ONLINE DRIVERS MEDIA

FSR ? more muscle = no news for ya!

For the average SuppVersity reader the sentence "Acute Post-Exercise Myofibrillar Protein Synthesis Is Not Correlated with Resistance Training-Induced Muscle Hypertrophy in Young Men" is not just the title of a recent paper in the open access journal PLOS|ONE, its also the experimental verification of a claim Ive made in almost all my articles about the acute effects of certain training modalities and/or supplements on myofibrillar protein synthesis and the corresponding increases in muscle size some people appear to expect from a 2h-long 10% increase in fractional protein synthesis (learn more).

And yes, practically speaking these findings imply that we have to question the real world significance of all the neat studies on the "superior muscle building effects" of whey protein, BCAAs and even more so leucine, in which the authors base their recommendations on acute increases in post-exercise protein synthesis.
In the corresponding experiment that was funded by the National Science and Engineering Research Council (NSERC) of Canada Cameron J. Mitchell et al. determined whether the acute myofibrillar protein synthesis measured acutely in training-naive subjects after their first bout of resistance exercise with protein consumption would correlate with the actual increase in muscle size after 16 weeks of resistance training.

Suggested read: "Protein Intake & Muscle Catabolism: Fasting Gnaws on Your Muscle Tissue and Abundance Causes Wastefulness " | more

Before the actual experiment began, the subjects, healthy young recreationally active normal-weight men (177 cm; body mass index = 26.4 kg/m²; men age 22 years) without previous strength training experience, underwent a magnetic resonance imagining (MRI) scans of their right thigh to determine muscle volume, a dual, energy x-ray absorptiometry (DXA) scan to assess whole body fat and bone-free mass (lean mass) and standardized strength tests to determine their maximal isotonic strength (often labeled the 1RM) for all training exercises.

After all baseline measurements (including baseline muscle protein synthesis) were recorded, the subjects completed 16 weeks of RT while ingesting a protein rich beverage (30g of the same whey protein of which Burd et al. showed in 2012 that it elicits a higher increase in MPS than casein) immediately after their exercise session and with breakfast on non-training days.

"Briefly, participants trained four times weekly with two upper and two lower body workouts. Lower body exercises are described above in the acute exercise session. Upper body exercises consisted of chest press, shoulder press, seated row, lat pulldown, bicep curl and tricep extension. The program was progressive in linear manner moving from 3 sets of 12 repetitions to 4 sets of 6  repetitions. At the end of the training period, MRI, DXA scans and strength testing were repeated." (Mitchell. 2014)

If you look at the above description of the workout (and supplementation regimen) you will probably agree that this is pretty much what the majority of resistance physique oriented gym-goers do.

Figure 1: Myofibrillar fractional protein synthesis rate (left) measured acutely after a single workout and changes in muscle volume (%) over the whole 16-week study period as a function of the 1-6h post-workout FSR (Mitchell. 2014).

People who hope that the often reported increases in fractional protein synthesis would pay off and yield increased net muscle gains and thus exactly what Mitchell et al. did not observe in their study, which could not establish the corresponding correlation between the actute increase in post-workout fractional protein synthesis (Figure 1, left) and the chronic change in muscle volume (Figure 1, right).

Figure 2: Changes in muscle volume (%) expressed relative to acute increases in 4E-BP (Mitchell. 2014).

If anything, it was the expression of the Eukaryotic translation initiation factor 4E-binding protein 1 aka 4E-BP1 one of the motors of protein synthesis, but not the increase in myofibrillar fractional protein synthesis that looked as if it could have any predictive value with respect to the increase in muscle volume, the young men experienced in the course of the 16-week training period.

After thinking about the implications of these findings for a minute, I do yet have to admit that the assumption that this would refute the previously invoked recommendations completely, is probably premature.
Reference:

• Burd, Nicholas A., et al. "Greater stimulation of myofibrillar protein synthesis with ingestion of whey protein isolate v. micellar casein at rest and after resistance exercise in elderly men." British Journal of Nutrition 108.06 (2012): 958-962.

It takes pains to maintain your gains!

You will certainly remember the shocking revelation that simply eating more protein is not going to prevent the diet induced muscle loss that occurs whenever you consume less energy than you expend (read up on "Protein Intake & Muscle Catabolism: Fasting Gnaws on Your Muscle Tissue and Abundance Causes Wastefulness" | go for it!)...

Dont rejoice, the study at hand does not refute this - protein is still unable to counter the increase in atrogin-1 and other muscle cannibalizing proteins, but there is a "tweak" by the means of which you can at least avoid that its pro-anabolic affects are also impaired.
What this "tweak" is? Well, thats easy: Heavy lifting. If you are familiar with the "muscle loss in zero gravity" research that has been conducted by and for the NASA in the past decades (e.g. Ferrando. 2002).this shouldnt surprise you. The NASA studies have after all shown quite conclusively that compared to bed-rest / chronic skeletal muscle unloading, starving yourself is almost "anabolic". No wonder that lifting heavy objects, and not dietary protein is the #1 when it comes to saving your muscular ass from shriveling away on a long and hard diet.

Why does resistance training work, if protein fails?

As discussed in "Protein Intake & Muscle Catabolism" (read it!), its not a question of the pro-anabolic effects. You, as a suppversity reader know that the p-AKT/mTOR pathway thats activated by protein feeding is sufficient to increase the influx of protein into the musculature. What your beloved protein cant do, though, is to reset a different switch: The "sacrifice muscle to fuel more fundamental metabolic demands switch" which is triggered whenever you are in a long(er) term energy deficit.

"Training For Gains: High Intensity, Low Volume Strength Gains Stick." | more

So what can be done then? Well,... as it is so often the case, the answer lies - once more - open before our eyes: Hit the weights, down the protein and kick your diets catabolic ass!

I know this sounds too easy, but if you take a peek at the weight loss diets of the average physique athlete and their appearance on stage, it stands out of question that the combination of resistance training and strategic protein supplementation spares muscle mass.

Now the verb "to spare", according to the Oxford English Dictionary, means "to leave (a person) unhurt" (OED.COM), which is - and you probably expected this already, not really accurate. Even the latest data from the School of Medical Sciences at the RMIT University in Melbourne and the Exercise Metabolism Research Group at the Department of Kinesiology of the McMaster University in Hamilton, Ontario, Canada, and the Canadian Sport Institute clearly demonstrates that you cannot switch the diet-induced protein wasting off, completely (Areta. 2014).

Figure 1: The large inter-individual differences make it virtually impossible to tell, whether the MURF-1 levels increased. The similarly catabolic (see overview in the middle) atrogin was yet significantly increased in the early (15g) and late phase (30g) after the workout during ED (Gumucio. 2013; Areta. 2014)

In the corresponding experiment, 16 young, healthy, resistance trained subjects (8 females, 8 males) who had been fed individualized pre-packaged meals delivering 45 kcal/kg FFM (macros: PRO / CHO / FAT 1.4-1.6, 3-3.5 and 0.5-1.5 g·kg BM) per day for five days before they went on a standardized energy 30% energy reduced diet containing approximately

• 1.4-1.6g protein per kg total body mass, 
• 4.0-4.5g carbohydrates per kg total body mass and
• 1.5-2.5g fat per kg total body mass

for another five days. At the end of this "ED" period and five days on rations with only 30kcal/kg fat free mass, all subjects performed a standardized leg press workout (warmup + 6 sets of 8 repetitions at ~80% 1 RM with 3 min rest between set) that was followed by the ingestion of either 15g or 30g of whey protein or an isocaloric placebo.

Figure 2: SLC7A5 AA transporter expression (left) and myofibrillar fractional protein synthesis (% / hour; Areta. 2014)

What a brief glance at the data in Figure 2 does tell you, though, is that resistance training will effectively counter, the diet-induced downregulation of the pro-anabolic response to protein. What it wont do, though is to increase the net protein retention to levels comparable to those on an energy balanced diet!
Contrary to what Areta et al. may have suspected the restoration of the protein synthetic response in the post-workout period did not restore the expression of the amino acid transporter gene SLC7A5 to normal. It is thus not surprising that...

Highly suggested read: " Evidence From the Metabolic Ward: 1.6-2.4g/kg Protein Turn Short Term Weight Loss Intervention into a Fat Loss Diet" | more

"[...] despite this elevation, exercise merely restored MPS [muscle protein synthesis] to a level that was similar to, but not exceeding, rates measured in EB [energy balance]. Accordingly, it appears the metabolic status of the muscle during short-term (5 days) ED [energy deficit] plus a ~10 h fast may dictate that contractile overload in isolation is not enough to increase MPS to values that otherwise would be observed when subjects are in EB." (Areta. 2014)

The results of this recent study do thus have to regarded as another nail an already boarded up coffin thats loaded with bro-scientific myths about "body recompositioning."
Unlike the non-existent changes in amino acid transporter expression, the observation that 30g of protein are more effective than 15g will probably not come as a surprise to you - notwithstanding the fac t that this was "the first [study] to determine the acute muscle anabolic response to resistance exercise with two different doses of protein ingested after exercise during short-term ED", by the way. About as unsurprising as the researchers (eventually unwarranted - I dont see a 20g protein group, here ;-) conclusion that their ...

"[...]results suggest that the optimal amount of protein to maximize the response to a single bout of resistance training while in ED may be above the level (20 g) found to maximize MPS post-exercise for individuals who are in EB." (Areta. 2014)

And my recommendation, not to worry too much about all the details. There are a couple of simple principles that have been working for generations of athletes thriving to cut weight without having to sacrifice muscle mass; and as you should know if youve read and memorized the "9 Simple Rules Every Dieter Must Follow" (go back) consuming 30g of protein with every meal and lifting heavy objects are both part of a set of rules thats rooted in bro- and supported by pro-science.
Reference: 

• Areta, José L., et al. "Reduced resting skeletal muscle protein synthesis is rescued by resistance exercise and protein ingestion following short-term energy deficit." American journal of physiology. Endocrinology and metabolism (2014). Ahead of Print.
• Ferrando, Arny A., Doug Paddon-Jones, and Robert R. Wolfe. "Alterations in protein metabolism during space flight and inactivity." Nutrition 18.10 (2002): 837-841.
• Gumucio, Jonathan P., and Christopher L. Mendias. "Atrogin-1, MuRF-1, and sarcopenia." Endocrine 43.1 (2013): 12-21.