Can excess protein be stored as body fat?

do-protein-shakes-make-you-fat

Introduction

It’s not uncommon to hear claims that dietary protein eaten in excess of some arbitrary number will be stored as body fat. Even those who are supposed to be reputable sources for nutrition information propagate this dogma. These claims however tend to drastically ignore context. While paging through one of my old nutrition textbooks, I came across a section in the protein chapter regarding amino acids and energy metabolism [1]. To quote the book directly:

“[E]ating extra protein during times of glucose and energy sufficiency generally contributes to more fat storage, not muscle growth. This is because, during times of glucose and energy excess, your body redirects the flow of amino acids away from gluconeogenesis and ATP-producing pathways and instead converts them to lipids […] The resulting lipids can subsequently be stored as body fat for later use.”

(pg. 198)

This is, more or less, supported by another textbook I own [2]:

“In times of excess energy and protein intakes coupled with adequate carbohydrate intake, the carbon skeleton of amino acids may be used to synthesize fatty acids.”

(pg. 213)

While these passages do take into account the metabolic state of the person, I still find these explanations (the first one especially) to be lacking, even borderline misleading. Indeed, more recent evidence is needed when talking about amino acid conversion to fatty acids and subsequent body fat storage. While the metabolic pathways to convert amino acids to fatty acids do in fact exist, the reality of the matter is that under almost no circumstance will this ever happen. In all honesty, I have yet to actually find a convincing scientific example where this happens. So, without much further ado, what is to follow is the long explanation as to why you shouldn’t worry about protein getting stored as body fat.

Protein digestion begins in the stomach and ends in the small intestine

While the physical breakdown of proteins does take place in the mouth, it’s not until the protein reaches the stomach that appreciable chemical breakdown occurs; this is facilitated by hydrochloric acid (HCl) and the enzyme pepsin (converted from its inactive form, pepsinogen). Once the initial protein denaturing and peptide cleaving is complete, the product polypeptides pass through the pyloric sphincter of the stomach and into the proximal small intestine.

The proximal small intestine (the duodenum to be exact) is where most of the digestion of proteins and virtually all of the absorption of amino acids occurs (a very small amount do get excreted in the feces). Here even more digestive enzymes are present to break down the remaining polypeptides into their individual amino acids along with some trace amounts of di- and tri-peptides. Once broken down completely, the free amino acids and di-/tri-peptides can then enter the cells of the small intestine where some (especially glutamine) are used for energy within the intestinal cells, with the remaining passing through into hepatic portal circulation. Those that do pass into circulation are destined for the liver.

Protein absorption claims

Before we head on over to the liver and discuss amino acid metabolism with regards to the initial claims, I would first like to touch upon another related (or variant) claim that some of you may have heard in the lay media or from an uneducated classmate, etc. It usually reads:

“The average person can only absorb 30 grams of protein at one sitting. Anything above that will be stored as fat.”

Unlike the claims in the introduction, this one offers no context whatsoever. Moreover, it’s downright moronic. And while this sounds like straw man argument readily poised for the takedown, I actually got this gem of wisdom from an online article written by a Registered Dietitian. Believe me; I couldn’t make this crap up if I wanted to (note: this is not to slander the RD profession, this is just an example which happened to involve someone who should know better).

For instance, let’s take someone who eats, dare I say it, 40 grams of protein in one sitting. If we are to assume only 30g are absorbed at a time, then it’s safe to say that the extra 10g will be excreted in the feces. If this were the case, most people would be egesting tiny sirloin steaks on a daily basis. Nevertheless, based on the initial argument, how are you supposed to store 10g of excess protein as body fat if you can’t even (allegedly) absorb it in the first place? Most people (who I can understand don’t have an advanced degree in nutrition) don’t realize the difference between utilization and absorption and make this fundamental error. I’m not quite sure what this woman’s excuse is, because in order to store or metabolize a nutrient (i.e. utilize it), it must first be absorbed into the body.

The bottom line is that your GI tract will take its sweet time absorbing protein, no matter the amount. Thirty grams is just an arbitrary number that has no roots in scientific evidence. For a more complete and in-depth review of this topic, I suggest reading a rather recent article by my friend and colleague, Alan Aragon.

At this point let us circle back to the initial claim, that excess protein, which has already been absorbed, during times of adequate energy and carbohydrate intake, is converted to fatty acids and stored as body fat.

Liver, the primary site for amino acid metabolism

As we’ve already covered, the amino acids released from the small intestine are destined for the liver. Over half of all the amino acids ingested (in the form of protein) are bound for and taken up by the liver. The liver acts almost as a monitor for absorbed amino acids and adjusts their metabolism (breakdown, synthesis, catabolism, anabolism etc.) according to the body’s metabolic state and needs [2]. It is here the initial claim comes into play. While the pathways for fatty acid synthesis from amino acids do exist, no argument there, the statement that all excess protein, under specified conditions, will be stored as fat ignores recent evidence.

[Enter one of the most tightly controlled studies of our time]

Bray GA, et al. 2012

In 2012, George A. Bray and colleagues [3] sought to examine whether the level of dietary protein affected body composition, weight gain, and/or energy expenditure in subjects randomized to one of three hypercaloric diets: low protein (5%), normal protein (15%), or high protein (25%). Once randomized, subjects were admitted to a metabolic ward and were force fed 140% (+1,000kcals/day) of their maintenance calorie needs for 8 weeks straight. Protein intakes averaged ~47g (0.68g/kg) for the low protein group and 140g (1.79g/kg) and 230g (3.0g/kg) for the normal and high protein groups, respectively.  Carbohydrate was kept constant between groups (41-42%), with dietary fat ranging from 33% in the high protein group to 44% and 52% in the normal and low protein groups, respectively. Lastly, during the course of the 8-week overfeeding period, subjects’ body composition was measured bi-weekly using dual x-ray absorptiometry (DXA; i.e. the “Gold Standard” for measuring body composition).

Results

At the end of the study, all subjects gained weight with near identical increases in body fat between the three groups (in actuality, the higher protein groups actually gained slightly less body fat than the lower protein group, however, this wasn’t significant). The group eating the low protein diet gained the least amount of weight (3.16 kg) with the normal and high protein groups gaining about twice as much weight (6.05 and 6.51 kg, respectively). See the chart below.

Bray Phillips Overfeeding ChartHowever, as you can see, the additional ~3 kg of body weight gained in the higher protein groups (15% and 25%) was due to an increase in lean body mass and not body fat. To quote the conclusions of the authors:

“Calories alone […] contributed to the increase in body fat. In contrast, protein contributed to changes in […] lean body mass, but not to the increase in body fat.”

While we can’t say for sure the exact composition of the lean mass that was gained, we can assuredly say that the extra protein was not primarily used for fat storage. My hunch is that the protein was predominantly converted to glucose (via gluconeogenesis) and stored subsequently as glycogen with the accompanying water weight. Either way, it wasn’t body fat.

Regroup

So before we continue, let’s just take a second for this sink in. These subjects were literally forced to eat ~1,000kcals more than what they needed to maintain their body weight for 8 full weeks (not an easy task for even the strong willed) and even then it was seen that the protein contributed to increases in lean body mass rather than body fat. Given the initial claim – that once energy, glucose and protein requirements are met all excess amino acids will get converted to fatty acids and stored as body fat – I find it hard to argue that those in the higher protein groups did not meet any of the aforementioned requisites. In reality, they far and away surpassed them, yet still did not gain additional body fat compared to the lower protein group. This is in stark contrast to what is traditionally thought.

In the end, however, we’re still left with the quintessential question underlying the entire concept, and that is: what is the maximal amount of protein (amino acids) that the body can effectively utilize before being converted to fatty acids and stored as body fat? Given the results of this study it appears that; this number is either way higher than three times the current RDA with concomitant hypercaloric intakes for weeks on end, or; it requires a similar overfeeding protocol drawn out over a longer period of time (i.e. greater than 8 weeks) at which point lean mass gains would most likely plateau and fat mass would accrue. Either way, both situations are highly unlikely in the general public and even those consciously trying to gain weight with higher intakes of protein and calories. Moreover, this upper extreme is likely to be highly individual and contingent upon other factors such as genetics, lifestyle, training status (if an athlete), etc. Unfortunately, we just don’t have the answers to these questions right now.

Conclusions

So, while we do biochemically possess the pathways needed to convert amino acids to fatty acids, the chances of that ever happening to a significant degree during higher protein intakes, even in the face of adequate energy and carbohydrates, are irrelevant given what we know about the extreme measures that need to be surpassed in order for any appreciable fat gain from protein to take place.

Indeed, overeating by ~1,000kcals/day for 8 weeks in combination with higher protein intakes did not amount to any additional gains in body fat compared to a lower protein, hypercaloric diet. Rather, excess protein in the face of overfeeding actually contributed to gains in lean body mass (be that what it may); quite the contrary to what textbooks and classrooms teach. In reality, the chances that excess protein contributes to body fat stores are insignificant, and arguably physically impossible under normal and/or reasonable hypercaloric conditions that most people/athletes might face on a daily basis. Only until theoretical extremes, either for protein intakes or calories or both are achieved, will there be any significant contributions to body fat from excess protein intake. This shouldn’t concern most people in the slightest.

References

1.            McGuire M, Beerman, KA.: Nutritional Sciences: From Fundamentals to Food. 2nd edn. Belmont, CA.: Wadsworth Cengage Learning; 2011.

2.            Gropper S, Smith, JL., Groff, JL.: Advanced Nutrition and Human Metabolism. 5th edn. Belmont, CA.: Wadsworth Cengage Learning; 2009.

3.            Bray GA, Smith SR, de Jonge L, Xie H, Rood J, Martin CK, Most M, Brock C, Mancuso S, Redman LM: Effect of dietary protein content on weight gain, energy expenditure, and body composition during overeating: a randomized controlled trial. JAMA 2012, 307:47-55.

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Red meat: back on the chopping block

red-meat

Introduction

In a recent article published last week in the prestigious Nature Medicine journal [1], researchers presented novel data on the pathogenesis of cardiovascular disease (CVD), arguing that it’s not the saturated fat (SFA) or cholesterol in your red meat that’s causing your arteries to clog; rather, it’s the carnitine. What’s more is that the media just can’t get enough of it. Indeed, both the New York Times and the Wall Street Journal (just to name a few) jumped on this story and put out articles with quotations from experts warning people against red meat consumption. While this type of alarmism is nothing new, especially with regards to red meat (remember last summer when red meat would just flat out kill you?), this new article is extremely interesting and does offer up a novel explanation for (part of) why red meat is constantly being associated with cardiovascular disease (CVD).

Nevertheless, in spite of the originality of this new paper and its potential implications for future health policy, we should remain critical of the paper’s content and not take giant leaps of faith in accepting new research findings as dogmatic fact (I’m looking at you vegans and vegetarians). Therefore, today’s goal is show you why you should not fear red meat, because it can, like all others foods, fit easily into anyone’s diet and impart beneficial effects on health: even heart-health!

Prevailing paradigm

It’s no news that the prevailing notion about red meat has been that its accompanying SFA and cholesterol are the primary driving forces behind the food’s association with CVD [2-5]. However, a recent meta-analysis refutes this assumption after showing no association between SFA and CVD [6]. While investigation into several other potential disease-causing mediators that commonly accompany red meat, such as salt [7] and heterocyclic compounds (you know, the char on your meat that gives it that “grill taste” you enjoy so much) [8] are proving to be less fruitful in the red meat-CVD debate – albeit salt is generating some interesting data with regards to autoimmune disease progression [9, 10] – today’s article looked at something no one had ever really considered before: carnitine.

Primer on carnitine

In order to save time, I have copied and pasted the following paragraph on carnitine from a previous article wherein I evaluated carnitine’s (null) effects on fat loss and performance. For those interested, you can see the full article here:

“Carnitine – named after the Latin word carnis, meaning ‘flesh’ – is a vitamin-like, water-soluble amine that can be obtained through dietary intake (for example: meat and milk) or by endogenous synthesis via S-adenosyl-methionine (SAM) and lysine in both the liver and kidneys. Almost all (~95-98%) of the bodily stores of carnitine are present in skeletal muscle and in the heart (with the remaining 2-5% in the liver, kidneys and plasma). Carnitine plays a pivotal role in both fat metabolism as well as carbohydrate metabolism […] Throughout most of the day (assuming you don’t sprint everywhere) the human body runs on a mixture of glucose, amino acids, and free fatty acids, with the majority of ATP coming from FFAs. However, in order to oxidize these FFAs (and yield energy in the form of ATP) each fatty acid must undergo a process called beta-oxidation. Beta-oxidation takes place within the matrix of the mitochondria of the cell. In order for the fatty acid to even make it into the matrix, it must rely on the help of carnitine to facilitate its transport in. Once inside, the fatty acids can undergo beta-oxidation and proceed to the Tricarboxylic acid (TCA) cycle and produce ATP.”

Furthermore, carnitine and its derivatives have shown huge promise in various pathological conditions, some of which happen to be to cardiovascular and heart disease [11-14]. While this may seem counterintuitive – even contradictory – to the published Nature Medicine article which argues that carnitine causes CVD, one has to remember that the physiology/biochemistry during a pathological condition is very different from that of a relatively healthy person. Indeed, the benefits of carnitine supplementation for certain cardiovascular and heart pathologies are due to the reduction in heart carnitine levels caused by the condition itself (usually the lack of oxygen to the heart, called ischemia) [13]. Therefore, it would not be wise to say that carnitine is contraindicated for those with heart disease because, in fact, supplementation with carnitine actually improves health under certain cardiovascular conditions. Like all things, nothing is ever black and white. So before I start getting ahead of myself, let’s actually examine the Nature article and see why carnitine might lead, or even (dare I say it) cause, cardiovascular and heart disease.

Biological rationale for carnitine’s role in CVD pathogenesis

The authors, in an attempt to unveil some earth-shattering mechanism for why red meat might be causing CVD, suggest that there could possibly be some type of microbe-dependent, diet-host mechanism that had previously been unexplored. In other words, perhaps the bacteria in our intestines are somehow contributing to CVD. Recent evidence in both human and animal models suggests a role for such a mechanism in a whole host of diseases, such as obesity [15-17] and type II diabetes [18]. Therefore, the idea for a similar rationale in CVD is not so farfetched.

In preliminary research, the authors identified a group of metabolites that were associated with CVD risk [19], wherein, upon further analysis, they found that the metabolite known as trimethylamine N-oxide (TMAO for short) was the primary candidate. Furthermore, the researchers also discovered that this metabolite happens to be a product of gut-dependent-choline metabolism, providing further evidence for a microbial role in CVD progression.

So how does carnitine fit into the picture? Well, carnitine is similar in structure to choline (they’re both trimethylamines) and therefore undergoes the same metabolism as choline (see figure below).

CVD pathogenesis

This in turn produces TMAO and increases plasma levels which could lead to CVD. While carnitine is present in other foods such as fish (a food commonly associated with improving CVD risk [20, 21]), the levels of carnitine are about 10-12 times higher in red meat [22]; potentially letting fish off the proverbial hook, so to speak. However, as it turns out, some types of fish are actually fairly high in TMAO [23]; lending less credence to the notion that only red meat (and not other forms of meat like fish) possibly leads to CVD.

Article findings

To keep things simple (because this article was a beast and I don’t feel like getting into every little methodological detail), I’m going to bullet point the major results. If you REALLY want to read the study, e-mail me and I’ll send it your way. The findings were as follows:

  1. Carnitine was associated with CVD
  2. Human gut microbes are required to form TMAO from carnitine
  3. Vegans and vegetarians produce much less TMAO than non-vegans, and this is primarily due to differences in gut bacteria composition
  4. A dose-dependent relationship between plasma levels of carnitine and CVD exists; however, TMAO was shown to be the driving force behind this association. Therefore, it is not the carnitine, per se, that potentially causes CVD. Rather, it’s TMAO.
  5. ApoE -/- (knockout) mice were shown to have a doubling of CVD progression when supplemented with carnitine or choline.
  6. TMAO inhibits cholesterol removal from peripheral tissues back to the liver in ApoE -/- mice. This, effectively, shifts the net balance towards cholesterol deposition and accumulation, which can progress to atherosclerosis and CVD/heart disease.

So, to briefly summarize, an association (not causation) between carnitine and CVD risk was established in humans, with subsequent rodent data to help provide the mechanistic justification as to why. However, as with all rodent data, there needs to be some reservation when trying to apply the findings to humans (Again, I’m looking at you vegans/vegetarians). ApoE -/- knockout mice have a genetic deletion that specifically causes them to develop dyslipidemia (high blood lipids) and atherosclerosis [24]. Indeed, even in the face of a regular chow, low cholesterol diet, these mice have blood cholesterol levels upwards of 400mg/dL (normal levels ~80mg/dL). This was more than sufficient to induce CVD, showing that plasma lipids do contribute to the pathogenesis of the disease. Therefore, it was shown that, in mice that already had CVD and severe dyslipidemia, a diet with supplemental carnitine exacerbated the disease; it did not cause it. Moreover, the levels of carnitine used to exacerbate the disease were beyond supraphysiological. The mice would have had to consume over 6lbs of red meat per day in order to reach the levels of carnitine they were supplemented with (~2g carnitine/day; the average cut of red meat contains ~70mg/100g [22]). This intake would be even greater for humans. Not realistic by any stretch of the imagination.

In the end, until subsequent research comes out involving more human-derived data, we just can’t translate preliminary and completely unrealistic rodent data into health policy-altering fact. Furthermore, there is substantial data in humans involving realistic intakes red meat that at least makes us think twice about red meat’s role in CVD. Indeed, this research shows actual improvements in traditional risk factors (like someone’s cholesterol levels (LDL and HDL) that do promote CVD) when beef is consumed alongside a reasonable diet (i.e. one with fruits and vegetables, etc.). While these studies do nothing to refute carnitine’s potential role in CVD progression, they do lend credence to the fact that red meat can be incorporated into a traditional heart-healthy diet which actually improves health. Whether or not carnitine/TMAO can exert their potential CVD-causing effects independent of an improved lipid profile and a realistic intake of red meat is far from established, and hard to believe. Obviously future research will need to address this concern.

Evidence to the contrary

Despite the craze after last week’s Nature Medicine article, the fact of the matter is that red meat can be incorporated into a diet that actually lowers one’s risk for CVD and heart disease, based on traditional risk factors, like total, LDL and HDL cholesterol levels. A non-exhaustive list of the research follows.

In 1994, Scott et al. [25] saw that, in free living subjects, a 5-week diet containing red meat had similar effects on lowering plasma total and LDL cholesterol when compared to a similar diet containing chicken. Five years later in 1999, Davidson and co. [26] also showed that, in free-living subjects consuming lean red meat, subjects lowered total and LDL cholesterol, as well as, raised HDL cholesterol to the same degree as those on a white meat diet. Fast forward to 2003, to quote the concluding remarks of Beauchesne-Rondeau et al. who examined the effects of beef, lean fish and poultry on lipoprotein profiles in hypercholesterolemic men (important line bolded) [27]:

[W]ith respect to [heart disease] risk, an AHA diet with a high [polyunsaturated to saturated fat ratio]  and high fiber content, regardless of the protein source, induced numerous favorable changes such as reductions in plasma total and LDL cholesterol and apo B, total and VLDL triacyl-glycerols, and total:HDL cholesterol in hypercholesterolemic men, and it overlapped the effects of protein sources on LDL apo B pre-viously observed in normocholesterolemic subjects.”

Finally, in a well-controlled study conducted last year, Roussell et al. [28] showed that, when incorporated into a well-balanced diet (again, plenty of fruits and vegetables) red meat can actually improve one’s heart health. This was evidenced by improvements in total and LDL cholesterol, as well as, plasma triglycerides. To quote the authors directly;

[These] results […] provide convincing evidence that lean beef can be included in a heart-healthy diet that meets current dietary recommendations and reduces CVD risk.”

Concluding remarks

So, even with the incorporation of red meat into someone’s diet, one can definitely improve their lipid profile and reduce their risk for CVD and heart disease, as long as that diet is sensible and contains reasonable amounts of fruits and vegetables, etc. The big thing to keep in mind is that, while new research like this may seem compelling and interesting, it’s often wrought with the media’s biased, sensationalist coverage. It’s important to keep in mind the overall context of one’s diet when evaluating the individual food constituents and their effects on someone’s health. Red meat should not be feared or vilified. Rather, it should be eaten and enjoyed, in moderation, like all other foods.

There is still a lot to be learned about carnitine and its role in CVD. As we have seen, under certain pathological conditions supplemental carnitine and its derivatives can be beneficial to patients with previous heart complications. Furthermore, it has yet to be shown why foods like fish, which have been shown to have the detrimental metabolite TMAO, are not usually associated with CVD. Lastly, I want to also point out that physical activity and life style modifications have yet to be mentioned in this discussion. Given my fitness-oriented readership, I feel the need to at least briefly mention that weight-loss and physical activity both affect the composition of one’s gut microbiota. Indeed, a couple of the strains of bacteria that were shown to be associated with carnitine metabolism in the Nature article were actually shown to be reduced in another study which observed overweight individuals who lost weight and increased their physical activity [29].

So, while the masses may buy into the media’s frenzy about red meat being evil, I’ll be firing up the grill this weekend and enjoying a nice steak.

References

1.            Koeth RA, Wang Z, Levison BS, Buffa JA, Org E, Sheehy BT, Britt EB, Fu X, Wu Y, Li L, et al: Intestinal microbiota metabolism of l-carnitine, a nutrient in red meat, promotes atherosclerosis. Nat Med 2013.

2.            Wilson PW, Kannel WB, Silbershatz H, D’Agostino RB: Clustering of metabolic factors and coronary heart disease. Arch Intern Med 1999, 159:1104-1109.

3.            Keys A: Coronary heart disease, serum cholesterol, and the diet. Acta Med Scand 1980, 207:153-160.

4.            Micha R, Wallace SK, Mozaffarian D: Red and processed meat consumption and risk of incident coronary heart disease, stroke, and diabetes mellitus: a systematic review and meta-analysis. Circulation 2010, 121:2271-2283.

5.            Bernstein AM, Sun Q, Hu FB, Stampfer MJ, Manson JE, Willett WC: Major dietary protein sources and risk of coronary heart disease in women. Circulation 2010, 122:876-883.

6.            Siri-Tarino PW, Sun Q, Hu FB, Krauss RM: Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr 2010, 91:535-546.

7.            Bibbins-Domingo K, Chertow GM, Coxson PG, Moran A, Lightwood JM, Pletcher MJ, Goldman L: Projected effect of dietary salt reductions on future cardiovascular disease. N Engl J Med 2010, 362:590-599.

8.            Hansen ES: International Commission for Protection Against Environmental Mutagens and Carcinogens. ICPEMC Working Paper 7/1/2. Shared risk factors for cancer and atherosclerosis–a review of the epidemiological evidence. Mutat Res 1990, 239:163-179.

9.            Wu C, Yosef N, Thalhamer T, Zhu C, Xiao S, Kishi Y, Regev A, Kuchroo VK: Induction of pathogenic T17 cells by inducible salt-sensing kinase SGK1. Nature 2013.

10.          Kleinewietfeld M, Manzel A, Titze J, Kvakan H, Yosef N, Linker RA, Muller DN, Hafler DA: Sodium chloride drives autoimmune disease by the induction of pathogenic T17 cells. Nature 2013.

11.          Malaguarnera M: Carnitine derivatives: clinical usefulness. Curr Opin Gastroenterol 2012, 28:166-176.

12.          Pauly DF, Pepine CJ: The role of carnitine in myocardial dysfunction. Am J Kidney Dis 2003, 41:S35-43.

13.          Mingorance C, Rodriguez-Rodriguez R, Justo ML, Alvarez de Sotomayor M, Herrera MD: Critical update for the clinical use of L-carnitine analogs in cardiometabolic disorders. Vasc Health Risk Manag 2011, 7:169-176.

14.          Serati AR, Motamedi MR, Emami S, Varedi P, Movahed MR: L-carnitine treatment in patients with mild diastolic heart failure is associated with improvement in diastolic function and symptoms. Cardiology 2010, 116:178-182.

15.          Backhed F, Manchester JK, Semenkovich CF, Gordon JI: Mechanisms underlying the resistance to diet-induced obesity in germ-free mice. Proc Natl Acad Sci U S A 2007, 104:979-984.

16.          Turnbaugh PJ, Gordon JI: The core gut microbiome, energy balance and obesity. J Physiol 2009, 587:4153-4158.

17.          Turnbaugh PJ, Hamady M, Yatsunenko T, Cantarel BL, Duncan A, Ley RE, Sogin ML, Jones WJ, Roe BA, Affourtit JP, et al: A core gut microbiome in obese and lean twins. Nature 2009, 457:480-484.

18.          Greiner T, Backhed F: Effects of the gut microbiota on obesity and glucose homeostasis. Trends Endocrinol Metab 2011, 22:117-123.

19.          Wang Z, Klipfell E, Bennett BJ, Koeth R, Levison BS, Dugar B, Feldstein AE, Britt EB, Fu X, Chung YM, et al: Gut flora metabolism of phosphatidylcholine promotes cardiovascular disease. Nature 2011, 472:57-63.

20.          He K, Song Y, Daviglus ML, Liu K, Van Horn L, Dyer AR, Greenland P: Accumulated evidence on fish consumption and coronary heart disease mortality: a meta-analysis of cohort studies. Circulation 2004, 109:2705-2711.

21.          Whelton SP, He J, Whelton PK, Muntner P: Meta-analysis of observational studies on fish intake and coronary heart disease. Am J Cardiol 2004, 93:1119-1123.

22.          Rigault C, Mazue F, Bernard A, Demarquoy J, Le Borgne F: Changes in l-carnitine content of fish and meat during domestic cooking. Meat Sci 2008, 78:331-335.

23.          Yancey PH: Organic osmolytes as compatible, metabolic and counteracting cytoprotectants in high osmolarity and other stresses. J Exp Biol 2005, 208:2819-2830.

24.          Pendse AA, Arbones-Mainar JM, Johnson LA, Altenburg MK, Maeda N: Apolipoprotein E knock-out and knock-in mice: atherosclerosis, metabolic syndrome, and beyond. J Lipid Res 2009, 50 Suppl:S178-182.

25.          Scott LW, Dunn JK, Pownall HJ, Brauchi DJ, McMann MC, Herd JA, Harris KB, Savell JW, Cross HR, Gotto AM, Jr.: Effects of beef and chicken consumption on plasma lipid levels in hypercholesterolemic men. Arch Intern Med 1994, 154:1261-1267.

26.          Davidson MH, Hunninghake D, Maki KC, Kwiterovich PO, Jr., Kafonek S: Comparison of the effects of lean red meat vs lean white meat on serum lipid levels among free-living persons with hypercholesterolemia: a long-term, randomized clinical trial. Arch Intern Med 1999, 159:1331-1338.

27.          Beauchesne-Rondeau E, Gascon A, Bergeron J, Jacques H: Plasma lipids and lipoproteins in hypercholesterolemic men fed a lipid-lowering diet containing lean beef, lean fish, or poultry. Am J Clin Nutr 2003, 77:587-593.

28.          Roussell MA, Hill AM, Gaugler TL, West SG, Heuvel JP, Alaupovic P, Gillies PJ, Kris-Etherton PM: Beef in an Optimal Lean Diet study: effects on lipids, lipoproteins, and apolipoproteins. Am J Clin Nutr 2012, 95:9-16.

29.          Santacruz A, Marcos A, Warnberg J, Marti A, Martin-Matillas M, Campoy C, Moreno LA, Veiga O, Redondo-Figuero C, Garagorri JM, et al: Interplay between weight loss and gut microbiota composition in overweight adolescents. Obesity (Silver Spring) 2009, 17:1906-1915.

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Protein supplementation and resistance training: worthwhile or worthless? – ARTICLE REVIEW

200010255-001

Muscle performance, size, and safety responses after eight weeks of resistance training and protein supplementation: a randomized, double-blinded, placebo-controlled clinical trial

Walter AA, Herda TJ, Costa PB, Ryan ED, Stout JR, Cramer JT.

Journal of Strength and Conditioning Research 2013, 25 February [Epub ahead of print]

PubMed: http://www.ncbi.nlm.nih.gov/pubmed/23442287

ABSTRACT: The purpose of this study was to examine the effects of two different types of protein supplementation on thigh muscle cross-sectional area, blood markers, muscular strength, endurance, and body composition after eight weeks of low- or moderate-volume resistance training in healthy, recreationally trained, college-aged men. One hundred and six men were randomized into five groups: low-volume resistance training with bio-enhanced whey protein (BWPLV; n=22), moderate-volume resistance training with BWP (BWPMV; n=20), moderate-volume resistance training with standard whey protein (SWPMV; n=22), moderate-volume resistance training with a placebo (PLA; n=21), or moderate-volume resistance training with no supplementation (CON; n=21). Except for CON, all groups consumed one shake before and after each exercise session and one each non-training day. The BWPLV, BWPMV, and SWPMV groups received approximately 20g of whey protein per shake, while the BWP groups received 5g additional polyethylene glycosylated (PEG) leucine. Resistance training sessions were performed three times per week for eight weeks. There were no interactions (p>0.05) for muscle strength and endurance variables, body composition, muscle cross-sectional area, and safety blood markers, but main effects for training were observed (p≤0.05). However, Albumin:Globulin ratio for SWPMV was lower (p=0.037) than BWPLV and BWPMV. Relative protein intake (PROREL) indicated a significant interaction (p<0.001) with no differences across groups at pre, however, BWPLV, BWPMV, and SWPMV had a greater intake than PLA or CON at post (p<0.001). The present study indicated that eight weeks of resistance training improved muscle performance and size similarly among groups regardless of supplementation.

Opening Comments

It’s common practice for many strength athletes and bodybuilders to consume protein supplements around and even during training. This practice is more or less supported by a growing body of literature over the past 10-15 years that suggests the ingestion of protein both before and after weight training for the purposes of maximizing muscle gain [1, 2]. Today’s article adds to the ever-growing compendium of research on protein supplementation, its safety, and its purported beneficial effects on body composition, muscular hypertrophy, strength, and endurance when added to a structured resistance training (RT) program. This study is conceptually novel in that it also tries to address the issue of optimal training volume alongside supplementation for RT gains.

With regards to protein supplement safety, the researchers site some weak data supporting a possible contraindication for supplement usage [3-5]. For those of you who have been following me for the past year know that I have already covered this topic before (i.e. the safety of higher protein diets). For those of you who are newcomers, I suggest you read my thorough examination of higher protein diets from last July. While my article doesn’t address protein supplementation, per se, it does address the majority of safety concerns of higher protein diets on a myriad of health topics. That being said, higher protein intakes are completely harmless unless you already have some preexisting kidney condition. For today, I will limit my analysis to the findings on protein supplementation, protein type, and its effects on body composition, muscular hypertrophy, strength and endurance. I will also briefly touch upon some of the observations on training volume and its effects on strength and muscle size given that it too is a hot topic in exercise science research.

In the end, the researchers saw no difference between the three supplement groups or between the supplement groups and the placebo (PLA)/control (CON) groups on improvements in body composition, muscle hypertrophy, strength or endurance. Moreover, they did not see any difference between training volumes on any of the muscular outcomes (i.e. they all got stronger and gained muscle to a similar degree in spite of overall training volume as well as supplement status). It can also be inferred from the study that protein timing, that is, consuming protein immediately after training (as was seen in the intervention groups) offered no further benefit over consuming protein – if at all – at some later point in time (as can be inferred by the lack of immediate protein ingestion after training for the PLA and CON groups). This, however, was not a primary goal of the study and will not be a point of focus in today’s review. Nevertheless, for those interested in the topic of nutrient timing, I would suggest accessing a recent, well-written comprehensive review by friend and colleague, Alan Aragon along with exercise science stud, Brad Schoenfled [6].

Moreover, despite what we already know about higher protein diets and their safety (ala my previous coverage), I should note that the researchers saw no adverse health outcomes (as assessed by various blood bio-markers) associated with the introduction of protein supplementation in conjunction with RT. Go figure.

As I’ve already alluded to, the authors wrap up their discussion by stating that, regardless of supplementation status and training volume, all groups showed significant improvements in all muscular outcomes. They also go on to suggest that lower training volume alongside protein supplementation may promote similar outcomes as training with higher volume; something that may be of interest to athletes who are recovering from an injury. I will respond to their conclusions later.

Study strengths

This study’s strengths include its rather large sample size (n=106), randomization, the blinding of subjects and researchers, study duration (8-weeks), and concept. In addition, supplementation adherence was tightly regulated, with subjects consuming the protein and PLA supplement in the lab, under the observation of the researchers, 30-minutes before, as well as, immediately following the RT bout. On non-training days, the treatment and PLA subjects were advised to consume 1 packet of the supplement in the morning, in the same manner as they had done in the lab. They were also instructed to return the empty packets in order to ensure compliance (which was, on avg., about 95%). I should also note that the supplementation dosage of 20g of whey protein is highly supported in the literature [2, 7, 8], with estimates ranging from 20-30g of high quality protein as being the “sweet spot,” as it were, for muscle protein synthesis (MPS). The additional leucine (5g) in the “bio-enhanced” groups seems like an exercise in idiocy more than anything else. Despite leucine being the primary dietary stimulus for MPS [9, 10], to my knowledge there is no strong data supporting the addition of leucine to an already adequate amount of protein for the enhancement of MPS. In fact, there is compelling data to the contrary [11, 12]. Either way, each group was receiving an adequate bolus of protein following training.

Three-day dietary recalls were also used to evaluate the diets between the groups, although no additional dietary instructions were given to the subjects besides to continue their usual dietary habits. Body composition was measured via hydrostatic weighing (aka underwater weighing), once considered the “Gold Standard” for body composition measurements. Despite more accurate methods out there (most notably DEXA and MRI), there are more error-prone methods (BOPPOD, BIA, skinfolds) that could make this study much worse. Muscle cross-sectional area (CSA) was also ascertained – albeit by a quite novel method that I was unaware of, called peripheral quantitative computerized tomography (pQCT). Based on the literature, pQCT is primarily used for supplemental measurements of bone mineral density alongside DEXA, although it has been recently validated for measurements of muscle CSA and proves to be quite reliable [13].

Study limitations

Unfortunately, the study’s limitations far outweigh its strengths. Firstly, despite the authors’ attempt at recruiting “recreationally trained males,” they fall short of eliminating “newbie” gains that may mask any effects of supplementation. For example, it was reported that half of the subjects participated in about 4 hours of aerobic exercise per week, while less than half of the subjects reported participating in about 3 hours of weightlifting per week. Anyone who is familiar with weight lifting knows that these subjects are neither athletes nor intermediate to advanced lifters. At the very best they’re entry-level beginners (more like untrained weightlifters), something even the authors saliently note in their discussion:

“Since the sample in the present study consisted of untrained or recreationally-trained healthy young men, it is possible that the profound effects of the resistance training alone… may overshadow any additional, smaller benefits of whey protein supplementation.”

Therefore, given the training status – or lack thereof – of the subjects, any results can only be applied to healthy, young, untrained and/or entry-level weightlifters. This is contrary to how the authors try to extrapolate their findings with regards to recommendations for athletes (tisk tisk).

Another disparaging limitation of the study was the failure to control for dietary/protein intakes. Case in point, failing to control for overall protein intakes led to a wide range of intakes between the groups (0.69-2.86g/kg bodyweight), with the PLA and CON groups leaning more towards the lower end of the range (0.69-1.96g/kg) and the supplement groups comprising the upper end (1.04-2.86g/kg). Nevertheless, given the subject’s baseline weights (ballpark avg. of 78kg or ~172lbs), the supplement groups were taking anywhere from ~80-225g of protein and the PLA and CON groups were slightly worse off with intakes ranging from 53-152g/day. So in other words, the researchers were looking at a clusterf***k of overlapping protein intakes, ranging from terrible to more-than-adequate, both inter- and intra-group-wise. Basically, some subjects that were receiving the supplement were getting less protein per day than some subjects not receiving the supplement at all. This could be another reason why no differences were seen between supplement and non-supplement groups.

Comments & Conclusions

Given the totality of information from the present study, most notably the untrained status of the subjects and the failure to control for protein intakes, we just can’t conclude that protein supplementation is worthless in the context of a sufficient, high-quality protein diet along with a structured RT program for intermediate to highly trained athletes/weightlifters. Probably the closest thing we have to an answer is a recent meta-analysis looking at protein supplementation and increases in muscle accretion and strength in a wide range of lifting populations [14]. In the end, however, protein supplementation’s beneficial effects may only apply to those hitting the lower end (1.2g/kg) of the recommended protein intake for strength/power athletes. This, however, probably has more to do with increasing overall intake rather than supplementation, per se.

In regards to protein type, I’m also not quite sure what the researchers were hoping to find by using leucine-enriched whey as the secondary supplement. The subjects were already receiving a bolus of whey protein which is to be considered adequate for muscle protein synthesis. Indeed, in 2009, Moore et al. [7] found that muscle protein synthesis displayed a dose response relationship to dietary protein ingestion, topping out at around 20g, while multiple studies by Koopman et al. have shown no benefit of additional supplemental free leucine when a sufficient amount of casein-hydrolysate was ingested post-workout [11, 12]. So, despite hopes of seeing differences in protein type, the results were doomed from the start. Instead, I would like to have seen a whole food source or something else vs. whey that might be of real-life significance and applicability. My hunch, however, is that it won’t matter in the long run as long as the whole food source is of high-quality protein (i.e. high in leucine and EAAs). This may be of some concern to those who are vegetarian and tend to be lacking in high-quality protein sources. In this case, whey would be a great addition to cover all their bases.

As far as training volume and strength/hypertrophy is concerned, it would be presumptuous to argue that, based on this study, increased training volume has little to no benefit on muscular outcomes when compared to fewer sets and therefore lower overall volume. In probably the most well-controlled study of its kind, Marshall et al. reported greater increases in 1RM strength on the squat in an 8-set/exercise group compared to a 1-set/exercise and 4-set/exercise group after 10 weeks of squat training [15]. What’s even more compelling about this study is that the 8-set/exercise group started out stronger than the 1-set and 4-set/exercise group yet still increased their 1RM by MORE than the 1-set and 4-set group. Let that sink in for a second… Despite being stronger from the start, the 8-set group got stronger, relatively, than the people who started out weaker. Usually, those who are weaker and less trained have the most to gain and, relatively, gain more strength than those who are already strong to begin with. In addition, only the 8-set group got significantly stronger in the squat after 3 weeks, showing an immediate effect of volume on strength gains. This has implications for those athletes trying to get stronger within a finite period of time. Either way, a growing body of evidence suggests that if you want to get bigger and stronger, you should increase your volume (i.e. do more sets) [16-21].

In the end, this study tells us nothing that we don’t already know; put novice trainees on a structured RT program and they’ll get bigger and stronger and improve their body composition. Shocker! Unfortunately, a poor research design made this study virtually useless to examine the practical effects of protein supplementation on muscular outcomes in athletes and weightlifters. Nevertheless, regardless of this study, logic dictates that protein supplementation will never be necessary in the face of already sufficient protein intakes (assuming there is an emphasis on high quality proteins, rich in leucine and EAAs); an assumption this is supported by a recent meta-analysis [14].

As it stands, current recommendations for protein intake for strength and power athletes range from 1.2-2.2g/kg of bodyweight [22-26]. Furthermore, in a well-written review by Kevin Tipton and Robert Wolfe [22], the authors note that protein intakes as high as 3.0g/kg aren’t harmful and may even be of some benefit to the athlete, while a more recent study showed that, in Korean bodybuilders, habitual intakes of ~4.3g/kg had no adverse health effects [27]. Nevertheless, regardless of overall intake, the most salient point Tipton and Wolfe make, and one that I happen to agree with above all else, is that, as long as protein intake doesn’t hinder the intake of other macronutrients (carbs/fats), there’s no reason not to consume higher amounts of protein (even up to 3-4g/kg although this is not necessary by any stretch) given that there is no inherent harm, even at the more “extreme” intakes. So, in the end, if you’re already taking in adequate, or even more than adequate amounts of protein on daily basis, without extra protein supplements, don’t waste your money. I am unaware of any studies comparing chronic whole food vs. protein powder consumption in conjunction with a training regimen.

Moral of the story: if you find that whey protein (or whatever powder you choose) is easier and more convenient than firing up the grill or slaving over a hot stove pre- and post-workout, than by all means, hit the powder. Personally, I enjoy the taste and love portability of whey protein powder (just shake and drink). Preferences aside, the key thing to remember is that there is nothing magical about protein supplementation, despite what the supplement companies are telling you. As of now, all it is is a way to further augment your total dietary protein intake, which, in the end, is all that matters.

To quote my friend and colleague, Alan Aragon:

“If this daily target [read: total] is achieved with both whole foods and supplements, then great – but supplementation should not be viewed as necessary or optimal.”

References

1. Cermak NM, Res PT, de Groot LCPGM, et al. Protein supplementation augments the adaptive response of skeletal muscle to resistance-type exercise training: a meta-analysis. Am J Clin Nutr. 2012;96(6):1454-64.

2. The science of muscle hypertrophy: making dietary protein count. Proc Nutr Soc. 2011;70:100-103.

3. Brenner BM, Meyer TW, Hostetter TH. Dietary protein intake and the progressive nature of kidney disease: the role of hemdynamically mediated glomerular injury in the pathogenesis of progressive glomerular sclerosis in aging, renal ablation, and intrinsic renal disease. NEJM 1982;307:652-659.

4. Martin WF, Armstrong LE, Rodriguez NR. Dietary protein intake and renal function. Nutr. Metab. (Lond) 2005;2:25.

5. Metges CC, Barth CA. Metabolic consequences of a high dietary-protein intake in adulthood: assessment of the available evidence. J Nutr. 2000;130:886-889.

6. Aragon AA, Schoenfeld BJ. Nutrient timing revisited: is there a post-exercise anabolic window? JISSN 2013;10(1):5.

7. Moore DR, Robinson MJ, Fry JL, et al. Ingested protein dose response of muscle and albumin protein synthesis after resistance exercise in young men. Am J Clin Nutr. 2009;89:161-8.

8. Symons TB, Sheffield-Moore M, Wolfe RR, Paddon-Jones D. A moderate serving of high-quality protein maximally stimulates skeletal muscle protein synthesis in young and elderly subjects. J Am Diet Assoc. 2009;109:1582-1586.

9. Stipanuk MH. Leucine and protein synthesis: mTOR and beyond. Nutr Revs. 2007;65(3):122-129.

10. Drummond MJ, Rasmussen BB. Leucine-enriched nutrients and the regulation of mammalian target of rapamycin signaling and human skeletal muscle protein synthesis. Curr Opin Clin Nutr Metab Care 2008;11(3):222-6.

11. Koopman R, Wegenmakers AJM, Manders RJF, et al. Combined ingestion of protein and free leucine with carbohydrate increases postexercise muscle protein synthesis in vivo in male subjects. Am J Physiol Endocrinol Metab. 2005;288(4):E645-53.

12. Koopman R, Verdijk L, Beelen M, et al. Co-ingestion of leucine with protein does not further augment post-exercise muscle protein synthesis rates in elderly men. Br J Nutr. 2008;99(3):571-80.

13. Cramer T, Palmer IJ, Ryan ED, et al. Validity and reliability of a peripheral quantitative computed tomography scanner for measuring muscle cross-sectional area. Med Sci Sports Exerc. 2007;39:S225-S226.

14. Cermak NM, Res PT, de Groot LC, et al. Protein-supplementation augments the adaptive response of skeletal muscle to resistance-type exercise  training: a meta-analysis. Am J Clin Nutr. 2012;96(6):1454-64.

15. Marshall PWM, McEwan M, Robbins DW. Strength and neuromuscular adaptation following one, four, and eight sets of high intensity resistance exercise in trained males. Eur J Appl Physiol. 2011;111:3007-3016.

16. Rhea MR, Alvar BA, Burkett LN, et al. A meta-analysis to determine the dose response for strength development. Med Sci Sports Exerc. 2003;35(3):456-464.

17. Peterson MD, Rhea MR, Alvar BA. Maximizing strength development in athletes: a meta-analysis to determine the dose-response relationship. J Strength Cond Res. 2004;18(2):377-382.

18. Wolfe BL, LeMura LM, Cole PJ. Quantitative analysis of the single- vs. multiple-set programs in resistance training. J Strength Cond Res. 2004;18(1):35-47.

19. Krieger JW. Single versus multiple sets of resistance exercise: a meta-regression. J Strength Cond Res. 2009;23(6):1890-1901.

20. Krieger JW. Single vs. multiple sets of resistance exercise for muscle hypertrophy: a meta-analysis. J Strength Cond Res. 2010;24(4):1150-1159.

21. Wernbom M, Augustsson J, Thomeé R. The influence of frequency, intensity, volume and mode of strength training on whole muscle cross-sectional area in humans. Sports Med. 2007;37(3):225-64.

22. Tipton KD, Wolfe RR. Protein and amino acids for athletes. J Sports Sci. 2004;22(1):65-79.

23. Wilson J, Wilson GJ. Contemporary issues in protein requirements and consumption for resistance trained athletes. JISSN 2006;3:7-27.

24. Rodriguez NR, DiMarco NM, Langley S, et al. Position stand of the American Dietetic Association, Dietitians of Canada, and the American College of Sports Medicine: nutrition and athletic performance. JADA 2009;109(3):509-27.

25. Kreider RB, Campbell B. Protein for exercise and recovery. Phys Sportsmed. 2009;37(2):13-21.

26. Campbell B, et al. International Society of Sports Nutrition position stand: protein and exercise. JISSN 2007;4:8.

27. Kim H, Lee S, Choue R. Metabolic responses to high protein diet in Korean elite bodybuilders with high-intensity resistance exercise. JISSN 2011;8:10.

Posted in Reviews | 9 Comments

Stoking the metabolic fire: does higher meal frequency increase metabolism and enhance fat loss?

Stoking the fire

Introduction

It has been a long-held belief in bodybuilding and health/fitness circles that eating more frequently throughout the day leads to an increase in metabolic rate and fat-loss. This is colloquially coined, “stoking the metabolic fire.”  In fact, this very concept has been disproved about 15 years ago [1], and still remains accurate to this day, with the most recent research showing no differences in 24hr energy expenditure, respiratory quotient (RQ), or fat oxidation [2]. For those of you who are less attuned to the popular bodybuilding and fitness dogma that I just mentioned, it usually goes something like this:

Gym-goer: “I want to lose weight. What’s the best way to go about doing so?”

Trainer: “Well, first off, you need to eat at least 6 meals per day, spaced 2-3 hours apart. That will ignite the metabolic furnace and enhance fat loss.”

It is here that the person recommending such strict, dogmatic claims shows his lack of knowledge in basic human physiology and biochemistry, not to mention a complete lack of respect for the person’s personal preferences when it comes to dieting.

Breaking it down

There are essentially four factors that affect a person’s overall energy expenditure throughout the course of a day (24EE). Those factors are basal metabolic rate (BMR; also termed resting metabolic rate [RMR]), diet induced thermogenesis of food (DIT; also known as the thermic effect of food [TEF]), exercise thermogenesis (EEx), and spontaneous movement, termed non-exercise activity thermogenesis (NEAT). Mathematically it looks something like this:

24EE = BMR + TEF + EEx + NEAT

Now, if increasing meal frequency in fact does lead to an increase in metabolic rate and fat loss, through whatever means, it would have to affect one of the above factors. Obviously increasing meal frequency will not directly alter EEx or NEAT, so we can cross those off the list immediately, leaving us with BMR and TEF as potential modifiable factors.

Let’s take a step back

However, before we analyze the two remaining variables, let’s consider what energy actually is and what food provides in the context of the body deriving energy from it and using it. Simply put, energy is the capacity to do work. It can neither be created nor destroyed; only transformed. This work can be biological (cellular function, transport of ions, etc.), chemical (breaking or building of bonds between atoms), mechanical (muscle contraction), osmotic, or electrical. Food is essentially potential energy that, when ingested, is oxidized and yields ATP for us to do work. It can also be stored (as glycogen, triacylglyceride, and muscle protein [although not a “true” storage form]) and subsequently “freed” during times when food is not present in order to provide us with an endogenous, readily available fuel source. So the question remains; does a simple manipulation of food intake (frequency of ingesting potential energy) promote a beneficial effect on energy expenditure (our ability to use that food to do work) so that we burn more calories, specifically those derived from our fat stores?

Basal metabolic rate (BMR)

The primary driving force behind 24EE, given that your EEx isn’t through the roof, is fat-free mass (FFM) [3]. Taking this one step further, FFM is the primary driving force behind BMR [4]. Therefore, a majority of the energy expended over the course of a day is dictated by BMR (i.e. how much FFM someone has). Knowing this, how can increasing meal frequency alter someone’s BMR? Plain and simple, it can’t. If anything it would have to indirectly increase BMR through increases in FFM, but this is irrelevant given that there is no indication that eating smaller more frequent meals increases FFM to a greater extent than does eating an isocaloric diet with fewer, larger meals; period. In a related vein, there is some equivocal research suggesting increases in BMR and TEF following exercise [5, 6]. However, most of the research was done in previously untrained men and women. So if anything, the increase in an athletic individual is likely to be negligible at best.  So now all we are left with is the thermic effect of food.

Thermic effect of food (TEF)

Quite simply, TEF is averaged out to ~10% of someone’s total caloric intake. So, if a given person ingests 3,000kcals over the course of the day, ~300kcals will be lost as heat through obligatory processes like absorption, digestion, and storage [3]. Also, as a point of interest, there has been some early research showing that obese individuals actually have reduced values of TEF (i.e. <10%), possibly increasing their risk for weight gain [7].

Nevertheless, will increasing meal frequency have any effect on TEF? Again, the answer is no [8]. In fact, in the acute studies showing non-significant increases in TEF based on meal frequency, it was shown that lower meal frequencies actually yielded the higher values of TEF [1, 9]. This is diametrically opposite of what many bodybuilders and fitness enthusiasts believe! Bottom line: increasing meal frequency doesn’t affect TEF to any significant degree.

Other factors to consider with meal frequency

From a practical standpoint, increasing meal frequency is a great way to increase an athlete’s caloric intake or possibly reducing a dieter’s feelings of hunger on a hypocaloric diet. Furthermore, there is research to suggest that the body anticipates meals based on fixed feeding patterns [10]. This is manifested in ghrelin (a hormone that causes sensations of hunger) signaling the brain that you are hungry because it is ‘expecting’ a meal. Therefore, those who might be considering dropping the number of meals they eat per day may experience an initial increase in hunger due to the ‘entrainment’ of ghrelin on your previous feeding pattern. This will eventually subside after the body adapts your new feeding routine.

Summary

In closing, there is no strong evidence to suggest an increase in metabolic rate and body fat oxidation by way of increased meal frequency. So whether you eat three times per day or six or more, the effects on metabolism will essentially be the same. As I mentioned before, BMR is dictated by FFM and TEF is essentially unchanged by when you eat your meals. Therefore, the only two logical modifiable factors when it comes to meal frequency are essentially non-modifiable to any significant degree. On the other side of the coin, things to consider when it comes to meal frequency are increased feelings of hunger with fewer meals during a hypocaloric diet and the possible increase in feelings of hunger with a shift in feeding pattern (from higher frequency to lower). Nevertheless, at the end of the day it comes down to personal preference and the person’s individual fitness/performance goals. If you find that eating more frequently throughout the day is tedious and difficult to follow, perhaps fewer, larger meals may be the way to go. There is no difference.

References

1. Bellisle F, McDevitt R, Prentice AM. Meal frequency and energy balance. Brit J Nutr. 1997;77(Suppl. 1):S57-S70.

2. Ohkawara K, Cornier M, Kohrt WM, Melanson EL. Effects of increased meal frequency on fat oxidation and perceived hunger. Obesity 2012. Epub ahead of print.

3. Ravussin E, Bogardus C. A brief overview of human energy metabolism and its relationship to essential obesity. Am J Clin Nutr. 1992;55:242S-5S.

4. Bogardus C, Lillioja S, Ravussin E, et al. Familial dependence of the resting metabolic rate. NEJM 1986;315(2):96-100.

5. Osterberg KL, Melby CL. Effect of acute resistance on postexercise oxygen consumption and metabolic rate in young women. Int J Sport Nutr Exerc Metab. 2000;10(1):71-81.

6. Sharhag-Rosenberger F, et al. Effects of one year aerobic endurance training on resting metabolic rate and exercise fat oxidation in previously untrained men and women. Metabolic endurance training. Int J Sports Med. 2010;31(7):498-504.

7. Schutz Y, Bessard T, Jéquier E. Exercise and postprandial thermogenesis in obese women before and after weight loss. Am J Clin Nutr. 1987;45:1424-32.

8. Taylor MA, Garrow JS. Compared with nibbling, neither gorging nor a morning fast affect short-term energy balance in obese patients in a chamber calorimeter. Int J Obes Relat Metab Disord. 2001;25(4):519-28.

9. Munsters MJ, Saris WH. Effects of meal frequency on metabolic profiles and substrate partitioning in lean healthy males. PLOS One 2012;7(6):e38362.

10. Frecka JM, Mattes RD. Possible entrainment of ghrelin to habitual meal patterns in humans. Am J Physiol Gastrointest Liver Physiol. 2008;294:G699-G707.

Posted in Diets | Tagged , , | 10 Comments

An objective look at L-carnitine supplementation for fat-loss and enhanced performance

Pill

Opening Comments

Over the past 25-plus years carnitine has received a lot of attention, both from researchers and supplement companies alike. Indeed, both camps are interested in carnitine’s role in fat metabolism; however, it is for two very different reasons. Researchers are primarily interested in the ergogenic capacity that carnitine may have to offer endurance athletes – namely carnitine’s glycogen sparing effect via increased fat oxidation – while supplement companies (and consumers) are mostly interested in carnitine for increased fat oxidation to enhance fat-loss and improve body composition. Being the skeptic that I am, today I will evaluate both sides of the aisle and make some final comments and conclusions about whether or not it’s practical to take carnitine supplements, be it for performance purposes or weight loss endeavors. As always, I will begin with some background information (with a little biochemistry thrown in there), follow it up with the pertinent research, and then end with some closing remarks and applications. Let’s get to it!

Rationale behind carnitine supplementation to improve performance

Before I actually get into the potential benefits of carnitine supplementation, I think it would be best to first cover the rationale behind taking carnitine for performance. In doing so, I will try to keep this as short as possible.

It has been well established that the body can use both carbohydrate and fat (in the form of free fatty acids) for muscular contraction [1]. However, the latter only remains true at low to moderate intensities. Indeed, as exercise intensity is increased (>75-85% VO2 max), the proportion of fat that is and can be used to fuel muscle contraction is decreased – if not completely inhibited – such that carbohydrate oxidation increases (see figure below) [2].

FFA ox

However, as moderate to intense exercise continues (as in a marathon or other endurance-type events) the reliance on FFAs is increased due to lowered glycogen stores and therefore less available glucose to fuel muscle contraction. This is important, because during the final leg of a race, runners, cyclists, etc. tend to speed up and may even sprint to the finish line. This would require additional glucose to fuel the high-intensity (>75% VO2 max) sprint. Depleting ones glycogen stores prior to the final stretch of the race could hinder the racer’s finish and (potentially) placement. It is from this paradigm that the theory of fat adaptation came about. Fat adaptation-ists believe that if one can shift their metabolism during moderate intensity exercise to exclusively rely on FFAs, then that person could potentially conserve glycogen stores for when they are needed most, like during the final stretch of a race (>75% VO2 max). Many dietary manipulations have been undertaken in order to help aid in this adaptation, however I will not cover those here as another entire article could be written on the subject. Rather, we will look at how carnitine may be able to facilitate this need (i.e. increase fat oxidation and spare glycogen) by first looking at some basic biochemistry behind fat metabolism (and thus carnitine’s role therein) that will lay the foundation for our discussion on whether or not carnitine can be used as an effective ergogenic and/or fat-loss aid.

Fat metabolism and carnitine’s role therein   

When talking about fat metabolism, it is important to note that there are various control points at which fat metabolism (in skeletal muscle) can be regulated. A recent review by Lawrence Spriet [3] eloquently states that fat metabolism can be regulated during exercise at six different ‘control points,’ one of which is FFA transport across the mitochondrial membrane (think back to high school biology class). It is at this point that carnitine is almost exclusively involved and where I will pick up the conversation.

Carnitine – named after the Latin word carnis, meaning ‘flesh’ – is a vitamin-like, water-soluble amine that can be obtained through dietary intake (for example: meat and milk) or by endogenous synthesis via S-adenosyl-methionine (SAM) and lysine in both the liver and kidneys. Almost all (~95-98%) of the bodily stores of carnitine are present in skeletal muscle and in the heart (with the remaining 2-5% in the liver, kidneys and plasma). Carnitine plays a pivotal role in both fat metabolism as well as carbohydrate metabolism (the latter I will briefly mention when needed) [4]. Throughout most of the day (assuming you don’t sprint everywhere) the human body runs on a mixture of glucose, amino acids, and free fatty acids, with the majority of ATP coming from FFAs. However, in order to oxidize these FFAs (and yield energy in the form of ATP) each fatty acid must undergo a process called beta-oxidation. Beta-oxidation takes place within the matrix of the mitochondria of the cell. In order for the fatty acid to even make it into the matrix, it must rely on the help of carnitine to facilitate its transport in. Once inside, the fatty acids can undergo beta-oxidation and proceed to the Tricarboxylic acid (TCA) cycle and produce ATP.

It is at this point that I would like to stop and regroup. The above paragraph is extremely important because it really lays out the basis (theoretically) for carnitine improving both performance and body composition. This however, operates under a couple of assumptions: 1) that carnitine translocation is the rate limiting step in fatty acid oxidation, meaning that; 2) increasing carnitine levels will equate to greater transport of fatty acids into the matrix and greater levels of oxidation; and lastly that, 3) you can indeed increase muscle levels of carnitine in the first place. Granted that all three of these factors are true, than yes, there may be a reasonable case for carnitine supplementation. The real question here is whether or not they hold up under scientific scrutiny.

Research against carnitine supplementation

Above, we just saw that carnitine helps “ship” FFAs into the mitochondria so that they can be oxidized to produce ATP. Therefore, potentially having more carnitine may mean more FFA oxidation and therefore a “sparing effect” on muscle glycogen stores which may lead to increased performance. Indeed, muscle carnitine levels decrease as exercise intensity increases [3]. It would make sense that low muscle carnitine levels would therefore lead to a decrease in FFA usage, given that this effect does hold true under high intensities. However, and counter intuitively, the highest FFA oxidation rates actually occur when carnitine levels are well below resting levels [3]. Furthermore, when fat availability in the blood is artificially increased during exercise (at 80% VO2 max), with no concomitant increases in carnitine, the muscle does indeed oxidize more fat [5]. This suggests that carnitine isn’t the rate limiting step during fat metabolism. Therefore, theoretically increasing muscle carnitine levels may not even amount to further increases in fat oxidation given that maximal rates are already being achieved with reduced levels of muscle carnitine and that artificially high levels of FFA are easily handled in the absence of additional carnitine as it is. Lastly, and most importantly, increasing muscular levels of carnitine has been shown time and time again to be quite futile.

In 1994, Barnett and colleagues showed that 14 days of carnitine supplementation (at 4g/day) did not significantly affect muscle levels of carnitine [6]. Similarly, in the same year, Vukovich et al. investigated the effects of carnitine supplementation on muscle carnitine concentrations and glycogen content during submaximal exercise [7]. Here, subjects ingested 6g/day of carnitine and still did not show any increases in muscular levels of carnitine. And if two weeks isn’t long enough to convince you, Wächter and co. [8] gave subjects 4g of carnitine per day for three months and still saw no increase in muscle levels of carnitine. Moreover, had you even thought about hooking up your at-home IV kit and mainlining your carnitine, you’d still be wasting your time as direct infusion has been shown to be unsuccessful [9, 10]. What’s more is that performance parameters such as perceived exertion, exercise performance, VO2 max, or markers of muscle substrate such as RER, VO2, blood lactate levels, leg FFA turnover, and post-exercise muscle glycogen content were all unaffected by the ingestion of 2-5g of carnitine per day (anywhere from one week up to three months) [11]. Thus, the majority of relevant data looking at the oral ingestion and infusion of carnitine has failed to increase muscular levels leading to a lack of improved performance. Therefore, if we still buy into the hypothesis that fat metabolism can be increased via an increase in muscle levels of carnitine we are sadly left with the realization that this is just not possible. Or is it…

Research supporting carnitine supplementation

Although we just saw that the vast majority of research shows that carnitine supplementation (of up to 3 months) has very little impact – if any – on muscle levels of carnitine, it doesn’t leave out the fact there are some studies that do show an impact of oral ingestion and infusion of carnitine on muscle concentrations. First we will examine the infusion studies.

Effective means of carnitine infusion

As noted earlier, straight infusion of carnitine has little impact on muscle levels of carnitine [9, 10]. However, infusion of carnitine alongside an infusion of insulin actually does have an impact on muscle levels [10]. What researchers saw was ~15% increase in muscle levels of carnitine. Although significant, this is not truly representative of the population taking carnitine because I don’t know about you, but I’m not willing to start injecting myself with physiologically high levels of insulin just to increase my muscle carnitine stores. Nevertheless, for those of you who may be considering this option, there may be an easier way.

Effective means of oral carnitine ingestion  

Indeed, it has been shown that oral ingestion of carnitine, alongside a rather large dose of carbohydrate (~80-94g), is able to effectively stimulate the “uptake” of carnitine as measured indirectly via plasma levels and urinary excretion [12, 13]. This is undoubtedly due to carbohydrates’ insulin stimulatory effect. Although 80-94g of carbohydrate is not unusual for a bodybuilder or weightlifter to consume in one sitting in the offseason or even in the earlier stages of dieting, the dosage may come into conflict during the later stages of prep (when carbs are being reduced) or for those who have lower CHO requirements by default (like the average American). Therefore, some practical limitations may come into play, especially when it means eating relatively high amounts of carbohydrate in order to gain what may be a trivial fat-burning effect from carnitine. What’s more is that although muscle levels of carnitine were indirectly seen to increase, there was absolutely no measure of improved body composition during the studies. However, what they did see was a reduction in glycogen breakdown at low intensity exercise (50% VO2 max), but this was effectively eliminated at intensities around 80% VO2 max. Either way, this does not reveal any convincing evidence that carnitine is a potent fat-burner or ergogenic aid even though major shifts in fuel metabolism can be seen; essentially showing a greater reliance on FFAs as a fuel source. These findings, nevertheless, are limited to conjectures about fat-loss in the long-term and are confounded by methodological issues that do not apply to the normal bodybuilder/fitness population or the endurance athlete – or anyone for that matter.

Conclusions

Although it may be physically possible to increase muscle levels of carnitine using relatively large amounts of carbohydrate repeatedly throughout the day, the fact still remains that there is limited convincing data that shows that carnitine is a potent fat-burner or ergogenic aid. Furthermore, when practical limitations come into play, the usefulness of carnitine as a fat-burner is undoubtedly overshadowed by the well-known effects of a solid caloric deficit in combination with increased physical activity (usually in the form of cardio). I should also note that carnitine has been implicated in aiding recovery from resistance exercise in both young and middle-aged populations [14-16] as well as increasing androgen receptor (AR) synthesis and therefore increasing cellular uptake up testosterone following weight training. This potentially leads to the activation various muscle synthetic pathways [17]. However, despite the potential beneficial basis of carnitine supplementation for muscle recovery and hypertrophy there just isn’t enough convincing data that shows supplemental carnitine will do jack-diddly in terms of sizeable gains in muscle mass accretion. We just don’t have the long-term studies necessary to make that conclusion. Conversely, there is some convincing evidence that transient elevations in anabolic hormones (due to exercise) such as testosterone and growth hormone are not closely associated with increases in muscle mass [18-20]. Therefore, increasing AR synthesis and testosterone uptake may be trivial in the larger scope of things.

The bottom line is that the beneficial role of carnitine for either exercise (be it endurance or resistance) or fat burning in young, healthy populations (especially the athlete) are, at this stage, completely theoretical and, most likely, trivial at best.

References

1. Asmussen E. Muscle metabolism during exercise in man. A historical survey; in Pernow B, Saltin B (eds): Muscle Metabolism during Exercise. New York, Plenum Press, 1971, pp. 1-11.

2. van Loon LJ, Greenhaff PL, Constantin-Teodosiu D, Saris WH, Wagenmakers AJ. The effects of increasing exercise intensity on muscle fuel utilisation in humans. J Physiol. 2001;536(Pt. 1):295-304.

3. Spriet LL. Metabolic regulation of fat use during exercise and recovery. Nestlé Nutr Inst Workshop Ser. 2011;69:39-53;discussion 53-8.

4. Constantin-Teodosiu D, Carlin JI, Cederblad G, Harris RC, Hultman E. Acetyl group accumulation and pyruvate dehydrogenase activity in human muscle during incremental exercise. Acta Physiol Scand. 1991;143:367-372.

5. Romjin JA, Coyle EF, Sidossis LS, et al. Relationship between fatty acid delivery and fatty acid oxidation during strenuous exercise. J Appl Physiol. 1995;79:1939-1945.

6. Barnett C, Costill DL, Vukovich MD, Cole KJ, Goodpaster BH, Trappe SW, Fink WJ. Effect of L-carnitine supplementation on muscle and blood carnitine content and lactate accumulation during high-intensity sprint cycling. Int J Sport Nutr. 1994;4(3):280-8.

7. Vukovich MD, Costill DL, Fink WJ. Carnitine supplementation: effect on muscle carnitine and glycogen content during exercise. Med Sci Sports Exerc. 1994;26(9):1122-9.

8. Wächter S, Vogt M, Kreis R, Boesch C, Bigler P, Hoppeler H, Krähenbühl S. Long-term administration of L-carnitine to humans: effect on skeletal muscle carnitine content and physical performance. Clin Chim Acta. 2002;318(1-2):51-61.

9. Brass EP, Hoppel CL, Hiatt WR. Effect of intravenous L-carnitine on carnitine homeostasis and fuel metabolism during exercise in humans. Clin Pharmacol Ther. 1994;55(6):681-92.

10. Stephens FB, Constantin-Teodosiu D, Laithwaithe D, Simpson EJ, Greenhaff PL. Insulin stimulates L-carnitine accumulation in human skeletal muscle. FASEB J. 2006; 20:377-379.

11. Stephens FB, Constantin-Teodosiu D, Greenhaff PL. New insights concerning the role of carnitine in the regulation of fuel metabolism in skeletal muscle. J Physiol. 2007;581(2):431-444.

12. Wall BT, et al. Chronic oral ingestion of L-carnitine and carbohydrate increases muscle carnitine content and alters muscle fuel metabolism during exercise in humans. J Physiol. 2011;589(4):963-973.

13. Stephens FB, Evans CE, Constantin-Teodosiu D, Greenhaff PL. Carbohydrate ingestion augments L-carnitine retention in humans. J Appl Physiol.. 2007;102:1065-1070.

14. Volek JS, Kraemer WJ, Rubin MR, et al. L-carnitine L-tartrate supplementation favorably affects markers of recovery from exercise stress. Am J Physiol Endocrinol Metab. 2002;282:E474-E482.

15. Kraemer WJ, Volek JS, French DN, et al. The effects of L-carnitine L-tartrate supplementation on hormonal responses to resistance exercise and recovery. J Strength Cond Res. 2003;17(3):455-62.

16. Ho JY, Kraemer WJ, Volek JS, et al. L-carnitine L-tartrate supplementation favorably effects biochemical markers of recovery and from physical exertion in middle-aged men and women. Metabolism 2010;58(8):1190-9.

17. Kraemer WJ, Spiering BA, Volek JS, et al. Androgenic responses to resistance exercise: effects of feeding and L-carnitine. Med Sci Sports Exerc. 2006;38(7):1288-96.

18. West DW, Phillips SM. Anabolic processes in human skeletal muscle: restoring the identities of growth hormone and testosterone. Phys Sportsmed. 2010;38(3):97-104.

19. West DW, Phillips SM. Associations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort after weight training. Eur J Apply Physiol. 2012;112:2693-2702.

20. West DW, Burd NA, Staples AW, Phillips SM. Human exercise-mediated skeletal muscle hypertrophy in an intrinsic process. Int J Biochem Cell Biol. 2010;42:1371-1375.

Posted in Reviews, Supplements | 9 Comments

Protein and muscle gain: Are we closer to an optimal dosing strategy? – REVIEW

Daytime pattern of post-exercise protein intake affects whole-body protein turnover in resistance-trained males.

Moore DR, Areta J, Coffey VG, Stellingwerf T, Phillips SM, Burke LM, Cleroux M, Godin JP, Hawley JA.

Nutrition & Metabolism 2012, 16;9(1):91 [Epub ahead of print]

PubMed: http://www.ncbi.nlm.nih.gov/pubmed

Background

The pattern of protein intake following exercise may impact whole-body protein turnover and net protein retention. We determined the effects of protein feeding strategies on protein metabolism in resistance-trained young men.

Methods

Participants were randomly assigned to ingest either 80g of whey protein as 8x10g every 1.5h (PULSE; n=8), 4x20g every 3h (intermediate, INT; n=7), or 2x40g every 6hr (BOLUS; n=8) after an acute bout of bilateral knee extension exercise (4×10 repetitions at 80% maximal strength). Whole-body protein turnover (Q), synthesis (S), breakdown (B), and net balance (NB) were measured throughout 12h of recovery by a bolus ingestion of [15N]glycine with urinary [15N]ammonia enrichment as the collected end-product.

Results

PULSE Q rates were greater than BOLUS (~19%, P<0.05) with a trend towards being greater than INT (~9%, P=0.08). Rates of S were 32% and 19% greater and rates of B were 51% and 57% greater for PULSE as compared to INT and BOLUS, respectively (P<0.05), with no difference between INT and BOLUS. There were no statistical differences in NB between groups (P=0.23); however, magnitude-based inferential statistics revealed likely small (mean effect +/-90%CI; 0.59+/-0.87) and moderate (0.80+/-0.91) increases in NB for PULSE and INT compared to BOLUS and possible small increase (0.42+/-1.00) for INT vs. PULSE.

Conclusions

We conclude that the pattern of ingested protein, and not only the total daily amount, can impact whole-body protein metabolism. Individuals aiming for maximize NB would likely benefit from repeated ingestion of moderate amounts of protein (~20g) at regular intervals (~3h) throughout the day.

Opening Comments

Today’s topic is likely going to gin up strong sentiment from both sides of the meal-frequency aisle when it comes to eating protein and gaining muscle. Indeed, the article above fires a clear shot across the bow at those consuming meals in the lower-frequency-range and thus fewer protein feedings (i.e. potential anabolic muscle-building events) throughout the day. It the literature it has been proposed that multiple (~3-4) protein feedings throughout the day are required in order to optimally gain muscle [1]. For most, this is not an issue given that multiple protein-rich meals are consumed in order to hit daily caloric needs anyway. However, in the past 5-10 years, a new take on dieting has emerged that – at the very least – makes us reconsider how lean mass is gained/preserved. I am of course referring to Intermittent Fasting (IF), a dieting protocol wherein participants fast for a majority of the day (~16-20hrs), complete their workout, and then consume anywhere from 1-3 meals within a short window of time (~4-8hrs on average).

Fewer protein feedings for attenuating muscle loss

Despite its recent surge in popularity, the scientific data behind IF is preliminary at best and includes data that closely characterizes people eating in the lower range of meal frequency (2 meals spread throughout the day) for weight loss as opposed to actual IF protocols (eating within a designated window post-workout). Nevertheless, the data does support at least equal benefits in terms of muscle retention during weight loss/maintenance when consuming fewer, and thus larger protein meals compared to smaller, more frequent ones [2-6]. Moreover, there may even be a slight advantage to doing so under maintenance conditions [4], although any advantages seen in body composition were verified using BIA rather than more accurate measures such as DEXA or MRI. I should also note that most studies were conducted in the absence of a structured training program. All areas for future study!

Optimal protein dosing strategy for muscle gain

On the other side of the coin, research looking at lower meal frequencies (read: fewer protein feedings) compared to higher meal frequencies and subsequent muscle gain have never really been conducted. To my knowledge, the study above is the first one of its kind to look at varying isonitrogenous diets in terms of dosing strategy and whole-body protein balance while not under hypocaloric conditions. Indeed, last month, a 6-week trial did look at varying isonitrogenous diets in terms of dosing strategy on body composition (and therefore muscle mass retention), but did so under hypocaloric conditions and noticed that both groups lost an equal amount of muscle tissue and body fat as measured by DEXA [6]. Unfortunately this does not get us closer to an ‘optimal dosing strategy’ for protein and muscle gain.

So, coming back to today’s study, there are some hefty limitations that do warrant a healthy dose of skepticism and criticism before we go jumping to conclusions about protein dosing and muscle gain. So without further ado, let’s dive right in!

Study strengths

The biggest strength of this study is its innovativeness, as it is – to my knowledge – the first study to look at varying isonitrogenous diets in terms of dosing strategy on whole-body protein retention in humans devoid of a caloric deficit. Other strengths include using resistance-trained males (eliminates “newbie” bias), controlling dietary intake 72h prior to testing (effectively standardizing all the participants), and instructing participants not to engage in any physical activity 72h before testing. I should note that the use of a DEXA to assess body composition was made. However, given the brevity of the study (12h), and no follow-up body composition measures, I see this as neither a strength nor a weakness.

Study limitations

The most glaringly obvious weakness is the acute nature of the study (12h in duration). Any relevant/practical conclusions about smaller, more frequent protein feedings as being optimal for muscle gain are completely speculative and will need longer-term trials in order to verify. Secondly, total protein intakes were 80g over the course of the study period (~0.9g/kg); an intake significantly less than what most trainees consume on a daily basis, and an intake that can be argued to be insufficient for optimal muscle gain [1].

Lastly, the researcher’s use of ammonia end-product to assess whole-body protein balance does not directly measure muscle protein synthesis (MPS); the one factor most people are concerned about when talking about protein ingestion following resistance training. To this end, the authors do cite the limitations of using whole-body tracer methodologies. To quote them;

A limitation of [this methodology] is the inability to delineate tissue-specific changes in protein metabolism.”

Indeed, a much better methodology would have been stable isotope infusion in conjunction with muscle biopsy so that actual MPS could be quantified and analyzed; not just net whole-body retention. Therefore, because they did not use stable isotope infusion, nor did they follow up with biopsy or subsequent body comp measures such as DEXA or MRI, we are left to speculate the true effects of protein dosing strategy on MPS and body composition. Truthfully, all we are left with is data using a poor surrogate for tissue specific muscle gain under insufficient dietary protein intakes.

Conclusions

Given the multitude of limitations contained within the study above, we just can’t say for sure that smaller, more frequent protein feedings are optimal for muscle protein accretion. To be blunt, it wasn’t truly looked at! In reality, all we know is that there was no significant difference between each protocol on whole-body protein balance over a 12h period (although a slight edge was seen in the 20gx4 group). Nevertheless, the overall effect speaks more to the importance of hitting total daily protein intake rather than focusing on dosing strategy when it comes to achieving an anabolic state. Moreover, had optimal protein intakes been achieved (i.e. >0.9g/kg and more in the range of 1.2-1.7g/kg), I believe that any differences – as slight as they were above – would effectively be negated.

So, where does this leave us? What is the take-home message? In a recent article by Alan Aragon on the lower threshold of meal frequency for optimizing muscle gain [7], Alan makes some practical recommendations (that I happen to agree with), based on the evidence to-date. To quote, Alan;

I would error on the safe side and go with three protein-rich meals as an ‘optimal minimum frequency’ for anabolism. It strikes a compromise between conservative practicality [and] exploiting the hypotheticals.”

For now we know that reducing meal frequency, and thus protein feedings, is more than effective when it comes to attenuating muscle loss during weight loss, as long as dietary protein is sufficient. However, we are still in the dark when it comes to optimal meal frequency, and thus protein feedings, when it comes to increasing muscle mass. The study above by no means opens the door to revealing this answer but rather puts it fingers on the handle so that we may start to investigate further. In the end, as long as you are hitting your daily goal of protein intake, I see no need to fret over dosing strategy. On the whole, most people who care about increasing muscle mass are already eating multiple protein-rich meals per day. If this sounds like you, then you are already ahead of the game.

References

1. Phillips SM, van Loon LJ. Dietary protein for athletes: from requirements to optimum adaptation. J Sports Sci. 2011;29(Suppl 1):S29-38.

2. Arnal MA, Masoni L, Boirie Y, et al. Protein pulse feeding improves protein retention in elderly women. Am J Clin Nutr. 1999;69(6):1202-8.

3. Arnal MA, Masoni L, Boirie Y, et al. Protein feeding pattern does not affect protein retention in young women. J Nutr. 2000;130(7):1700-4.

4. Stote KS, et al. A controlled trial of reduced meal frequency without caloric restriction in healthy, normal-weight, middle-aged adults. Am J Clin Nutr. 2007;85(4):981-8.

5. Soeters MR, et al. Intermittent fasting does not affect whole-body glucose, lipid, or protein metabolism. Am J Clin Nutr. 2009;90(5):1244-51.

6. Adechian S, Balage S, Remond D, et al. Protein feeding patter, casein feeding, or milk-soluble protein feeding did not change the evolution of body composition during a short-term weight loss program. Am J Physiol Endocrinol Metab. 2012;303(8):E973-82.

7. Aragon A. What’s the lower threshold of meal frequency for optimizing muscle gain? AARR 2012 May;2-5.

Posted in Protein, Reviews | Tagged , , , | 1 Comment

Sodas and Childhood Obesity – ARTICLE REVIEW

A Trial of Sugar-free or Sugar-sweetened Beverages and Body Weight in Children

Janne C. de Ruyter, Margreet R. Olthof, Jacob C. Seidell, and Martijn B. Katan

NEJM September 21, 2012

Full Text: http://www.nejm.org/doi/pdf/10.1056/NEJMoa1203034

Background

The consumption of beverages that contain sugar is associated with overweight, possibly because liquid sugars do not lead to a sense of satiety, so the consumption of other foods in not reduced. However, data are lacking to show that the replacement of sugar-containing beverages with noncaloric beverages diminishes weight gain.

Methods

We conducted an 18-month trial involving 641 primarily normal-weight children from 4 years 10 months to 11 years 11 months of age. Participants were randomly assigned to receive 250ml (8oz.) per day of sugar-free, artificially sweetened beverage (sugar-free group) or a similar sugar-containing beverage that provided 104kcal (sugar group). Beverages were distributed through schools. At 18 months, 26% of the children had stopped consuming the beverages; the data from children who did not complete the study were imputed.

Results

The z score for the body-mass index (BMI, the weight in kilograms divided by the square of the height in meters) increased on average by 0.02 SD units in the sugar-free group and by 0.15 SD units in the sugar group; the 95% confidence interval (CI) of the difference was -0.21 to -0.05. Weight increased 6.35kg in the sugar-free group as compared with 7.37kg in the sugar group (95% CI for the difference -1.54 to -0.48). The skin-fold thickness measurements, waist-to-height ratio, and fat mass also increased significantly less in the sugar-free group. Adverse events were minor. When we combined measurements at 18 months in 136 children who had discontinued the study with those in the 477 who completed the study, the BMI z score increased by 0.06 SD units in the sugar-free group and 0.12 SD units in the sugar group (P=0.06).

Conclusions

Masked replacement of sugar-containing beverages with noncaloric beverages reduced weight gain and fat accumulation in normal-weight children.

 

Opening comments

Today’s article has a high likelihood of being taken way out of context – something that is not allowed here. Some may argue that this article tries to answer one of the most pressing questions of the 21st century, and that is, “what is the cause of childhood obesity?” However, this article does not due certain methodological weaknesses leaving us wanting for more. Instead, the article shows us exactly what we’ve known all along, and that is, when you eat fewer calories, you gain either less weight or no weight at all. In today’s article, we’re talking about the former. So without further ado, I will show you why this article doesn’t prove that sodas cause obesity before it gets taken way out of context on every news channel around… because it most certainly will.

Introduction & Results

The article begins with acknowledging the concomitant rise in both sugary beverage consumption and obesity in children. The authors postulate this correlation is due to soda’s inability to compensate for calories at subsequent meals – a topic I covered thoroughly back in April. Indeed, the literature to-date suggests that liquid calories do not have the same effect on satiety that solid foods do. Therefore, sodas may promote increased food intake (or lack of calorie displacement) by virtue of sugar’s vehicle (liquid medium) rather than the sugar itself. However, none of this was evaluated in today’s study.

Lastly, the authors note the lack of convincing evidence suggesting sodas’ causational role in obesity due to other collinear factors such as fast food consumption (which usually coincides with soda consumption) and lack of physical activity (or as they put it, increased television watching). Therefore, they sought to examine the effect of replacing soda with a masked, calorie-free soda substitute on weight gain (further adding to the lack of causational data).

In the end, both groups (those who drank the sugar-sweetened soda and those who drank the diet soda) gained weight and fat mass (as expected given their age). However, the group receiving the sugar-sweetened soda gained more weight (16lbs vs. 14lbs) and more fat mass than the sugar-free group (3.5lbs vs. 2.3lbs).

Study Strengths

Strengths of the study include double-blind randomization of participants, an 18 month study duration, large sample size (n = 477), and urinary sucralose measures to assess the sugar-free group’s adherence to the intervention. Other strengths include custom-made sodas which were designed to taste identical (this eliminates subject bias) and teachers’ reminders and physical watching of the children consuming the beverages in school (ensures adherence).

Study Weaknesses

Unfortunately, the study is filled with more weaknesses than strengths. First and foremost, there was no mention of diet or physical activity of any of the 477 participants who completed the study. Secondly, 26% of participants dropped out for unspecified reasons. Thirdly, skinfold measurements and BIA were used to assess body composition, both of which are highly prone to human error. Now don’t get me wrong, I am not naïve enough to think that all 477 kids could have been DXA’d. However, a subset of participants could have been analyzed using DXA to confirm skinfold and BIA measurements. Lastly and most importantly, assuming that the two groups’ diets were identical at baseline, the addition – or in this case the subtraction – of one soda per day (104 kcal) for 18 months resulted in the sugar group potentially receiving over 56,000 kcals MORE than the sugar-free group. All this proves is that if you consume more calories, you gain more weight. WOW, huge shocker there!

Comments and conclusions

It’s not surprising that the sugar-free group gained less weight than their sugary counterparts; the researchers theoretically removed over 56,000 calories from the sugar-free group’s diet over an 18 month period! Furthermore, suspicions of increased food intake caused by soda intake were never even evaluated. In order for that to happen there needed to be some form of assessment of diet over the 18 month period. This, however, was mistakenly left out. On the bright side, this study does lend some credence to efforts to reduce soda intake in children, despite showing no causational effects of soda on obesity whatsoever. Remember, sodas are an easy and readily available source of nutrient-poor calories; that is all. Sodas don’t cause obesity more so than does an extra equi-caloric serving of brown rice each day. If you want to enjoy that can of soda you have to remember to eat less of other things throughout the day (whether or not this is possible in free-living populations is the TRUE question and one that was nowhere close to being answered in this study). Therefore, although the aim was to examine the effects of replacing a chronically consumed sugar-sweetened soda with a diet alternative on weight gain, I would suspect similar findings with ANY food source being substituted with a calorie-free alternative.

Bottom-line: consume fewer calories; you’ll gain less weight if you do.

Posted in Reviews | 2 Comments