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 | 7 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 , , | 6 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 | 4 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

Roundtable Interview with Layne Norton PhD, Eric Helms and Alan Aragon

Introduction

Before I begin I just want to take a minute to thank (for the thousandth time) Layne, Eric and Alan for humbly doing this e-mail interview with me. For those of you who don’t know who these men are, you can skip to the end of the interview (for their website links below) and get educated. For the rest of you, introductions are not necessary. In short, I cannot thank them enough for taking the time to answer my questions. I specifically chose to ask the questions that I did because I noticed that every interview these guys do they pretty much answer the same damn questions over and over. To be quite honest, I find it a waste of their time, and mine, to hear the same responses repeated… and repeated… and repeated. Hopefully you will find today’s interview a little more substantive, meaningful, and fun.

In conclusion, each one of these gentlemen has had a profound impact on me and my life, in more ways than one, and without them I can honestly say that I would not have pursued a degree in nutrition nor would I have had the courage to ever start up Calories in Context; and for that, I can never thank them enough. So, before I get too carried away (because I could write an entire article on how these guys have impacted me), I hope you all enjoy what Layne, Eric and Alan had to say as much as I did. So without further ado, let’s get to it!

Me: What spurred your interest in nutrition/fitness and inevitably made you want to study it in college (be it undergraduate/graduate/doctoral)?

Alan: I think anyone in his right mind has an innate obsession with carbohydrate, protein, and fat :) …  Just kidding, sort of. I originally was a graphic design major in college. Back when I first got into training and nutrition in the late 80′s and early 90′s, personal training wasn’t considered a real job yet, so I was advised against pursuing a fitness-related degree. At a certain point I said, ‘Screw this, I need to go after what I’m genuinely interested in.’ I was torn between going into exercise science or nutrition, but since, at the time, my ambition was to be a trainer, I figured that my certifications would cover the exercise side, so I went for the nutrition degree. I ended up getting my graduate degree in nutrition as sort of an afterthought, but I ended up really enjoying the process of writing and teaching. The rest is bro-history.

Plenty of my colleagues tell me that I should get a doctorate, but I can’t be more satisfied with my current career trajectory, so fixing what ain’t broke isn’t really an option. There was a time that everyone encouraged me to become an RD [Registered Dietitian], but I didn’t feel the strong impetus to do so; same with getting a PhD. Thus far, it hasn’t been a career handicap in the slightest.

Eric: I fell in love, head over heels, absolutely obsessed with bodybuilding, lifting and getting stronger. I tend to get consumed by things I’m passionate about. So really it was hard to see anything else for me as a potential study topic as nothing else held my interest and intrigue in the same way.

Layne: For me it was pretty simple. I started lifting weights in high school to get more attention from girls and try to stop bullies from picking on me. Over time lifting transformed from something I did out of lack of self-esteem to something I did because I loved it. As I read more and more about training and nutrition I realized that there was a huge gap in the advice that every expert in a magazine recommended. I would read one article that said to do one thing, then read another contradicting it. So I decided to start researching for myself. That turned into a passion for research over time.

Me: What aspect(s) about yourself has/have made you as successful as you are today? In essence, what separates you from everyone else out there?

Alan: This is a tremendously tough question to answer. I’m not sure, so I’m just gonna’ ramble. I think part of my success is a result of being as real and honest as possible whenever I try to convey ideas. I’ve been told that I’m good at taking complex information and distilling it into concrete terms that most people can understand. That, plus I’m skeptical as hell, since most information pumped out in this industry is purely crap. I have an impressive list of clients, but a lot of other guys have that too. I guess none of those would separate me from everyone else. So, I really don’t know…

One thing I noticed that might separate me is that I know how to laugh at shit; too many people at the top of their fields are far too wrapped up in appearing polished or being politically correct. It stiffens them up, and their real colors and personality never show, and they end up unnoticed among the hordes of people trying to make names for themselves.  People also tend to be too wrapped up in preserving a god-like aura. We’re all just humans, so we shouldn’t take ourselves so damn seriously every minute we’re in the public eye. One thing I learned early on in the game is that it’s okay to be wrong about stuff, and that it’s actually a sign of diligence and integrity to adjust your position on any given topic depending on how the evidence evolves.

Eric: First of all, I really don’t think I’m separate from everyone else out there. Sure, I’m unique, I’m me. There is only one me, but there is only one everyone for that matter. But, I get what you are trying to ask: “why is it you are interviewing me, why isn’t someone else a relatively well-known name in this field?”

For me, I think it comes down to being genuine. I’m not trying to sell something, I’m not trying to push anything, and I don’t have an agenda. I just want to share my passion and help people. That, coinciding with a relatively extroverted personality and a very dedicated and focused approach to bodybuilding and powerlifting and the science related to it, has put me where I’m at. I also think having grown up immersed in online forums and the internet helped me transfer my information and “get myself out there” during the boom of social media with less of a struggle than some others who might have been less comfortable with this medium.

Layne: To be quite frank, I feel like I just want it more than many other people and worked my butt off over a long period of time.  Even before I was well known in the industry, I would spend tons of time each day answering 60-70 emails from people, asking for nothing in return.  I spent hours each day on bodybuilding forums answering questions and giving out free advice.  I would write articles for free for any website or magazine that would print them.  I was willing to do whatever I possibly could to get my philosophies out there.  On top of that I was taking full time classes, doing research, and of course lifting every day.  But I loved it, so it never felt like work.  But I have always said that I feel like success is a battle of attrition.  Everyone gets discouraged at various points and wants to quit, the difference is who can keep going and putting one foot in front of the other when those rough patches hit.  Anyone can be motivated when things are going well.  What separates people is who can stay motivated when everything is going to crap.

Me: Why do you think people enjoy the information that you put out? What makes it hit home for them? 

Alan: I kind of live a dual life in terms of the information I put out. On one side, I write for various lay publications, where getting all freaky and technical isn’t really gonna’ help anyone. On the other hand, in my monthly research review, I can really slam folks with jargon and complexity when the topic lends itself, knowing that the readership will be familiar with the terms and concepts. I think that it’s important to be sensitive and in-tune with the audience, and this audience varies in my case. I was just on a call today with one of the senior editors of Men’s Health who is putting a story together on various fitness/nutrition myths. I was asked whether or not people “need” a post-exercise shake, like it’s often pushed in the fitness and bodybuilding magazines. I proceeded to explain that there is a continuum of importance for these sorts of tactics, and the vast majority of Men’s Health readers will reap all the benefit they could possibly need by simply nailing their protein target for the day. The rest is just nitpicking toward what might hypothetically clinch that extremely narrow edge, which might be important for elite competitors, but not relevant to weekend warriors.

Eric: You know to be honest, I couldn’t say. I just do my thing. There are billions of people on the planet, and I figure that there are enough people out there that can relate to me that I really don’t have to “do” anything or be anyone besides myself.  I’ve always found that when you are honest, genuine and real, most people can relate to you. And if they have coinciding interests, they are open to what you have to say.

Layne: Probably because I don’t try to BS people with magic tricks.  Anyone who follows me on twitter knows I hate ‘guruism.’ (Term coined by Bret Contreras).  Guruism is when people make up outlandish BS to try to sell people that they have some magic secret that will give people the key to unlocking unbelievable results.  That’s complete crap.  80-90% of this stuff is hard work and dedication.  You can have a terrible approach, but if you work really hard over a really long period of time you will get results. However, this doesn’t mean that they are optimal.  I’m the first to tell people that there are no secrets.  Certainly there are small tweaks to be made to try to optimize things, but if you are looking for some magic ‘secret’, sorry, I don’t have it. 

Me: Where do you see the field of nutrition/exercise science heading in the next 10 years?

Alan: I see it all going to hell in a hand-basket… Hah! Seriously though, I’m excited for what’s to come as research marches on, bringing us closer and closer to understanding how to either simplify or modify training or dietary protocols for the better. The field itself has gradually gained legitimacy (I’m talking about training in particular), and organizations such as the NSCA & NASM have really put their necks out and made strong efforts to raise the barriers toward being considered worthy of being a practitioner in the field. An interesting thing I’ve noticed – but saw coming for quite some time – is the growing interest in solidifying a nutrition certification for those who aren’t interested in standard/traditional collegiate routes governed by the ADA (recently changed to the AND). I think that as much of an eyesore as they may be to the old guard of dietetics administration, newer organizations such as the ISSN are really going to make some deep inroads into the traditional model, as they continue to capture the interest (& preference) of fitness professionals seeking to bolster their credibility in nutritional knowledge.

In general, I see continued growth of the allied health and fitness fields. This is always going to be a double-edged sword, since the fitness field attracts nutcakes and quacks like bees to honey, but at least the nutjobs give me plenty to write about in the spirit of protecting the public from false information.  My hope is that the allied health and fitness professions place a continued emphasis on research-based guidelines, and also an emphasis on critical thinking. I’m not sure if the latter will ever happen to a satisfactory degree, but we can always hope.

Eric: I think the internet becoming more and more involved is a good thing in many ways. It adds speed, transparency and ease of collaboration. I can write a paper with someone I’ve never physically met. I can hook up with a professor at a university on the other side of the planet and discuss research. My thoughts and ideas are open to the criticism of everyone with an internet connection. So I think information will become higher quality slowly but surely through better collaboration and because there will be more people to check the t’s and dot the i’s.

Layne: I honestly am very excited about it.  For decades researchers were just viewed as lab junkies; people who were knowledgeable but had no clue how to apply it.  But right now I know dozens of competitive bodybuilders, lifters, and enthusiasts doing their PhDs or advanced degrees in a relevant field.  I think that the merging of research and practical application is going to provide a lot of the answers we have been searching for.

Me: Similarly, where do you see yourself in the next 10 years?

Alan: If all goes as planned, I see myself doing exactly what I’m doing now. Perhaps the only change would be more volunteer outreaches to younger folks (high school and early college) where I can talk about what it takes to succeed, and how important it is to find out what it is that interests them so they can make a great life of it. It kills me to know that so many students think they have to fit into a conventional/socially expected career mold whether they hate it or not.

Eric: In ten years, I know one thing is for sure. I’ll be happy, pursuing my goals and making awesome human connections. That’s all I know 100% for sure. But, based on my current trajectory, I will have been a PhD for half a decade, and maybe have done some teaching at the university level, published some studies in the field, and possibly gotten bored and started to pursue a second PhD in sports psychology or something.

Also, I will be a veteran competing in the professional ranks in natural bodybuilding, becoming more competitive with each outing. Lastly, I hope to have gotten myself closer to the elite status in raw drug free powerlifting, and maybe I’ll even have put up a respectable total in Olympic weightlifting that I have just started to dabble in. Possibly I’ll be coaching some weightlifters too!

Layne: I guess that’s a weird question for me.  I don’t necessarily have a 10-year plan.  My approach has always been to keep my head down and keep working hard and the opportunities would take care of themselves.  So far, I have been right, so I plan to stick with the game-plan.  Overall in my life, I want to leave a legacy of someone who worked their tail off, treated people right, and did things with a lot of integrity.  That might sound silly, but integrity and character are things I take extremely seriously.

Me: If there is one piece of wisdom that every beginner weight-lifter out there should absolutely have, what should it be?

Alan: One piece of wisdom? That’s a toughie. If I could pick just one, it would be that achieving big goals takes time – plenty of time. Despite what the multitude of online rip-off ads promise (i.e., “shortcuts” or “secrets”), developing a high level of athletic skill or physique development is a matter of several years of mind-numbingly consistent, hard work. Remember there’s no such thing as a short path to greatness, so enjoy the long haul.  I’ve actually compiled a list of these types of tips, just Google “Wisdom & Wisecracks.”

Eric: Learn from everyone. A smart person who is dedicated to personal growth can find a gem of knowledge or wisdom from literally everyone. As soon as you write someone off, you’ve closed an avenue for growth. Humble yourself, and see everything as an opportunity for growth and learning. Also, patience is the most valuable attribute you can have. My success in lifting and bodybuilding has little to do with my next 3 months of thinking and planning and everything to do with setting myself up for long term goals. I envision where I will be years from now, and then ensure I get there by putting in the work. In less words: humility, openness, patience, hard work.

Layne: Patience.  This is not going to happen overnight.  Please see my comments about success being a battle of attrition.  Success in lifting/bodybuilding is no different. 

Me: Are there any mistakes that you’ve made in the past, specifically with regards to training and nutrition, that you look back on and say, “What the hell was I thinking?!” And if so, what steps did you take to correct those mistakes and learn from your errors?

Alan: Perhaps my biggest training mistake was, as a beginner, following the popular bodybuilding split where each body part is bludgeoned with a high volume once a week. This was straight from the magazines, so how could it be wrong, right? It was blasphemy to train any other way than my idols in the mags. But then I did more reading and experimenting, and although the bro-split worked to a certain degree, cutting volume in half and doubling frequency made a huge difference. I’ve tried increasing frequency further, but cannot maintain it for more than short periods without recovery suffering. Another training mistake I’ve made in more recent times is constantly striving to lift heavier, focusing on the ‘stats’ rather than the feel. That was a good recipe for injury, especially for someone who wasn’t specifically concerned with powerlifting.

Nutrition-wise, perhaps the biggest mistake I made, funny enough, was not having an awareness at all of what might optimize gains in terms of protein and total calories. I knew that nutrition was important, but I never realized just how important it was, and how far off I was missing optimal targets. I just pretty much winged it; figuring things would work themselves out as long as I trained hard. It made a huge difference when I hunkered down and applied research-based findings towards my goals. I’ve mentioned in past interviews that a big mistake I made was being unaware of timing benefits, but eventually came to figure out that the timing had mostly to do with getting the right amount of carbs, protein, and fat within a 24-hour period.

One more mistake I want to add has more to do with philosophy rather than nutrition or exercise per se. I didn’t question enough of the concepts I was taught, either in a formal or informal setting. I often took the words of highly decorated ‘authorities’ as a matter of fact. It turns out that they were not omniscient, and neither is anyone else. Everything is open to dispute, and everything should be questioned. There’s nothing wrong with getting to the origin of any given claim, and seeing if that basis is solid or just pulled out of someone’s hot rear end.

Eric: Oh god, so many. If you aren’t making mistakes you aren’t trying hard enough and you aren’t pushing the envelope enough and you aren’t stretching yourself outside of your comfort zone. But honestly, I wouldn’t go back and change anything. Because I’ve tried every workout program and nutritional concept out there and because I’ve done every exercise, program, and diet on the planet, intelligent and otherwise, I have a vast amount of experience to draw from.

Learning is not accomplished by hoarding information, it only starts there, and that is the tip of the ice berg. Going out and putting all the theories and concepts into play is how you truly learn. We are human adults, we learn by doing. Nearly a decade of reading things, trying things, teaching things to others and coaching others has taught me that action is the way you learn something completely (if there is such a thing) and embody knowledge.

Layne: Sure.  I did all the guru stuff like eating 8 times per day, taking 100g of dextrose after a training session, downing 30g of glutamine per day, doing fasted cardio, etc.  But I would not take it back; those experiences were still valuable.  Mistakes are only bad if you don’t learn from them.

Me: Who has made the biggest impact on you in terms of who you are today, and what about that person sets them apart from anyone else in your life?

Alan: Dude, these questions are intense! I’m used to being asked, “What’s the one carb to avoid in order to not get teh luv handelz

To answer your question, I would have to say that career-wise, there are two people. One of them was one of my graduate professors named Brian Koziol. He was big on picking apart research and digging into the methodological strengths and weaknesses of the various studies that shape our beliefs of what’s what in sports nutrition. He also genuinely seemed to care about whether or not students actually learned anything, in contrast to other professors who appeared to just go through the motions of a job that they weren’t necessarily passionate about.

The other person who heavily influenced my career is a guy named Lyle McDonald. He’s relatively unknown to the general Dr. Oz masses, but very well known to those in the nerdier recesses of the internet (especially Facebook). A debate I had with Lyle on his forum several years back exposed to me the fact that I didn’t know as much as I thought, and that I had grown complacent and casually reliant on my education level at the time. This led me to gather up my balls and get started on my monthly research review, which is a cornerstone of my career to the present day. Lyle is a one-of-a-kind person. More innate brilliance than he knows what to do with. Far too much going on in his mind than formal degrees can contain. I’m not too proud to point out when someone has talent, and as far as the nutrition and dieting stuff goes, Lyle is in a class by himself. His reach of influence has been vast – on not just me, but many others. He’s not the most warmly adored figure in the industry, but I gotta’ give credit where credit is due.

Eric: I wouldn’t be able to list just one person. But I have some members of my family and some close friends who have shown me truly what unconditional love is, what being genuine and authentic means, and I’ve watched people achieve balance and happiness in life through living life authentically and I have emulated this with great success.

I have learned that belief in one’s self is the key to all success. The only true barriers to success are self-imposed. We are the gatekeeper to our own success in life and when we can truly understand that and take control over our own self perceptions and beliefs we can achieve great things. Not that I have mastered this, that never happens! But, because of my family and some of my close friends I at least know what I am attempting to master! A short list would include my fellow coaches at 3DMuscleJourney, and some of my close family.

Layne: Obviously my parents probably had the biggest impact on me.  They taught me a lot of what I know about hard work, how to treat people, and integrity.  Outside of them, definitely my grandfather.  He was my personal hero and the greatest man I have ever met.  If I ended up being half the man he was, I would consider myself an enormous success.

Me: What is your greatest accomplishment to-date, and what makes it so special that it surpasses everything else in your life?

Alan: Oh man, more deep questions… My greatest accomplishment to-date is finding the right girl and marrying her. This was just dumb luck, or extreme fortune, depending on how you look at it. And no, I didn’t just say this so I can show it to her this interview and enjoy the reaction to follow.

Aside from that, I’ve been extremely thrilled to influence the career paths of various individuals. For example, Daniel Yeh and John McMahan of Citadel Nutrition have personally thanked me for helping them make the decision to pour their vital resources into their supplement company. Essentially, they put everything on the line to chase what they believed in (and were passionate about), and now they’re seeing the fruits of their courage and diligence. It’s hugely gratifying to know I played a part in that. Will Citadel Nutrition exist in 10 years? 5 years? Another year? Nothing is certain, especially in the cut-throat industry that sports supplements is. However, my hunch is that they’ll continue to do well, and knowing that I contributed to their sense of integrity is priceless.

Other standout accomplishments were being invited to speak at various conferences including the Fitness Summit and NSCA Personal Trainer’s Summit. The thing about these engagements was that I was invited to speak. I didn’t have to apply to get these opportunities. The fact that they approached me, as opposed to me approaching them, tells me that I’ve reached a certain level of value in the industry that even the big boys notice. Along these lines, one of the most profound events in my career was getting invited onto the staff at Men’s Health magazine as their go-to nutrition guy. Plenty of opportunities flourished as a result of top guys in the publishing industry like Adam Bornstein and Adam Campbell being fans of my work. Men’s Health is the largest magazine of its kind in the world, many times over. For them to recognize me as someone who could fulfill their position of authority in their targeted market (post-college bros and struggling dads) was just tremendous for me.  Being invited to serve on Fitocracy’s advisory board by the founders Dick Talens and Brian Wang was a biggie as well, no pun intended.

Another big milestone for me was getting invited onto the peer review board of the ISSN by the founder himself, Dr. Jose Antonio. If there is any formal “stamp” that I am as nerdy as some folks think I am about criticizing research, then this is definitely it. This also lets me know that the time and effort I’ve spent in fulfilling my interest in the objective study of training and nutrition has not gone unnoticed by the academics in the ivory tower.  Along these lines, I’m collaborating with Eric Helms and Peter Fitschen on a bodybuilding-related article that will be published in a peer-reviewed journal. It’s almost finished; they’re just waiting on me, hahahaha! It will be a kick to finally make it into “The Pubmedz” – especially with an article that isn’t the run of the mill in biomedical circles.

Last but not least, my own accomplishments tend to pale in comparison to what my clients have accomplished – permanent improvements in their habits, and the life-long implementation of sound principles that they were open-minded enough to incorporate into their lifestyles.  To think that I’ve influenced real people’s everyday lives is mind-blowing to me. I know you asked for a single accomplishment, but I couldn’t help but take a trip down memory lane and recall the roses among the thorns in my path.

Eric: I can’t compare apples to oranges in my life, and I’ve done a few things that I’m proud of and happy about up to this point in my life, so I won’t be able to list one thing. I also know that I will continue to do more things that I see as great accomplishments, that’s the purpose of my life in many ways.

But, I would say marrying my wife Barbara is huge, that has brought me so much happiness, enjoyment, fulfillment and a partnership that makes my life amazing. I would also say that I am very proud of finding my way into my graduate work at the Auckland University of Technology. Once I decided I wanted to get my PhD I managed to find a way despite there not being any programs locally that I was qualified for, that sparked my interest or that I could get funding for. I kept hunting, I kept looking, and when an opportunity presented itself I grabbed it and wouldn’t let go. I don’t know how the studies are going to go overseas, but honestly just getting out there and doing it is a huge accomplishment.

Also, getting my natural pro card is a huge accomplishment for me. That has been a goal since I first started lifting, and I think the biggest barrier to achieving it was the self-doubt that I’ve overcome in the process. Convincing myself that I COULD achieve this goal at all was probably the biggest factor in acquiring it. I learned through this process that I could be successful at anything in life even if it required some hard work over a long time period against significant odds.

Layne: Marrying my wife Isabel and staying married.  I see so many phony relationships and people who don’t truly understand what it means to be on the ‘same team.’  My wife and I may fight, but at the end of the day we know that we have each other’s back and we love each other very much.  One of my life long goals is to NEVER be divorced. I met Isabel, fell in love with her, and love her even more today.  But we worked very hard at our relationship, just like everything else, to try to become more in tune with each other and compromise more.  We aren’t perfect by a long shot, but we are always trying.  So having a successful relationship with the love of my life is my greatest accomplishment.  If I do a good job raising kids in the future, then my family will become my greatest accomplishment I think.  As for personal stuff, completing my PhD is what I am most proud of, as it was the ONLY thing in my life I ever wanted to quit at one point. 

Me: We all know that the best ergogenic aid is some kick-ass music. Are there any bands that you just can’t lift without? 

Alan: I actually can’t stand the idea of dealing with any musical delivery implements on me while training. I just get in there and mentally block out whatever music is playing. However, driving to the gym, I have personalized playlists that include the Devin Townsend Project, Strapping Young Lad, Meshuggah, Lamb of God, Pantera, Mastodon, Killswitch Engage, Animals as Leaders, Skyharbor, Solution 45, Timfy James, Hacktivist, and others slipping my mind at the moment. On an amusing note, I occasionally watch Aragorn’s speech at the Black Gate before driving out to the gym.

Eric: What I listen to when I lift it very much depends on my mood. Sometimes it’s play time for me, and while I play hard (very hard), it’s not the same as when I am feeling aggressive in terms of my mood. I like more upbeat, funky music when I’m in this mood. For example, I found myself singing off key really loudly to Journey’s “Don’t Stop Believing” in the middle of a set a week ago, lots of fun.

Other times I go in there andI am hyped up and r eady to kill shit. I get pretty focused sometimes and I definitely relieve tension through training, and something aggressive like Disturbed, Rage Against the Machine, Eminem, Tech n9ne or really anything hard and heavy, rock or hip hop can be appropriate for me.

Lastly, sometimes I like silence when I’m training in a more introspective state; it can almost be a little more of a daily ritual, or practice. In times like these I prefer to train alone, do my thing and I enjoy just the sound of the iron and the plates.

Layne: Absolutely.  Disturbed, Chimaira, 30 Seconds to Mars, Sevendust, Skillet, Papa Roach, Filter, Hatebreed, and Shinedown are some of my favorites. 

Me: What is your favorite nutrition and or exercise-related topic to discuss/debate/write about?  

Alan: I really don’t have a favorite. The more challenging and controversial, the better, because it’s more stimulating.  I have a particular fondness for the macronutrients, since each one of them has its own ongoing war of beliefs in terms of optimal amount, type, timing, and distribution for a number of goals.  As far as training goes, I’m currently interested in the mechanisms of hypertrophy, and thankfully, I have guys like Brad Schoenfeld and Bret Contreras to bounce ideas off of in that department, since they’re deep in the thick, greasy trenches of that line of research. It’s intriguing to think that counter-intuitive aspects like metabolic fatigue could, in concurrence with hormonal factors, contribute to muscle growth (& strength) beyond merely a focus on progressive mechanical/tension-related factors alone. I always anticipate the victory of simplicity (e.g., more weight on the bar = more inches on the gunz), but the odd/esoteric findings can often grab me since they force me to re-think whatever paradigm that’s currently holding me captive.

Eric: My favorite topic changes so often to be honest. I really enjoy the kinesological aspects of movement, why people move certain ways in certain movements, how we can optimize it for specific goals, and how we can improve or correct faulty movement patterns. I also really enjoy the topic of nutritional approaches for both muscle gain and fat loss. Lastly, I’d say I really enjoy the discussion of weight training programming. Periodization, peaking, programming and customizing this to the individual lifter is very fun to talk about.

Layne: Definitely protein.  Did my PhD on protein metabolism and obviously it holds a special place in my heart haha. 

Me: What is one nutritional, physiological, or exercise -based topic that you wished you knew more about? Have you done anything to help expand your knowledge about it?

Alan: Everything…. Seriously, nothing stands out. Well, hold on. I think that I can stand to brush up on biostatistics. It’s not something that excites me (yet), but that’s a sign that I’m behind on it and need to firm up my grip. Time to contact James Krieger and Aaron Fanning (James might see this interview, but Aaron might not).

Eric: There is a whole lot more than just one topic I wish I knew more about! And I continually focus on these things to round out my knowledge. When not studying protein intake in strength athletes (my thesis topic), in my spare time I have been studying substrate utilization, metabolism, exercise endocrinology, in-depth muscle physiology and digestion.

Layne: Definitely would love to learn more about physiological and psychological responses to resistance training and periodization.  I’ve done a ton of reading, but I still feel like the programming aspect of periodization may be where I need more improvement. 

Me: What is your favorite non-exercise/nutrition-related book? What makes it such an excellent read?

Alan: I rarely read anything that isn’t related to nutrition & training. There’s just not enough time in the day. However, I recently got done reading – of all things – a fictional book called The Bronze Bow by Elizabeth Gorge Speare. What makes it an excellent read? Just everything about it kicked my ass. I don’t know how else to describe it.

Eric: I have to name just one book, seriously? Well, let me start by saying that I’m an avid science fiction and fantasy geek and I play role playing games (and I mean real table top RPGs, not ones on computers) and I probably read a couple books per month that are totally unrelated to fitness. I also have gone through periods where I really enjoyed philosophy, spirituality, and other weird topics. So asking me for one book that stands out is impossible!

Among the books in the philosophy/spirituality/personal-growth realm, I’d say the following books really helped me to grow and to change my perspective: The Way of the Peaceful Warrior by Dan Millman, The Alchemist by Paulo Coelho, The Prophet by Kahlil Gibran and Zen and the Art of Motorcycle Maintenance by Robert Pirsig. Although there are a lot of other books too that stand out.

Among the books in the science fiction/fantasy realm, I’d say the following books really were my favorites and really sucked me in: The Lord of the Rings Trilogy and The Hobbit by JRR Tolkien, The Game of Thrones series by George RR Martin, The Prince of Nothing Trilogy by R Scott Bakker (and the follow up series), The Kingkiller Chronicles by Patrick Rothfuss, The Hyperion Cantos by Dan Simmons, The Ender books by Orson Scott Card, The Dune books by Frank Herbert,  and the Ringworld books by Larry Niven. To be honest though, there are a lot more that stand out; it’s not a comprehensive list.

Layne: Well, it’s a tie.  I loved Dave Ramsey’s book The Total Money Makeover, not so much because I needed a lot of help saving money but because it was motivating to read about how powerful sacrifice can be and it reinforced what my parents taught me about money and success.  I also really enjoyed Tim Tebow’s book Through My Eyes because I love the guy’s work ethic and how he has proved people wrong every step of the way. 

Me: Can we (the readers) expect anything exciting (events, publications, travels, etc.) from you in the upcoming weeks/months/years?

Alan: AARR being posted on the projected date each month (although the universe might actually implode if that happens).  Other than that, I’ll be speaking in at least one of the NSCA conferences in 2013, and of course the Fitness Summit that I’ve been doing each year since 2008.

Eric: I am working on a lit review paper on evidence based approaches to natural bodybuilding with Alan Aragon and Peter Fitschen at the moment that we are just about ready to submit for publication that should be very cool. I’m also going to be involved with a number of projects during my graduate school work over the next 4 years at AUT that will involve a lot of topics, but will mainly involve protein intake in strength athletes during hypocaloric periods. My thesis is looking at this specifically, and I will be attempting to get my findings published and I’ll probably be taking part in publishing a bunch of other sports-science related papers over the course of the of my grad studies.

Also, in November I will be speaking in New Zealand at the Sports Performance Research Institute SPRINZ) conference on protein intake for athletes, and also at the FITex personal training conference on protein supplementation. These conferences are kind of like the equivalent of the NSCA CSCS and CPT conferences here in the states.

Layne: Oh yea, lots of stuff.  I just re-launched my website www.biolayne.com with a totally new design, more content and way more interaction so I’m updating that several times per week.  I also recently was selected as Dan Soloman’s replacement as the announcer for the Mr. Olympia contest so I’m excited to do that.  I could have never imagined watching the Olympia at home on my TV 11 years ago, that someday I would be calling the play by play… it’s insane.

Me: Where can we (the readers) learn more about what you do, the services you offer, and the information that you put out?

Alan: http://alanaragon.com/researchreview

Eric: www.3dmusclejourney.com

Layne: Definitely through my website www.biolayne.com as well as Facebook: www.facebook.com/LayneNorton, Twitter: www.twitter.com/biolayne, and YouTube:www.youtube.com/biolayne

Me: Thank you all again! It is greatly appreciated.

Alan: Thanks so much for the exceptionally challenging and fun interview, Dylan. I really enjoyed this, and am very thankful that there are folks like yourself to help me carry the torch.

Eric: My pleasure. Thanks, Dylan!

Layne: My pleasure, thanks for the opportunity.

And thank you, the readers, for making this all worthwhile! Look out for a new article in the coming days! Until then…

 

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