Interesting Study, But Opposite Of Others...

[NWlifter]

Reading some studies tonight, this one was a 'whoa'...

http://www.pnas.org/content/109/35/E2353

Moreover, we show that muscle hypertrophy after pharmacological blockade of this pathway occurs without significant satellite cell proliferation and fusion to myofibers and without an increase in the number of myonuclei per myofiber....................All of these findings are consistent with satellite cells playing little or no role in myostatin/activin A signaling in vivo and render support that inhibition of this signaling pathway can be an effective therapeutic approach for increasing muscle growth even in disease settings characterized by satellite cell dysfunction.

(or maybe that's only short term?) An excerpt from the study below coincidentally states this, which is what I thought: whereas skeletal muscle hypertrophy is permitted in the absence of satellite cells in the short term (2), it is attenuated in the long term (3), which indicates that satellite cells are essential for continued hypertrophic adaptation to loading.)

 

[NWlifter]

Now I find another one that is contradictory to what we've heard....

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4871801/

With this study we investigated the role of nonsteroidal anti-inflammatory drugs (NSAIDs) in human skeletal muscle regeneration. Young men ingested NSAID [1200 mg/d ibuprofen (IBU)] or placebo (PLA) daily for 2 wk before and 4 wk after an electrical stimulation–induced injury to the leg extensor muscles of one leg.

Activation of satellite cells and the regeneration of human skeletal muscle are expedited by ingestion of nonsteroidal anti-inflammatory medication.

 

[Blade]

First one: it is true that hypertrophy can occur without SC activation-proliferation-differentiation, as long as the myonuclear domain is preserved. At some point, you can’t grow a bigger muscle without the SC process increasing the myonuclei pool.

Second one: EMS induced injury isn’t a prerequisite nor a good model for muscle growth, and it is most likely modulating the extreme inflammation down to a more manageable level that caused a higher SC response here.

 

[NWlifter]

First one: it is true that hypertrophy can occur without SC activation-proliferation-differentiation, as long as the myonuclear domain is preserved. At some point, you can’t grow a bigger muscle without the SC process increasing the myonuclei pool.

OK, good, that's how I thought things were

Second one: EMS induced injury isn’t a prerequisite nor a good model for muscle growth, and it is most likely modulating the extreme inflammation down to a more manageable level that caused a higher SC response here.

True, but oddly NSAIDS helped, usually studies show they hinder, that inflammation is more stimulating and things like Ibuprofen will lower the response. At least that's what I had heard years ago.

 

[Blade]

Exactly. They will help if inflammation is excessive, as in this study, but under normal circumstances there will be only moderate inflammation and NSAIDS will be counterproductive.

 

[NWlifter]

Exactly. They will help if inflammation is excessive, as in this study, but under normal circumstances there will be only moderate inflammation and NSAIDS will be counterproductive.

Ah ok, that would fit a couple others I've seen too, that said
* NSAIDS may help hypertrophy in older people but not younger
and
* The non or low responder types that have a kind of 'over' inflammation response have more hypertrophy with NSAIDS

Question: Have you ever seen a study that checked satellite cell activity with various training frequencies? I searched like crazy last night and can't find that scenario. All I find is that satellite cell activity can increase and peak anywhere from a day or two up to 5 days after a bout and may stay high for up to 10 or 12 days after a bout. But I can't find anything on repeated bouts with various frequency.