NBME 15

[Wanderer HitchHiker]

During an experiment of muscle contraction, intracellular Ca is decreased after a substance is administered to a muscle preparation obtained from experimental animal. which of the following best explains why contraction is inhibited in this case?

A- Ach release increase
B- Depolarization a long T-tubules is enhanced
C- Myosin binding sites on actin remain covered with TROPONIN C !!
D- Na influx is increased
E- Tropomyosin is dettached from actin

Answer keys say C which doesn't make sense for me. Troponin C does not cover myosin binding sites, tropomyosin does
I think the answer is D .. because of Na/Ca exchange ... increased Na influx explain the decrease in Ca concentration and the ceasing of contraction !
so if the substance added is ATP that would activate both SERCA and Na/K ATPase pump which will decrease cytoplasmic concentration and decrease contraction ... i think it makes sense, what did i miss?

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[orangetea]

Tropomyosin is blocking myosin-binding

sites on the actin filament. Released

Ca2+ binds to troponin C (TnC), shifting

tropomyosin to expose the myosin-binding

sites.

 

[Wanderer HitchHiker]

Yes i know that but the choice answer (C) mentions that these sites are covered with troponin C which is not accurate !!

 

[The.Supinator]

Yes i know that but the choice answer (C) mentions that these sites are covered with troponin C which is not accurate !!

fair enough, i'm assuming your looking for troponin I which blocks the binding site? either way its still the best answer, tropoinin I,C,T is ONE complex, so its not completely wrong, still best answer, what other answer would be better?

 

[Wanderer HitchHiker]

I already said that i think D ... Na influx would decrease Ca level and inhibit contraction. it's the reverse of the mechanism of action of digoxin.
I just don't trust the answer keys because it has a lot of silly mistakes, so i would appreciate if anyone who had this NBME online provide me with the right answer

 

[The.Supinator]

Na influx D, That's still not the best answer sodium influx starts the action potential outside the cell, from there the ryanodine receptors and their release of calcium takes over, the question asks about intracellular calcium, sodium is 3 steps back at least. The answer is 100 percent C, I took this nbme online and it is C for sure.

 

[Wanderer HitchHiker]

dude, the question is not talking about action potential or excitation contraction coupling ... it's about lusitropy and relaxation.
again i'mnot talking about voltage gated Na channels i'm talking about Na/Ca exchanger !! you got what i mean?

 

[The.Supinator]

Bro I think you need to Lusitrop with those exclamation points lol. So the answer still cannot be sodium influx (and it is not)

1st) You need to understand that this is skeletal muscle and one key thing to know that the majority of the calcium homeostasis is done by SERCA, not by the na/ca exchanger your referring to, but this is more of an aside but important to know when answering questions.

2nd) lets say that exchanger mattered, how would decreasing the intracellular calcium cause more of an influx of the sodium exchanger? if the point of the exchanger is to relax the skeletal muscle how would decreasing the intracellular calcium cause the sodium to increase in influx, i.e. why would the rate of exchange increase if there is less calcium in the cell? and even then it still not answering question directly, "how does decreased calcium cause relaxation" sure the sodium calcium exchanger helps with relaxation, but that's not really answering question.

3rd) Digoxin works on cardiac muscle so well because contraction is very dependent on calcium induced calcium release, there is no one of that in skeletal muscle. This is exactly the reason why digoxin doesn't work on skeletal muscle that well, because calcium homeostasis in skeletal muscle is controlled by serca.

4th) C is the correct answer on the online nbme bro.

 

[foxyMD16]

Bro I think you need to Lusitrop with those exclamation points lol. So the answer still cannot be sodium influx (and it is not)

1st) You need to understand that this is skeletal muscle and one key thing to know that the majority of the calcium homeostasis is done by SERCA, not by the na/ca exchanger your referring to, but this is more of an aside but important to know when answering questions.

2nd) lets say that exchanger mattered, how would decreasing the intracellular calcium cause more of an influx of the sodium exchanger? if the point of the exchanger is to relax the skeletal muscle how would decreasing the intracellular calcium cause the sodium to increase in influx, i.e. why would the rate of exchange increase if there is less calcium in the cell? and even then it still not answering question directly, "how does decreased calcium cause relaxation" sure the sodium calcium exchanger helps with relaxation, but that's not really answering question.

3rd) Digoxin works on cardiac muscle so well because contraction is very dependent on calcium induced calcium release, there is no one of that in skeletal muscle. This is exactly the reason why digoxin doesn't work on skeletal muscle that well, because calcium homeostasis in skeletal muscle is controlled by serca.

4th) C is the correct answer on the online nbme bro.

Very helpful and agree. Thank-you.