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"No sun, no diabesity protection." The evidence is equivocal and the number of studies low, but there is evidence that this statement could be true.

Ok, its November and not exactly sunny in the Northern hemisphere, but if you look back at the months June-August, how much sun exposure did you actually get, this year? Hardly any? Well, thats bad news, because a recent review of the scant scientific evidence suggests that there is "a role of recreational sun exposure in reducing odds of T2DM incidence" (Shore-Lorenti. 2014).

In view of the fact that the contemporarily available evidence is not exactly comprehensive, you should yet consider the following overview of the potential effects and mechanism as a "work in progress".
As Shore-Lorenti et al. point out, the recent International Diabetes Federation (IDF) Diabetes Atlas (6th edition) describes a snapshot of the global diabetes burden in 2013 and projects this forward to the year 2035.1 Cur rently, an estimated 382 million global citizens have diabetes, costing around $1437 USD in 2013 for each person affected by the condition. Projections based on current trends predict that 592 million people will be living with diabetes by 2035; one in ten people will be affected, with an inordinate amount of fund ing required globally to treat diabetes and manage diabetic com plications ($627 billion USD in 2035).

And while scientists are feverishly searching for a solution for the diabesity epidemic, the ongoing research into the effectiveness of vitamin D supplementation in diabetes have yielded inconsistent results (Mitri. 2011). Against that background it appears almost negligent that only few scientists have yet taken a closer look at the factors that trigger vitamin D sufficiency or rather the global low vitamin D epidemia.

Lack of sun"low vitamin D" - thats not all!

Figure 1: Australians who use sunscreen chronically have 50% reduced vitamin D levels (Matsuoka. 1988)

A lack of sufficient (unprotected) sun exposure - previous studies have shown that chronic sunscreen use decreases circulating concentrations of 25-hydroxyvitamin (Figure 1 | Matsuoka. 1988) - is one of the factors of which researchers speculate that it contributes to the development of vitamin D deficiency even in those of us who live in areas with a high annual sun-exposure.

Now, if restoring the 25-OHD (vitamin D) levels to normal does not work the anti-diabetic magic it is supposed to do and our D-levels are low due to insufficient sun-exposure, it appears only logical to assume that a lack sun-exposure and not a lack of vitamin D is one of the factors that contributes to the ever-increasing rates of diabesity - in conjunction with the usual subjects, obviously: The consumption of a junk-food diet and a lack of exercise, which is without doubt the #1 reason people in the Western Obesity Belt develop obesity, diabetes and the other characteristics of the metabolic syndrome.

Against that background its all the more surprising that evidence for an association between sun exposure and fasting serum glucose level is scarce.

"Typically, the lowest glucose levels occur during summer and levels peak in winter or early spring. One of these analyses [Shore-Lorenti et al. reviewed] went beyond simply observing trends in fasting glucose throughout the year: fasting plasma glucose was positively correlated with a measure of available sun and inversely correlated with temperature." (Shore-Lorenti. 2014)

The study, the researchers from the University of Melbourne have in mind was conducted by Suarez, L. & Barrett-Connor, E. in 1988, already.
If you look at the data Suaraez & Barret-Connor generated, you can see - even without their statistical sophisticated analysis - that there is a significant correlation between possible sun exposure (Figure 1, left) and the fasting plasma glucose levels (Figure 1, right).
Since physical activity may follow a similar circannual rhythm, its yet difficult to exclude that the effects Suarez & Barret-Connor observed were not corroborated (or corrupted?) by an increase in physical activity. However, Shore-Lorenti et al. believe that ...

"[...c]onsidering that the unadjusted analyses and three of four of the studies included in the best evidence synthesis (including the study adjusting for physical activity) are in agreement, it is possible that future research may confirm that sun exposure reduces fasting glucose" (Shore-Lorenti. 2014).

Shore-Lorenti et al. also point out that the highest level of evidence (moderate) for an association between sun exposure and T2DM outcomes in adults originates from the study by Lindqvist et al. (2010). In their paper, the researchers from the Karolinska University Hospital report a reduction in odds of developing T2DM given increased recreational (rather than occupational) sun exposure. 

Figure 2: Leisure time sun exposure is associated with a significantly reduced risk (up to 50%!) of developing T2DM in Swedish adults (Lindqvist. 2010)

In subjects with a low BMI the beneficial effect of using the tanning bed and sunbathing is even more pronounced (-60% risk). In the obese, however, it is significantly reduced (-10%) compared to the average reductions you see in Figure 2.

The fact that only leisure time, but not occupational sun exposure was linked to a significant reduced risk of developing type II diabetes may, as Shore-Lorenti et al. point out be due ...

"[...] to the frequency of sun exposure (perhaps leading to tolerance), duration, intensity and site of exposure (sun protective clothing and behaviour differences between the two settings), or perhaps selection biases for such work (for example, fair-skinned people may avoid occupational sun exposure or a less healthy lifestyle may be associated with manual labour)."

Incidentally, a similar disparity between recreational and occupational sun exposure is well described for risk of developing melanoma (Chang. 2009).

A review by Chen et al. (2008) provides low-level evidence for an association between sun exposure and fasting insulin levels; fasting serum insulin was higher in summer than in winter. Overall, the results are yet inconclusive. A fact, Shore-Lorenti et al. ascribe to "the lack of adjustments made by the included study – particularly for BMI" (Shore-Lorenti. 2014)
Overall, we are thus left with the above overview (Table 1) as a conclusion of which the mere number of "unkown"s and "inconsistent"s tell you that we are not yet at the point to draw a water-proof conclusion.
References:

• Chang, Yu-mei, et al. "Sun exposure and melanoma risk at different latitudes: a pooled analysis of 5700 cases and 7216 controls." International journal of epidemiology (2009): dyp166. 
• Chen, Shui-Hu, et al. "Community-based study on summer-winter difference in insulin resistance in Kin-Chen, Kinmen, Taiwan." Journal of the Chinese Medical Association 71.12 (2008): 619-627.
• Lindqvist, Pelle G., Håkan Olsson, and Mona Landin-Olsson. "Are active sun exposure habits related to lowering risk of type 2 diabetes mellitus in women, a prospective cohort study?." Diabetes research and clinical practice 90.1 (2010): 109-114.
• Mitri, J., M. D. Muraru, and A. G. Pittas. "Vitamin D and type 2 diabetes: a systematic review." European Journal of Clinical Nutrition 65.9 (2011): 1005-1015.
• Nelemans, P. J., et al. "An addition to the controversy on sunlight exposure and melanoma risk: a meta-analytical approach." Journal of clinical epidemiology 48.11 (1995): 1331-1342.
• Shore?Lorenti, Catherine, et al. "Shining the Light on Sunshine: a systematic review of the influence of sun exposure on type 2 diabetes mellitus?related outcomes." Clinical endocrinology (2014).
• Suarez, L., and E. Barrett-Connor. "Seasonal variation in fasting plasma glucose levels in man." Diabetologia 22.4 (1982): 250-253. 

You wont see the same effects with pineapple/juice (Aiyegbusi. 2011).

Proteases are as any Wikipedia user will lean enzymes that break down proteins (proteolysis) by hydrolyzing the peptide bonds that link amino acids together in the polypeptide chain forming the protein.

Proteases have evolved multiple times, and different classes of protease can perform the same reaction by completely different catalytic mechanisms. Proteases can be found in animals, plants, bacteria, archaea and viruses. And proteases can be found on among the favorite supplements of naturopath.
Up to today, however proteases could not be found on the list of scientifically proven performance enhancers. With the latest study from the University of Tasmania, the latter has changed: According to the results Shing et al. published in the latest issue of the European Journal of Sport Science, bromelain, a protease that can be found among others in several foods, most prominently pineapple, can reduce (a) the subjective feelings of fatigue and (b) help to maintain testosterone concentration in competitive cyclists taking part in a six-day cycle stage race.

The former is what Shing et al. conclude based on the results of a study that involved fifteen highly trained cyclists [age: 22, years, height: 1.79, body mass: 68.69]. In the corresponding randomized, double-blind, placebo-controlled trial

• 8 of the cyclist 1000mg of bromelain per day, while
• 7 of the cyclists got a visually identical placebo supplement

which was consumed daily across six days of competitive racing. Blood was collected from each cyclist on days one, three and six of racing and analysed for creatine kinase (CK), myoglobin, lactate dehydrogenase (LDH) and testosterone.

Figure 1: Changes in CK and testosterone during the 6 days of competitive cycling (Shing. 2015).

The results of the study show significant elevations in CK activity (this protein is indicative of muscle damage), LDH activity (this protein is necessary to get rid of lactate) and myoglobin concentration in both groups. What was different, though was that the testosterone concentrations of the athletes who received the bromelain supplement tended to maintain stable, while those of the subjects in the placebo group decreased significantly over the course of the 6-day race period.

In conjunction with the perceived feeling of fatigue with was lower in the bromelain group on day four of racing (P = 0.01), the results of the study at hand to this in fact suggest that the consumption of 1,000mg of bromelain can have beneficial effects on some, albeit not directly performance relevant parameters in trained athletes.
References:

• Aiyegbusi, Ayoola I., et al. "A comparative study of the effects of bromelain and fresh pineapple juice on the early phase of healing in acute crush achilles tendon injury." Journal of medicinal food 14.4 (2011): 348-352.
• Pavan, Rajendra, Sapna Jain, and Ajay Kumar. "Properties and therapeutic application of bromelain: a review." Biotechnology research international 2012 (2012).
• Shing, Cecilia M., et al. "Acute protease supplementation effects on muscle damage and recovery across consecutive days of cycle racing." European journal of sport science ahead-of-print (2015): 1-7.

Believe it or not, but the question "low or high carb for breakfast" is non-sense, because there is no general answer. It depends on who is asking and what he is going to spend the rest of his day.

Before we can start reviewing the contemporary literature, we will have to define the term "breakfast" as the first meal in the day which is eaten in the AM. This definition differs from the "literal" one, Ive used in a previous article with the title "Circadian Rhythmicity - "Breakfast" or "Breaking the Fast"? Fasting as Zeitgeber & All About King, Prince & Pauper" (read it) and is thus in line with the mainstream idea of standing up, showering and... yes, you got it: having breakfast.

If you google "breakfast" and "obesity" youre served a colorful potpourri of "pro breakfast" articles which will inform you about "facts" like "Eating a big breakfast fights obesity and disease" (ScienceDaily), or "Breakfast Combats Obesity and Diabetes in Young People" (medscape).
Could all these "experts" be wrong? For the obedient average Joe this sounds crazy. Like one of those theories from your average Internet conspiracy theorist, but if you look at the actual evidence you have to admit:"A definitive conclusion can be made concerning the role of breakfast skipping in weight change." (McCrory. 2014)

The reasons for our cluelessness are manifold

There is for example a very good reason I anteceded this article with a definition of "breakfast". The latter is after all something you wont find in the average study, which could therefore consider eating a donut at 11am in as much as "breakfast", as it would discard having a protein shake immediately after you wake up as "not breakfast".

If we look at the actual "average Joe" (according to US National survey data), were getting into even more trouble. This guy was eating 2.76 meals in 1971–75, while he is now up to 2.96 in 1999–2002 (Kant. 2007).

In other words: Americans eat more frequently these days, but are still fatter

Obviously frequency alone doesnt tell us whether one of those "almost three" meals was actually the holy breakfast. I mean, if it wasnt its obvious the Americans became fatter and fatter - right (sarcasm)? The data we are interested in, is thus not the total number of meal (if you want to know more about that, take a look at "Many Small Meals Suck!" | go for it!). The data we are interested in is the data in Figure 1, the number of non-obedient US citizens who dont listen to the well-meant advice from the USDA and simply skip one of their holy meals.

Figure 1: Prevalence of skipping meals (breakfast, lunch, dinner) and snacking in the US, 2009–10 (McCory. 2014).

As McCorey highlights in a recent review (2014), their number rose. This seems to be a contradiction. I mean, if the number of meal skippers increases, shouldnt the number of meal (on average) decrease, when it in fact rose from 11% to 18%? Well, it should, if it was not for the snackers and grazers who either skip breakfast and snack all-day or are over-obediently grazin on 20+ small meals per day.

Figure 2: Prevalence of breakfast skipping among US men and women (USDA)

Whats interesting, is that we will find that the was a decrease in breakfast skippin from 2002 to 2009, of which I am pretty sure that it was (at least partly) mediated by headlines like the ones I quoted in the introduction to this article (USDA)

USDA shows a slight decrease in the prevalence of breakfast skippingin both men and women by about 4%. If not having breakfast was the root cause of the obesity epidemic, the average American should thus have lost a few pounds over the past decade - right?

Right! This should be the case if breakfast was the mythical "lean-maker" the "experts" want us to believe. The figures, i.e. the constantly increasing rate of obesity, dont disprove that (those who dont eat breakfast could simply gain even more weight), but they certainly put another "?" behind the statement that having breakfast has anti-obesogenic effects.

23% of males and 20% of females skip lunch!

Apropos "?", I am missing one, here! One behind the consequences of skipping lunch. With all the upheaval about skipping breakfast, people seem to have forgotten that lunch, not breakfast, was the most commonly skipped meal among most age groups in 2009–10. In most age groups, 23% of males and 20% of females are skipping this important (?) meal... and are - you bet - having an unhealthy snack later in the afternoon.
Anyway! This is the breakfast skipping research summary and no afford to dig up the two or three studies that dealt with skipping lunch explicitly. Lets thus, just for the time being, assume breakfast does in fact keep you lean. How on earth would eating some extra-food do that, when we all agree that the root cause of the obesity epidemic is after all the ravenousness of the average Westerner and the ways in which his / her diet multiplies these effects...oh, I guess the latter will lead us right to one of the answer to our question.

Proposed reasons for the anti-obesity effects of breakfast

I am not sure if I will be able to list all of them, but the following list of explanations that have been brought forward to explain the cross-sectionally observed negative association between body weight and breakfast eating is probably pretty comprehensive:

• skipping breakfast leads to lower satiety than if breakfast had been eaten, thus 
• overeating will ensue later in the day, which
• over time would result in weight gain

What? Yeah, in the end, this is all the "breakfastpromoters" have to tell you: Its an overcompensation for the energy missed at breakfast they blame the alleged fattening effects of not having breakfast on. As McCroy points out, in whats probably the most recent peer-reviewed analysis of the contemporary evidence, one could easily imagine another scenario

"in which breakfast skipping could result in no weight change over time, if breakfast skipping does not lead to overeating (i.e., if there is perfect compensation for the missed meal), or to weight loss if there is lack of compensation." (McCrory. 2014)

In his review McCory provides an enlightening overview of each of these possible scenarios, I dont want to keep from you. The“control” in this imaginary case study is a habitual breakfast eater with energy needs of 2000kcal/day, whose energy intake distribution across breakfast, lunch, snacks and dinner is 2000 kcal/day and therefore who is maintaining body weight.

Figure 3: Theoretical models illustrating different types of breakfast skippers vs. a habitual breakfast eater (McCrory. 2014).

There are potentially three types of habitual breakfast skippers: those with perfect compensation and maintain body weight, those who overcompensate and gain weight, and those who undercompensate and lose weight over time. In his consecutive review, in which McCrory considered only studies in adults (?18 years on average) and focusing primarily on experimental studies (short-term acute feeding trials or longer-term feeding trials) and longitudinal studies (prospective or retrospective, with the outcome of body weight change), the scientists from the Purdue University draws the following conclusions:

• Acute feeding studies on breakfast skipping effects on energy intake and appetite later in the day show equivocal results.
• Longer-term (2–3 weeks) randomized controlled trials do not show effects of breakfast skipping on weight change.
• In prospective studies with 3.7–10 years follow-up, individuals who consume breakfast more frequently gain less weight.

McCrory also points out that the lack of standardization is a major obstacle that makes it difficult, if not impossible to compare the results from different labs / different experimental setups.
References:

• Brown, Andrew W., Michelle M. Bohan Brown, and David B. Allison. "Belief beyond the evidence: using the proposed effect of breakfast on obesity to show 2 practices that distort scientific evidence." The American journal of clinical nutrition 98.5 (2013): 1298-1308.
• Kant, Ashima K., and Barry I. Graubard. "Secular trends in the association of socio-economic position with self-reported dietary attributes and biomarkers in the US population: National Health and Nutrition Examination Survey (NHANES) 1971–1975 to NHANES 1999–2002." Public health nutrition 10.02 (2007): 158-167.
• McCrory, Megan A. "Meal skipping and variables related to energy balance in adults: A brief review, with emphasis on the breakfast meal." Physiology & Behavior (2014).

Pancakes al cacao & your gut: Bad grains and good cacao?

There is an increasing amount of interesting scientific publications on the role of the gut microbiome in health and disease. Unfortunately, the evidence on what exactly influences the number and types of bacteria in our gut in a beneficial way and even what exactly a "beneficial way" actually is, is yet largely unknown.

In todays installment of the SuppVersity Short News, I am going to take a closer look at a selection of recent studies that may shed at least some light at the previously mentioned questions.

• Cacao as a gut microbiome modulator - The first study were going to look at deals with cacao. Cacao and its effect on the gut microbiome. In said study, 3-week-old Wistar and Brown Norway rats were fed, for 4 weeks, either a standard diet or the following three isoenergetic diets containing increasing proportions of cocoa flavonoids from different sources: one with 0·2 % polyphenols (from conventional defatted cocoa), and two others with 0·4 and 0·8 % polyphenols (from non-fermented cocoa, very rich in polyphenols).
  
  

  Only the regular theobromine containing cacao did also reduce the weight gain in the three-week study (Massot-Cladera. 2014).

  What the scientist found, when they analyzed the serum Ig concentrations, faecal IgA levels, microbiota composition and IgA-coating bacterial proportion at the end of the study and compared them to those at the beginning was a significant beneficial effect on the mucosal IgA levels and microbiota composition from all supplements. The 0.2 % cacao diet which contained a higher proportion of theobromine and fibre, however, had a more profound impact on the aforementioned parameters - in spite of the fact that there was less cacao in the diet. Obviously, the caffeine-like bitter alkaloid from cacao is contributes to the beneficial effects of cacao in a similar way as the polyphenols.
  
  As the body weight data in Figure 1 shows, the theobromine containing conventional cacao was also the only one that was able to reduce the diet induced weight gain in the rats. This could, but does not necessarily have to be related to the higher levels of Bacteroides, Bifidobacterium and Lactobacillus bacteria in the gut of the rodents that received the "cheap" conventional cacao.
• Acidic water triggers type I diabetes - probably by modulating the gut microbiome - No, I am not trying to advertise bicarbonate, here. I am just reporting the results of a recent study from the Medical University of South Carolina which found that a stain of mice thats particularly susceptible to type I diabetes developed insulitis and hyperglycemia rapidly, only when the mice were maintained on acidic pH water (AW).
  
  

  Suggested Article: "High Dietary Acid Load Doubles Risk of Type II Diabetes in Lean Individuals! Causative or Corollary? Plus: Are Grains, not Meats the Main Offenders in Our Diet?" | read more.

  The scientists also observed that this effect could be countered by fecal transplants and was obviously triggered by changes in the diversity of the gut flora that occurred, when the pH of drinking water was in the acidic range and were probably related to the proinflammatory cytokine response in the intestinal mucosa.
  
  As you as a SuppVersity reader know previous studies in humans have already shown that a "High Dietary Acid Load Doubles Risk of Type II Diabetes in Lean Individuals!" (read more) - Who knows, this could also be related to the effect on the gut microbiome!?
• Gluten and whole grains as modulators of the gut microbome - In two recent randomized cross-over trials, researchers from the University of Copenhagen determined the impact of dietary gluten or whole grains on the gut microbiome and host metabolic health.
  
  What the researchers found was what the recent backlash against gluten and "healthy" whole grains on the internet would suggest the already overweight "[p]articipants had slightly elevated fasting glucose levels and increased waist circumference" (Ibrügger. 2014).
  

  Table 1: Overview of the products used in the randomized controlled cross-over trials (Ibrügger. 2014)

  Whether thats related to the effects on the gut microbome is unfortunately something I cant tell you, yet. Why? Well, the currently available paper refers to a future publication that would outline the detailed results. All I can tell you now is that the study used the products listed in Table 1 and, more importantly, that it is its high statistical power, which, due to the large sample size and the crossover design, "allows detecting even small diffrences in the outcome variables" (Ibrügger. 2014).

References:

• Ibrügger, S., et al. "Two Randomized Cross-Over Trials Assessing the Impact of Dietary Gluten or Wholegrain on the Gut Microbiome and Host Metabolic Health." J Clin Trials 4.178 (2014): 2167-0870.
• Massot-Cladera, Malen, et al. "Impact of cocoa polyphenol extracts on the immune system and microbiota in two strains of young rats." British Journal of Nutrition 112.12 (2014): 1944-1954.
• Sofi, M. Hanief, et al. "pH of drinking water influences the composition of gut microbiome and type 1 diabetes incidence." Diabetes 63.2 (2014): 632-644.

Protein before workouts "accelerates protein catabolism"? That sounds worse than it actually is (photo BSN).

Most of you will probably consume a protein shake after their workout. Probably whey, if youve read all SuppVersity articles, maybe 25g whey + 10g casein (learn why), or something like that. But what do you do before your workouts? Do you consume a protein shake 60-90 minutes before your workout? If so, you will be shocked about the conclusion of a recent study from the Tokyo University of Agriculture which says: "[...]  pre-exercise protein supplementation taken in excess may accelerate protein catabolism" (Hasegawa. 2014).

But is it actually possible that consuming more protein (albeit at the wrong time) will have a negative impact on your gains?
Before we can answer this important question it is necessary to take a look at the actual design of the randomized cross-over study.

Figure 1: Graphical overview of the experimental protocol (Hasegawa. 2014)

The participants, six healthy male university students [21.2 (±0.3) years, 173.6 (±2.8) cm, and 62.7 (±2.8)kg] with no allergies to egg white or soy, the two protein sources the effects of which the researchers initially wanted to compare, underwent three 8-day testing periods with an exercise at the end (the 8-day intervals were separated by at least seven days).

"Each  testing period began on Day-1 and ended the meat-free diet  consisting of grains, beans, and milk, and 24- hour urine sample collection on Day-8 (Figure 1). Participants were allocated into  one of three groups; egg white protein (E), soy protein (S), and mineral water control (C) group with no additive, and all were carried out this study protocol three times, and asked not to change their lifestyle behaviors." (Hasegawa. 2014). 

The result of this study should remind you of the "Protein-Wheysting" Article | more is not always better!

On Day-5, the day of the workout, the  participants arrived at the  laboratory at 8:00 AM, and had a breakfast consisting of a rice ball (energy, 355 kcal; protein, 6.7 g; carbohydrate, 78.1 g). At 9:30 AM, after the baseline blood sample collection and perceived muscle soreness (MS) measurements, the subjects received one of the three test beverages which contained

• 20 g of egg protein,
• 20g of soy protein, or
• an isoenergetic placebo without protein

that had been dissolved in 200ml of mineral water. 90 minutes later, at 11:00 AM, the previously untrained participants started a resistance training protocol that involved seated rows, flys, leg extensions, and leg presses.

The exercises were performed for three sets of 10 repetitions at ~80% of a predetermined 1-RM with one min rest between sets and two minutes between each exercise.

Figure 2: no significant difference in perceived fatique, but a significant reduction in peak muscle soreness in the soy (grey blocks) vs. the control (white triangles) group (Hasegawa. 2014).

As you can see in Figure 2, the initially mentioned negative effects of the protein supplement were not the only significant inter-trial differences the scientists observed; and whats more, the significantly decreased muscle soreness in response to both protein powders (the peak levels differed statistically significantly only for control vs. soy) stands in stark contrast the mainstream interpretation of protein breakdown (which is "protein breakdown = muscle loss").

How is that possible? Increased protein breakdown and reduced muscle soreness?

So, here we are with an obvious contradiction between the reduced muscle soreness (Figure 2) and the scientists claim that "pre-exercise protein supplementation taken in excess may accelerate protein catabolism" (Hasegawa. 2014)... you already guessed it: The contradiction depends on the false assumption that "protein catabolism" means "catabolism of muscle protein", which is not generally the case and in this specific case certainly wrong.

Figure 3: Urinary nitrogen excretion measured for 72h after the workout (Hasegawa. 2014)

The process we are talking about here is thus most likely not an increase in "mucle catabolism" but rather about the absence of a reduction in protein wasting, i.e a "protein sparing" mechanism that wont be triggered if there is plenty of protein around during the workout.
References:

• Baty, Jacob J., et al. "The effect of a carbohydrate and protein supplement on resistance exercise performance, hormonal response, and muscle damage." The Journal of Strength & Conditioning Research 21.2 (2007): 321-329.
• Hasegawa, Yuko, et al. "Effect of Egg White Protein Supplementation Prior to Acute Resistance Training on Muscle Damage Indices in Untrained Japanese Men." Monten. J. Sports Sci. Med. 3 (2014) 2: 5–12.
• Rasmussen, Blake B., et al. "An oral essential amino acid-carbohydrate supplement enhances muscle protein anabolism after resistance exercise." Journal of Applied Physiology 88.2 (2000): 386-392.
• Wycherley, Thomas Philip, et al. "Timing of protein ingestion relative to resistance exercise training does not influence body composition, energy expenditure, glycaemic control or cardiometabolic risk factors in a hypocaloric, high protein diet in patients with type 2 diabetes." Diabetes, Obesity and Metabolism 12.12 (2010): 1097-1105.