Disuse atrophy of muscles (SPOILER for NBME 13)

[mclee0033]

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What actually causes this? Choices:

Decreased glycogen synthesis (only liver makes it right. maybe liver makes less when muscle not being used?)
Increased phosphatidyl degradation
Increased protein degradation
Mitochondrial damage
Necrosis of muscle fibers


I don't really think any of them are...except maybe decreased glycogen synthesis. I didn't chose that because it's not the muscle that makes glycogen, it's the liver. Maybe I over-thought this question.

 

[sharklasers]

I remember I got this question right, I don't remember exactly what I put though.

Based on seeing it again now, I would assuming increased protein degradation.

Hypertrophy you have increased protein synthesis.
Atrophy would logically have increased protein breakdown.

 

[mclee0033]

Why would you have increased protein degradation though?

 

[FIREitUP]

Why would you have increased protein degradation though?

you're not using the muscles so there will be ubiquitination of cytoskeletal proteins (as well as actin/myosin, most likely) leading to a decrease in cell size=atrophy

 

[MDSlacker]

I got it right and I put increased protein degradation. The way I thought about it was basically just applying it to everyday logic. If you work out for a few weeks you get stronger because you are making new muscle. You make the new muscle via protein (hence why you drink protein shakes). If you stop working out for a while you get weaker and the reason you get weaker is due to disuse atrophy from protein breakdown.

It's not glycogen b/c if it were decreased glycogen then that would be that you would basically be getting leaner when you stopped working out and that's clearly not true. There isn't any necrosis or mitochondrial damage because that would be pretty severe and if you start working out again then you can still regain that muscle.

 

[Oreoomar]

What actually causes this? Choices:

Decreased glycogen synthesis (only liver makes it right. maybe liver makes less when muscle not being used?)
Increased phosphatidyl degradation
Increased protein degradation
Mitochondrial damage
Necrosis of muscle fibers


I don't really think any of them are...except maybe decreased glycogen synthesis. I didn't chose that because it's not the muscle that makes glycogen, it's the liver. Maybe I over-thought this question.

http://en.wikipedia.org/wiki/Muscle_atrophy#Pathophysiology
"Muscle atrophy occurs by a change in the normal balance between protein synthesis and protein degradation. During atrophy, there is a down-regulation of protein synthesis pathways, and an activation protein degradation. The particular protein degradation pathway which seems to be responsible for much of the muscle loss seen in a muscle undergoing atrophy is the ATP-dependent ubiquitin/proteasome pathway."