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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.

Asian foods are low in SFAs. So the researchers had to add it to the pan.

From a physiological perspective, the observation researchers from the Nakamura Gakuen University, the  Akita University, the Chiba University and the University of Copenhagen appear counter-intuitive, why should fat increase the insulin response to a meal. The presence of fat in a meal should slow down the absorption of glucose, right?

Obviously you havent read my previous article on the fallacies of adding fat to glucose in the false believe that the reduced digestive speed would reduce the post-prandial insulin spike ("True or False? Adding Fat to A Carby Meal Lowers Insulin Response." | read more) - a highly suggested read you may want to read either, before or after you devour todays SuppVersity article.
Dont worry, todays article still has something new to offer. While the previously reported data dealt with acute responses to high(er) fat meals, Itoh et al. (2014) whose study is available as an "ahead of print paper" on the website of Nutrition Research, looked at the effects of sub-chronic, not acute high saturated fat intakes.

Figure 1: Graphical overview of the procedure  (Itoh. 2014)

In that, they conducted an intervention study to investigate the insulin and plasma GIP responses in 11 healthy women, including a dietary control. Subjects were provided daily control meals (F-20; saturated fatty acids/monounsaturated fatty acids/polyunsaturated fatty acids [S/M/P] ratio, 3:4:3) with 20 energy (E) % fat, followed by 2 isoenergetic experimental meals for 7 days each. All meals were standard Japanese meals, the recipes for both experimental meals were identical, only a different cooking oil was used.
Talking about "test meals" (I dont like to call them thus, as they were consumed for a couple of days and not just for a "test), these meals comprised 60 E% carbohydrate, 15 E% protein, and 30 E% fat with the fat being distributed as follows:

• in the high saturated fatty acid meal (FB-30): S/M/P, 5:4:1; 
• in reduced saturated fatty acid meal (F-30): S/M/P, 3:4:3

Tests were conducted after two days on the FB-20 meal (pre) and at the end of the FB-30 and F-30 phases (see Figure 1), before and 30, 60, and 120 minutes after a meal tolerance test.

Figure 2: Comparison of glucose, insulin, and C-peptide levels after the control, F-30, and FB-30 meals (Itoh. 2014)

Interestingly, the plasma glucose responses did not differ between F-20 and FB-30 or F-30. The insulin levels, on the other hand, were higher after the FB-30 than after the F-20 (P<.01).

The GIP response, i.e. the response of the non-satiating non-fat burning insulin release triggering brother of GLP-1 (learn more) that does neither reduce hunger, not appetite nor improve glucose control (increased amount of insulin used to store away the same amount of glucose; cf. Edholm. 2010), after the FB-30 was higher than that after the F-30 (P< .05).

"In addition, the difference in the incremental GIP between FB-30 and F-30 correlated significantly and positively with that of the insulin." (Itoh. 2014)

The scientists believe that their results clearly prove, what scientists have believed for quite some time, now: "a high saturated fatty acid content stimulates postprandial insulin release via increased GIP secretion." (Itoh. 2014)
References:

• Boden, Guenther, et al. "Mechanisms of fatty acid-induced inhibition of glucose uptake." Journal of Clinical Investigation 93.6 (1994): 2438.
• Edholm, T., et al. "Differential incretin effects of GIP and GLP?1 on gastric emptying, appetite, and insulin?glucose homeostasis." Neurogastroenterology & Motility 22.11 (2010): 1191-e315.
• Itoh, Kazue, et al. "High saturated fatty acid intake induces insulin secretion by elevating gastric inhibitory polypeptide levels in healthy individuals." Nutrition Research (2014).
• Nuutila, P., et al. "Glucose-free fatty acid cycle operates in human heart and skeletal muscle in vivo." Journal of Clinical Investigation 89.6 (1992): 1767.
• Roden, Michael, et al. "Mechanism of free fatty acid-induced insulin resistance in humans." Journal of Clinical Investigation 97.12 (1996): 2859.

Can you hit the fat hard with choline?

I want to be honest with you. I am a huge fan of choline and truly believe that it is hugely under-appreciated, but the prominent relative (not absolute) increase in body fat loss in study at hand must be interpreted with caution - no matter how statistically significant the "choline advantage" may be.

Before we can get to said "cautious interpretation", lets briefly take a look at what exactly Gehan Elsawy, Osama Abdelrahman, and Amr Hamza from the Zagazig University and the Mansoura University in Egypt did to produce a 100% increase in body fat loss in their 22 female study participants (15 taekwondo and 7 judo athletes).
The idea was to clarify the magnitude of rapid body mass reduction among Egyptian judokas, in order to identify the scientific basis and justification for such practices. In that, the researchers were particularly interested in the effects of choline supplementation on bodymass reduction and leptin levels among their females taekwondo and judo athletes.

The athletes were divided into two groups, according to their body mass; the experimental group contained ten female athletes, and the control group twelve female athletes. At the time of enrollment, all the subjects were healthy, according to a medical information questionnaire, and none of the subjects had any specific dietary restrictions. Exclusion criteria included the use of any medication or supplement during the previous six months.

2.0g per day divided in two 1.0g doses of choline did the trick

For one week prior to a competition, the athletes in the experimental group took choline tablets (1.0 g) twice daily with a meal, equaling a total daily dose of 2.0 g (the scientists dont provide any information on the form of choline, they used, but their references suggest that it was PS, i.e. phosphatidylcholine). The control group received a placebo, and they participated in usual training (with 75% training intensity) at the same time as the choline group four times per week.

"According to Anni et al. (2011), choline supplementation appears to be safe and the authors recommend taking approximately 2.5 g one hour before a prolonged exercise session. The effective dose in sport studies is 0.2 g phosphatidylcholine 90% per kg of the body mass, which equals 2.1 g of choline for an 80-kg athlete. There is no requirement for a loading or maintenance phase and choline supplementation up to one hour before exercise has been shown to be effective in reducing fatigue." (Elsawy. 2014)

There was no standardized diet, there were no diet logs and there was no recording of training intensity and volume.
Things that were assessed are body weight, body fat (see red box above), serum and urinary choline, as well as back and leg strength.

Figure 1: Changes in leptin, plasma choline, body fat (%), BMI, leg & back strength within the last week of precompetition dieting with or without the addition of 2g of choline (undisclosed form) in a recent study by Elsawy et al. (2014).

Statistically significant differences were observed for plasma choline (obviously), leptin and the change in body fat (-1% vs. -2% in the choline group). It would be nice if we also knew if this affected the food and/or water intake and/or if we had confirmation from DEXA and caliper data that the body fat difference was more than just body impedance b*s* - unfortunately, none of these data are available.
References:

• Elsawy et al. "Effect of Choline Supplementation on Rapid Weight Loss and Biochemical Variables Among Female Taekwondo and Judo Athletes." Journal of Human Kinetics volume 40/2014, 77-82.
• Hanin I, Ansell GB. "Lecithin: Technological, Biological, and Therapeutic Aspects". Plenum Press, NY, 180-181; 1987.
• Slater, Gary. "Assessing Body Composition of Athletes." Sports Nutrition for Paralympic Athletes (2014): 189.
• Wurtman RJ, Hirsch MJ, Growdon JH. "Lecithin consumption raises serum-free-choline levels." Lancet, 1977; 2: 68-69