ONLINE DRIVERS MEDIA

Todays SuppVersity News will provide you with "confirmation" rather than "innovation", I suppose

With my recent article on the non-existance of protein-related osteoporosis (read more) and the short news post about the unique satiating effects of protein snacks (read more), theres been quite some protein lovin here at the SuppVersity as of late. Usually, I would try to avoid having yet another "protein article" in the same week, but for the most recent study on "Dietary Protein Distribution", I will make an exception and I bet, you wont mind! Why? Well, what about what follows the "Dietary Protein Distribution" in the title of said paper?

"...Influences 24-h Muscle Protein Synthesis in Healthy Adults"

By now, you may feel reminded of a recent review by Alan Aragon and Brad Schoenfeld (Aragon. 2013), the results of which (learn more) are not refuted by the results of the study at hand.
What the study does tell us, is simple: "The consumption of a moderate amount of protein at each meal stimulated 24-h muscle protein synthesis more effectively than skewing protein intake toward the evening meal." (Mamerow. 2014)

In other words: Dont cram all your protein into one meal!

I guess in view of past articles on related topics (e.g. "2x40g, 4x20g or 8x10g of Whey? Which Feeding Strategy Yields the Greatest Net Protein Retention?" | read more; or "Protein Timing Reloaded: A Reminder on the Importance of Repeated 20g Pulses for Optimal Protein Synthesis" | read more), this insight is not really going to surprise you.

Figure 1: Fractional protein synthesis at breakfast (left), when the difference was most pronounced (+30%) and rel. calculated 24h fractional protein synthesis (right) with EVEN vs. SKEWED protein distribution (Mamerow. 2014)

What may surprise you, though is the simple fact that this study, which was a joint venture of scienfitsts from the Division of Rehabilitation Sciences at the Department of Nutrition and Metabolism, and Department of Internal Medicine at the University of Texas Medical Branch and the Department of Food Science and Human Nutrition at the University of Illinois at Urbana (Mamerow. 2014) is the first study to conclusively show that spreading a relatively high protein intake (1.2g/kg body weight) across the day is superior to the large steak the average intermittent faster may be washing down with a triple protein shake in the evening.

With an average age of 37 years the 8 healthy, normal-weight adult men and women who participated in the study at hand were neither rodents, nor elderly individuals, and - contrary to what you may expect if you look at the italicized names of the Institutions the scientists who were involved in this study are working at - they were not in need of rehabilitation after an injury - they were average Joes (n = 5) and Janes (n= 3).

This is not about rodents, elderly people or injured athletes

As you can see in the overview in Table 1, the subjects consumed three square meals, i.e. breakfast, lunch and dinner in the course of the 7-day study period. The previous reference to intermittent fasting is thus obsolete - eating a minimal amount of protein in the morning and at noon is after all very different from eating nothing at all. 

Table 1: Seven-day mean energy and macronutrient intake in healthy adults consuming diets with an EVEN or SKEW protein distribution (Mamerow. 2014)

As the scientists point out, the total 24-h protein, carbohydrate, and fat consumption in the SKEW and EVEN conditions was not different.

"Both diets exceeded the RDA for protein [0.8 g/(kg d)] by ~50%. The SKEW diet met the RDA for protein during the evening meal alone. In all versions of the EVEN and SKEW menus used in this study, the animal-to-vegetable protein ratio was ~2:1." (Mamerow. 2014)

By using a 7-d crossover feeding design with a 30-d washout period, the scientists were thus able to measure the influence of protein timing, on the changes in muscle protein synthesis.

The latter was measured thrice, i.e. after each of the three meals, and used to calculate the twenty-four-hour mixed muscle protein fractional synthesis rates on days 1 and 7 after the ingestion of EVEN-ly or SKEW-edly distributed protein diets.
Reference:

• Aragon, Alan Albert, and Brad Jon Schoenfeld. "Nutrient timing revisited: is there a post-exercise anabolic window?." Journal of the International Society of Sports Nutrition 10.1 (2013): 5.
• Mamerow, Madonna M., et al. "Dietary Protein Distribution Positively Influences 24-h Muscle Protein Synthesis in Healthy Adults". J. Nutr. January 29, 2014 jn.113.185280 [ahead of print].

"Go slow, grow fast" - does it really work this way?

I have to admit that I didnt have time to write "complete" article, so I will just work out an introduction and a bottom line to a never-finished draft that discusses an - in my humble opinion -  still unresolved question:  "Does the time under tension, which must not be confused with the simple number of reps let alone the set, matter when it comes to strength or muscle gains?"  As I said, based on my knowledge of the contemporary literature this is still an unresolved issue. Mostly, because slow (by necessity) means "light weight" and is hard / impossible to distinguish from the rep-number.

The methodological issues are probably also part of the reason that it would be an exaggeration to say that there are only "few" studies that investigate the influence of the time under tension (TUT) on hypertrophy or strength gains - but alas, I have collected the science-crumps for you. So here you go (for a preliminary list):

• Figure 1: Myofibrillar fractional protein synthesis (%/h; Burd. 2012)

  Low load + slow movement = high TUT ? increased protein synthesis -- The 175% increase in muscle protein synthesis in response to leg extensions that were performed with a TUT of 6s in the concentric, and 6s in the eccentric phase of the movement Nicholas A. Burd et al. report in their a 2012 paper in the Journal of Physiology is one of the is one of the few very concrete results from studies that were designed to isolate the effect of the time under tension (Burd. 2012).
  
  In view of the pathetic load (30% of the 1RM) and the matched volume, the practical relevance of these figures is yet highly questionable. For me personally, it is thus more surprising that the difference between ...
  
  • doing 12, 7 and 6 reps @ 30% of the 1 rep max to failure for 198±10 s 119±9 and 90±7s, respectively (SLOW condition w/ TUT of 606), and 
  • performing the same number of reps with the same weight, this time obviously not to failure, within 25±2s, 14±1s, and 11±1s, respectively,
  ...was not even more pronounced than the +/- 49% difference (175% vs. 126%) Burd et al. observed in their eight young male subjects after performin three sets of unilateral leg extensions. 
• Longer TUT, greater anaerobic energy expenditure - Inspite of the fact that it appears logical that longer times under tension would be associated with increases in energy expenditure, you as a SuppVersity reader know very well that not all things that exercise and nutrition science is not necessarily logical.
  
  In view of the overall scarcity of literature it is thus more than worth mentioning that Christopher B. Scotts 2012 study into the effects of time-under-tension and weight lifting cadence on aerobic, anaerobic, and recovery energy expenditures found that both, the anaerobic (=glyoclytic) energy expenditure and post energy oxygen consumption (EPOC) were significantly increased, when you train with a cadence of 4:1 or 1:4 and a corresponding TUT of 25s instead of 1.5:1 (TUT = 15s).

  Figure 2: Anaerobic energy expenditure, post exercise oxgen consumption and total energy expenditure (all in kJ) in the low TUT (1.5:1.5; 15s) vs. high TUT trials (Scott. 2012)

  It is thus only logical (you see, sometimes there is logic in exercise science ;-) that the total energy expenditure in the 25s TUT trials was ~30% higher than in the 15s TUT trial with its 1.5s up : 1.5 down cadence (see Figure 2).
  
  In view of the fact that the majority of us are hopefully not hitting the gym to "burn calories" (learn why thats simply dumb), these findings are interesting, but of similarly irrelevant as the previously cited increases in protein synthesis in the Burd study.
• Concentric tension time is key to muscle growth -- I know that broscience dictates otherwise, but the evidence from a human study by Gillies, Putman & Bell suggests just that: Its the concentric portion of the exercise that stimulates skeletal muscle hypertrophy in response to leg presses, parallel squats, knee extensions and knee flexions in 28 healthy young women with previous strength training experience (Gillies. 2006).

  Figure 3: Fiber area (µm²) of type I & II fibers before and after the 9-week training intervention (Gillies. 2006)

  As you can see in Figure 3, the baseline fibre size(s) of the subjects were yet so different that the participants that had been randomized to the group with an emphasis on the concentric phase (4:1 cadence) had an unfair growth advantage compared to the ladies in the eccentric emphasis group.
  
  In view of the fact that the eccentric emphasis group did also record greater strength gains, it appears unwarranted to change your training regimen from explosive / fast concentric vs. slow eccentric movements to the "concentric emphasis" pattern with its 4s : 1s cadence that was used in the study at hand. 
• Heavy and fast or "slow" and long - it does not even matter -- In 2006 and thus 6 years before the previously discussed study by Burd et al., Michiya Tanimoto and Naokata Ishii, two scientists from the University of Tokio conducted a similar, yet more realistic study which compared
  

  • Figure 4: Cross-sectional area of the knee extensor before (open bars) and after (solid bars) LST, HN, and LN exercise training for 12 wk (Tanimoto. 2006)

    a low-intensity training regimen [ 50% of onerepetition maximum (1RM)] with slow movement and tonic force generation (3 s for eccentric and concentric actions, 1-s pause, and no relaxing phase; LST), to a
  • a high-intensity training regimen ( 80% 1RM) with normal speed (1 s for concentric and eccentric actions, 1 s for relaxing; HN), and 
  • a low-intensity with normal speed training regimen (same intensity as for LST and same speed as for HN; LN)
  and found what most of you will probably already have expected: As far as muscle growth there was no difference to be seen between the LST and the HN regimen after 12 weeks. The LN = low-intensity, normal speed training on the other hand sucked was a total waste of time and did not increase the size of the quadriceps muscle that had been hammered with three sets thrice a week at all.

References: 

• Burd, N. A., Andrews, R. J., West, D. W., Little, J. P., Cochran, A. J., Hector, A. J., ... & Phillips, S. M. (2012). Muscle time under tension during resistance exercise stimulates differential muscle protein sub?fractional synthetic responses in men. The Journal of physiology, 590(2), 351-362. 
• Gillies, E. M., Putman, C. T., & Bell, G. J. (2006). The effect of varying the time of concentric and eccentric muscle actions during resistance training on skeletal muscle adaptations in women. European journal of applied physiology, 97(4), 443-453.
• Scott, C. B. (2012). The effect of time-under-tension and weight lifting cadence on aerobic, anaerobic, and recovery energy expenditures: 3 submaximal sets. Applied Physiology, Nutrition, and Metabolism, 37(2), 252-256. 
• Tanimoto, M., & Ishii, N. (2006). Effects of low-intensity resistance exercise with slow movement and tonic force generation on muscular function in young men. Journal of Applied Physiology, 100(4), 1150-1157.

If you want other to see your pump, you got to be ripped. If not, why care about reductions in BMR?

If you remember my posts about the first generation, arginine-based pre-workout products you will be aware that the only pump they produced was the word "pump" in their name or product description. The reason was and still is simple. The mere provision of l-arginine, which is a precursor to nitric oxide does not lead to an increase in nitric oxide production. Why? Well, think of a building a house: Just buying some concrete wont make you a proud home owner, either ;-)

The bad thing: Arginine didnt work. The good thing: This means it didnt decrease your BMR, either

Against that background its quite astonishing that arginine and citrulline based pre-workout products have dominated the top-seller lists of the big supplement vendors for decades. A fact thats probably partly due to other potential benefits of these amino acids, of which one - you as a SuppVersity reader know that - could be fat loss | learn more about the potential fat loss effects.
With more and more people openly declaring that they would no longer waste money on "good tasting, but expensive and disfunctional products", they industry was yet pressed to develop alternatives. Luckily, our body has two options it can chose from, when producing nitric oxide.

Fortunately, the industry has developed better alternatives...?

You know option #1, the arginine ? nitric oxide pathway, and - with all the hype and hyperbole that surrounded the introduction of the first nitrate supplements - I am pretty sure, you know the other one as well, the nitrate-nitrite ? nitric oxide pathway

Figure 1: The Arginine- and the Nitrate-Nitrite - NO pathway are the yin and yan of nitric oxide production (Lundberg. 2008).

As the illustration (Figure 1) I have "borrowed" from a comment by Jon. O. Lundberg et al. (2008) illustrates quite nicely, the arginine and nitrite nitric oxide pathway are the yin and yan of NO production.

With the "yan", i.e. the nitrate-nitrite ? nitric oxide pathway being a relatively "new kid on the NO block", that recycles (=reduces) inorganic anions nitrate and nitrite to form bioactive NO in blood and tissues during physiological hypoxia.

It goes without saying that there is a bottle neck to this process as well, but the rate limiting availablility of oxygen which hampers the argine-based NO generation by NOS becomes limited as oxygen levels fall is actually a signal for the nitrate–nitrite ? nitric oxide to really kick in.

There is more yin and yan, here

If you take a closer look at the results of a study in the America Journal of Clinical Nutrition (Figure 2), you will yet have to realize that there is "more yin and yan", here than youd probably hope for. According to the data scientists from the venerable Karolinska Institutet in Stockholm, Sweden, present in their paper, "[d]ietary inorganic nitrate reduces the RMR." (Larsen. 2014)

Figure 2: VO2 consumption (marker of fatty acid oxidation) and basal metabolic rate (BMR) relative to means (left), thyroid hormone (T3, T4) levels after 3-d dietary intervention with sodium nitrate (Larsen. 2014)

Whut? Yes, you read Larsen et al. right: In their randomized, double-blind, crossover study, in the course of which the Swedish scientists measured the resting metabolic rate (RMR) of 13 perfectly healthy 18–49 y olds (17 women) via indirect calorimetry after a 3-d dietary intervention with sodium nitrate (NaNO3 @ 0.1mmol/kg body weight) or a placebo (NaCl), Larsen, Schiffer, Ekblom et al. observed a statistically and (probably) physiologically significant reduction BMR reduction of 4.2% which correlated strongly to the degree of nitrate accumulation in saliva (r²= 0.71) and fits in nicely with the reduced O2 consumption of which Bailey et al. were the first to observe it in response to nitrate supplementation during exercise (Bailey. 2009).

Interestingly, these effects were not - as you may have been speculated - brought about by changes in thyroid hormone status. And the subjects insulin sensitivity, glucose uptake, plasma concentration of isoprostanes, as well as their total antioxidant capacity were unaffected, as well.
Reference:

• Bailey, Stephen J., et al. "Dietary nitrate supplementation reduces the O2 cost of low-intensity exercise and enhances tolerance to high-intensity exercise in humans." Journal of Applied Physiology 107.4 (2009): 1144-1155.
• Hotta, Yuji, et al. "Oral l?citrulline supplementation improves erectile function and penile structure in castrated rats." International Journal of Urology (2014).
• Larsen, Filip J., et al. "Dietary inorganic nitrate improves mitochondrial efficiency in humans." Cell metabolism 13.2 (2011): 149-159.
• Lundberg, Jon O., Eddie Weitzberg, and Mark T. Gladwin. "The nitrate–nitrite–nitric oxide pathway in physiology and therapeutics." Nature Reviews Drug Discovery 7.2 (2008): 156-167.
• Neuzillet, Y., et al. "A randomized, double?blind, crossover, placebo?controlled comparative clinical trial of arginine aspartate plus adenosine monophosphate for the intermittent treatment of male erectile dysfunction." Andrology 1.2 (2013): 223-228.

Maximal protein synthesis requires protein, but how much exactly you need will depend on your age - the older you are the more PWO protein youll need.

Scientists from the University of Auckland were fed up with the lack of information about the differential response in protein synthesis in response to the ingestion of various amounts of protein. Accordingly, Randall F. D’Souza et al. conducted a study to characterize the changes in intramuscular levels of EAAs and BCAAs and the expression of the "protein pump" p70S6K at Thr389, a marker of protein synthesis, in response to resistance exercise and graded ingestion of whey protein in older men.

As a regular SuppVersity reader you will probably already think: "Where is the actual measurement of the fractional protein synthesis?" The unfortunate answer: Its not there.
Previous research had show that the ingestion of graded amounts of high-quality protein such as whey after resistance will maximize with "only" 20g of egg protein (Moore. 2009) or whey (Witard. 2014) in young men. Multiple studies in older adults (>60 years), on the other hand, suggest that they exhibit a lower anabolic signaling and MPS response to protein feeding, resistance exercise, and the combination of feeding and exercise when compared to young men (Cuthbertson. 2005; Fry. 2011; Burd. 2013). Scientists call this phenomenon age-related "anabolic resistance" (Yang. 2012b).

Figure 1: In contrast to the fractional protein synthesis in the elderly, which increases with increasing amounts of protein, the FSR of young men shows a ceiling effect at 20g+ whey protein (Yang. 2012a; Moore. 2009)

As you can see in Figure 1 from a 2012 study by Yang, the same 20g of extra-whey (total dose 40g) that was useless in young men, lead to a significant increase in protein anabolism in elderly men. Compared to young men, the MPS response to feeding 40 g of protein was yet still slightly lower in older vs. count men (Yang. 2012a; Churchward Venne. 2013b).

What is particularly relevant for the study at hand, and the previously criticized absence of actual MPS measurements is the fact that deficits in feeding induced p70S6K phosphorylation may at least partially underpin anabolic resistance in aged skeletal muscle (Cuthbertson. 2005), which is why measuring the p70S6K phosphorylation in older human subjects (mean age 71 years) in response to the graded ingestion of whey protein after a leg workout consisting of three sets of 8–10 repetitions of bilateral barbell smith rack squat, 45°leg press, and seated knee extensions at 80% of the subjects predetermined 1R is not as irrelevant at it may initially have seemed.

Workout + supplements, thats the "whey to go" ;-)

The exercises were performed in a circuit manner with 1 min rest between each exercise and 3 min rest between subsequent sets, the exercise protocol took approximately 20 min to complete. Following completion of the exercise protocol, subjects were immediately provided with a fixed-volume (350 mL) beverage, containing a flavored noncaloric placebo, or oneof the four doses of whey protein concentrate (10 g, 20 g, 30 g, or 40 g).

Figure 2: Intramuscular amino acids. This figure is a heat map which shows groups means fold changes from the resting fasted condition. Green represents a decrease in amino acid content, white represents no change, and red represents an increase in amino acid content (D’Souza. 2014)

Subjects were instructed to ingest the beverage within 2 min and were required to ingest the total volume provided. Following consumption of the supplements, subjects rested in a supine position throughout the 4 h of post-exercise recovery with additional muscle biopsy samples collected at 2 and 4 h post exercise.

Figure 3: Higher protein intake = higher increase in p70S6K phosphorylation (left graph). This increase is linearly associated with intramuscular leucine levels (right graph | both from D’Souza. 2014)

As you can see in Figure 3, there was a similar dose-dependent increase in p70S6K as it was observed previously for MPS in skeletal muscle of elderly subjects by Yang et al. (2012b). In fact, the fold change in the phosphorylation of p70S6K (Thr389) at 2 h post exercise was correlated with the dose of whey protein consumed (r =0.51,P<001) and was found to be significantly correlated with intramuscular leucine content (r =0.32,P=0.026).

Moreover, the intramuscular BCAAs, and leucine in particular, appear to be important regulators of anabolic signaling in aged human muscle during post-exercise recovery via reversal of exercise-induced declines in intramuscular BCAAs.
References:

• Burd, N. A., S. H. Gorissen, and L. J. van Loon. 2013.  Anabolic resistance of muscle protein synthesis with aging. Exerc. Sport Sci. Rev. 41:169–173.
• Churchward-Venne, T. A., N. A. Burd, C. J. Mitchell, D. W. West, A. Philp, G. R. Marcotte, et al. 2012. Supplementation of a suboptimal protein dose with leucine or essential amino acids: effects on myofibrillar protein synthesis at rest and following resistance exercise in men. J. Physiol. 590:2751–2765.
• DSouza, Randall F., et al. 2014. Dose?dependent increases in p70S6K phosphorylation and intramuscular branched?chain amino acids in older men following resistance exercise and protein intake. Physiological Reports 2.8: e12112.
• Churchward-Venne, T. A., L. Breen, and S. M. Phillips. 2013a. Alterations in human muscle protein metabolism with aging: protein and exercise as countermeasures to offset sarcopenia. BioFactors 40:199–205.
• Churchward-Venne, T. A., C. H. Murphy, T. M. Longland, and S. M. Phillips. 2013b. Role of protein and amino acids in promoting lean mass accretion with resistance exercise
  and attenuating lean mass loss during energy deficit in humans. Amino Acids 45:231–240.
• Churchward-Venne, T. A., L. Breen, D. M. Di Donato, A. J. Hector, C. J. Mitchell, D. R. Moore, et al. 2014. Leucine supplementation of a low-protein mixed macronutrient beverage enhances myofibrillar protein synthesis in young men: a double-blind, randomized trial.
  Am. J. Clin. Nutr. 99:276–286.
• Cuthbertson, D., K. Smith, J. Babraj, G. Leese, T. Waddell, P. Atherton, et al. 2005. Anabolic signaling deficits underlie amino acid resistance of wasting, aging muscle. FASEB J. 19:422–424.
• Moore, D. R., M. J. Robinson, J. L. Fry, J. E. Tang, E. I. Glover, S. B. Wilkinson, et al. 2009. Ingested protein dose response of muscle and albumin protein synthesis after resistance exercise in young men. Am. J. Clin. Nutr. 89:161–168.
• West, D. W., and K. Baar. 2013. May the Force move you: TSC-ing the mechanical activation of mTOR. J. Physiol. 591:4369–4370.
• West, D. W., N. A. Burd, J. E. Tang, D. R. Moore, A. W. Staples, A. M. Holwerda, et al. 2009a. Elevations in ostensibly anabolic hormones with resistance exercise enhance neither training-induced muscle hypertrophy nor strength of the elbow flexors. J. Appl. Physiol. 108:60–67 .
• West, D. W., G. W. Kujbida, D. R. Moore, P. Atherton, N. A. Burd, J. P. Padzik, et al. 2009b. Resistance exercise-induced increases in putative anabolic hormones do not enhance muscle protein synthesis or intracellular signalling in young men. J. Physiol. 587:5239–5247.
• Witard, O. C., S. R. Jackman, L. Breen, K. Smith, A. Selby, and K. D. Tipton. 2014. Myofibrillar muscle protein synthesis rates subsequent to a meal in response to increasing doses of whey protein at rest and after resistance exercise. Am. J. Clin. Nutr. 99:86–95
• Yang, Y., L. Breen, N. A. Burd, A. J. Hector, T. A. Churchward-Venne, A. R. Josse, et al. 2012a. Resistance exercise enhances myofibrillar protein synthesis with graded intakes of whey protein in older men. Br. J. Nutr. 108:1780–1788.
• Yang, Y., T. A. Churchward-Venne, N. A. Burd, L. Breen, M. A. Tarnopolsky, and S. M. Phillips. 2012b. Myofibrillar protein synthesis following ingestion of soy protein isolate at rest and after resistance exercise in elderly men. Nutr. Metab. 9:57.

Is there something to the good vs. bad fat shenanigan, after all?

Only recently scientists from the Texas Tech University report that a PUFA-rich high-fat meal led to a greater diet-induced thermogenesis in normal-weight premenopausal women compared with SFA- or MUFA-rich high-fat meals.

Reason enough to take a closer look at this and previous studies investigating the diet-induced thermogenic effects of PUFA-, MUFA- and SFA-rich meals and to conduct a reality check wrt to the question whether these differences actually matter - I mean, will you get and stay lean by upping your PUFA intake? Lets take a look!
In the initially mentioned study, Hui C. Clevenger, Amanda L. Kozimor, Chad M. Paton and Jamie A. Cooper explored the effect of three HF meals enriched with different fatty acids (MUFAs, PUFAs or SFAs) on metabolism in premenopausal women of normal weight. In that, the metabolic parameters of interest included postprandial energy expenditure (EE), which is then used to calculate DIT, and substrate oxidation, which included respiratory exchange ratio (RER), fat oxidation and carbohydrate (CHO) oxidation.

Based on previous research in men of normal weight, the Texas Tech researchers hypothesized that the diet induced thermogenesis (DIT) and fat oxidation would be the highest after the PUFA- and MUFA-rich meals and lowest after the SFA-rich meal in premenopausal women - a result of which you already know that it was only partly confirmed.

Figure 1: Diet-induced thermogenesis and respiratory exchange rate (higher RER = lower fatty acid oxidation vs. higher CHO oxidation) in the 5h after the test meal (Clevenger. 2014)

The data in Figure 1 does after all tell you that the expected MUFA-induced increase in diet-induced thermogenesis did not occur. PUFAs, on the other hand did the job, Clevenger et al. expected them to do. They increased the DIT by an ostensibly whopping 14% over the DIT the scientists observed in response to the ingestion of the high MUFA and SFA liquid meals that had been prepared with the same base of 8 fl oz (237 ml) of chocolate Ensure(R) with soy lecithin and Nesquik (R, but contained different additional dietary fatty acids added depending on the treatment condition:

• Table 1: Liquid meal nutrient composition breakdown (Clevenger. 2014).

  The PUFA-rich meal was ‘base’ plus sunflower oil and flaxseed oil, with 42% of total energy coming from PUFA.
   
• The MUFA-rich meal was ‘base’ plus canola oil and extra virgin olive oil, with 42% of total energy coming from MUFA.
  
  
• Finally, the SFA-rich meal was ‘base’ plus butter, coconut oil and palm oil, with 40% of total energy coming from SFA. 

As the data in Table 1 indicates, the nutrient profiles didnt differ much. The fatty acid composition, on the other hand did, with the SFA meal being the only one with measurable amounts of Butyric, Caprioc, Caprylic, Capric, Lauric, Myristic and Hepatedic acid. Fatty acids of which previous research indicate that they induces an obesity-linked proinflammatory gene expression profile in adipose tissue of subjects at risk of metabolic syndrome (van Dijk. 2009).

High MUFA diets, on the other hand, have been shown to potentiate the effects of weight loss in obese NIDDM patients (Low. 1996). They are the major group of fatty acids in the one oil, everyone appears to agree that its health (Olive oil). And last but not least, even the allegedly unhealthy omega-6s have been shown in randomized controlled to reduce liver fat and modestly improve metabolic status, without weight loss, when compared to high saturated fat diets (Bjermo. 2012).

All of these effects / this evidence could potentially be more important than the increase postprandial thermogenesis in the study at hand - so the ultimate question is: Does DIT even matter?
References:

• Bjermo, Helena, et al. "Effects of n? 6 PUFAs compared with SFAs on liver fat, lipoproteins, and inflammation in abdominal obesity: a randomized controlled trial." The American journal of clinical nutrition 95.5 (2012): 1003-1012.
• Clevenger, Hui C., et al. "Acute effect of dietary fatty acid composition on postprandial metabolism in women." Experimental physiology (2014): expphysiol-2013.
• Westerterp, Klaas R., et al. "Dietary fat oxidation as a function of body fat." The American journal of clinical nutrition 87.1 (2008): 132-135.

Trp and its metabolite 5-HTP may be particularly useful for female sugar cravings and binges.

Can l-tryptophan help you lose body fat? If you look at the results of the latest study from the University for Health Sciences, Medical Informatics and Technology it would seem that the answer to this question may be "Possibly, yes, but..." Before we come to the implications I would yet like to take a closer look at said study which shows that a lack of tryptophan (Trp) during diets does not just affect the biosynthesis of serotonin, but may also be associated with increased susceptibility for mood disturbances and carbohydrate craving. Accordingly, "strategies to supplement Trp while dieting could be highly useful in treating uncontrolled weight gain or in preventing neuropsychiatric symptoms" (Strasser. 2014).
As Strasser et al. point out, both overweight and obesity go hand in hand with significant increases in low-grade inflammation. The latter is not just the reason that obesity increases the risk of cardiovascular disease, though. Recent evidence suggests that it is also associated with errors in the kynurenine (Kyn) pathway, in which tryptophan is broken down to kynurenine which in turn has been associated with increased risk of depressive symptoms, cognitive deficits in schizophrenia, Alzheimers and, as mentioned before, cardiovascular disease. Weight loss, on the other hand,

"[...] has been shown to improve or prevent many of the aforementioned conditions. Bariatric surgical intervention in patients with adiposity was found not to improve tryptophan breakdown rates and other signs of immune activation and inflammation [4], whereas caloric restriction is known to be a strong activator of protective metabolic pathways, thereby leading to lower blood pressure, improved blood lipids, and reduced inflammatory markers, including CRP [9]. Still, little is known about the effects of an extreme short-term hypocaloric diet on Trp metabolism and changes in inflammatory biomarkers" (Strasser. 2014).

The study Barbara Strasser, Ken Berger and Dietmar Fuchs conducted was thus designed to assess the effect of a 2-week caloric restriction weight loss diet on Trp breakdown, leptin, and inflammatory biomarkers in over weight adults.
The scientists randomized 27 overweight and 11 obese participants (22 men and 16 women, mean age 52.8 ± 9.1 years) from the health center Lanserhof, Innsbruck–Lans, into two diet groups:

• a very low kcal diet group (VLCD; Ø 600 kcal/ day) and 
• a low kcal diet group (LCD; Ø 1,200 kcal/day). 

Only healthy subjects with BMI [25 kg/m²] between the ages of 35 and 70 years were accepted for the study. A physician performed physical examinations on all subjects before the study. Subjects were excluded if they consume any anti-inflammatory drugs (e.g., ibuprofen or aspirin) or supplements (such as antioxidants or fish-oil capsules). None from either group was involved in regular training programs.

Figure 1: Changes in body composition pre- vs. post (Strasser. 2015).

As the measurements of body composition, which were just like the energy intake and biologic markers conducted in all subjects before and after the 2-week energy restriction intervention period, indicate, both diets lead to significant reductions in body mass - and that almost exclusively in form of body fat.

Table 1: Biologic markers before and after a 2-week very low kcal diet (VLCD) or low kcal die (LCD) in 38 overweight subjects (mean ± SD)

"Data for biologic markers are shown in Table [1]. Fasting blood glucose declined significantly (P < 0.05) in the LCD group with no significant changes in insulin sensitivity in both groups after 2 weeks of caloric restriction. Weight loss diet lowered leptin levels in both groups, although not reaching the level of significance. Inflammatory biomarkers were not significantly altered during the trial, although there was a tendency toward an increase in IL-6 and TNF-a in the LCD group" (Strasser. 2015).

In contrast to what the researchers expected, both the Trp and Kyn concentrations decreased significantly by 21 and 16 % for VLCD and by 15 and 17 % for the LCD group, respectively, with no significant difference between groups. Practically speaking, this means that the ratio of Kyn/Trp concentrations did not change significantly in both groups.
A significant reduction in Phe concentrations was only seen after VLCD. Neopterin and Tyr levels remained unchanged during the trial. Which leaves us with only one significant finding:

"Trp concentrations decreased significantly with a caloric restriction weight loss diet, and lowest Trp concentrations were observed in the group of individuals with the lowest calorie intake." (Strasser. 2015)

This reduction in Trp levels may well induce a disturbance in the biosynthesis of neurotransmitter 5-hydroxytryptamine (5-HT | Anderson. 1990), and appears to be associated with an increased susceptibility for depression (Widnet. 2002; Raison. 2009). Strasser et al. highlight:

Figure 2: The consumption of tryptophan-free amino acid supplements leads to highly significant increases in hunger ratings in healthy female subjects (Rieber. 2010).

"Because Trp is precursor in various biochemical pathways, e.g., it is hydroxylated by tryptophan-5-hydroxylase (T5H) into the intermediate product 5-hydroxy-tryptophan, which by decarboxylation is further converted to neurotransmitter 5-HT (serotonin), and because substrate saturation of T5H is only about 50 % (Dantzer. 2011), changes in plasma Trp levels may have an immediate impact on brain serotonin levels" (Strasser. 2014).

Experiments in which Trp was acutely depleted (in many studies by administering BCAAs | see red boy) support this assumption. Young et al. (2013), for example, confirmed that the acute depletion of tryptophan will lead to low serotonin and subsequently lower mood and increased aggression, although results vary somewhat between studies with similar participants.

Figure 3: Correlations between changes in tryp:LNAA ratio and appetite ratings (Gendall. 2000).

For the link to obesity, though, the correlation (r-values in Figure 3) between high Trp:LNAA (BCAAs, tyrosine, phenlylanine) and a reduction carbohydrate cravings, general hunger and binge eating is yet way more important - and that specifically for women, who appear more vulnerable than men both to the diet-induced reductions in Trp and to its consequences for brain serotonin function (Anderson. 1990).

Ah, and in case you are asking yourself why carbohydrate / sugar binges are a common consequence of low tryptophane:LNAA ratios, its important to know that increases in glucose and insulin in response to high carbohydrate meals will trigger an increase in brain tryptophan and serotonin synthesis (Benton. 2002). This is why the effects of low tryptophan or high LNAA (BCAA, tyrosine, phenylalanine) levels are more pronounced if you avoid dietary carbohydrates.
References:

• Anderson, I. M., et al. "Dieting reduces plasma tryptophan and alters brain 5-HT function in women." Psychological medicine 20.04 (1990): 785-791. 
• Benton, David. "Carbohydrate ingestion, blood glucose and mood." Neuroscience & Biobehavioral Reviews 26.3 (2002): 293-308.
• Cangiano, Carlo, et al. "Eating behavior and adherence to dietary prescriptions in obese adult subjects treated with 5-hydroxytryptophan." The American journal of clinical nutrition 56.5 (1992): 863-867.
• Cangiano, Carlos, et al. "Effects of oral 5-hydroxy-tryptophan on energy intake and macronutrient selection in non-insulin dependent diabetic patients." International journal of obesity and related metabolic disorders: journal of the International Association for the Study of Obesity 22.7 (1998): 648-654.
• Ceci, F., et al. "The effects of oral 5-hydroxytryptophan administration on feeding behavior in obese adult female subjects." Journal of neural transmission 76.2 (1989): 109-117.
• Cui, Y., T. F. Lee, and L. C. H. Wang. "Thermoregulatory responses following injection of 5-hydroxytryptamine into the septohippocampal complex in rats." Pharmacology Biochemistry and Behavior 45.4 (1993): 935-939.
• Dantzer, Robert, et al. "Inflammation-associated depression: from serotonin to kynurenine." Psychoneuroendocrinology 36.3 (2011): 426-436. 
• Fernstrom, John D. "Branched-chain amino acids and brain function." The Journal of nutrition 135.6 (2005): 1539S-1546S.
• Gendall, Kelly A., and Peter R. Joyce. "Meal-induced changes in tryptophan: LNAA ratio: effects on craving and binge eating." Eating behaviors 1.1 (2000): 53-62. 
• Le Feuvre, R. A., L. Aisenthal, and N. J. Rothwell. "Involvement of corticotrophin releasing factor (CRF) in the thermogenic and anorexic actions of serotonin (5-HT) and related compounds." Brain research 555.2 (1991): 245-250.
• Nieuwenhuizen, Arie G., et al. "Acute effects of breakfasts containing ?-lactalbumin, or gelatin with or without added tryptophan, on hunger,‘satiety’hormones and amino acid profiles." British journal of nutrition 101.12 (2009): 1859-1866.
• Raison, Charles L., et al. "CSF concentrations of brain tryptophan and kynurenines during immune stimulation with IFN-?: relationship to CNS immune responses and depression." Molecular psychiatry 15.4 (2009): 393-403.
• Rieber, N., et al. "Acute tryptophan depletion increases experimental nausea but also induces hunger in healthy female subjects." Neurogastroenterology & Motility 22.7 (2010): 752-e220.
• Strasser, Barbara, Ken Berger, and Dietmar Fuchs. "Effects of a caloric restriction weight loss diet on tryptophan metabolism and inflammatory biomarkers in overweight adults." European journal of nutrition (2014): 1-7.
• Widner, Bernhard, et al. "Neopterin production, tryptophan degradation, and mental depression—What is the link?." Brain, behavior, and immunity 16.5 (2002): 590-595.
• Young, Simon N. "The effect of raising and lowering tryptophan levels on human mood and social behaviour." Philosophical Transactions of the Royal Society B: Biological Sciences 368.1615 (2013): 20110375.