Monday, April 4, 2016

Human Study Provides New Insight into How NSAIDs Speed Up Satellite Cell Recruitment & Muscle Repair in Youngsters

No, I still do not recommend the chronic (ab-)use of NSAIDs, bro.
No, this is not the first study about the effects of NSAIDs on muscle gains I discuss here at, but it is certainly one of the more interesting ones. The study which is about to be published in the FASEB Journal was designed to investigate the role of nonsteroidal anti-inflammatory drugs (NSAIDs) in human skeletal muscle regeneration.

As you may remember, previous studies have yielded conflicting evidence with respect to the ability of NSAID to accelerate muscle healing and thus accelerater and ultimately shorten the adaptational process.
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In the study at hand, the authors did therefored recruit 32 untrained, but healthy young men and randomly assigned them to consume either 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.

To assess, whether the ingestion of ibuprofen would, as the scentists suspected alter satellite cell response and time course of regeneration in the experimentally injured skeletal muscle of young healthy men, biopsies were collected from the vastus lateralis muscles before and after stimulation (2.5 h and 2, 7, and 30 d) and were assessed for satellite cells and regeneration by immunohistochemistry and real-time RT-PCR. In conjunction with the likewise measured length of the telomeres, the scientists expected to be able to determine the actual effect of NSAIDs on the post-exercise recovery process.
Figure 1: CD68 and CCL2 are only two markers of the damage/repair process that show a clear phase-shift (meaning earlier elevation = earlier repair) with IBU. Furthermore the ibuprofen "preload" prevented the formation of collage (right) in the muscle after 30 days (Mackey. 2016).
What the researchers found was appears to be a clear advantage... initially: After injury, and compared with PLA, IBU was found to augment the proportion of ActiveNotch1+ satellite cells at 2 d [IBU, 29 +/- 3% vs. PLA, 19 +/- 2% (means +/- SEM)], satellite cell content at 7 d [IBU, 0.16 +/- 0.01 vs. PLA, 0.12 6 0.01 (Pax7+ cells/fiber)], and to expedite muscle repair at 30 d.

The bad news is that the chronic consumption of NSAIDs is nothing a healthy individual should consider - even if it prevents your muscle from collagen depositions (see Figure 1, right); and still, if we could get the benefits observed in the study at hand without the potential long-term side effects of common NSAIDs, they could be a game changer... at least for elderly individuals, in whom the recruitment of satellite cells and thus process of muscle repair appears to be impaired by aging.
The statement that NSAIDs could be particularly beneficial for elderly is more than an unsupported hypothesis. In February, I already wrote about the type-I-specific muscle-building effects of COX-inhibitors | learn more.
So what? No, this is not an endorsment of NSAIDs and I still cannot recommend the chronic ingestion of NSAIDs as muscle builders. I have to admit, though, that I am pretty impressed by the way ibuprofen helped the repair of myofibers in the later stages of regeneration and mediated a more rapid return of satellite cells and muscle extra-cellular matrix (ECM) gene expression levels to baseline values.

As Mackey et al. point out, NSAIDs (in this case IBU) is eventually shifting the entire time course of satellite cell, myofiber - and that without effects on muscle telomere length in human skeletal muscle in vivo. In view of the highly damaging electrostimlation method, it does yet remain to be seen how beneficial effect of NSAID ingestion are when the damate to the muscle is less pronounced and thus in a more physiological range  | Leave a comment and tell me what you think on Facebook!
  • Mackey, Abigail L., et al. "Activation of satellite cells and the regeneration of human skeletal muscle are expedited by ingestion of nonsteroidal anti-inflammatory medication." The FASEB Journal (2016): fj-201500198R.