Dukan Diet

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.

You as a SuppVersity reader should know that there is no "instant gratification" with  "doing cardio" and that doing it "in the zone" is totally 90s... 1990s, even ;-)

For decades, the "Fat Burning Zone" has been one of the holy grails of exercise sciences. Then somebody realized that maximizing the ratio of fat : glucose thats are being used as fuel during a workout doesnt really have an effect on weight loss and all of a sudden papers with titles like "Changes in peak fat oxidation in response to different doses of endurance training" (Rosenkilde. 2013) have become a rarity... although, if you look closely, you will realize that this is actually not another investigation into the realms of the "Fat Burning Zone", but an afford to quantify the effect of regular "cardio training" on your bodies ability to oxidize fat, instead of glucose.

Dont worry its not really about the "fat burning zone"

Luckily Rosenkildes most recent paper, which happens to be the third spinoff of the high (600kcal/day) vs. medium (300kcal/day energy expenditure from "cardio") training volume that already taught us (you can read more about the exact exercise protocol in the previous SuppVersity articles, below) ...

• Learn more about the "Fallacy of Working Out To Burn Calories"

  how futile it is to work out like a maniac if fat loss is your goal ("Some HIIT For Life & Less LISS For More! How to Burn 27,300 Kcal Extra W/out Losing a Single Extra Pound of Fat!" | read more) and 
• how messed up the die hard belief that "exercise" just makes you hungry actually is and what the effects of endurance exercise on appetite and energy intake are ("Exercise: Does It Really Make You Hungry? The More You Train, The Less Hungry You Are." | read more)

In this second serving of the data, we can now learn whether regular endurance training increases peak fat oxidation in a dose-dependent fashion.

Figure 1: Pre & post respiratory exchange ratio (lower value = higher ratio of fatty acid : glucose oxidation) in sedentary control and 300kcal/day group, left; changes in the expression of mitochondrial enzymes (Rosenkilde. 2013)

As you can see in Figure 1 the outcomes of the experiment were not exactly surprising: While there was a persistent increase in fatty acid oxidation and the expression of the facilitative mitochondrial complexes, i.e. enzymes in the mitochondrial respiratory chain, the daily endurance training volume (MOD: 300kcal/day vs. HIGH: 600kcal/day energy expenditure during endurance training) had no effect on the effect size.

So, if its not the volume, what determines the increase in fatty acid oxidation?

Rosenkilde have probably asked themselves something similar to the above, when they realized that there were no meaningful differences between the subjects in the medium vs. high dose cardio groups. The statistical analyses the researcher conducted did yet reveal, that

• VO2peak, generally regarded as a marker of cardio-respiratory fitness,
• fat free mass, the weight of everything (incl. bones, organs, etc.) thats not fat, 
• cycling efficiency, the power output at a given VO2 peak, and the
• mitochondrial complexes II–V, enzymes that facilitate the oxidation of fatty acids,

were all associated with higher increases in fatty acid oxidation, while the observed changes in fasting plasma insulin, glucose, FFA, or glycerol had no prognostic value with respect to the increase in fatty acid oxidation.
References: 

• Crane, J. D., MacNeil, L. G., & Tarnopolsky, M. A. (2013). Long-term Aerobic Exercise Is Associated With Greater Muscle Strength Throughout the Life Span. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, 68(6), 631-638.
• Harber, M. P., Konopka, A. R., Douglass, M. D., Minchev, K., Kaminsky, L. A., Trappe, T. A., & Trappe, S. (2009). Aerobic exercise training improves whole muscle and single myofiber size and function in older women. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 297(5), R1452-R1459.
• Ozaki, H., Loenneke, J. P., Thiebaud, R. S., Stager, J. M., & Abe, T. (2013). Possibility of leg muscle hypertrophy by ambulation in older adults: a brief review. Clinical interventions in aging, 8, 369.
• Rosenkilde, M., Reichkendler, M. H., Auerbach, P., Bonne, T. C., Sjödin, A., Ploug, T., & Stallknecht, B. M. (2014). Changes in peak fat oxidation in response to different doses of endurance training. Scandinavian Journal of Medicine & Science in Sports.