contractions are a voluntary activity not involuntary.  Therefore, no a muscle contraction is not only in response to that reflex arc, but that is how it occurs through an involuntary response mediated by the nervous system itself.
 
7.  Do pacemaker only posses the ability to produce and spread APs or do they also have contractile activity?

Smooth muscle pacemaker cells posses the ability to produce and spread APs AND have contractile activity.  In the cardiac system, in contrast, pacemaker cells have very limited contractile properties and do not initiate contraction, but mostly just initiate and propagate APs.  We will discuss those in greater detail within the cardiovascular module.

4 comments:

  1. Hi Dr. J,
    On the practice quiz for smooth muscle question 11 asks about the latch state. I thought that when the actomyosin was dephosphorylated while still being latched on it kept the contraction much longer without using ATP. (step 4) The answer has the step (3) of the phophorylated actomyosin going back to phosphorylated MLC. Can you help me understand?
    Thank you
    Lisa Roberts

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    1. What you are describing as the latch state is correct. I believe that that question is, therefore, miss keyed. I apologize for that. Indeed, latch state IS when the actomyosin is dephosphorylated while still in connection with each other.

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  2. Alpha 2 adrenergic receptors are inhibitory for cAMP-and have nothing to do with calcium release. So is it possible that we are talking about alpha 1 receptors? Furthermore, how do the beta and gamma subunits initiate the IP3 system? It is not in the lecture notes or the textbook.

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    Replies
    1. I am unsure what you are referring to in terms of alpha 2 vs. alpha 1, but vascular smooth muscles contain alpha 1 adrenergic receptors and indeed the activation of that receptor causes contraction. Activation of the alpha 2 receptor, in contrast typically causes relaxation of smooth muscles.

      The IP3 receptor pathway is not activated by the beta-gamma subunits, but by the activation of the alpha subunit of the Gq protein through the activation of phospho-lipase C.

      I am unsure where your questions are coming from as they are not referring to things I discussed in class, but hopefully these help. If there are specific areas you are referring to please let me know so that I can be of more help.

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