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Cramer MJ, Dumke CL, Hailes WS, Cuddy JS, Ruby BC.

Int J Sport Nutr Exerc Metab. 2015 Oct;25(5):448-55.


Soylent: a suboptimal solution to first-world

By Alan Aragon

Copyright November 1st, 2015 by Alan Aragon


11 Eric Helms interrogated about recomp & magic.

By Alan Aragon

A closer look at the claim that a carb is a carb.

By Alan Aragon

Longer inter-set rest periods enhance muscle

strength and hypertrophy in resistance-trained
Schoenfeld BJ, Pope ZK, Benik FM, Hester GM, Sellers J,
Nooner JL, Schnaiter JA, Bond-Williams KE, Carter AS,
Ross CL, Just BL, Henselmans M, Krieger JW. J Strength
Cond Res. 2015 Nov 20. [Epub ahead of print] [PubMed]

The anabolic response to a meal containing

different amounts of protein is not limited by the
maximal stimulation of protein synthesis in
healthy young adults.
Kim IY, Schutzler S, Schrader A, Spencer HJ, Azhar G,
Ferrando AA, Wolfe RR. Am J Physiol Endocrinol Metab.
2015 Nov 3:ajpendo.00365.2015 [PubMed]

Probiotic supplementation attenuates increases in

body mass and fat mass during high-fat diet in
healthy young adults.
Osterberg KL, Boutagy NE, McMillan RP1, Stevens JR,
Frisard MI, Kavanaugh JW, Davy BM, Davy KP, Hulver
MW. Obesity (Silver Spring). 2015 Oct 14. doi:
10.1002/oby.21230. [PubMed]

Postexercise glycogen recovery and exercise

performance is not significantly different between
fast food and sport supplements.

Alan Aragons Research Review November 2015

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A closer look at the claim that a carb is a carb.

By Alan Aragon
There has been a long-standing debate in both clinical and sports
nutrition circles over how much food choices matter, as opposed
to mere macronutrition. A carb is a carb, goes the mantra. We
never hear that a fat is a fat, or protein is protein. Why is this?
The idea of a wide range of quality and effectiveness of different
protein sources is readily accepted. Weve all seen protein
sources ranked on the basis of their amino acid profile.1 A
greater proportion of essential amino acids (EAAs) translates to
higher quality, and among those EAAs, if a given protein source
has a higher branched chain amino acid (BCAA) content, it
receives an even higher ranking.
With fats, it isnt as much about ranking as it is about attaining
the right balance of fatty acid types.2 For example, consuming a
predominance of industrial (as opposed to ruminant) trans fatty
acids puts cardiovascular health at risk.3 Under-consuming
omega-3 fatty acids while over-consuming omega-6 fatty acids
is another ill-advised move.4 Yet another example is that a high
intake of linoleic acid-rich vegetable oils can pose adverse health
effects, while linoleic acid-rich nuts have reams of support in the
literature for their health benefits.5,6
Context has a tremendous impact here. So, how did carbs earn
the seal of indifference? Its mainly because context is neglected.
Lets look at just how much a carb is a carb within the
context of health, athletic performance, and body composition.
A carb is not a carb when it comes to health. However, dosage
matters as much as food source when it comes to the health
aspects of carbs. An obvious example here is added sugars (also
called extrinsic sugars, as opposed to the intrinsic sugars in dairy
and fruit). There is now an abundance of research showing that
added sugars consumed in excess can not only lower overall diet
quality, but also increase risk factors for the metabolic
syndrome. However, its important to remember that these
effects are seen largely in conditions where the dose of added
sugar is unrealistically high.7 Current added sugar cut-off points
from the major health organizations range from approximately
10-25% of total calories.8 Bear in mind that the last thing I want
to do is paint a binary picture of good carbs versus bad carbs to
be avoided. Clearly, theres room for all types in the diet,
including added sugars, which simply need to be moderated
more cautiously than intrinsic sugars (which are accompanied by
other compounds that can mitigate disease).

plant-derived) that contribute to the prevention of chronic

diseases.9 And to reiterate, dose always matters. The less glucose
control an individual has, the more caution must be applied to
dosing, regardless of the form or food source.
Athletic performance
A carb is not a carb when it comes to athletic performance. In
the pre-exercise period leading up to endurance competition,
glycemic index (GI), a foods ability to raise blood glucose
levels, is largely inconsequential to performance.10 However, for
the goal of maximizing the rate of post-exercise glycogen
resynthesis, high-GI carb sources are superior.11
A proprietarily engineered, very high-molecular weight glucose
polymer (trade name Vitargo) was seen to have significantly
faster gastric emptying and glycogen resynthesis rates than a
glucose monomer & oligomer-based solution.12 Glucose (and
polymers of glucose such as maltodextrin) are high-GI, but
Vitargos GI is estimated to be approximately 37% higher.
Vitargo was seen to outperform a maltodextrin-based solution
for improving time trial performance after glycogen depletion. 13
This has applications for athletes required to compete with
glycogen-depleted muscles very soon after depletion.
During endurance exercise, a carb is not a carb, since the type
and form of carb influence gastric emptying, gastric comfort,
rate of absorption, rate of delivery to working muscles, and
ultimately performance. Glucose and fructose have separate
intestinal transporters, so providing a mix of glucose and
fructose during endurance exercise has been consistently shown
to enhance performance compared to a single carbohydrate
source.14-16 As a practical reminder, sucrose (table sugar) is a 1:1
ratio of fructose:glucose, which is similar to the 0.8:1 ratio of
fructose:glucose that has been repeatedly demonstrated as the
performance.15,16 I personally would like to see performance
trials involving Vitargo ingestion during exercise, compared
with the ingestion of typical sports beverages containing a mix
of multiple transportable carbohydrates. To my knowledge, this
research has not yet been done (or at least not yet published).
Body composition

Just as food sources of linoleic acid (e.g., corn oil versus

walnuts) can lean toward opposite health effects, the same is true
for sugar sources in the diet (e.g., sugar-sweetened beverages
versus whole fruits). There is a multitude of carbohydratedominant foods (typically unrefined or minimally refined, and

If the claim that a carb is a carb was ever relatively correct,

its in the context of body composition. However, this largely
depends on the foods ability to influence eating behavior via its
effect on reward signals in the brain.17 The ability of different
foods to have different neurobiological effects on eating
behavior weakens the claim that a carb is a carb. Foods vary
widely in their ability to induce satiety and control appetite. In
classic research by Holt et al,18 white potatoes were the runaway
winner out of 38 common foods tested for satiating effect. Other
highly satiating foods were oatmeal, oranges, apples, brown
pasta, and baked beans. Toward the bottom of the satiety ranks
were ice cream, crisps, Mars candy bars, doughnuts, and cake,
with croissants being the least satiating of all the foods tested.
Note that I only gave examples of carb-rich foods; protein and
fat-rich foods were also tested. The point is, appetite control (or
lack thereof) can ultimately affect body composition. This is not
to say that the only options are either an all-croissant & ice

Alan Aragons Research Review November 2015

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cream diet or an all-potato & oatmeal diet. However, if appetite

control is the objective, more highly satiating carbohydrate
sources can benefit the dieter, especially if they fit his or her
personal preferences.
In addition to the various health concerns of overconsumption,
added/extrinsic sugar has been accused of inhibiting fat loss in
dieting conditions compared to other carb sources. However,
research has demonstrated this fear to be false at least under
controlled conditions where total calories are matched. A 6-week
trial by Surwit et al19 compared 43% versus 4% of the total
calories as sucrose for 6 weeks in hypocaloric conditions. No
significant differences bodyweight or body fat loss (assessed via
DXA) were seen between the high- and low-sucrose groups.
Those who buy into the carb-insulin hypothesis of fat gain
believe that high-GI carbs ability to raise insulin levels makes
them more potent agents of fat gain or inhibition of fat loss.
People are free to make any claim they want, but what does the
research evidence say? In short, it says theyre wrong. Lets look
briefly at insulin first, then move on to GI. A recent tightly
controlled metabolic ward study by Hall et al20 found that a 30%
energy deficit imposed via dietary fat reduction caused greater
net body fat loss than an isocaloric/isonitrogenous condition
where carbohydrate was reduced. Insulin levels were higher in
the condition where more body fat was lost.
Holt et al, authors of the satiety index,18 compiled an insulin
index of common foods21 and found that beef and fish elicited
higher insulin responses than porridge and al dente pasta. Does
this mean fish and beef are inherently more fattening? Of course
not. As for the opposite claim that the lipolytic effect of
glucagon elicitation by these foods counteracts lipogenic effects
of insulin, thats false as well, since glucagon elevations have
failed to increase lipolysis in humans in vivo.22,23
As for GI, its inherent influence on fat loss or fat gain is highly
questionable. The body of research to-date has largely failed to
match macronutrition and fiber between higher- and lower-GI
conditions.24 Fat loss tends to favor higher protein and/or higher
fiber intakes thats a no-brainer. Despite these discrepancies,
GI has still failed to consistently or robustly influence body
composition or fuel oxidation in well-controlled studies.25 A
recent study by Sacks et al26 finally did control macronutrition
and fiber, and found no significant effect of GI on insulin
sensitivity, blood lipids, or systolic blood pressure. But that
belongs in the discussion about health. In diets predominated by
whole & minimally refined foods, where macronutrition is
optimized and fiber is adequate, the mere concept of GI becomes
virtually useless for both health and body composition.


Millward DJ, Layman DK, Tom D, Schaafsma G. Protein quality

assessment: impact of expanding understanding of protein and amino acid
needs for optimal health. Am J Clin Nutr. 2008 May;87(5):1576S-1581S.
de Lorgeril M, Salen P. New insights into the health effects of dietary
saturated and omega-6 and omega-3 polyunsaturated fatty acids. BMC
Med. 2012 May 21;10:50. [PubMed]
Da Silva MS, Julien P, Prusse L, Vohl MC, Rudkowska I. Natural RumenDerived trans Fatty Acids Are Associated with Metabolic Markers of
Cardiac Health. Lipids. 2015 Sep;50(9):873-82. [PubMed]

Alan Aragons Research Review November 2015


Taha AY, Cheon Y, Faurot KF, Macintosh B, Majchrzak-Hong SF, Mann

JD, Hibbeln JR, Ringel A, Ramsden CE. Dietary omega-6 fatty acid
lowering increases bioavailability of omega-3 polyunsaturated fatty acids
in human plasma lipid pools. Prostaglandins Leukot Essent Fatty Acids.
2014 May;90(5):151-7. [PubMed]
5. Ros E. Health benefits of nut consumption. Nutrients. 2010 Jul;2(7):65282. [PubMed]
6. Ros E. Nuts and CVD. Br J Nutr. 2015 Apr;113 Suppl 2:S111-20.
7. Rippe JM, Angelopoulos TJ. Sucrose, high-fructose corn syrup, and
fructose, their metabolism and potential health effects: what do we really
know? Adv Nutr. 2013 Mar 1;4(2):236-45. [PubMed]
8. Refer to the July 2015 issue of AARR, p.12-13 for a discussion of the sugar
guidelines of the major organizations.
9. Boeing H, Bechthold A, Bub A, Ellinger S, Haller D, Kroke A, LeschikBonnet E, Mller MJ, Oberritter H, Schulze M, Stehle P, Watzl B. Critical
review: vegetables and fruit in the prevention of chronic diseases. Eur J
Nutr. 2012 Sep;51(6):637-63. [PubMed]
10. Ormsbee MJ, Bach CW2, Baur DA3. Pre-exercise nutrition: the role of
macronutrients, modified starches and supplements on metabolism and
endurance performance. Nutrients. 2014 Apr 29;6(5):1782-808. [PubMed]
11. Poole C, Wilborn C, Taylor L, Kerksick C. The role of post-exercise
nutrient administration on muscle protein synthesis and glycogen synthesis.
J Sports Sci Med. 2010 Sep 1;9(3):354-63. [PubMed]
12. Piehl Aulin K, Sderlund K, Hultman E. Muscle glycogen resynthesis rate
in humans after supplementation of drinks containing carbohydrates with
low and high molecular masses. Eur J Appl Physiol. 2000 Mar;81(4):34651. [PubMed]
13. Stephens FB, Roig M, Armstrong G, Greenhaff PL.Post-exercise ingestion
of a unique, high molecular weight glucose polymer solution improves
performance during a subsequent bout of cycling exercise. J Sports Sci.
2008 Jan 15;26(2):149-54. [PubMed]
14. Rowlands DS, Thorburn MS, Thorp RM, Broadbent S, Shi X. Effect of
graded fructose coingestion with maltodextrin on exogenous 14C-fructose
and 13C-glucose oxidation efficiency and high-intensity cycling
performance. J Appl Physiol (1985). 2008 Jun;104(6):1709-19. [PubMed]
15. O'Brien WJ, Stannard SR, Clarke JA, Rowlands DS. Fructose-maltodextrin
ratio governs exogenous and other CHO oxidation and performance. Med
Sci Sports Exerc. 2013 Sep;45(9):1814-24. [PubMed]
16. Jeukendrup A. A step towards personalized sports nutrition: carbohydrate
intake during exercise. Sports Med. 2014 May;44 Suppl 1:S25-33.
17. Egecioglu E, et al. Hedonic and incentive signals for body weight control.
Rev Endocr Metab Disord. 2011 Sep;12(3):141-51. [PubMed]
18. Holt SH, Miller JC, Petocz P, Farmakalidis E. A satiety index of common
foods. Eur J Clin Nutr. 1995 Sep;49(9):675-90. [PubMed]
19. Surwit RS1, Feinglos MN, McCaskill CC, Clay SL, Babyak MA,
Brownlow BS, Plaisted CS, Lin PH. Metabolic and behavioral effects of a
high-sucrose diet during weight loss. [PubMed]
20. Hall KD, et al. Calorie for Calorie, Dietary Fat Restriction Results in More
Body Fat Loss than Carbohydrate Restriction in People with Obesity. Cell
Metab. 2015 Sep 1;22(3):427-36. [PubMed]
21. Holt SH, Miller JC, Petocz P. An insulin index of foods: the insulin
demand generated by 1000-kJ portions of common foods. Am J Clin Nutr.
1997 Nov;66(5):1264-76. [PubMed]
22. Bertin E, Arner P, Bolinder J, Hagstrm-Toft E. Action of glucagon and
glucagon-like peptide-1-(7-36) amide on lipolysis in human subcutaneous
adipose tissue and skeletal muscle in vivo. J Clin Endocrinol Metab. 2001
Mar;86(3):1229-34. [PubMed]
23. Gravholt CH, Mller N, Jensen MD, Christiansen JS, Schmitz O.
Physiological levels of glucagon do not influence lipolysis in abdominal
adipose tissue as assessed by microdialysis. J Clin Endocrinol Metab. 2001
May;86(5):2085-9. [PubMed]
24. Lopes da Silva MV, de Cssia Gonalves Alfenas R. Effect of the glycemic
index on lipid oxidation and body composition. Nutr Hosp. 2011 JanFeb;26(1):48-55. [PubMed]
25. Daz EO, Galgani JE, Aguirre CA. Glycaemic index effects on fuel
partitioning in humans. Obes Rev. 2006 May;7(2):219-26. [PubMed]
26. Sacks FM, et al. Effects of high vs low glycemic index of dietary
carbohydrate on cardiovascular disease risk factors and insulin sensitivity:
the OmniCarb randomized clinical trial. JAMA. 2014 Dec

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bolstered via protein supplementation (24 g whey) in addition to

the subjects pre-existent dietary habits.
Longer inter-set rest periods enhance muscle strength
and hypertrophy in resistance-trained men.
Schoenfeld BJ, Pope ZK, Benik FM, Hester GM, Sellers J,
Nooner JL, Schnaiter JA, Bond-Williams KE, Carter AS, Ross
CL, Just BL, Henselmans M, Krieger JW. J Strength Cond Res.
2015 Nov 20. [Epub ahead of print] [PubMed]
PURPOSE: The purpose of this study was to investigate the
effects of short rest intervals normally associated with
hypertrophy-type training versus long rest intervals traditionally
used in strength-type training on muscular adaptations in a
cohort of young, experienced lifters. DESIGN: Twenty-one
young resistance-trained men were randomly assigned to either a
group that performed a resistance training (RT) program with 1minute rest intervals (SHORT) or a group that employed 3minute rest intervals (LONG). All other RT variables were held
constant. The study period lasted
8 weeks with subjects performing
3 total body workouts a week
comprised of 3 sets of 8-12
repetition maximum (RM) of 7
different exercises per session.
Testing was carried out pre- and
post-study for muscle strength
(1RM bench press and back
squat), muscle endurance (50%
1RM bench press to failure), and
muscle thickness of the elbow
flexors, triceps brachii, and quadriceps femoris via ultrasound imaging. RESULTS: Maximal
strength was significantly greater for both 1rm squat and bench
press for long compared to short. Muscle thickness was
significantly greater for long compared to short in the anterior
thigh and a trend for greater increases was noted in the triceps
brachii,(p = 0.06) as well. Both groups saw significant
increases in local upper body muscle endurance with no
CONCLUSIONS: The present study provides evidence that
longer rest periods promote greater increases in muscle strength
and hypertrophy in young resistance-trained men.
SPONSORSHIP: None listed.
Study strengths
An immediate strength that anyone should detect instantly is that
Brad Schoenfeld is the lead investigator (see, I troll my friends
not only in the public domain, but also the private domain :)).
This study is the first to ever examine the effect of varying
interset rest duration (rest interval) on muscular endurance as
well as maximal strength. Comparing a 1-minute vs. 3-minute
rest interval diligently addresses gaps in the literature, given that
previous research has compared 2 vs 5 min,1 1 vs. 2.5 min,2 and
1 vs. 4 min.3 The measurement of muscle thickness via
ultrasound is a step up in sensitivity & sophistication compared
to more crude anthropometric measures such as circumference.
Subjects were resistance-trained, which minimized the
confounding potential of newbie gains. Anabolism was
Alan Aragons Research Review November 2015

Study limitations
The authors acknowledged several limitations. The trial duration
was relatively short (8 weeks), dietary tracking and reporting
was absent (this is a common logistical limitation with training
studies). A renovation of the university gym during the trial and
resultant use of alternate machines with a different mode of
action (and thus different load schemes) prevented an accurate
assessment of volume load. A final limitation the authors
acknowledged was that muscle thickness assessed via ultrasound
was taken at the midpoint of the muscle, which does not rule out
possible undetected changes at the proximal and distal regions of
the muscle.

The authors hypothesized that short rest intervals (1 min) would

be more conducive to muscle growth and endurance while long
rest intervals (3 min) would better promote maximal strength.
However, while the latter hypothesis was correct (3-min rest
yielded markedly greater gains in 1RM squat and bench), 3-min
rest was superior to 1 min for inducing hypertrophy, as seen in
the above table. An exception was a lack of difference in
hypertrophy of the lateral thigh. Also contrary to what was
hypothesized, while muscular endurance increased in both
conditions, rest duration did not have any differential impact.
While the better-known mechanisms behind increased endurance
via shorter sets were in play (e.g., increased buffering capacity),
the longer rest interval may have also increased endurance
capacity since, increases in maximal muscular strength may be
associated with a reduced cost when performing tasks with the
same absolute submaximal load.
In terms of practical application, the present findings indicate
that a 3-minute rest interval is superior to a 1-minute rest interval
for the goals of not just maximal strength, but hypertrophy as
well. Shorter rest periods in the 30 to 60-second range have been
recommended as appropriate for maximizing hypertrophy,
presumably due to effects on anabolic hormone levels.4
However, the present study does not support that, and is more in
agreement with a recent literature review by Henselmans &
Schoenfeld,5 which also favored longer rest intervals for the goal
of hypertrophy. Further research is needed to examine the
effectiveness of mixed-duration rest intervals.
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The anabolic response to a meal containing different

amounts of protein is not limited by the maximal
stimulation of protein synthesis in healthy young
Kim IY, Schutzler S, Schrader A, Spencer HJ, Azhar G,
Ferrando AA, Wolfe RR. Am J Physiol Endocrinol Metab. 2015
Nov 3:ajpendo.00365.2015 [PubMed]
PURPOSE: We have determined whole body protein kinetics i.e.,
protein synthesis (PS), breakdown (PB), and net balance (NB) in
human subjects in the fasted state and following ingestion of ~40g
(moderate protein, or MP) that has been reported to maximized the
protein synthetic response or ~70g (higher protein, HP) protein,
more representative of the amount of protein in the dinner of an
average American diet. DESIGN: Twenty three healthy young men
who had performed prior resistance exercise (X-MP or X-HP) or
time-matched resting (R-MP or R-HP) were studied during a primed
continuous infusion of L-[2H5]phenylalanine and L-[2H2]tyrosine.
Subjects were randomly assigned into an exercise (X, n=12) or
resting (R, n=11) group, and each group was studied at the two
levels of dietary protein intake in random order. PS, PB, and NB
were expressed as increases above the basal, fasting values (mg/kg
LBM/min). RESULTS: Exercise did not significantly affect protein
kinetics and blood chemistry. Feeding resulted in positive NB at
both levels of protein intake: NB was greater in response to the meal
containing HP (p<0.00001). The greater NB with HP was achieved
primarily through a greater reduction in PB and to a lesser extent
stimulation of protein synthesis (for all, p<0.0001). HP resulted in
greater plasma EAA responses (p<0.01) vs. MP, with no differences
in insulin and glucose responses. CONCLUSIONS: In conclusion,
whole body net protein balance improves with greater protein intake
above that previously suggested to maximally stimulating muscle
protein synthesis because of a simultaneous reduction in protein
breakdown. SPONSORSHIP: The project was financially
supported by a grant from National Cattlemen's Beef Association.
The project was partially supported by Pepper Center Grant
AG028718 and an award from the National Center for Advancing
Translational Sciences (NCATS).

Study strengths
This is the first study to ever examine the whole-body, net
anabolic response (protein synthesis, protein breakdown, and net
balance) of a moderate (40 g) dose of protein vs. a large (70 g)
dose within a mixed meal with and without prior resistance
exercise. Protein kinetics at the muscle level as well as the
whole-body level were assessed. Subjects underwent a 3-day
dietary normalization period prior to testing, where food was
provided via the metabolic kitchen. A dietitian assessed nutrient
intake and compliance via pictures of the meals (taken by the
subjects). A minimum of 80% compliance was required for
subjects to undergo the metabolic study.
Study limitations
This study was very well controlled and executed, but its
inevitably limited by its acute (short-term) nature. Acute
responses to protein feeding do not necessarily reflect
adaptations that occur in the long-term. Another possible
limitation was that the results might only apply to the specific
food sources used for the test meals (beef patties, other
Alan Aragons Research Review November 2015

macronutrient sources not listed), as well as the macronutrient

breakdown of the meals themselves, whose order of caloric
dominance was carbohydrate > fat > protein. Finally, subjects
were not trained, so it remains speculative whether the results
would reliably apply to athletic populations.
The main findings were three-fold: 1) whole-body net protein
balance protein synthesis minus breakdown increased in both
doses but was greater with 70 g protein than 40 g. Reduced
protein breakdown (PB) was the largest contributor to the
increase in net balance. 2) Muscle protein synthesis (MPS), was
not significantly different between the two protein doses. 3)
Prior exercise did not influence protein kinetics at either dose.
The authors speculated that this lack of effect of exercise could
have been due to the 40 g dose being high enough on its own to
maximize muscle protein synthesis (MPS). They also speculated
that an insulin-mediated suppression of protein breakdown (with
carbohydrate playing a role in this) could have contributed to the
lack of influence of exercise.
The traditionally presumed protein dose that maximizes the
acute anabolic response is approximately 20-35 g, with the
higher end (even up to 40 g) applying to older subjects.6-10
However, the authors contend that this is based on an incomplete
picture of the anabolic response since it only examines protein
synthesis while ignoring protein breakdown. They assert that the
idea that protein breakdown is a minor or insignificant factor is
not based on mixed meals, and thus has limited application.
Recent work from the present studys lab found that MPS was
greater with protein dosed at 1.5 g/kg vs. 0.8 g/kg, regardless of
distribution pattern through the day (33/33/33% vs
15/20/65%).11 Perhaps the strongest support for these findings is
previous work by Adechian et al,12 who found no significant
between-group differences in body composition change in a 6week comparison of whey vs casein consumed in a pulse meal
pattern (8/80/4/8%) vs a spread pattern (25/25/25/25%).
However, it should be noted that Adechian et als work is
challenged by Arciero et al,13 who saw that a more spread-out
distribution of protein had superior effects on body composition
compared to a more concentrated pattern (6 vs 3 meals).
The idea that 20-35 g maximizes the anabolic response applies
only to protein kinetics within muscle. Ill end this discussion by
quoting the authors salient rebuttal to the traditional focus on
MPS, and neglect for whole-body protein balance:
It is likely that increases in whole body PS likely reflected
increases in PS [protein synthesis] in tissues other than muscle,
such as gut (14) as we did not find increases in MPS with HP
compared to MP. Consistent with this notion, it was reported
that feeding and concomitant insulin response increase gut
tissue net protein synthesis (13). Stimulation of gut protein
synthesis is potentially beneficial, particularly in a situation
where MPS has been already maximized. Proteins retained in
the gut can be released into the circulation as a consequence of
gut protein turnover, and then be used for MPS (14). This
mechanism could be particularly important overnight, in which
the fasting state is predominated by PB, which resultant
negative NB [net balance].

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Probiotic supplementation attenuates increases in

body mass and fat mass during high-fat diet in healthy
young adults.

the effects would persist in the long-term. Another limitation I

would add is that the results seen in this study might not be
relevant to athletic populations.

Osterberg KL, Boutagy NE, McMillan RP1, Stevens JR, Frisard

MI, Kavanaugh JW, Davy BM, Davy KP, Hulver MW. Obesity
(Silver Spring). 2015 Oct 14. doi: 10.1002/oby.21230. [PubMed]
OBJECTIVE: The objective was to determine the effects of the
probiotic, VSL#3, on body and fat mass, insulin sensitivity, and
skeletal muscle substrate oxidation following 4 weeks of a high-fat
diet. METHODS: Twenty non-obese males (18-30 years)
participated in the study. Following a 2-week eucaloric control diet,
participants underwent dual X-ray absorptiometry to determine
body composition, an intravenous glucose tolerance test to
determine insulin sensitivity, and a skeletal muscle biopsy for
measurement of in vitro substrate oxidation. Subsequently,
participants were randomized to receive either VSL#3 or placebo
daily during 4 weeks of consuming a High-fat (55% fat),
hypercaloric diet (+1,000 kcal day-1 ). Participants repeated all
measurements following the intervention. RESULTS: Body mass
(1.42 0.42 kg vs. 2.30 0.28 kg) and fat mass (0.63 0.09 kg vs.
1.29 0.27 kg) increased less following the High-fat diet in the
VSL#3 group compared with placebo. However, there were no
significant changes in insulin sensitivity or in vitro skeletal muscle
pyruvate and fat oxidation with the High-fat diet or VSL#3.
CONCLUSIONS: VSL#3 supplementation appears to have
provided some protection from body mass gain and fat
accumulation in healthy young men consuming a High-fat and highenergy diet. SPONSORSHIP: This study was funded by VSL
Pharmaceuticals, Inc.

Study strengths
This study is conceptually strong, as it adds to an interesting but
scant body of research showing the effectiveness of probiotic
supplementation for fat loss.14,15 Diets were planned via software
by a registered dietitian who created 7-day rotating menus.
Breakfast was prepared daily by research staff, and subjects
consumed it under their supervision (breakfast contained the
1000 kcal surplus-yielding milkshake that housed either the
placebo or the probiotic supplement). A cooler containing the
remainder of the days food was provided to take home. Body
composition was assessed via dual X-ray absorptiometry (DXA).

As seen above, the main finding was that the probiotic

supplement (VSL#3) resulted in significantly less bodyweight
and body fat gain compared to placebo after 4 weeks in a 1000
kcal, high-fat energy surplus. In terms of the actual numbers,
VSL#3 gained 0.88 kg less total mass and 0.66 kg less fat mass
than the placebo group. If one were to present this data for the
purpose of selling the supplement, it can accurately be said that
the placebo group gained twice as much fat. However, the net
difference (0.66 kg) can be viewed as relatively minor. But, you
can also speculate that if this effect persisted for several months
or years, it could amount to a substantial prevention of fat gain.
Unfortunately, the study was only 4 weeks. No significant
difference was seen in the secondary outcomes (circulating
endotoxin concentrations, proinflammatory cytokines, insulin
sensitivity, and skeletal muscle substrate metabolism), which
leaves unanswered questions about potential mechanisms.

The authors acknowledged four limitations of the study. 1) The

sample size (20 subjects) was small, which opens the possibility
of being statistically underpowered. 2) The results might be
limited to the subject profile healthy, young, normal-weight
males. Effects in other poulations such as women or the elderly
are unknown. 3) Compliance to the instruction to maintain
habitual physical activity was not assessed. Therefore,
differences in body composition due to changes in physical
activity cannot be ruled out. 4) It is unknown which specific
strains of probiotics were responsible for the mitigation of body
fat gain. Furthermore, the mechanism(s) responsible for the antilipogenic effects of the probiotics are poorly understood and
require further research in order to be elucidated. To these
acknowledged limitations, I would add that the study was
relatively short (4 weeks), so it remains unknown whether or not

The authors speculate that there are four potential mechanisms

through which VSL#3 may work its anti-lipogenic magic: 1)
reduced energy harvesting at the gut level via alterations in gut
microflora; 2) less lipase activity resulting in reduced lipid
absorption and increased fecal fat excretion; 3) increased energy
expenditure and whole-body fat oxidation from increased GLP-1
secretion;16 3) increased inhibition of lipoprotein lipase by
increased angiopoietin-like protein-4;17 4) increased sympathetic
nervous system activity innervating and raising brown adipose
tissue thermogenesis.18 Ultimately, this study supports and
extends the findings of previous research showing the promise of
probiotic supplementation for fat loss (or in this case, inhibition
of fat gain). However, I wonder just how effective this
supplementation might be in exercising populations. I also
wonder what the effects would be in conditions where energy
expenditure is objectively assessed (for example, via doubly
labeled water). I would also love to see an independent/noncommercially vested study, preferably with a longer duration.

Alan Aragons Research Review November 2015

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Study limitations

Page 6

Postexercise glycogen recovery and exercise
performance is not significantly different between fast
food and sport supplements.
Cramer MJ, Dumke CL, Hailes WS, Cuddy JS, Ruby BC. Int J
Sport Nutr Exerc Metab. 2015 Oct;25(5):448-55. [PubMed]
BACKGROUND & PURPOSE: A variety of dietary choices are
marketed to enhance glycogen recovery after physical activity. Past
research informs recommendations regarding the timing, dose, and
nutrient compositions to facilitate glycogen recovery. This study
examined the effects of isoenergetic sport supplements (SS) vs. fast
food (FF) on glycogen recovery and exercise performance.
METHODS: Eleven males completed two experimental trials in a
randomized, counterbalanced order. Each trial included a 90-min
glycogen depletion ride followed by a 4-hr recovery period.
Absolute amounts of macronutrients (1.54 0.27 gkg-1
carbohydrate, 0.24 0.04 gkg fat-1, and 0.18 0.03gkg protein-1)
as either SS or FF were provided at 0 and 2 hr. Muscle biopsies
were collected from the vastus lateralis at 0 and 4 hr post exercise.
Blood samples were analyzed at 0, 30, 60, 120, 150, 180, and 240
min post exercise for insulin and glucose, with blood lipids analyzed
at 0 and 240 min. A 20k time-trial (TT) was completed following
the final muscle biopsy. RESULTS: There were no differences in
the blood glucose and insulin responses. Similarly, rates of glycogen
recovery were not different across the diets (6.9 1.7 and 7.9 2.4
mmolkg wet weight- 1hr-1 for SS and FF, respectively). There
was also no difference across the diets for TT performance (34.1
1.8 and 34.3 1.7 min for SS and FF, respectively.
CONCLUSIONS: These data indicate that short-term food options
to initiate glycogen resynthesis can include dietary options not
typically marketed as sports nutrition products such as fast food
menu items. SPONSORSHIP: None listed.

The main findings were a lack of significant difference in

glycogen resynthesis (as seen above), blood glucose & insulin,
blood lipids, and TT performance (34.1 1.8 and 34.3 1.7 min
for SS and FF, respectively). One of the important things you
wont get from reading the abstract are the specific foods
compared, which are as follows:

Study strengths
This study examines a practical question for athletes who do not
have a preference for, cannot afford, or cannot readily access
engineered sports products. In addition to assessing the rate of
glycogen resynthesis, a time trial (TT) was done in order to
compare the practical/performance effects of each protocol. A
crossover design enabled all the subjects to undergo both
treatments, which minimizes confounding from inter-individual
differences, and also alleviates the compromised statistical
power of a small sample size (11 subjects).
Study limitations
The authors acknowledged three limitations: 1) The lifestyle of
subjects between trials cannot be controlled, so this opens up the
possibility of confounding variation in physical activity and
resting glycogen levels. 2) Despite training and calibration,
human error can occur with the use of instrumentation. 3)
Participants were recruited by convenience, not randomly
sampled. However, random ordering of treatments was utilized
in a cross-over design. Id add that the results might be limited to
the subject profile (young, recreationally active males).
Questions remain about effects in advanced competitors with
less time available for recovery between events. In addition, the
results might be limited to the dietary agents compared. Its
possible that differences might have been detected in a
comparison using different foods & products.

The authors concluded that their isocaloric, isomacronutritional

comparison of fast food vs. engineered sports supplement
feedings in optimized carbohydrate dosing for glycogen
resynthesis (1.54 g/kg at 0 and 2 hrs post-depletion) did not yield
differences in muscle recovery or subsequent exercise
performance. Also, the fast food feeding did not differently
affect blood lipids, as well as glucose & insulin, compared to the
sports supplements. Although these findings are not very
surprising to me, they must be quite disappointing for companies
that produce sports beverages, bars, Bloks, and chews.

Alan Aragons Research Review November 2015

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Page 7


Ahtiainen JP, Pakarinen A, Alen M, Kraemer WJ, Hkkinen

K. Short vs. long rest period between the sets in
hypertrophic resistance training: influence on muscle
strength, size, and hormonal adaptations in trained men. J
Strength Cond Res. 2005 Aug;19(3):572-82. [PubMed]
2. Buresh R, Berg K, French J. The effect of resistive exercise
rest interval on hormonal response, strength, and
hypertrophy with training. J Strength Cond Res. 2009
Jan;23(1):62-71. [PubMed]
3. Villanueva MG, Lane CJ, Schroeder ET. Short rest interval
lengths between sets optimally enhance body composition
and performance with 8 weeks of strength resistance
training in older men. Eur J Appl Physiol. 2015
Feb;115(2):295-308. [PubMed]
4. de Salles BF, Simo R, Miranda F, Novaes Jda S, Lemos A,
Willardson JM. Rest interval between sets in strength
training. Sports Med. 2009;39(9):765-77. [PubMed]
5. Henselmans M, Schoenfeld BJ. The effect of inter-set rest
hypertrophy. Sports Med. 2014 Dec;44(12):1635-43.
6. Moore DR, Robinson MJ, Fry JL, Tang JE, Glover EI,
Wilkinson SB, Prior T, Tarnopolsky MA, Phillips SM.
Ingested protein dose response of muscle and albumin
protein synthesis after resistance exercise in young men. Am
J Clin Nutr. 2009 Jan;89(1):161-8. [PubMed]
7. 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 Sep;109(9):1582-6.
8. Phillips SM, Van Loon LJ. Dietary protein for athletes:
from requirements to optimum adaptation. J Sports Sci.
2011;29 Suppl 1:S29-38. [PubMed]
9. Yang Y, Breen L, Burd NA, Hector AJ, Churchward-Venne
TA, Josse AR, Tarnopolsky MA, Phillips SM. Resistance
exercise enhances myofibrillar protein synthesis with graded
intakes of whey protein in older men. Br J Nutr. 2012 Nov
28;108(10):1780-8. [PubMed]
10. Pennings B, Groen B, de Lange A, et al. Amino acid
absorption and subsequent muscle protein accretion
following graded intakes of whey protein in elderly men.
Am. J. Physiol. 2012; 302:E9929. [PubMed]
11. Kim IY, Schutzler S, Schrader A, Spencer H, Kortebein P2,
Deutz NE, Wolfe RR, Ferrando AA. Quantity of dietary
protein intake, but not pattern of intake, affects net protein
balance primarily through differences in protein synthesis in
older adults. Am J Physiol Endocrinol Metab. 2015 Jan
1;308(1):E21-8. [PubMed]
12. Adechian S, Balage M, Remond D, Mign C, QuignardBoulang A, Marset-Baglieri A, Rousset S, Boirie Y,
Gaudichon C, Dardevet D, Mosoni L. Protein feeding
pattern, 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 Oct 15;303(8):E973-82. [PubMed]

Alan Aragons Research Review November 2015

13. Arciero PJ, Ormsbee MJ, Gentile CL, Nindl BC, Brestoff
JR, Ruby M. Increased protein intake and meal frequency
reduces abdominal fat during energy balance and energy
deficit. Obesity (Silver Spring). 2013 Jul;21(7):1357-66.
14. Kadooka Y, Sato M, Imaizumi K, et al. Regulation of
abdominal adiposity by probiotics (Lactobacillus gasseri
SBT2055) in adults with obese tendencies in a randomized
controlled trial. Eur J Clin Nutr 2010;64:636-643. [PubMed]
15. Sanchez M, Darimont C, Drapeau V, et al. Effect of
Lactobacillus rhamnosus CGMCC1.3724 supplementation
on weight loss and maintenance in obese men and women.
Br J Nutr 2014;111:1507-1519. [PubMed]
16. Yadav H, Lee JH, Lloyd J, Walter P, Rane SG. Beneficial
metabolic effects of a probiotic via butyrate-induced GLP-1
hormone secretion. J Biol Chem. 2013 Aug
30;288(35):25088-97. [PubMed]
17. Aronsson L1, Huang Y, Parini P, Korach-Andr M,
Hkansson J, Gustafsson J, Pettersson S, Arulampalam V,
Rafter J. Decreased fat storage by Lactobacillus paracasei is
associated with increased levels of angiopoietin-like 4
protein (ANGPTL4). LoS One. 2010 Sep 30;5(9). pii:
e13087. [PubMed]
18. Tanida M1, Shen J2, Maeda K2, Horii Y2, Yamano T2,
Fukushima Y2, Nagai K2 High-fat diet-induced obesity is
attenuated by probiotic strain Lactobacillus paracasei ST11
(NCC2461) in rats. Obes Res Clin Pract. 2008 Sep;2(3):I-II.

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Page 8

Soylent: a suboptimal solution to first-world problems.

By Alan Aragon

involvement with the formulation of Soylent is not completely

clear, but it could be an ongoing partnership since the formula
has changed several times since its inception. Heres a shot of
the ingredients of the latest powdered version (v1.5):

Soylent is a meal replacement product formulated in early 2013
by software engineer Rob Rhinehart, who since has inexplicably
raised over 3 million dollars to support the venture via crowd
funding. This is the largest sum of publicly donated money ever
generated for a food product. It was released into the market in
early 2014. What makes Soylent different from other meal
replacement drinks? Mainly its marketing and lack of flavor. It
doesnt have a singular focus on weight loss. Rather, the
campaign is directed towards eliminating the productivitykilling, time-robbing inconvenience of going out and fetching
or worse yet, preparingreal food. Furthermore, strong appeals
are made to consumers disdain for expending any kind of effort,
yet equally strong appeals are made to consumers desire for
good health. Another potent marketing tactic is the promise of
saving the environment by not being wasteful. In short, Soylent
hits consumers in the deep feels, not just the superficial stuff.
Quoting the website:

Well, there it is! Above are the contents of a product described

on the website as a nutritional profile that is optimized for the
average adult human, using guidelines from the Institute of
Medicine, United States FDA, and our physician team. Before
even discussing macro- and micronutrition, keep in mind that
ingredients are listed in order of amount within the mix,
beginning with the highest. Does a predominance of canola oil,
sunflower oil, maltodextrin, and modified food starch sound like
the optimization of health? Heres the ingredient list of the more
recently released pre-mixed drink (v2.0):

Soylent frees you from the time and money spent shopping,
cooking and cleaning, puts you in excellent health, and vastly
reduces your environmental impact by eliminating much of the
waste and harm coming from agriculture, livestock, and foodrelated trash.

Suboptimal ingredients
Soylent claims to be nutritionally complete, to the degree of
covering all human macro- and miconutritional requirements.
Rhinehart apparently is no dummy, so he wisely employed Dr.
F. Xavier Pi-Sunyer, a professor of medicine at Columbia
University, as their advisor in developing the product. I have
known of Pi-Sunyer for at least a decade. He wrote an excellent
peer-reviewed critique of the glycemic index in 2002,1 and its
still one of my favorite papers. The extent of Pi-Sunyers

Well, there you go! Optimized human nutrition from a

predominance of maltodextrin, soy protein isolate, high-oleic
algal oil, isomaltulose, and rice starch. Please do not miss my
sarcasm, dear reader. Having refined carbohydrates, subpar

Alan Aragons Research Review November 2015

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Page 9

protein, and refined oils as your diets foundation doesnt even

deserve the dignity of being called suboptimal. Id call it pisspoor subsistence.
Suboptimal macros
The macronutritional breakdown of a serving of the powder is
listed as 500 kcal, 20 g protein, 57 g carbohydrate, and 23 g fat
(15%P, 45%C, 40%F). The pre-mixed drink is listed as 400 kcal,
20 g protein, 37 g carbohydrate, and 21 g fat (20%P, 33%C,
The website claims that Soylents nutritional profile is based on
the Institute of medicines (IOM) guidelines, but thats just
not true. The Acceptable Macronutrient Distribution Ranges
(AMDRs) set by the IOM lists 20-35% of total energy as the
appropriate fat intake for adults.2 Soylents 40-47% fat
proportion is significantly higher than what the IOM
recommends. And of course, this high fat content comes at the
expense of protein and carbohydrate. It is well-established that
the RDA for protein (0.8 g/kg) is not optimal. In many cases, its
flat-out insufficient. Protein consumed at double the RDA (1.6
g/kg) has repeatedly outperformed the RDA for preserving lean
mass and reducing fat mass in hypocaloric conditions.3,4 In order
for an 80 kg (176 lb) person to consume protein at 1.6 g/kg via
Soylent, this would require 6.4 servings (3200 kcal in powder, or
2560 kcal in drink form). This makes Soylent a bad choice for
those dieting for weight/fat loss, especially since higher protein
intakes have the advantages of increased satiety, lean mass
preservation, and thermic effect.5

form. This is a tell-tale indicator of keeping production costs

low. Magnesium oxide has been shown to have substantially
poor bioavailability compared to other forms such as magnesium
citrate.7-9 Compounding this issue, approximately half of the US
population fails to consume adequate amounts of magnesium.10
The other micronutrient that stands out is vitamin D. An
estimated 30-50% of the general population are vitamin Ddeficient,11 so its important to get this nutrient right. Vitamin D3
(cholecalciferol) is the preferred form due to its superior
bioavailability and functional capacity for numerous biological
roles. Soylent contains vitamin D2 (ergocalciferol), which is not
only inferior at raising total vitamin D levels, but has actually
been shown to lower serum D3 levels.12
Suboptimal taste
How does it taste? In short: not good. However, some truly
weird people find it tolerable. Soylent was designed to have a
bland taste, but it obviously cant have zero flavor, since certain
flavoring agents are necessary to mask the nasty-tasting
ingredients in the formula. Heres a rather entertaining video of
people trying it. Soylents taste has been hilariously described as
such: Soylent 2.0 tastes like a chalkboard-eraser-Elmer's-glue
smoothie, but it really is convenient and, if not tasty, palatable.
That sounds like a euphemistic way of saying that it tastes like
the way prison feels.

Soylent claims to be inexpensive ($2.42 USD per 400 kcal). But

as the saying goes, you get what you pay for. Calling something
optimized when it should be called economized is irritating.
On that note, a couple of things stand out (not in a good way)
about their micronutritional sources. Magnesium is in the oxide

Pi-Sunyer FX. Glycemic index and disease. Am J Clin Nutr. 2002

Jul;76(1):290S-8S. [PubMed]
2. Manore M. Exercise and the Institute of Medicine recommendations
for nutrition. Curr Sports Med Rep. 2005;4(4):193-8. [PubMed]
3. Layman DK, Evans E, Baum JI, Seyler J, Erickson DJ, Boileau RA.
Dietary protein and exercise have additive effects on body composition
during weight loss in adult women. J Nutr. 2005 Aug;135(8):1903-10.
4. Layman DK1, Evans EM, Erickson D, Seyler J, Weber J, Bagshaw D,
Griel A, Psota T, Kris-Etherton P. A moderate-protein diet produces
sustained weight loss and long-term changes in body composition and
blood lipids in obese adults. J Nutr. 2009 Mar;139(3):514-21.
5. Leidy H, Clifton P, Astrup A, Wycherley T, Westerterp-Plantenga M,
Luscombe-Marsh N, et al. The role of protein in weight loss and
maintenance. Am J Clin Nutr. 2015; pii: ajcn084038. [Epub ahead of
print]. [PubMed]
6. Food and Nutrition Board, Institute of Medicine. Dietary Reference
Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol,
Protein, and Amino Acids. 2005. [Summary PDF]
7. Lindberg JS, Zobitz MM, Poindexter JR, Pak CY. Magnesium
bioavailability from magnesium citrate and magnesium oxide. J Am
Coll Nutr. 1990 Feb;9(1):48-55. [PubMed]
8. Firoz M, Graber M. Bioavailability of US commercial magnesium
preparations. Magnes Res. 2001 Dec;14(4):257-62. [PubMed]
9. Walker AF, Marakis G, Christie S, Byng M. Mg citrate found more
bioavailable than other Mg preparations in a randomised, double-blind
study. Magnes Res. 2003 Sep;16(3):183-91. [PubMed]
10. Rosanoff A, Weaver CM, Rude RK. Suboptimal magnesium status in
the United States: are the health consequences underestimated? Nutr
Rev. 2012 Mar;70(3):153-64. [PubMed]
11. Wacker M, Holick, MF. Vitamin D - effects on skeletal and
extraskeletal health and the need for supplementation. Nutrients. 2013
Jan 10;5(1):111-48. [PubMed]
12. Lehmann U, Hirche F, Stangl GI, Hinz K, Westphal S, Dierkes J.
Bioavailability of vitamin D(2) and D(3) in healthy volunteers, a
randomized placebo-controlled trial. J Clin Endocrinol Metab. 2013
Nov;98(11):4339-45. [PubMed]

Alan Aragons Research Review November 2015

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The IOMs fiber guidelines are not met either. Fiber content is
3g in both the powder serving and the bottled drink. The IOMs
recommended intake for total daily fiber for adults 50 years and
younger is 38 g for men and 25 g for women.6 For those over 50,
this is reduced to 30 & 21 g, respectively, due to decreased food
consumption. This means that if youre not over 50, youd have
to consume approximately 8-12 servings of Soylent in order to
hit the recommended fiber intake. Thats 3200-4800 kcals
worth of the drink, and 4000-6000 kcal of powder. Alternatively,
you can eat whole- & less-refined foods, and meet your fiber
requirements in a lot less calories (you can also experience the
joy of chewing).
Suboptimal micros


Page 10

Eric Helms interrogated about recomp & magic.

By Alan Aragon
Alright Eric, thanks again for continuing this interrogation
series. While I was toiling indefatigably (ya like that?) on the
completion of the latest issue of AARR, you and Menno
Henselmans got into a rather epic debate/discussion over
various aspects of energy balance and body composition
change. The cool thing is that you both had some great learning
moments and you also came to some common resolutions
(while I'm sure certain disagreements still exist).
The prevailing conventional wisdom says that weight gain
beyond transient fluctuations requires the sustaining of an
energy surplus over time. Same thing with an energy deficit for
weight loss. Obviously, this doesn't take into account what goes
on with fat mass versus lean mass.
Getting to the first set of questions... Body fat can obviously be
lost in a caloric deficit, there are endless examples of this in the
vast literature involving weight loss experiments. What's also
been seen repeatedly in the literature is a simultaneous loss of
fat and gain in lean mass during hypocaloric & eucaloric
conditions. However, what has been disputed is the idea that
net losses in fat can occur in a sustained energy surplus wherein
net gains in total bodyweight occur. In other words, a scenario
where gains in lean mass exceed losses in body fat (with both
phenomena occurring). Please give me your thoughts on this,
and include any standout examples in published research that
support of the possibility of this scenario.
Did I like your use of "indefatigably"? Simple answer:
indubitably I did! First, let me say again, honor to be
"interrogated" by you Alan. It's all good cop and no bad cop with
you. I get the proverbial donuts and coffee, but no sleep
deprivation or threats of prison. So again, much appreciated for
letting me grace the pages of the AARR!
Much to talk about here. Indeed the debate with Menno was
enlightening for me (hopefully for both of us). Speaking for
myself, I definitely came away with new perspectives. While I
didn't have a shift in my perspective on protein per se (which
was the topic of the debate), I did experience shift in perspective
after the debate took an odd left turn towards the nature of
energy balance. For a brief bit of background, I shared the key
studies on trained lifters performing resistance training while
dieting to present my case, and then to make his case Menno
cited a handful of studies where fat was lost and represented
them as dieting studies.

weight over 2 to 6 month periods. I vehemently denied these

studies were dieting studies and stated that bodyweight is
determined by energy balance. Menno correctly pointed out that
I was wrong to say that bodyweight is dictated by energy
balance. To prove his case he cited the large differences in the
energy content of muscle versus body fat. He then stated that
any study in which fat is lost, is in fact the result of a caloric
deficit. So, I dug into the studies he presented and back
calculated the energy balance for each study group based on the
changes in fat mass and fat free mass, and ended up finding out
that we were both wrong.
Most importantly, on my part it is incorrect to state that
bodyweight change is determined by energy balance, more
correctly, body tissue mass change is determined by energy
balance. While I understood that body fat and lean body mass
had vastly different energy densities and water contents for the
same volume and weight of tissue, I'd never truly considered that
you can in fact gain weight in a deficit. Likewise, while Menno
had the presence of mind to consider this, he didn't think it was
possible to lose fat in a surplus. We both found out we were
wrong when I went through and did the math.
To answer your question, fat loss can actually happen in a
supposedly sustained surplus where net gains in total
bodyweight occur (due to the lean mass gained weighing more
than the fat mass lost). To prove my point I have to get into
some math, there is no way around it unfortunately. But believe
it or not, there are two examples just in the studies that Menno
brought up in the debate. I'll use one to illustrate the point. In
the less recent of the two studies by Dr. Jose Antonio and
colleagues on very high protein diets, fat loss during a surplus
occurred only in the 4.4g/kg (2g/lbs) protein group. Over the 8
week study period, these subjects gained 1.9kg of lean body
mass while losing 0.2kg of fat mass:
When using lab methods of measuring changes in body
composition, changes in water are calculated as a part of lean
body mass, while changes in fat mass are that only of actual fat,
not adipose tissue (which includes some water). Thus, there are
9434.4 kcal per kg of fat mass, and 1815.2 kcal per kg of lean
mass using the arguably most accurate and up to date energy
values from Dr. Hall in his 2007 paper on this
To calculate the net energy balance of these subjects you need
only add the surplus required to deposit 1.9kg of lean mass to the
deficit required to metabolize 0.2kg of fat mass. Doing so yields
a net energy surplus of 1562 kcal over this 8 week period, which
on average is a ~28 kcal surplus per day. So indeed, fat loss
occurred during a surplus.

I called foul, pointing out that the studies were not dieting
studies because a caloric deficit was not enforced. I also
emphasized that out of the 12 cohorts of subjects represented in
the 5 studies, 7 cohorts gained weight, 2 cohorts maintained
weight, and the remaining 3 lost only 100-300 grams of body

Now to give you my thoughts, first this is a group mean not what
necessarily occured in every subject in this group, but most
likely fat loss and lean mass gains did occur during a slight
surplus in enough of the subjects or the mean would likely look
different. Second, obviously the magnitude of fat loss here is
incredibly small. 200g of fat lost in 8 weeks is nothing you
would even notice. Thirdly, 1.9kg of lean body mass is not as

Alan Aragons Research Review November 2015

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Page 11

impressive as it sounds, as this includes the water content in the

body overall, and also the inherent water content of hydrated
muscle. The actual contractile protein added to the body is a
fraction of this, and not even all of the 1.9kg would be hydrated
muscle. I point out the practical realities of these body comp
changes just so people don't think magic is occurring. Finally,
for those who might think "this throws the '3500 calorie rule' out
the window!", I disagree and here is why.
The subjects gained a net 3.7lbs, which if you used the old
"3500kcal per pound rule" to roughly estimate the surplus, you'd
estimate the subjects would have been in a ~230kcal surplus per
day, so you'd overestimate the surplus by 200kcals. First off, in a
practical setting that wouldn't be too terrible. Simply using an
inappropriate maintenance calorie estimation equation or even
an appropriate equation but an inappropriate activity multiplier
would produce similar if not greater errors. But more
importantly, it wouldn't be an issue at all in a practical setting.
The metabolic cost of synthesizing muscle is so great that it has
been estimated that it "costs" 4 to 5 times the energetic value of
muscle to synthesize it (Williams, M.H., Nutrition for health,
fitness, & sport. 2005: McGraw-Hill Science Engineering).
What this means, is that if you are not in a study setting, but
rather in a practical one, and you set up a lean gaining diet based
on the "3500 calorie rule", you wouldn't be far off at all. To
prove my point, let's say you accurately determined maintenance
calories (which is actually not always a fair assumption) to be
3000kcal per day. Then, if you wanted to try to put on half a
pound of (hopefully) lean mass per week for 8 weeks like these
subjects did, you'd attempt to increase your calories by 250/day
using the 3500 kcal rule (as a side note gaining half a pound of
week is probably around the fastest a trained natural lifter should
go to avoid fat gains, see last AARR's "Less Recent Gem"). Now
interestingly enough, if you were successful in synthesizing that
amount of muscle (like the subjects were), the energetic cost of
building that muscle would be so high that TDEE would rise
from heat generation to the point where you were actually in a
much smaller surplus than the intended 250 kcal per day. Since
the cost of building the muscle is 4 to 5 times the metabolizable
energy of it, you'd only end up in a 40-50kcal surplus at most per
day over the 8 weeks. Interestingly, this is only a 10-20 calories
different than the surplus of the subjects in this study. So while it
is true that you might only be in a ~50kcal surplus rather than
the 250 kcal surplus you prescribed yourself, you wouldn't
know it because you aren't a subject in a laboratory. In fact,
using the "3500 calorie rule" in this hypothetical example would
actually lead you to think that the "3500 kcal rule" estimation
held up quite nicely. So basically, let's not throw the proverbial
baby out with the bathwater. Due to the fact in the real world we
can't differentiate between adipose tissue and pure fat mass, the
3500 calorie rule is a perfectly fine estimation for a fat loss
caloric intake prescription, and due to the cost of synthesizing
muscle, the 3500 kcal rules is a perfectly fine estimation for a
lean gain caloric intake prescription.

immediately/automatically grasp the calculation (based on

the 2007 Hall paper Eric cited):
Fat-free mass (FFM), within the context of this discussion is
referring to hydrated muscle, which has an energy density of
7.6 MJ/kg. This converts to 1815.2 kcal/kg. The energy density
of body fat is much greater than that of muscle. Fat's energy
density is estimated at 39.5 MJ/kg. This converts to 9434.4
kcal/kg. So, in Antonio et al's recent study comparing high vs
super-high protein intakes, the following occurred during 8
weeks: 1.9 kg FFM was gained, 0.2 kg FM was lost. What
follows is the translation of these tissue masses into calories,
ending off with the net balance:
1.9 x 1815.2 (the energy density of FFM) = 3448.88 kcal (gained)
0.2 x 9434.4 (the energy density of FM) = 1886.80 kcal (lost)
3448.88 - 1886.80 = 1562.08 kcal (net surplus)
So, a net caloric surplus of 1562.08 kcal was spread over 8
weeks (56 days), and this translates to an average daily surplus
of approximately 28 kcal/day, since 1562.08 56 = 27.89.
Great points, Eric. I'd like to acknowledge a few things, and
raise some of my own discussion points as well. First, I agree
with your conclusion that we can't throw out the "3500 kcal
rule" because it covers unforeseen increases in energy
expenditure, which are a reality in many cases. The fact of the
matter is that it's very common for programmed caloric
surpluses (via increased intake) to be overtaken by concurrent
increases in total training output (more weight moved &/or
reps &/or sets done), which ironically, were fueled by the
increased energy intake. In short, programmed surpluses can
rather easily be "swallowed up" by increases in training
variables, not to mention training adaptations themselves
which can ramp up maintenance energy requirements.
Adding to this, some individuals ramp up non-exercise activity
thermogenesis (NEAT) to extraordinary degrees. I'm certain
you're familiar with Levine et al's 1999 study, where 8 weeks of
running a 1000 kcal surplus resulted in a mean storage of only
432 kcal; the rest was dissipated through an increase in NEAT.
This increase in NEAT among the subjects was as high as 692
kcal/day. These findings reinforce the idea that, as you
mentioned, surpluses can potentially be under-programmed to
a degree where they soon disappear. The results also support
the idea that people who think they're "hard gainers" may
actually just be "NEAT freaks" who hyper-respond to caloric
intake increases by increasing subconscious/unconscious
energy output.

Speaking directly to the readership: I wanna provide some

background to Eric's explanation, for the readers who don't

That was sharp of you to break down just how small the
absolute changes were. Quoting you: "200g of fat lost in 8
weeks is nothing you would even notice." Agreed. In imperial
terms, 200 g is less than half a pound in 8 weeks. Yup, that's a

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tiny amount. Furthermore, we must keep in mind a couple of

important things. First off, we're putting a certain degree of
faith in the accuracy of body composition estimation. In this
case it was via air displacement plethysmography (Bod Pod),
which has its limitations (as do all methods), including highly
variable individual results. Secondly, subjects self-reported their
intake, which is a common compromise in research due to
feasibility constraints Preparing & providing subjects all of their
intake is ideal, but it's rare since it's cost-prohibitive.
Unfortunately, self-reported intake is notoriously inaccurate.
So, it's possible that one or both of the aforementioned caveats
could confound the data we're looking at, I'd say that this
discussion will always be somewhat speculative until more
tightly controlled conditions are carried out, of course with
optimized macros and resistance training. Imagine such a study
where all intake is provided, and energy expenditure is tracked
objectively via doubly labeled water. We can dare to fantasize,
right? I know, it's not gonna happen anytime soon (or ever). It's
already a massively difficult undertaking to do studies that are
far less controlled.
A commonly held assumption is that simultaneous fat loss &
muscle gain (recomposition, or "recomp") only happens to a
significant degree in beginners and to a lesser degree in
intermediates - both of whom have extra fat to lose in the first
place. This makes sense from the fundamental standpoint that
the closer you come to your maximal potential for muscle gain
and/or leanness, the lesser those changes are (down to being
negligible, the further along you are towards your genetic
ceiling in either muscle gain or fat loss). Let's take a look at
some of the research that gets referenced in discussions about
recomp in trained subjects.
In Antonio et al's high-protein study which you cited earlier, has
been used to support the idea that trained subjects, not just
beginners, can experience recomp. Indeed, the subjects
apparently gained muscle and lost fat, despite resistance
training regularly for the last 8.9 6.7 years at an average of 8.5
3.3 hours per week. However, this doesn't necessarily mean
that they're advanced trainees near their potential. The
baseline body fat levels of the high-protein and control group
were 16.3 & 15.1%, respectively. If this was an all-female
sample, a case can be made that subjects were in fact close to
their potential for leanness, but these were the mean values of
a mix of men and women. No specifics of the male-female
breakdown were given. Antonio et al's follow-up study is has
also been cited to support the recomp phenomenon in trained
subjects in a caloric deficit, but the baseline body fat levels of
the high-protein & control groups were 18.3 & 20.2%,
respectively. Notably, approximately 70% of the subjects were
male, which is a strong indication that these subjectsalthough
trainedwere not particularly lean.

follow-up here). While recomp was seen in the face of an

energy deficit lasting 4-12 weeks, with LBM gains occurring only
in the slow weight loss group. However, toward my previous
point, the baseline body fat levels of the subjects were not
particularly low in this group, men and women averaged 17 &
27%, respectively.
This brings me to the practical point that it's generally not
realistic for very lean individuals (e.g., men in the low-teens or
less, and women in the low-20's or less) to expect a meaningful
degree of fat loss in sustained hypercaloric conditions within
the context of a program designed for the primary goal of
muscle gain. I would also say that it's generally not realistic for
most 'trained' subjects to experience muscle gain in a sustained
caloric deficit unless the resistance training stimulus is novel, as
in the case of Garthe et al, which involved elite athletes in
sports that were largely endurance-based and/or did not
involve a predominant demand for strength, power, and mass.
Alan I completely agree on all points. Just to add a few more
points, the subjects in Garthe were elite athletes, but that doesn't
mean they were necessarily "elite" in terms of resistance
training. In fact, if you look at the design of the original study,
and the follow up on the same subjects, you find three things: 1)
The subjects actually added 4 days of resistance training to their
weekly training schedule during the dieting phase. This is a huge
increase in training volume and highlights the fact that to be able
to to do this, they were likely doing sport specific training
almost exclusively prior to this point. 2) Additionally, the lean
body mass gains were predominantly in the upper body, which is
not surprising given the nature of sport specific training as it
tends to predominantly train the lower body. Thus, they were
essentially "upper body newbies". 3) To give credence to this
speculation, in the follow up study the lean body mass they had
gained, was no longer present. Guess what also wasn't present:
the additional 4 days of weight training that had been added.

What about elite athletes, who in many cases represent the

profile of an "advanced" trainee? In Garthe et al's initial
study examining fast versus slow weight loss (0.7 vs 1.4%/wk)
involved elite athletes from a broad range of sports (long-term

So really, this is not a study showing that elite resistance trained

individuals can gain muscle mass in a surplus. Rather, this is a
study showing that lean body mass gains can occur in a deficit, if
the deficit is small (as they only occurred in the slower weight
loss group), and if the subjects aren't already very lean, and
predominantly in muscle groups that are not well trained. That
said I do believe that "recomp" can occur in well trained lifters,
but I don' think the magnitude would be comparable to what
Garthe observed. But that said, as you pointed out in last month's
AARR in the Less Recent Gems, "bulking" really doesn't work
well for trained folks anyway. In the specific study cited last
month, the faster weight gain produced similar gains in strength
and lean body mass, but with five times the gain in fat mass than
the slower gaining approach. So while we could argue that
"recomp" is a slow and inefficient approach to gaining lean body
mass for well trained lifters, we also have to acknowledge that
gaining muscle mass at all is a slow and inefficient process in
trained lifters, and only a very small surplus is needed to
effectively put on lean body mass anyway. So in essence, the
process of gaining almost looks like recomping anyway. This is
something in the well trained natural lifting community we often
jokingly call "gaintaining" (much like your culking) whereby
you eat nearly or just over maintenance calories and simply

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focus on trying to make gains in the weight room in terms of

Also, I want to point out that "getting leaner" can occur during a
gaining phase even if you actually gain body fat. For example,
let's say over a year a new lifter goes from 180lbs to 200lbs. Not
an unreasonable amount of weight gain for a newbie in his first
year of lifting at this size. Let's say the 20lbs gained were 18lbs
muscle, and 2lbs fat. If he started at 15% bodyfat, he'd begin
with 27lbs of fat and 153lbs of muscle. At the end of the 6
months, he'd finish with 29lbs of fat and 172lbs of muscle and
he'd be 14.5% bodyfat because he gained a lot more muscle than
fat. Thus, he would be leaner in terms of body composition
despite a gain of 2lbs of bodyfat.
Additionally, I just want to point out that when we are "back
calculating" energy balance by body comp changes, the
inaccuracy of food reporting doesn't really matter. The changes
in body mass show us what energy was "deposited" as lean or fat
mass, and what was "withdrawn" as decreases in lean or fat
mass. So the energy balance over time (on average) is entirely
calculated by changes in body composition. However, that does
make your point about the Bod Pod very important indeed. And
I agree, while these errors tend to get reduced in group data, it is
very possible that there was actually not a net surplus in place in
the Antonio study, considering how small the calculated surplus
was. A small error could completely account for this.
Additionally, as much as I think Dr. Hall's calculations for the
energy contents of tissues makes sense, there are some
assumptions built in which could make that speculation incorrect
as well.
As a final highly speculative point, I have been thinking about
the nature of NEAT. In research NEAT is often quantified
simply by calculating it as the remainder of TDEE after RMR,
TEF and exercise activity are calculated. Given the "cost" of
building muscle, the gaps in our understanding of what exactly
contributes to NEAT and the inconsistency with which adaptive
increases in NEAT are reported in response to overfeeding (such
as in Levine 1999), I wonder if it is possible that at least part of
the variance and inconsistency could possibly be caused by
when muscle is gained or not? Perhaps in many studies where an
adaptive increase in TDEE is reported via NEAT, we are
actually seeing an increase in TDEE due to the process of
building muscle mass? And when it does not occur, it is partially
due to muscle not being synthesized? I don't know, something
totally speculative but just an interesting thought I had.
Thanks once again for the great information, Eric!
Eric Helms is a co-owner of 3D Muscle Journey
( 3DMJ is dedicated
to providing evidence-based information,
community support, and holistic coaching to
drug-free lifters. Hes coached hundreds of
athletes, attained professional status with the
INBA and competed internationally in rawpowerlifting with the IPF. He holds two masters;
in exercise science and also nutrition for physique
and strength sport. He is pursuing his PhD
researching auto-regulation in powerlifting at
AUT in New Zealand. Check out Eric' books on nutrition and training at

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As with most things in life, it's all about tradeoffs, choosing

objectives, and maximising the utility of available resources. So
one one extreme, you can corral a small number of people in
metabolic wards and strictly control everything about their lives
(nutrition, stress, sleep, activity, social interaction, etc.) for a
short period of time (before they revolt or before you run out of
money b/c this is a ridiculously expensive option) or you can run
a well designed long-term observational study of a large
population using appropriate controls for the major
social/socioeconomic/other factors. Or a study design
somewhere in the middle that focuses on a more narrowly
focused research question; that's why we have a body of
literature/collection of studies with which to fill in (and continue
to refine) the big picture. But as with most things in life, you
can't have it all, at least not all at the same time.
Molly Gregas

If you have any questions, comments, suggestions, bones of

contention, cheers, jeers, guest articles youd like to submit, or
any feedback at all, send it over to

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