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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.

Fight your fat with a high intensity interval training program thats similar to that of pro-/amateur boxers.

Actually, it should not surprise you that the latest study from the University of Western Sydney shows that boxing training (HIIT) in adults with abdominal obesity is (a) feasible and may (b) elicit a better therapeutic effect on obesity, cardiovascular, and health-related quality of life (HRQoL) outcomes than an equivalent dose of brisk walking (MICT).

What may surprise you, though, is that Birinder S Cheema et al. still feel that more "[r]obustly designed randomized controlled trials are required toconfirm these findings and inform clinical guidelines and practice for obesity treatment" (Cheema. 2015).

In view of the ever-increasing number of studies that show that HIIT training is vastly superior to moderate or even low-intensity exercise in obesity treatment, the guidelines should have been changed all along. But lets forget about politics for the moment. In the study at hand, the basically healthy, yet overweight or obese study participants performed only one of the following training programs:

• Boxing training - Four 50-min sessions of supervised boxing training per week - The interval-based exercises were preceded by a 5 min warm-up of continuous skipping at a self-selected intensity. Intervals were prescribed at 2:1 (i.e. 2 min of high-intensity activity followed by 1 min of rest (standing or pacing) between intervals and exercises). Three intervals of each of the following five exercises were performed for a total of 30 min of high-intensity effort: (1) heavy bag, (2) focus mitts, (3) circular body bag, (4) footwork drills, and (4) skipping. The total amount of physical activity (excluding warm up and rest periods) was computed as 30 min x 6 metabolic equivalents (MET) per minute = 180 MET min [24]. During the high-intensity bouts, participants were instructed to exercise at a rating of perceived exertion of 15-17/20 (“hard” to “very hard”) with the goal of achieving >75% of age-predicted maximal heart rate (i.e. 220-age; HRmax).
• Walking training - Four 50-min sessions of supervised brisk walking training - Participants were instructed to begin each session with a 5-min gradual warm-up and walk as quickly as possible for the remainder of the session (45 min). The total amount of physical activity (excluding warm up) was computed as 45 min x 4 metabolic equivalents (MET) per minute = 180 MET-min.

Needless to say that the boxing group trained at a significantly higher intensity each week versus the brisk walking group (p < 0.05) - intense enough for two participants to require modifications to their exercise program.

Figure 1: Changes in physique markers and parameters of real world well-being (Cheema. 2015).

Since both participants were able to continue the exercise intervention, both still saw similar beneficial effects as their peers who trained according to the original boxing HIIT protocol. These benefits included...

• Figure 2: Significant improvements in markers of cardiovascular health were achieved only with HIIT boxing, not with brisk walking (Cheema. 2015).

  having a lower attrition rate (n = 0 vs. n = 2) than the subjects in the walking group
• greater improvements in body fat percentage (p = 0.047),
• more pronounced reductions in systolic blood pressure (p = 0.026) and central aortic pressure (augmentation index | AIx; p < 0.001)),
• significantly more pronounced improvements in fitness (VO2Max), physical functioning and vitality, as well as
• greater improvements in health-related quality of life scores

over time. The walking group on the other hand, did not improve any clinical outcomes, and experienced a worsening of vitality (p = 0.043).
References:

• Arena, Ross, et al. "Should high-intensity-aerobic interval training become the clinical standard in heart failure?." Heart failure reviews 18.1 (2013): 95-105. 
• Ashor, Ammar W., et al. "Exercise Modalities and Endothelial Function: A Systematic Review and Dose–Response Meta-Analysis of Randomized Controlled Trials." Sports Medicine (2014): 1-18.
• Cheema, Birinder S., et al. "The feasibility and effectiveness of high-intensity boxing training versus moderate-intensity brisk walking in adults with abdominal obesity: a pilot study." BMC Sports Science, Medicine and Rehabilitation 7.1 (2015): 3.
• Gillen, J. B., et al. "Acute high?intensity interval exercise reduces the postprandial glucose response and prevalence of hyperglycaemia in patients with type 2 diabetes." Diabetes, Obesity and Metabolism 14.6 (2012): 575-577.
• Guiraud, Thibaut, et al. "High-intensity interval training in cardiac rehabilitation." Sports medicine 42.7 (2012): 587-605.

Its not just about more protein its about significantly more protein and - possibly - also about whey!

Just to make sure: Yes, I know the study I am about to discuss in todays SuppVersity article is a rodent study - a rodent study by researchers from the University College Cork and the University College Dublin (Mc Allan. 2014).  And yes, I know that you aint no fury little mouse or rat...

... but I do also know that the beneficial metabolic effects of high protein intakes appear to be even more, not less pronounced in human beings and will thus not mention 500x that the assumption that wed see similar benefits in men and women would obviously require experimental confirmation... alright?

Now that we are clear, dear non-dams and non-bucks...

... you are probably already drooling at the sought of reading yet another "high protein is good for you" study. Dont worry I am not going keep you on the tenderhooks longer than absolutely necessary. What is necessary, though is a very brief summary of the study design, which was designed to elucidate the effects macronutrient quality and composition on energy balance and the gut microbia - probably two of the hottest topics in todays discussions on the health and fitness bulletin boards of this world.
As the Irish researcher point out, their goal was to investigate how changes to protein quality (casein versus whey protein isolate; WPI) and the protein to carbohydrate (P/C) ratio within a high fat diet (HFD) impacts on the aforementioned parameters. The questions the experiment was supposed to answer were thus:

• Protein Quality ? Would adding whey protein on top of an obesogenic high fat rodent diet yield to a different weight and microbiota response than casein protein?
• Protein Quantity ? Would diets with 20%, 30% or 40% of the total energy intake from protein have different effects on body weight and microbiota in the rodents?

In view of the fact that casein is the standard protein in many of the high fat diets that are used in experiments like this, the study would thus also be able to give us an idea of whether or not the use of the slow-releasing IGF-1 boosting dairy protein contributes to the obesogenic effects.

As it turned out, the analysis of issues related to question #2, i.e. "Would diets with 20%, 30% or 40% of the total energy intake from protein have different effects on body weight and microbiota in the rodents?" did produce the more intriguing results, though.

Figure 1: Weight gain, fat and lean mass, as well as energy intake and respiratory exchange ratio (RER) after 21-weeks on diets with different amounts of whey protein in them (McAllan. 2014),

If you take a look at the data in Figure 1, its easy to see that (a) in comparison to casein (data from casein experiment not shown, because it was not discussed in detail | maybe there will be a follow up paper!?), WPI at a similar energy content normalised energy intake, increased lean mass and caused a trend towards a reduction in fat mass (P= 0.08). You may find that surprising, but its actually been known for quite some time now that whey buffers many of the ill-health effects of high fat diets in rodents.

Figure 2: Adipose tissue mRNA expression of selected genes (McAllan. 2014)

Although the addition of whey protein did not alter the oxygen consumption or locomotor activity, it was able to ...

• reduce the plasma leptin and liver triacylglycerold levels, and...
• attenuate the reduction in adipose FASN mRNA 

in HFD-fed mice (compared to what the researchers observed in rodents on the casein chow). Moreover, a high throughput sequence-based analysis of faecal microbial populations revealed that the

"[...]microbiota in the HFD-20% WPI group clustering closely with HFD controls, although WPI specifically increased Lactobacillaceae/Lactobacillus and decreased Clostridiaceae / Clostridiumin HFD-fed mice." (McAllan. 2014)

To understand the potential implications of these changes we will have to take a closer look at the recent evidence linking Clostridiaceae and Lactobacillaceae to the diabesity epidemic:

• Lactobacillus reuteri has anti-breast-cancer effects as well  (Lakritz. 2014).

  certain types of clostridiaceae are characteristic for obesity prone animals; their transplanation to normal mice will make them similarly vurnerable to the obesogenic effects of HFDs (Duca. 2014); similar differences, i.e. higher levels of clostridiaceae in obese individuals, have been observed in human studies, as well (Ferrer. 2013)
• lactobacilli, above all those of the reuteri type, have recently been used in several studies for their anti-obesogenic (Million. 2013a, b), anti-autoimmune (Forsberg. 2013), anti-caries (Stensson. 2013), anti-helicobacter plyori (Francavilla. 2013), pro-vitamin-D (Jones. 2013), and a whole host of other beneficial effects; for other types of lacutobacilli researchers have observed that they exert similar anti-obesity effects that may be mediated by the intestinal productino of the anti-obesity isomer of CLA, i.e. trans?10, cis?12?conjugated linoleic acid (Lee. 2007)

If we look at the previously listed metabolic effects, these changes in the make-up of the gut microbiome obviously correspond with the remarkable health improvements that occured in the whey-fed rodents.

High protein, low carb - What does it do?

Table 1: Plasma amino acid levels (mmol/L); blue bars to the right indicate sign. inter-group difference (McAllan. 2014)

Contrary to what youd expect based on appetite increasing effects researchers ascribe to high protein diets (Weigle. 2005), the increase in protein-to-carbohydrate ratio (P/C) did not lead to measurable reductions in energy intake, but ....

"[...]the highest ratio [40% of the total energy intake from protein] reduced HFD-induced weight gain, fat mass and plasma triacylglycerol, non-esterified fatty acids, glucose and leptin levels, while it increased lean mass and oxygen consumption." (McAllan. 2014)

As the scientists point out, similar effects were observed on adipose mRNA expression, where the highest ratio of protein to carbohydrates reduced HFD-associated expression of UCP-2 (a protein that has the fat stores eat themselves up), the inflammatory marker TNF-alpha and CD68 a gylcoprotein that messes with LDL cholesterol.

On the other hand, the (really) high protein diet increased the diet-associated expression of the b3-adrenergic recepto (b3-AR), lipoprotein lipase, a water soluble enzyme that hydrolyzes triglycerides in lipoproteins, such as those found in chylomicrons and very low-density lipoproteins (VLDL), as well as the expression of insulin receptors and the glucose transporters GLUT4 - all of which should be old acquaintances of loyal SuppVersity readers.

References: 

• Duca, Frank A., et al. "Replication of obesity and associated signaling pathways through transfer of microbiota from obese prone rat." Diabetes (2014): DB_131526.
• Forsberg, Anna, et al. "Pre?and post?natal Lactobacillus reuteri supplementation decreases allergen responsiveness in infancy." Clinical & Experimental Allergy 43.4 (2013): 434-442.
• Jones, Mitchell L., Christopher J. Martoni, and Satya Prakash. "Oral Supplementation With Probiotic L. reuteri NCIMB 30242 Increases Mean Circulating 25-Hydroxyvitamin D: A Post Hoc Analysis of a Randomized Controlled Trial." The Journal of Clinical Endocrinology & Metabolism 98.7 (2013): 2944-2951.
• Lakritz, Jessica R., et al. "Beneficial bacteria stimulate host immune cells to counteract dietary and genetic predisposition to mammary cancer in mice." International Journal of Cancer (2014).
• Lee, K., et al. "Antiobesity effect of trans?10, cis?12?conjugated linoleic acid?producing Lactobacillus plantarum PL62 on diet?induced obese mice." Journal of applied microbiology 103.4 (2007): 1140-1146.
• McAllan, Liam, et al. "Protein Quality and the Protein to Carbohydrate Ratio within a High Fat Diet Influences Energy Balance and the Gut Microbiota In C57BL/6J Mice." PLOS ONE 9.2 (2014): e88904.
• Million, M., et al. "Correlation between body mass index and gut concentrations of Lactobacillus reuteri, Bifidobacterium animalis, Methanobrevibacter smithii and Escherichia coli." International Journal of Obesity (2013a).
• Million, Matthieu, and Didier Raoult. "The role of the manipulation of the gut microbiota in obesity." Current infectious disease reports 15.1 (2013b): 25-30.
• Stensson, Malin, et al. "Oral Administration of Lactobacillus reuteri during the First Year of Life Reduces Caries Prevalence in the Primary Dentition at 9 Years of Age." Caries research 48.2 (2013): 111-117.
• Weigle, David S., et al. "A high-protein diet induces sustained reductions in appetite, ad libitum caloric intake, and body weight despite compensatory changes in diurnal plasma leptin and ghrelin concentrations." The American journal of clinical nutrition 82.1 (2005): 41-48.