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In general, you have to count and limit your weekly HIIT sessions. Doing as much as humanly possible, could yet make sense, when youre preparing for Olympia 2016 and realize 5 weeks before the event that you have been lingering for too long ;-)

I think as a SuppVersity reader you know by now that "more wont yield more" - no matter if we are talking about supplements or exercise. Now, while weve had countless examples of the "more aint more" principle thats also at the heart of the "Three Simple Rules of Supplementation" (read article) for supplements (e.g. zinc, chromium, etc.) and the simple notion that eating less wont always result in greater weight loss, evidence for the pro-anabolic / adaptive effects of exercise in general, and non-steady state cardio, in particular is scarce. Against that background its all the more important for us to cherish the publication of a paper from the Norwegian University of Science and Technology and the St Olav University Hospital in Trondheim Norway, Roy told me about by messaging me via the SuppVersity Facebook Page.

"More HIIT doesnt help more, either"

I guess the above would be the elevator pitch for the mythical "turbo lift" in Star Trek. For someone like yourself who has learned never to swallow "expert" wisdom just like that, the statement "more HIIT doesnt hep more, either" obviously wont be satisfying.

Figure 2: Illustration of the training in the low frequency (LF) and high frequency (HF) group.

If you look at the illustration above, you will already know somewhat more about the "more" in the previous sentence. As you can see, the parameter that has been modified is not the volume, its the frequency!  - and thus one of the parameters of which many gymrats think that it could hardly be high enough (AM + PM training, 7 days a week - does that ring a bell?). What this people ignore is the simple truth that ...

... adapatation takes time and training more often does not accelerate this process!

In the end, I am actually quite surprised to see that the net VO2 "gain" the scientists measured in the subsequent detraining phase (see Figure 2) was identical. Or, more explicitly, that packing 24 training sessions into three weeks did not blunt the mitochondrial adaptation processes that are responsible for the increase in VO2max, altogether.

Figure 2: VO2max and heart rate values of the 16 healthy subjects before / after high vs. low frequency HIIT (Hatle. 2014)

If we are brutally honest, though, there is obviously an advantage for the 24 sessions in 8 weeks version of this training protocol (see Figure 3, as well). The VO2max scores were after all identical only in the "catch-up" up period in week 11 and due to the rapid decline after week 12 the benefits faded equally rapid in both groups when the 19 healthy, normalweight, but non-athletic subjects returned to their usual laziness (detraining = not training at all).
References:

• Hatle H, Støbakk PK, Mølmen HE, Brønstad E, Tjønna AE, et al. "Effect of 24 Sessions of High-Intensity Aerobic Interval Training Carried out at Either High or Moderate Frequency, a Randomized Trial." PLoS ONE 9(2). (2014): e88375. doi:10.1371/journal.pone.0088375

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.