Novel Perspectives on Protein Consumption: 36% Decrease In Myostatin, With Low Protein (0.1g/kg BW) Diet, But...

What happens to your muscle, when you train on a low protein diet?

With the publication of Alan Aragon's and Brad Schoenfeld's excellent paper "Nutrient timing revisited: is there a post-exercise anabolic window?" (Aragon. 2013), the over-estimated importance of the so-called window of opportunity after a workout has been knocked back into reasonable shape. Neither of the two would yet probably tell you to copy the experimental design of a recently published study that was conducted by a team of researchers from the Maastricht University in The Netherlands, the McMaster University in Canada and the University of Nottingham in the UK.

Protein "starvation" and growth potential

Much contrary to the average "window of opportunity study", Snijders et al. did not look at the benefits of post-workout protein supplementation, but at the detriments of not consuming any protein before and after a workout.
To this ends, the scientists put their 21 ± 2 year old male subjects on iso-caloric (=same amount of total kcal) diets with highly different protein content. While

• Table 1: Subject data (Snijders. 2013)

  the normal protein group (NPD) feasted on 1.2g protein/kg↳ 88/474/60g PRO/CHO/FAT

the poor guys in

• the low protein group (LPD) received only 0.1g of protein/kg↳ 11/502/56g PRO/CHO/FAT

over the course of the 4 day tightly controlled study period. After following this diet for one day the subjects had to perform a single bout of resistance exercise which consisted of two different exercises, each of which was performed for six:

• horizontal leg press machine - 6 sets x 10 reps @ 75% of the 1RM
• leg extesions - 6 sets x 10 reps @ 75% of the 1RM

The equipment they used were standard Technogym machines and thus as representative of what the average trainee may find in his gym as the antroprometric, body composition and fitness data of the study participants (see Table 1) was representative of the average novice trainee's stats.

Figure 1: Total number of myostatin(+) satellite cells per type II fiber - left; rel. change (% of baseline) in type I+II fiber SC number and size 72h after the workout - right; (Snijders. 2013)

It is thus not unrealistic to assume that the data the scientists got from muscle biopsies of the vastus lateralis that were collected before and 12, 24, 48, and 72 h after the workout are representative of what would happen to any young, normally trained individual, on a quasi no-protein fast:

• A note on satellite cells: As Snijders et al. point out. Mere protein synthesis appears to be enough for short term growth, in the longer run, however, "SCs are required to provide additional myonuclei to allow muscle fiber hypertrophy". That's old news. The thing the study at hand adds, though, is the fact that the exercise induced recruitement of satellite cells "does not affect the increase in muscle fiber SC". The study at hand is thus the first to show that "the SC response to exercise is essentially dissociated from dietary protein intake and is likely evolutionary conserve" (Snijders. 2013).
  No acute differences in the net reduction in myostatin(+) satellite cells (SCs) - The fast won't have any effects on the number of myostatin(+) satellite cells (SC), in general. In other words, the training will acutely losen the "protein synthesis brake" irrespective of whether you consume or don't consume enough protein.
• Persistent decreases in myostatin(+) satellite cells only in the LPD group - The restoration of the number of myostatin(+) SCs in the fast twitch type II muscle fibers of the vastus will however be blunted - or, put differently, the myostatin expression will remain suppressed for at least 72h.
• Overall increases in total satellite cell content and size around the muscle fibers - The crowding of satellite cells around type I and type II fibers (Figure 1, right) is a crucial step in postworkout recovery, because the SCs "are thought to be the sole source for providing new myonuclei, thereby supporting skeletal muscle reconditioning" (Snijders. 2013).

Unfortunately we do not have the corresponding protein synthesis data, but I would bet that the ostensibly "negative" increase myostatin the subjects in the normal protein group experienced after 48h (+86%) and 72h (+88%) is actually a good indicator that the muscular protein pool was replenished (or even supercompensated) at this time point.

From the Intermittent Thoughts on Building Muscle you will probably remember that the increase in myostatin and the corresponding reduction in protein synthesis would be a perfectly normal - in fact, a very healthy response. A response that prevents the development of huge, but dysfunctional skeletal muscle (learn more). Consequently, we would have to interpret the myostatin reduction in the low protein group as a reaction to the loss, or at least constantly low skeletal muscle protein, a status the consequences of which are similar to those that occur, when you empty your glycogen stores: The muscle cells will do their best to replenish the said nutrient. In this case, this means that lower myostatin and generate an anabolic potential that cannot be fulfilled, though, as long as there is no protein to be "pumped" into the muscle.
References:

• Aragon, A. A., & Schoenfeld, B. J. (2013). Nutrient timing revisited: is there a post-exercise anabolic window?. Journal of the International Society of Sports Nutrition, 10(1), 5.
• Snijders, T., Verdijk, L. B., McKay, B. R., Smeets, J. S., van Kranenburg, J., Groen, B. B., ... & van Loon, L. J. (2014). Acute Dietary Protein Intake Restriction Is Associated with Changes in Myostatin Expression after a Single Bout of Resistance Exercise in Healthy Young Men. The Journal of nutrition, jn-113.