12 The effects of low-intensity resistance training

with vascular restriction on leg muscle strength in

older men.
Karabulut M, et al. Eur J Appl Physiol. 2010
Jan;108(1):147-55. [Pubmed]

14 Interview with Michael Krivyan.

By Alan Aragon
Copyright © December 1st, 2011 by Alan Aragon
Home: www.alanaragon.com/researchreview
Correspondence: aarrsupport@gmail.com 17 Nutrient timing – lingering controversy &
confusion.
By Alan Aragon

2 “Ah-ha” moments in 2011: pre-apocalypse edition. 18 Corrections have been made in previous issues.
By Alan Aragon By Alan Aragon

7 Effect of Dietary Protein Content on Weight Gain,

Energy Expenditure, and Body Composition
During Overeating.
Bray GA, et al. JAMA. 2011 2012;307(1):86-87. [JAMA]
8 Exercise dose and insulin sensitivity: relevance for
diabetes prevention.
Dubé JJ, et al. Med Sci Sports Exerc. 2011 Nov 2. [Epub
ahead of print] [Pubmed]

9 Effects of 4 weight-loss diets differing in fat,

protein, and carbohydrate on fat mass, lean
mass, visceral adipose tissue, and hepatic fat:
results from the POUNDS LOST trial.
de Souza RJ, et al. Am J Clin Nutr. 2012 Jan 18. [Epub
ahead of print] [Pubmed]

10 Fish-oil supplementation enhances the effects of

strength training in elderly women.
Rodacki CL, et al. Am J Clin Nutr. 2012 Jan 4. [Epub ahead
of print] [Pubmed]

11 Cardiac autonomic dysfunction in anabolic steroid

users. Critiqued by James Heathers
Maior AS, et al. Scand J Med Sci Sports. 2012 Jan 18. doi:
10.1111/j.1600-0838.2011.01436.x. [Epub ahead of print]
[Pubmed]

Alan Aragon’s Research Review – December 2011 [Back to Contents] Page 1


“Ah-ha” moments in 2011: pre-apocalypse edition.
By Alan Aragon
_________________________________________________________________
Pictured above: a crop circle near Silbury Hill in Wiltshire, England, which appeared on Aug 3, 2004   that’s different from celiac disease, defined as non-celiac
_________________________________________________________________
Another year has whizzed by, and it’s time to attempt to justify
that ever-so-rapid ‘whizzing.’ The following points are
numbered, but not listed in any order of importance. One of the
challenges of acknowledging noteworthy tidbits is making sure
that there aren’t any mere repetitions of ‘ah-ha’ moments in the
past. However, certain things actually do warrant a certain
degree repetition when they show remarkable staying power
through the test of time. What follows is an exposé of what made
an impression on me in 2011. While I’ve typically done this as a
Lay Press or Special Section article in the past, I’ve decided to
lean into it this time, and do a more in-depth feature article.
1. It looks like the Paleo diet’s popularity is still growing. I
can’t confirm whether this is due to an increase in people
subscribing to its supposed merits, or a population-wide
increase in cognitive decline & blind faith. However, a
positive result of this increased popularity is that more
researchers in the academic realm have caught wind of the
Paleo diet fad. Here are some eloquent & illuminating quotes
from a recent review by Knight, critiquing the popular diets
that rely upon an evolutionary rationale:1
“Not only is our knowledge of prehistoric eating habits
inevitably hazy, but the massive social and ecological
changes that have occurred since the Stone Age have
irrevocably changed the foods available to us. It is not
clear why Sears privileges macronutrient ratio as the
defining feature of healthy diet – a pragmatic possibility is
that it is relatively easy for today’s dieters to mimic. At any
rate, Sears uses the Neo-Paleolithic data selectively in
what appears to be a post-hoc rationalisation of his
macronutrient paradigm.”
“The representations of Stone-Age diet, health and lifestyle
that I have discussed in this section are consistently
contradictory and unsupported by scientific and historical
evidence. It is striking, for example, that Sears’s claims
Alan Aragon’s Research Review – December 2011
about the macronutrient composition of Paleolithic diet
are not substantiated even in the specific paper that he
himself cites in support of his figures. Instead, authors like
Sears and Atkins betray a discursive pressure to make the
foodways of other times and other places fit their own pre-
conceived notions of healthy diet.”
2. On the topic of Paleo, we know that grains as a group have
gotten a bad rap, but it’s often a case of throwing the baby
out with the bathwater. It’s gluten, not grains per se, that’s
the potential offender. The prevalence of celiac disease (a
gluten-dependent autoimmune disorder) affects an estimated
0.3-1.2% of the population.2 This wide range exists mainly
because diagnosis is so convoluted & difficult. However,
non-celiac gluten sensitivity (gluten intolerance symptoms
minus the classic biomarkers of celiac disease) and wheat
allergy may be flying under the radar, affecting more people
than previously thought. To quote a review by Bizzaro et al:2
“More recently, however, progress has been made toward
the hypothesis that a form of gluten intolerance exists
gluten intolerance or gluten sensitivity (GS), and it is
estimated that for every person who has CD, there are at
least six or seven people who have GS. Therefore, wheat
allergy, CD, and GS combined together may affect about
10% of the general population.”
Given the above concern, the Paleo crowd decided to kip up
to a broad brush and paint all grains as evil & unfit for human
consumption. This is a careless mistake, since not all grains
contain gluten. In fact, there’s quite a range of gluten-free
grains to choose from. Here’s a handy-dandy chart for the
small segment of the population it might concern:
Gluten‐Containing Grains  Gluten‐Free Grains 
ƒ Barley  ƒ Amaranth 
ƒ Rye  ƒ Buckwheat 
ƒ Triticale  ƒ Corn 
ƒ Wheat – including  ƒ Millet 
bulgur, durum, faro,  ƒ Montina (Indian rice 
kamut, semolina, spelt   grass) 
  ƒ Oats* 
ƒ Quinoa 
ƒ Rice 
ƒ Sorghum 
ƒ Teff 
ƒ Wild rice  
*Oats are a naturally gluten-free grain, but there have been
instances of gluten contamination in factories producing multiple
grain products. Companies that specialize in uncontaminated
gluten-free grains are: Avena Foods, Bob’s Red Mill, Cream Hill
Estates, Gifts of Nature, GF Harvest, Gluten Solutions.
On a related note, Williams wrote a fairly thorough literature
review of the health effects of grains that was published after
my grains article in the October 2011 AARR. To quote him:3
“The totality of evidence shows that consumption of up to
50% of all grain foods as core refined-grain foods (defined
as foods based on refined grains without significant added
[Back to Contents] Page 2
 fat, sugar, or sodium) is not associated with any increase
in disease risk. Nonetheless, eating more whole-grain
foods remains an important health recommendation, and
most consumers will need to reduce their current
consumption of refined grains to no more than one-third to
one-half of all grains in order to meet the targets for
whole-grain foods. It needs to be noted that this conclusion
about refined grains only applies to core refined-grain
cereal foods.”
Something to keep in mind about grain research is that most
of it is industry-sponsored. This undoubtedly biases it
towards a preponderance of positive outcomes. However, the
abundant convergence of evidence from epidemiological and
controlled studies simply does not support the fear-
mongering of the Paleos. In my personal observations in the
field, judicious – as opposed to reckless – consumption of
grains has never been problematic for any of my clientele
across the continuum of sports & fitness goals.
3. Being obese can screw with your vitamin D status. It seems
that people will go to great lengths to blame everything
except gluttony & sloth for the onset and progression of
obesity, claiming that a lack of vitamin D causes obesity.
Well, fat chance – it’s the opposite way around. Over a
decade ago, Wortsman et al found that the impaired vitamin
D status in obese subjects was due to the decreased
bioavailability of vitamin D3 from cutaneous (skin-mediated)
and dietary sources because of the compound’s
deposition/entrapment in the adipose tissue.4
4. It’s been almost exactly 2 years since my blog post critiquing
Dr. Robert Lustig’s fructose lecture. We all know that many
feathers got ruffled over that one, and undies continue to get
bunched-up over it until the present day. I recently got into a
debate with a forum member about how I presented the
USDA Economic Research Service (ERS) data as changes in
percentage points rather than percentage change. He then
realized that even listing the figures as percentage change
would be of limited use since the total kcals increased during
that period. So, he finally settled on the (somewhat desperate)
suggestion that I put the focus on net changes in energy
intake per food group.
I considered the forum member’s suggestion and re-
examined the ERS data. The values of the original post were
based on the 1970-2007. As of this writing, the dates range
from 1970-2009, where total energy intake increased from
2169 to 2594 kcal, which is an increase of 425 kcal:5
 
Proportional Change Net Change
Food Group (% of total kcals) (in kcals)   that’s still on its way to press challenges the idea that fast-
 
Meat, eggs & nuts -3 +10
Dairy -2 -6
Fruit 0 +17
Vegetables -1 -7
Flour & cereal products +4 +187
Added fats/oils & dairy fats +4 +185
Caloric sweeteners -2 +38
Alan Aragon’s Research Review – December 2011
Looking at the data, the proportional changes (in terms of
increases and decreases) are understandably disparate from
the net hikes & drops in actual energy consumed per food
group. Clearly, proportional decreases occurred in
meat/eggs/nuts, dairy, vegetables, and yes – caloric
sweeteners. The latter point is what I stressed in my blog
post. On the other hand, taking a look at net changes, the
only kcal decreases are in dairy & vegetables, and these are
miniscule. The most substantial kcal increases are in
flour/cereal products and added fats/oils & dairy fats. The net
increase in caloric sweetener intake is substantially less than
the increase in the two latter groups.
So, while I learned that it can be helpful to look at actual
changes in kcal intake – as opposed to only proportional
changes, this still does not change the main points I made in
my blog post. Specifically, total kcal intake is substantially
greater in the present day than in 1970, and this is combined
with an increase in sedentary living due current technologies
that facilitate prolonged periods of sitting and clicking.
And of course, the other point I made still stands: sugar
cannot be selectively singled out as the bad guy. Caloric
sweetener intake has proportionally decreased, and its net
increase of 38 kcal per day is almost times less than the kcal
increases from flour & cereal products, as well as added fats
& dairy fat. The fact that HFCS consumption has increased
since 1970 is offset by the fact that the use of other caloric
sweeteners has decreased to almost a stalemate in caloric
sweetener consumption. A final point worth re-emphasizing
is that this is survey research, which is inherently about as
reliable as Kai Green or Victor Martinez peaking properly at
every show they enter.
5. As I mentioned in last year’s “Things I learned in 2010”
article, rats are not a reliable model for predicting human
metabolic responses to carbohydrate. Every time a rodent-
based carbohydrate study pops up in the press, just remember
that the critters’ conversion of carbohydrate to fat has the
potential to be 10 times the rate of humans.6 Recently, I
came across research by Suryawan et al, who found that
humans and rats have vastly different muscle and liver
concentrations of BCAT & BCKD, the respective enzyme
systems involved with the first and second steps of BCAA
catabolism.7 This calls into question the predictability of not
just carbohydrate metabolism in humans when using rodent
models, but also that of protein metabolism.
Recent rodent research by Wilson et al showed the potential
for leucine (or carbohydrate) supplementation to prolong the
anabolic effect of a meal.8 However, other rodent research
absorbing leucine-rich protein must be consumed at metered
points throughout the day in order to maximize anabolism or
anticatabolism. It potentially holds more weight than Wilson
et al’s study, since it didn’t merely measure acute effects.
Adechian et al conducted 2 separate experiments comparing
3 different high-protein diets.9 They found that under 3
weeks of hypocaloric conditions, no significant difference in
the sparing of lean mass occurred between rodents that
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 consumed casein, whey (referred to in this study as milk
soluble protein), or a mix of casein & whey. This lack of
difference was seen regardless of whether the daily diets
were consumed over a 12-hour period or a 2-3-hour period.
Interestingly, this lack of agreement between acute effects
and longer-term effects is similar to what’s been seen in
humans.
6. Resistance training to failure, at both high (90% 1RM) and
low (30% 1RM) intensities, can cause an increased anabolic
sensitivity of muscle to protein feedings that can last up to 24
hours.10 This short-term finding can potentially explain – at
least partially – the lack of differential outcomes in recent
non-acute research comparing different placements of protein
feedings relative to the resistance training bout.
7. There might actually be something slightly magical about the
classic night-time carb-heavy gut-bomb. And I’d emphasize
“might” because the evidence base for this is still relatively
thin & racked with important limitations. However, in
controlled studies, the results are strikingly consistent. Martin
Berkhan has already done a good job of compiling the
research in this area, so I’m not going to recount all of it.11
Nevertheless, the most recent study in the saga is truly
provocative. In a 6-month trial with a larger-than-typical
subject sample, Sofer et al saw greater reductions in total
weight, fat mass, and waist circumference in subjects who
consumed the majority of their carbs at dinner, as opposed to
a more evenly spread consumption throughout the day in the
control group.12 A slightly lesser drop in leptin was seen in
the experimental group, which the authors speculate is what
led to greater satiety/lower hunger levels. Furthermore, the
experimental group had better improvements in measures of
glucose control, lipids, insulin sensitivity, and inflammation.
If the study went on any longer, you’d think that the subjects
in the experimental group would develop superpowers. These
type of results are just begging for a follow-up study to either
confirm or challenge them. Would a structured training
protocol neutralize the differences between the groups?
Would the same effects be seen in a similar design carried
out in non-obese subjects? We don’t know – yet. I personally
wouldn’t expect the ‘magic’ to appear in all conditions, but
then again, the results seen here were not expected either.
8. In a 2006 literature by La Forgia et al, the much-hyped
excess postexercise oxygen consumption (EPOC, also called
the afterburn) effect got the wind sucked out of its sails. After
examining the collective data, the authors concluded that
EPOC comprises only 6-15% of the expenditure of the
exercise bout.13 So, figure a typical training bout that burns
500 kcal might burn an extra 50 kcal afterward – which is
hardly worth dancing over.
However, Knab et al recently threw a small wrench into that
dismissal.14 They found that 45 minutes of cycling at 72.8%
of VO2max (about 86.7% of max heart rate) burned 519 kcal
during the activity, and an additional 190 kcal in the 14 hours
following. This is an afterburn of 37% of the training bout’s
expenditure, which is a lot more than the 6-15% afterburn
cited in LaForgia et al’s review. The results of Knab et al’s
Alan Aragon’s Research Review – December 2011
study are strengthened by the use of a controlled metabolic
chamber, as opposed to other studies in this area that have
used open-circuit means (ie, the Douglas bag method) which
are more highly subject to error. Apparently, training for
nearly an hour at ass-busting intensity can pay some
handsome dividends in terms of residual energy expenditure.
Still, it’s important to remember that intensity and risk
(musculoskeletal, cardiac, & other) directly correlate with
each other, so more intensity is not always better from the
standpoint of training longevity.
9. Longer is not necessarily better when it comes to inter-set
rest duration for strength & power goals. Alcaraz et al
compared the effects of 2 protocols.15 A high-resistance
circuit (HRC) consisted of 6 exercises done in succession
(upper & lower-body exercises were alternated), with 35
second rest between each exercise. This was compared with
a traditional strength training protocol (TS) consisting of the
same 6 exercises, but with 3 minutes of passive rest between
sets of the same exercise. This study showed that the use of
high loads in circuit fashion was as effective as TS for
increasing maximal strength, upper-limb peak power, and
lean mass. Importantly, HRC was better than TS at
decreasing body fat and increasing peak cycling power. To
top things off, HRC training bouts were significantly shorter
than TS (55-78 versus 105-125 minutes). This type of circuit
has potential applications for home gyms and relatively
empty commercial gyms. It certainly wouldn’t go over well
at Gold’s gym in peak traffic hours if someone tried to
reserve multiple stations for their personal circuit.
This study was novel in its use of high intensity (of load)
with short rests. Previous research by Campos et al compared
lighter loads & short rests with heavier loads & longer rests.
Unsurprisingly, the latter has been superior to the former for
the goal of gaining maximal strength, while the opposite was
true for the goal of building local muscular endurance.16 The
ability to efficiently kill two birds with one stone as seen in
Alcaraz et al’s study15 comes with the price of finding a
training venue that will actually allow that to happen. Of
course, another viable option is to stick with traditional
strength training – which has been getting the job done on a
global scale for the last half-century.
Other research in this vein has also captured my attention and
got me pondering my current perspective. Souza-Junior et al
compared the strength & hypertrophy effects of a
conventional/constant inter-set rest interval protocol (2
minutes) with a decreasing inter-set rest protocol which
started at 2 minutes, & decreased 15 seconds every 2 weeks,
until there was 30 seconds of inter-set rest in the final 2
weeks.17 Both groups were administered creatine. No
significant between-group differences in isokinetic peak
torque increases or maximal strength gains were seen. A non-
significantly greater increase in arm cross-sectional area
occurred in the decreasing-rest group. The study’s design &
applicability limitations were the duration (8 weeks), subject
profile (recreationally active, but not necessarily highly
trained), and load intensity (8-10 RM). Examining the latter
study led me to previous work with the same design, except
[Back to Contents] Page 4
 without creatine supplementation.18 The outcomes were
similar, notably the lack of difference in strength & size gains
between groups. Interestingly, maximal bench press strength
(1RM) in the decreasing-rest group was 10% greater than that
of the constant-rest group.
10. Along the lines of the previous point, there might possibly
be some metabolic, hormonal, or other poorly understood
‘magic’ conducive to size & strength gains in programs that
incorporate shorter rest intervals. A highly intriguing aspect
of the two aforementioned studies was the similar size &
strength gains despite the lower total work volume in the
decreasing-rest groups.17,18 This lesser volume would
normally be expected to compromise size & strength
adaptations, but that was not the case. To quote the authors’
speculations of how this might occur:17
“However, short rest periods also increase the metabolic
and hormonal response to resistance training. The
increased hormonal response (growth hormone, IGF-1)
with short rest periods indicates a more anabolic
environment that could result in increased muscle
hypertrophy.”
A very interesting but unreplicated study by Goto et al
putting 2 groups of subjects on a 6-week hypertrophy phase,
which was followed by a 4-week phase that compared
strength training versus combination training.19 the twice-
weekly training sessions consisted of leg presses and leg
extensions. In the combination group, 5 high-load/long-rest
(90% 1RM, 3 minute rests) sets followed by a 30-second
rest before performing a high-rep/low-load (50% 1RM) set
caused superior maximal strength and muscular endurance
gains compared to the 5 high-load/long-rest sets alone. It’s
also worth mentioning that cross-sectional area was also
greater in the combination group, but not to a degree of
statistical significance. The authors concluded the
following:
“Although the precise mechanism for its effects remains
unclear, the present regimen with combined high- and
low-intensity resistance exercises may be useful, at least
occasionally, in various kinds of sports that require
muscular strength and endurance simultaneously.”
Unfortunately, it’s not certain whether or not the
combination group prevailed due simply to a higher training
volume. This treatment imbalance could easily have been
fixed by adding an extra high-load/long-rest set to the
comparison arm on the final phase of the experiment.
Nevertheless, it’s apparent that strategic inclusion of shorter
rest periods and/or lower loads into otherwise traditional
strength training programs won’t likely hurt size & strength
gains, and might actually enhance them. A specific
application would be to incorporate a drop-set to the end of
each set progression (reducing the load by 25-50% in order
to continue on to the next set with minimal rest).
It should be noted that Goto et al’s subjects were not trained
or highly conditioned.19 In fact, part of the participant
recruiting criteria was a minimum of 6 months without any
regular exercise prior to joining the study. This brings me to
Alan Aragon’s Research Review – December 2011
my next point: untrained subjects have been seen to gain
strength at similar rates regardless of rest periods ranging
from 1-3.5 minutes.20,21 This brings me to my next point,
that inter-set duration can be manipulated according to the
development of the trainee. Lengthening the rest interval
between sets of the same exercise can serve as a
programming tool of progression. My preference is to begin
with the minimal amount of rest required to keep progress
moving along (this obviously will vary with the individual’s
goals and current level of conditioning). Finding the
minimum inter-set rest length for any given exercise also
saves time. This time-savings obvious, but it’s not always
practiced, especially among folks without tight schedules.
To quote Gentil et al:20
“Our data suggest that gains in maximum strength in
nontrained men are not dependent on the length of the
rest interval between sets. Therefore, personal trainers
and strength coaches can advise beginning lifters to use
short rest intervals to make best use of their time in the
weight room.”
Recent reviews have suggested 3-5 minutes of inter-set rest
for the goal of developing maximum strength.22,23 Ironically,
those same reviews also suggest a rest interval of 30-60
seconds for the goal of hypertrophy. That’s a fairly large
difference, and the middle ground (2-minute rests) tends to
miss the spotlight. This is why it’s important to note that in
trained subjects, 2-minute rest intervals have caused similar
strength gains to 4-minute24 & 5-minute rest intervals.25 The
latter studies challenge the necessity or optimality of the
commonly cited 3-5-minute range. Perhaps the smartest
thing to do is first get the goal straight (for example,
powerlifting vs bodybuilding vs general/casual fitness),
which should dictated by personal preference. Then, spend
the majority of the time in the training zone that’s most
conducive to the individual’s goal, tolerance, and training
status.
11. BCAA supplementation might benefit those who endurance-
train to exhaustion in fasted, glycogen-depleted conditions.
Gualano et al gave subjects a BCAA dose of 300 mg/kg (or
a maltodextrin placebo) for 3 days.26 On the second day,
subjects were put through a glycogen depletion protocol,
and on the third day, they underwent exercise testing in a
10-hour fasted state. To be clear, no food was consumed
after the glycogen depletion protocol the day before testing.
During testing (time to exhaustion at 80% of anaerobic
threshold; appx 9.9 km/hr or 6 mi/hr), the BCAA group had
a slightly lower RER (indicating greater fat oxidation),
higher plasma glucose levels, and 17.1 % longer time to
exhaustion compared to placebo.
The speculated mechanism for these effects is the potential
of BCAA supplementation to spare glycogen by providing
tricarboxylic acid (TCA) cycle intermediates. The authors
admit that this proposed mechanism is under intense debate,
but what can’t be argued are the results they saw. The
practical application here is quite limited, but some fringe
populations such as pre-contest bodybuilders and anyone
seeking to preserve endurance performance under fasted,
[Back to Contents] Page 5
 low-glycogen conditions might want to take note of these
findings.
Keep in mind that the subjects were not endurance-trained,
so these results may not apply to athletic or highly trained
populations. Furthermore, this study measured the effects of
a single exercise bout, so effects over the longer-term are
unknown. In addition to the small sample size (n=7), a final
limitation to consider is that habitual diet was not mentioned
in the text, let alone analyzed. As such, it’s unknown
whether or not the BCAA dose (300 mg/kg, which for an 80
kg person would be 24 g) simply brought a sub-optimal
habitual protein intake up to par.
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in Gluten Intolerance. Clin Rev Allergy Immunol. 2010 Dec
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strength, size, and hormonal adaptations in trained men. J
Strength Cond Res. 2005 Aug;19(3):572-82. [Pubmed]
26. Gualano AB, et al. Branched-chain amino acids
supplementation enhances exercise capacity and lipid
oxidation during endurance exercise after muscle glycogen
depletion. J Sports Med Phys Fitness. 2011 Mar;51(1):82-8.
[Pubmed]
[Back to Contents] Page 6

Effect of Dietary Protein Content on Weight Gain,
Energy Expenditure, and Body Composition During
Overeating.
Bray GA, et al. JAMA. 2012 Jan 4;307(1):47-55 [JAMA]
CONTEXT: The role of diet composition in response to overeating
and energy dissipation in humans is unclear. Objective To evaluate
the effects of overconsumption of low, normal, and high protein diets
on weight gain, energy expenditure, and body composition. DESIGN,
SETTING, & PARTICIPANTS: A single-blind, randomized
controlled trial of 25 US healthy, weight-stable male and female
volunteers, aged 18 to 35 years with a body mass index between 19
and 30. The first participant was admitted to the inpatient metabolic
unit in June 2005 and the last in October 2007. INTERVENTION:
After consuming a weight-stabilizing diet for 13 to 25 days,
participants were randomized to diets containing 5% of energy from
protein (low protein), 15% (normal protein), or 25% (high protein),
which they were overfed during the last 8 weeks of their 10- to 12-
week stay in the inpatient metabolic unit. Compared with energy
intake during the weight stabilization period, the protein diets
provided approximately 40% more energy intake, which corresponds
to 954 kcal/d (95% CI, 884-1022 kcal/d). MAIN OUTCOME
MEASURES: Body composition was measured by dual-energy x-ray
absorptiometry biweekly, resting energy expenditure was measured
weekly by ventilated hood, and total energy expenditure by doubly
labeled water prior to the overeating and weight stabilization periods
and at weeks 7 to 8. RESULTS: Overeating produced significantly
less weight gain in the low protein diet group (3.16 kg; 95% CI, 1.88-
4.44 kg) compared with the normal protein diet group (6.05 kg; 95%
CI, 4.84-7.26 kg) or the high protein diet group (6.51 kg; 95% CI,
5.23-7.79 kg) (P = .002). Body fat increased similarly in all 3 protein
diet groups and represented 50% to more than 90% of the excess
stored calories. Resting energy expenditure, total energy expenditure,
and body protein did not increase during overfeeding with the low
protein diet. In contrast, resting energy expenditure (normal protein
diet: 160 kcal/d [95% CI, 102-218 kcal/d]; high protein diet: 227
kcal/d [95% CI, 165-289 kcal/d]) and body protein (lean body mass)
(normal protein diet: 2.87 kg [95% CI, 2.11-3.62 kg]; high protein
diet: 3.18 kg [95% CI, 2.37-3.98 kg]) increased significantly with the
normal and high protein diets. CONCLUSIONS: Among persons
living in a controlled setting, calories alone account for the increase in
fat; protein affected energy expenditure and storage of lean body
mass, but not body fat storage. TRIAL REGISTRATION:
Clinicaltrials.gov: NCT00565149 SPONSORSHIP: This study was
supported in part by the US Department of Agriculture grant 2010-
34323-21052 and by funding from Louisiana State University.
Study strengths
This study is the first to compare the overfeeding effects of
varying protein levels under tightly controlled conditions.
Subjects lived in the metabolic unit throughout the trial. All
intake was provided by metabolic kitchen. Resting & total
energy expenditure was measured via doubly labeled water,
and body composition was measured via DXA.
Study limitations
There’s little practical utility in the inclusion of a low-protein
treatment (5% of total kcals), that has obvious proteolytic
potential, and is far below the norm. A more practical set of
proportions to compare would be something like 15%, 25%, &
35% (or even 40%) protein. The latter proportion would better
exploit the metabolic inefficiency of a (truly) high proportion
Alan Aragon’s Research Review – December 2011
of protein, thus potentiating an energy ‘wasting’ effect. As it
stands, the highest-protein arm was 26%, which isn’t high
compared to what’s typically consumed in fitness circles.
Furthermore, the “high protein” arm is still somewhat mis-
labeled since its dominant macronutrient was carbohydrate.
Comment/application
Before I comment further, the exact breakdowns of each
overfeeding treatment are not listed in the abstract, so I’ll list
them here, along with protein gram amounts in order to draw
more concrete implications:
ƒ Low-protein diet: 6% protein (47 g), 42% carb, 52% fat.
ƒ Normal-protein diet: 15% protein (139 g), 41% carb, 44% fat.
ƒ High-protein diet: 26% protein (228 g), 41% carb, 33% fat.
The main finding of this study was the lack of significant
differences in fat gain between groups despite the proportional
differences in protein intake. The authors thus concluded that,
“…calories are more important than protein while consuming
excess amounts of energy with respect to increases in body fat.”
Unsurprisingly, the low-protein group lost LBM while the
normal & high-protein groups gained LBM (2.87 & 3.18 kg,
respectively). Each group’s baseline protein intake was slightly
less than 100 g. Notably, the high-protein group, whose protein
intake was 3.0 g/kg, gained slightly more LBM than the normal
protein group, whose intake was 1.8 g/kg. This challenges the
commonly assumed upper limits of protein dosing for maximal
gains in LBM, which are typically cited to be 1.8-2.2 g/kg.1-3
As expected, resting & total energy expenditure did not increase
in the low-protein groups, but did in the normal & high-protein
groups. This was likely due to the higher metabolic cost of
protein turnover. Energy intake between groups was not
significantly different (low-protein: 3866 kcal; normal-protein:
4088 kcal; high-protein: 3873 kcal). Despite these factors, the
latter two groups gained about twice the weight as the low-
protein group. While this would appear to be a violation of the
basic weight gain & loss principles of thermodynamics, there’s
still a plausible explanation. Given enough time (more than the 8
weeks of overfeeding in the present study), gains in lean mass
would plateau while fat gains would continue and eventually
narrow the weight difference – with the main impeding factor
being the loss of LBM in the low-protein group. Indeed, the low-
protein group gained slightly more fat than the other groups, but
not to a statistically significant degree. Would this small amount
accumulate over time, yielding measurable differences in fat
gain? That’s tough to forecast in the present conditions, but if a
structured training protocol was implemented, it would likely
expose an adipokinetic disadvantage in the low-protein group.
Another thing to bear in mind is that muscle tissue is about 75%
water, while fat mass is 10-15% water. The carbohydrate content
was virtually identical between the diets, so the higher-protein
diets may have had an additional advantage for glycogen (& thus
water) storage due via muscle gain, while the low-protein diet
had a distinct disadvantage in this regard, further contributing to
the difference in weight gain. In any case, one can only hope for
a follow-up study with a longer duration & a training regimen. A
more practical (& relevant) twist would be to compare the
overfeeding effects of different proportions of dietary
carbohydrate while keeping protein intake sufficient & matched.
[Back to Contents] Page 7
Exercise dose and insulin sensitivity: relevance for
diabetes prevention.
Dubé JJ, et al. Med Sci Sports Exerc. 2011 Nov 2. [Epub ahead
of print] [Pubmed]
PURPOSE: Exercise improves insulin resistance and is a first
line for the prevention and treatment of type 2 diabetes. The
extent, however, to which these response are dose-dependent is
not known. The purpose of this study was to examine whether or
not exercise dose was associated with improvements in insulin
sensitivity following four months of exercise training in
previously sedentary adults. METHODS: Fifty-five healthy
volunteers participated in a 16-week supervised endurance
exercise intervention with a pre/post intervention design. Insulin
sensitivity was assessed by euglycemic hyperinsulinemic clamp,
peak oxygen uptake by a graded exercise test and body
composition by DXA. The exercise intervention consisted of 3
to 5 sessions/week with a minimum of 3 sessions supervised. A
ramped exercise prescription protocol was used to achieve 75%
of peak HR for 45 minutes/session. Exercise dose, expressed as
average kcal expended per week, was computed as the product
of exercise intensity, duration and frequency. RESULTS:
Improved insulin sensitivity was significantly related to exercise
dose in a graded dose-response relationship. No evidence of
threshold or maximal dose-response effect was observed. Age
and gender did not influence this dose-response relationship.
Exercise intensity was also significantly related to improvements
in insulin sensitivity, while frequency was not.
CONCLUSIONS: This study identifies a graded dose-response
relationship between exercise dose and improvements in insulin
sensitivity. The implication of this observation is of importance
for the adaptation of exercise prescription in clinical situations.
SPONSORSHIP: ADA clinical Research Award (B.H.G),
ACSM research grant (F.A.), NIH R01 (AG20128), NIH GCRC
(5M01RR00056) and Obesity Nutrition Research Center
(1P30DK46204).
Study strengths
A very practical & important question was investigated, since
being sedentary plays a key role in the development of type 2
diabetes. Since exercise is effective ‘medicine’, it’s important
to establish the proper dose. This study is innovative since it’s
the first to ever investigate a dose-response relationship
between exercise dose (average weekly duration, frequency, &
intensity) and insulin sensitivity. The volume & intensity
gradations were within realistic limits, done 3-5 days per week,
as follows... Weeks 1-4: 60-70% max HR for 30 minutes per
session. Weeks 5-8: 60-70% max HR for 40 minutes per
session. Weeks 9-16: 75% max HR for 45 minutes per session.
A minimum of 3 of the 5 sessions were supervised, which
bolstered compliance and insured proper execution.
Study limitations
As the authors acknowledged, the results might be limited to
the subjects’ profile (previously sedentary, as opposed to
trained/active/athletic). Furthermore, the results might not
translate exactly in the case of different exercise modes (ie,
cycling vs running) or types (ie, strength-type training vs
endurance-type training). Another potential limitation was the
Alan Aragon’s Research Review – December 2011
lack of dietary control or analysis; subjects were merely
instructed to maintain their usual habits. The authors did not
include weight loss (or fat loss) into their regression model.
Although this simplifies the analysis, it still leaves open
questions about the relative contribution of fat loss versus
exercise dose to improvements in insulin sensitivity. Notably,
subjects lost an average of 3.2 kg (7 lb) fat mass. A non-
exercising weight loss comparison arm would have made the
design more comprehensive. Alternatively, the diets could have
been programmed for weight maintenance despite the
progression of exercise dose, in order to rule out fat loss as a
contributing factor. In their defense, the authors cited research
by Kirwan et al, who saw improved insulin sensitivity without
weight loss in obese type 2 diabetics after 7 consecutive days
of exercise training (50-60 minutes total per session, consisting
of a combination of treadmill & cycling at 80-85% max HR).4
Comment/application
The main finding was a positive dose-response relationship
between exercise and improvements in insulin sensitivity,
measured via glucose infusion rate (GIR). GIR is an index
primarily of insulin sensitivity in muscle. As seen in the chart
above, BMI & fat mass decreased significantly as well, but as
mentioned earlier, these outcomes were not part of the study’s
aim. Importantly, neither a lower nor an upper threshold of
effectiveness was seen. It might not have been entirely
practical to exploit the upper end of exercise dosing in attempt
to seek a plateau in insulin sensitivity. However, it would have
been interesting, since there indeed are endurance athletes
(casual & competitive) who train more than 3-5 days per week
for 45 minutes at 75% max HR. An interesting finding was that
exercise intensity (average kcals burned per minute) was
significantly associated with improved insulin sensitivity,
while frequency (sessions per week) was not.
According to the latest Physical Activity Guidelines for
Americans, adults should do at least 150 minutes of moderate-
intensity physical activity.5 This figure is based on
epidemiological data, which makes it subject to considerable
error. Testing the validity of this guideline, the authors of the
present study ran a regression model which found that a
weekly training volume of 900 kcal/week had no significant
association with improved insulin sensitivity. They thus
concluded that this commonly prescribed lower threshold of a
moderate 150 minutes per week might not be enough to
universally mitigate cardiometabolic risk. Still, the authors
ultimately take a more general stance on the issue of physical
activity, as evidenced in the text’s concluding statement:
“It appears that, in term of improving insulin sensitivity, more
is likely better than a little, and a little is better than nothing.”
[Back to Contents] Page 8
Effects of 4 weight-loss diets differing in fat, protein,
and carbohydrate on fat mass, lean mass, visceral
adipose tissue, and hepatic fat: results from the
POUNDS LOST trial.
de Souza RJ, et al. Am J Clin Nutr. 2012 Jan 18. [Epub ahead
of print] [Pubmed]
BACKGROUND: Weight loss reduces body fat and lean mass,
but whether these changes are influenced by macronutrient
composition of the diet is unclear. OBJECTIVE: We
determined whether energy-reduced diets that emphasize fat,
protein, or carbohydrate differentially reduce total, visceral, or
hepatic fat or preserve lean mass. DESIGN: In a subset of
participants in a randomized trial of 4 weight-loss diets, body fat
and lean mass (n = 424; by using dual-energy X-ray
absorptiometry) and abdominal and hepatic fat (n = 165; by
using computed tomography) were measured after 6 mo and 2 y.
Changes from baseline were compared between assigned
amounts of protein (25% compared with 15%) and fat (40%
compared with 20%) and across 4 carbohydrate amounts (35%
through 65%). RESULTS: At 6 mo, participants lost a mean
(±SEM) of 4.2 ± 0.3 kg (12.4%) fat and 2.1 ± 0.3 kg (3.5%) lean
mass (both P < 0.0001 compared with baseline values), with no
differences between 25% and 15% protein (P ≥ 0.10), 40% and
20% fat (P ≥ 0.34), or 65% and 35% carbohydrate (P ≥ 0.27).
Participants lost 2.3 ± 0.2 kg (13.8%) abdominal fat: 1.5 ± 0.2 kg
(13.6%) subcutaneous fat and 0.9 ± 0.1 kg (16.1%) visceral fat
(all P < 0.0001 compared with baseline values), with no
differences between the diets (P ≥ 0.29). Women lost more
visceral fat than did men relative to total-body fat loss.
Participants regained ‫׽‬40% of these losses by 2 y, with no
differences between diets (P ≥ 0.23). Weight loss reduced
hepatic fat, but there were no differences between groups (P ≥
0.28). Dietary goals were not fully met; self-reported contrasts
were closer to 2% protein, 8% fat, and 14% carbohydrate at 6
mo and 1%, 7%, and 10%, respectively, at 2 y.
CONCLUSIONS: Participants lost more fat than lean mass
after consumption of all diets, with no differences in changes in
body composition, abdominal fat, or hepatic fat between
assigned macronutrient amounts. This trial was registered at
clinicaltrials.gov as NCT00072995. SPONSORSHIP:
Supported by the National Heart, Lung, and Blood Institute
(grant HL073286) and the General Clinical Research Center,
NIH (grant RR- 02635).
Study strengths
This study is definitely going to make people mad – both in the
academic and lay sectors. But, this makes it interesting. A
strength of the study was its long duration. Also, the sample
size was large (226 subjects completed the study). Body
composition was assessed via dual X-ray absorptiometry
(DXA), and visceral & hepatic fat was measured by computed
tomography (CT). The 4-treatment design was an ambitious
attempt at covering all of the main macronutritional variations
in weight loss diets. The assessment of biomarkers of nutrient
intake served as an indirect means of tracking compliance.
Study limitations
Dietary intake was self-reported. This is a common limitation
because of the astronomical expense of providing subjects all
of their food & beverage intake throughout the length of the
Alan Aragon’s Research Review – December 2011
study. This logistical limitation is often the Achilles heel of the
validity of the results. In the present case, the authors the
subjects’ intake did not meet the targets set for each
macronutrient at either the 6-month or 2-year checkpoint (more
on this in the comments section). An additional limitation
common to diet research was the lack of structured/standardized
training, and also the absence of any direct (or indirect)
assessment of energy expenditure.
Comment/application
The main finding was a lack of significant difference among
the diets in any of the parameters tested (body composition,
subcutaneous fat, visceral fat, & hepatic fat). It’s notable that
lean mass loss at 6 months was slightly greater in the 15%
protein than the 25% protein group, and also in the respective
high-carbohydrate group compared with the low-carbohydrate
group. It’s also notable that these trends disappeared by the 2-
year mark. Women lost more visceral fat relative to total body
fat than men did. Another noteworthy finding was that
collectively, fat loss was double the lean mass loss. This isn’t
too surprising because it’s fairly well-established that in
overweight & obese subjects, fat mass is more readily reduced
than lean mass. This scenario progressively becomes the
opposite as individuals get leaner. The study’s main
shortcoming – the subjects’ failure to hit the macronutrient
targets to sufficiently differentiate the treatments – is worth
further discussion. The following quote illustrates the authors’
admission of this confounder:
“We wished to see contrasts of 10%, 20%, and 30% between
amounts of protein, fat, and carbohydrate, respectively;
however, self-reported dietary data suggested the observed
contrasts were closer to 2%, 8%, and 14% at 6 mo and 1%, 7%,
and 10% at 2 y, respectively.”
Further narrowing the differences between diet groups was the
potential for underreporting dietary intake. The targeted energy
deficit was 750 kcal below daily maintenance requirements,
which in a simplified sense, would enable an average loss of 1-
1.5 lb (0.45-0.68 kg) per week. On the lower end, this would
amount to 10.9 kg (24 lb) lost in 6 months. However, at the 6-
month point, the average total weight loss was 6.3 kg (13.9 lb).
This is a 42.2% discrepancy, which is explainable by the
tendency of dieters to underreport their intake. Coincidentally,
Lichtman et al found that obese subjects who claimed to be
“diet resistant” actually underreported their energy intake by an
average of 47%.6
The authors spend a good portion of the text playing up the
strengths of their study in attempt to distract from the fact that
the originally intended design simply was not carried out. They
thus concluded that this trial serves as evidence that total
calories, not macronutrient composition, is what matters for fat
loss, as long as the diet falls within the general limits outlined
in the Institute of Medicine’s Acceptable Macronutrient
distribution Range (ADMR). This conclusion is faulty because
the ADMR’s protein range for adults is 10-35% of total
energy.7 In the present study, protein intakes ranged more
narrowly (18-23% at 6 months, 20-21% at 2 years). This is also
signficantly above the ADMR’s lower end. Given such small
differences in protein intake overall, the lack of difference in
body composition is not surprising.
[Back to Contents] Page 9

Fish-oil supplementation enhances the effects of
strength training in elderly women.
Rodacki CL, et al. Am J Clin Nutr. 2012 Jan 4. [Epub ahead of
print] [Pubmed]
BACKGROUND: Muscle force and functional capacity
generally decrease with aging in the older population, although
this effect can be reversed, attenuated, or both through strength
training. Fish oil (FO), which is rich in n-3 (omega-3) PUFAs,
has been shown to play a role in the plasma membrane and cell
function of muscles, which may enhance the benefits of training.
The effect of strength training and FO supplementation on the
neuromuscular system of the elderly has not been investigated.
OBJECTIVE: The objective was to investigate the chronic
effect of FO supplementation and strength training on the
neuromuscular system (muscle strength and functional capacity)
of older women. DESIGN: Forty-five women (aged 64 ± 1.4 y)
were randomly assigned to 3 groups. One group performed
strength training only (ST group) for 90 d, whereas the others
performed the same strength-training program and received FO
supplementation (2 g/d) for 90 d (ST90 group) or for 150 d
(ST150 group; supplemented 60 d before training). Muscle
strength and functional capacity were assessed before and after
the training period. RESULTS: No differences in the pretraining
period were found between groups for any of the variables. The
peak torque and rate of torque development for all muscles (knee
flexor and extensor, plantar and dorsiflexor) increased from pre-
to posttraining in all groups. However, the effect was greater in
the ST90 and ST150 groups than in the ST group. The activation
level and electromechanical delay of the muscles changed from
pre- to posttraining only for the ST90 and ST150 groups. Chair-
rising performance in the FO groups was higher than in the ST
group. CONCLUSIONS: Strength training increased muscle
strength in elderly women. The inclusion of FO supplementation
caused greater improvements in muscle strength and functional
capacity. SPONSORSHIP: This study had no funding source.
Study strengths
This is a very “outside the box” line of investigation, and thus
makes for an interesting study – particularly since fish oil has
multiple other benefits, minimal downsides, and it’s cheap. This
is the first study to examine the effects of fish oil
supplementation on muscle strength & functional capacity.
Exercise sessions were supervised by the research staff and
qualified instructors. Verbal encouragement was given during
the sessions.
Study limitations
Subjects averaged 64 years of age, and results may or may not
similarly translate to younger populations. Furthermore, the
subjects were previously sedentary, opening more questions
about the applicability of the results to the trained or athletic
population. Although dietary intake was tracked (via food
frequency questionnaire), there were no efforts to analyze the
habitual intakes of fish or omega-3 fatty acids. Also, the actual
dose of fish oil was curiously low (2 g of oil yielding 0.7 g of
combined EPA & DHA). Previous research has typically aimed
Alan Aragon’s Research Review – December 2011
to provide roughly 2 g of combined EPA & DHA. As such, the
low dose in the present study can either be viewed as more
vulnerable to a type I error (false positive), or it can be viewed
as a practical/efficient/economical discovery. In any case, it
would have been useful (although not as logistically feasible) to
investigate a dose-response relationship between fish oil dose &
effects on strength & functionality. The authors themselves
acknowledge that the results should be viewed caution due to the
small number of subjects, and that larger trials with different
combinations of training and treatment length are warranted.
A final potential limitation was the subjects’ sub-optimal
habitual diet, which they were instructed to maintain throughout
the study. Of particular note was their low protein intake. At an
average of 55.5 g/day, this amounted to roughly 0.9 g/kg. It’s
possible that the beneficial effect of fish oil on the strength-
related parameters would only apply to these dietary conditions.
However, it should be noted that a recent study by Mojtahedi et
al did not find any direct benefit of sufficient protein intake on
muscular strength & functionality in a similar population
(women, average age 65).8 A protein intake of 52.5 g/day was
compared with 102.5 g/day. Mojtahedi et al’s study differed
from the present one primarily due to its hypocaloric conditions
& the subjects’ significant weight loss; no weight loss occurred
in the present study.
Comment/application
The main finding was that neuromuscular response, measured by
strength & functional capacity, was positively affected by low-
dose fish oil supplementation during a resistance training
program. Additional effects were not seen as a result of getting a
head start on supplementation (90 or 150 days) prior to
beginning the training program. No changes in body mass were
seen in any group. The higher rate of torque development (RTD)
in the fish oil groups indicated improved muscle contractility,
which in older populations is important for carrying out
activities of daily living. The fish oil groups also showed greater
muscle activation, measured by electromyography. The authors
speculate that this was due to fish oil’s ability to increase
membrane fluidity & acetylcholine sensitivity, thus improving
muscle function. Improved membrane fluidity may have
facilitated impulse transmission & faster muscle contraction.
The results of the present study are reminiscent of recent work
by Smith et al, who found that a combined EPA & DHA dose of
3.36 g caused a robust increase in the acute muscle protein
anabolic response to hyperinsulinemia-hyperaminoacidemia in
healthy young and middle-aged aduilts.9 Specifically, in
response to insulin and amino acid infusion, the fish oil
supplementation caused a significant increase in fractional
synthesis rate, and a substantial (roughly 50%) increase in the
activation of the mTOR/p70S6K signaling pathway – which is
considered an important control point for muscle protein
synthesis. Importantly, this positive effect was seen in both
younger and older individuals… Back to the present study, the
authors concluded that fish oil supplementation in conjunction
with strength training increases functional strength via
enhancing neuromuscular response, a favorable effect for the
elderly population, which often is compromised in this regard. It
might be time to chalk up yet another positive effect of fish oil.
[Back to Contents] Page 10

Cardiac autonomic dysfunction in anabolic steroid
users. Critiqued by James Heathers
Maior AS, et al. Scand J Med Sci Sports. 2012 Jan 18. doi:
10.1111/j.1600-0838.2011.01436.x. [Epub ahead of print]
[Pubmed]
PURPOSE: This study aimed to evaluate if androgenic-anabolic
steroids (AAS) abuse may induce cardiac autonomic dysfunction in
recreational trained subjects. DESIGN: Twenty-two men were
volunteered for the study. The AAS group (n = 11) utilized AAS at
mean dosage of 410 ± 78.6 mg/week. All of them were submitted to
submaximal exercise testing using an Astrand-Rhyming protocol.
Electrocardiogram (ECG) and respired gas analysis were monitored
at rest, during, and post-effort. Mean values of VO(2) , VCO(2) ,
and V(E) were higher in AAS group only at rest. The heart rate
variability variables were calculated from ECG using MATLAB-
based algorithms. RESULTS: At rest, AAS group showed lower
values of the standard deviation of R-R intervals, the proportion of
adjacent R-R intervals differing by more than 50 ms (pNN50), the
root mean square of successive differences (RMSSD), and the total,
the low-frequency (LF) and the high-frequency (HF) spectral power,
as compared to Control group. After submaximal exercise testing,
pNN50, RMSSD, and HF were lower, and the LF/HF ratio was
higher in AAS group when compared to control group.
CONCLUSIONS: Thus, the use of supraphysiological doses of
AAS seems to induce dysfunction in tonic cardiac autonomic
regulation in recreational trained subjects. SPONSORSHIP: None
listed.
Study strengths
This paper reports a population of self-selected anabolic-
androgenic steroid (AAS) users as having cardiac autonomic
dysfunction as compared to a control population. This fits well
with a broad pattern of AAS demonstrating cardiac and
circulatory dysfunctions.10,11
Much can be said about the findings – they demonstrate a broad
pattern of autonomic dysfunction and impaired exercise recovery
associated with the AAS-using group, who demonstrate both
lower levels of heart rate variability (the beat-to-beat differences
in the heart which correspond to autonomic flexibility and
parasympathetic nervous system dominance) at rest and
immediately after exercise. There are a number of ways of
measuring heart rate variability, and differences between
methods are sometimes relevant in interpretation, but this study
demonstrates broad dysfunctions in all the typical measures.
Study limitations
However, detailed consideration of the above would be
imprudent. It should be noted that there are straightforward
matters of adequate statistical and procedural control in this
study which were not addressed. By themselves, these may be
minor points but overall point to a significant collective source
of error.
Firstly, the presence of sympathomimetics, drugs which
stimulate the sympathetic nervous system, was not measured.
This is extremely important to control in a study which measures
the differences between groups as levels of heart rate variability.
Alan Aragon’s Research Review – December 2011
Clenbuterol, ephedrine, and a variety of other legal or illegal
stimulants are capable of having a profound effect on baseline
autonomic variables.
Likewise, there is an enormous and unanalyzed difference in
baseline breathing rate. AAS users breathe at 18 cpm, controls at
10cpm. 18 cycles per minute is almost formally tachyapnea - a
clinically elevated breathing rate. This is undoubtedly
significant, and seeing as the measurement of parasympathetic
function is determined by measuring respiratory sinus
arrhythmia - the fluctuations in the heart rate caused by
breathing - there is most likely a big interaction with the
eventual result.
Finally, as is so often the case in this type of literature, no
determination was made of training age, training experience or
training volume. This is absolutely critical when comparing any
kind of sequelae between subjects - in its absence, we are always
left with the chicken-or-egg question: that is, are people who
train harder and under more systemic stress using anabolic
steroids (in order to accelerate their recovery, for example), or
are there direct effects of anabolic steroids which create
autonomic dysfunction?
These are just errors of process, however the paper makes a
basic but extremely serious statistical error. The paper lists the
group of AAS-using athletes as having a BMI of 28, with the
standard error of mean listed as 2.5. This is extremely unlikely.
In a sample of 11 people, this means the standard deviation of
this group is around 8.3. If this is the case, the group includes
both the largest possible people, but also some AAS-using
athletes who are bordering on being clinically underweight.
Likewise, the weight of the sample is listed as 85.1kg with a
SEM of 6.8kg. This is also extremely unlikely, as it means the
sample likely varies between an emaciated 40kgs to a Jay-
Cutler-esque 130kgs.
The simplest explanation is that what the authors have listed as
SEM is actually SD – standard deviation. They are both
legitimate ways of reporting variation, and this would be a minor
error... if the change to these figures didn't imply that there is
now a clear statistical difference between the AAS and non-AAS
using participants in BMI – as might be expected, the AAS
group is larger.
In other words, the study is comparing an AAS-using group
*with significantly more muscle mass* to a control group of
weight training non-drug users. As fat free mass is the
overwhelming determinant of resting metabolic rate, accounting
for more than 60% of the variance in a recent model,12 this is a
likely contributor to elevated basal SNS activity. This is not an
academic criticism as much as a perfectly adequate alternative
explanation.
It is absolutely imperative that research in this area is well-
conducted. AAS-using populations are in no way typical 'drug
users' – lifetime users are typically older, better educated, and
often extremely sceptical of research which investigates the
disruption posed by AAS under the assumptive basis of “steroids
are bad”. Thus, in no way is the process of understanding the
significance or dangers of AAS use helped by research which is
insufficiently controlled and reported.
[Back to Contents] Page 11

The effects of low-intensity resistance training with
vascular restriction on leg muscle strength in older
men.
Karabulut M, et al. Eur J Appl Physiol. 2010 Jan;108(1):147-55.
[Pubmed]
PURPOSE: The purpose of this study was to investigate and
compare the effects of two types of resistance training protocols
on the adaptation of skeletal muscle strength in older men.
METHODS: Thirty-seven healthy male subjects (50-64 years)
participated in this study. Subjects were assigned to one of three
groups: high-intensity (80% 1-RM) resistance training (RT80);
low-intensity (20% 1-RM) resistance training with vascular
restriction (VR-RT20); and a control group (CON) that
performed no exercise. Subjects in both exercise groups
performed three upper body (at 80% 1-RM) and two lower body
exercises either with (20% 1-RM) or without (80% 1-RM)
vascular restriction three times a week for 6 weeks. RESULTS:
As expected, the RT80 and VR-RT20 groups had significantly
(p < 0.01) greater strength increases in all upper body and leg
press exercises compared with CON, however, absolute strength
gains for the RT80 and VR-RT20 groups were similar (p >
0.05). It should be noted that the percentage increase in leg
extension strength for the RT80 group was significantly greater
than that for both the VR-RT20 (p < 0.05) and CON groups (p <
0.01), while the percentage increase in leg extension strength for
the VR-RT20 group was significantly (p < 0.01) greater than that
for the CON. CONCLUSIONS: The findings suggested that leg
muscle strength improves with the low-load vascular restriction
training and the VR-RT20 training protocol was almost as
effective as the RT80 training protocol for increasing muscular
strength in older men. SPONSORSHIP: None listed.
Study strengths
This study treaded some novel ground. To my knowledge, the
only other study with a direct comparison of high-intensity/non-
occluded vs low-intensity/occluded on strength measures was
conducted over a decade ago. In the latter study, Takarada et al
found that isometric elbow flexor strength increased by 18.4% in
the occluded arm (at 30-50% 1RM) and 22.6% in the other non-
occluded arm (80% 1-RM).13 However, strength was measured
via isokinetic dynamometer. The present study used a range of
common, gym-based exercises, which makes the results
potentially more relevant to the real-world. Another strength this
study has over most of its predecessors was the testing of both
upper and lower-body strength.
Study limitations
The results might be limited to the subject profile – males aged
50-64 years, recreationally active, but not involved with regular
structured training. Results could be different if highly
trained/experienced strength/power athletes were used. Another
limitation is the use of 1RM, which can be great for athletes
whose sport concentrates on maximal strength & power.
However, for other goals that involve more of a mix of strength
and endurance, single-repetition strength is a marginally relevant
metric. Although 1RM is a common index of strength, a more
widely applicable index would be the number of repetitions done
Alan Aragon’s Research Review – December 2011
at a submaximal load, such as 85-90% 1RM. An even more
comprehensive example of testing strength/power performance
in a more practical manner than simply 1RM was recently done
in a study by Lee et al (this study examined betaine’s effect,
but that’s beside the point).14 I’ll specify the testing protocol
here to save you some digging, as well as to illustrate my
forthcoming points in the comment section. Here’s Lee et al’s
testing protocol: After a 5-minute warm-up of low-intensity
cycling, subjects performed the following challenge; each
exercise was separated by a 2-minute rest (in addition to tallying
reps, a force plate was used to measure power & force):
ƒ 4 sets × 3 repetitions of vertical jump separated by 2‐minute rests 
ƒ Maximal effort isometric squat  
ƒ 3 repetitions of squat jump at 30% 1RM 
ƒ 3 sets back squat to fatigue at 85% 1RM separated by 2‐minute rests 
ƒ Maximal effort isometric bench press 
ƒ 3 repetitions of bench throw at 30% 1RM 
ƒ 3 sets of bench press to fatigue at 85% 1RM  
Comment/application
The main findings were that vascular restriction (occlusion)
applied to low-intensity resistance training (20% 1RM) caused
similar strength gains to traditional, non-occluded, high-intensity
resistance training (80% 1RM). As depicted below, the only
significant difference was in the leg extension, where the
traditional training caused greater strength gains from baseline to
the end of the 6-week period. Occluded and traditional training
increased leg extension strength by 19.1% and 31.2%,
respectively.
Nevertheless, this difference was minor within the context of the
overall similarity in gains across the range of upper- & lower-
body exercises tested, including a lack of significant different in
leg press strength gains. One of the ‘selling points’ of low-
intensity occlusion training seen here is that less work volume
(sets x number of reps per set x load) was required to achieve
similar results as traditional training. Another attractive feature
is that it causes less muscle damage.15,16 These features have
generated interest in its role for rehabilitation and training the
elderly. However, it has not been directly compared against
traditional strength training in testing protocols such as the one I
outlined previously, which more closely resembles the demands
of sports involving a mix of strength, power, and endurance.
Another thing to consider is that low-intensity occlusion training
is substantially less time-efficient, often requiring 2-3 times
more repetitions per set than high-intensity work.
[Back to Contents] Page 12
1. Phillips SM, Van Loon LJ. Dietary protein for athletes:
From requirements to optimum adaptation. J Sports Sci.
2011;29 Suppl 1:S29-38. [Pubmed]
2. Campbell B, et al. International Society of Sports Nutrition
position stand: protein and exercise. J Int Soc Sports Nutr.
2007 Sep 26;4:8. [Pubmed]
3. Wilson J, Wilson GJ. Contemporary issues in protein
requirements and consumption for resistance trained
athletes. J Int Soc Sports Nutr. 2006 Jun 5;3:7-27. [Pubmed]
4. Kirwan JP, et al. Effects of 7 days of exercise training on
insulin sensitivity and responsiveness in type 2 diabetes
mellitus. Am J Physiol Endocrinol Metab. 2009
Jul;297(1):E151-6. [Pubmed]
5. US Department of Health & Human Services. 2008 Physical
Activity Guidelines for Americans. [HHS]
6. Lichtman SW, et al. Discrepancy between self-reported and
actual caloric intake and exercise in obese subjects.N Engl J
Med. 1992 Dec 31;327(27):1893-8. [Pubmed]
7. FNB/IOM. Dietary Reference Intakes for Energy,
Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein,
and Amino Acids. 2005 [National Academies Press]
8. Mojtahedi MC, et al. The effects of a higher protein intake
during energy restriction on changes in body composition
and physical function in older women. J Gerontol A Biol
Sci Med Sci. 2011 Nov;66(11):1218-25. [Pubmed]
9. Smith GI, et al. Omega-3 polyunsaturated fatty acids
augment the muscle protein anabolic response to
hyperinsulinaemia-hyperaminoacidaemia in healthy young
and middle-aged men and women. in Sci (Lond). 2011
Sep;121(6):267-78. [Pubmed]
10. Payne JR, et al. Cardiac effects of anabolic steroids. Heart.
2004 May;90(5):473-5. [Pubmed]
11. Karila TA, et al. Anabolic androgenic steroids produce
dose-dependent increase in left ventricular mass in power
atheletes, and this effect is potentiated by concomitant use
of growth hormone. Int J Sports Med. 2003 Jul;24(5):337-
43. [Pubmed]
12. Johnstone AM, et al. Factors influencing variation in basal
metabolic rate include fat-free mass, fat mass, age, and
circulating thyroxine but not sex, circulating leptin, or
triiodothyronine. Am J Clin Nutr. 2005 Nov;82(5):941-8.
[Pubmed]
13. Takarada Y, et al. Effects of resistance exercise combined
with moderate vascular occlusion on muscular function in
humans. J Appl Physiol. 2000 Jun;88(6):2097-106.
[Pubmed]
14. Lee EC, et al. Ergogenic effects of betaine supplementation
on strength and power performance. J Int Soc Sports Nutr.
2010 Jul 19;7:27. [Pubmed]
15. Fujita T, et al. Increased muscle volume and strength
following six days of low-intensity resistance training with
restricted muscle blood flow. Int J KAATSU Train Res 4: 1-
8, 2008. [IJKTR]
16. Abe T, et al. Day-to-day change in muscle strength and
MRI-measured skeletal muscle size during 7 days KAATSU
resistance training: a case study. Int J KAATSU Train Res
1: 71-76, 2005. [IJKTR]

Alan Aragon’s Research Review – December 2011 [Back to Contents] Page 13


Interview with Michael Krivyan.
By Alan Aragon
________________________________________________________________
I’ve known Mike for quite some time on the message boards, and
have always regarded him as one of the most knowledgable &
helpful members of the community. What finally motivated me to
approach him for an interview was his recent victory in
bodybuilding competition. I find it interesting when anyone who
doesn’t work in the industry maintains this level of passion for
fitness. Heaven knows that if I wasn’t in the fitness industry,
there’s a good chance I’d look like a chewed piece of bubble
gum. Without further ado, let’s throw some questions at Mike.
________________________________________________________________
Please tell the readers a bit about how you got into
bodybuilding (ie, how old were you, what sparked the
interest, & what factors contributed to your decision to
compete). Also, please outline your competitive history.
As a reader of AARR, I'd first like to thank you for the
opportunity to share my views and experiences with your
audience.
You’re welcome, and thank YOU!
I was never a big fan of sports growing up, though I was always
a huge fan of food. Fast food, junk food, home-cooked food—
you name it, I ate a lot of it. This recipe for disaster quickly
transformed me from a skinny adolescent into an overweight
teenager. Years went by without any change until one day, a
spark went off inside me. I became furious and disgusted with
myself for the unhealthy lifestyle that I'd been following and
decided that I'd had enough—I was going to turn my life around.
I walked into the gym in 2005 at the age of 19 in an effort to lose
weight and improve my overall fitness. When I experimented
with lifting weight, I found that it was something I actually
enjoyed, which sparked a new desire to build muscle and
become stronger. By 2008, I was in the gym every day.
Without much knowledge of nutrition and training, however,
results came slowly. Though I’d eliminated most junk food
from my diet, I was still overeating. Over the next few years, I
gained muscle but was still unable to find that elusive six pack.
In late 2009, when I was 24 years old, I realized my mistake and
shifted the focus to my nutrition. It was the missing piece of the
puzzle that was holding me back from being lean again. In just a
few months of closely monitoring my calorie intake, my abs
were popping and I had muscle definition I‘d never dreamed of.
The results ignited my passion for nutritional science.
I had no intention of competing until a trainer at my gym
commented on my physique and recommended that I enter a
local bodybuilding show that was only 3 weeks away. I initially
thought he was crazy and shrugged it off. However, after giving
the idea a few hours of thought, I made the decision to compete
later that night. I stepped on stage for the first time in May 2010
at the NPC Long Island Bodybuilding, Fitness & Figure
Championships and took 2nd in the Bantamweight class. For the
Alan Aragon’s Research Review – December 2011
next 12 months I worked on building muscle and learning as
much as possible about advanced concepts of nutrition. I
competed in the same show in May 2011 and took 2nd again,
this time in the Lightweight class. Less than 2 months later, I
competed in the NPC Hudson Valley Bodybuilding, Fitness,
Figure, Bikini & Physique Championships, winning 1st in
Novice Lightweight and 1st in Open Lightweight.
Congrats on the placings and the win of both the novice &
open classes. I'm interested in what you currently do as a
career, and how you fit the bodybuilding lifestyle in with
your 'day job.' are there any ongoing challenges, or is it
basically a piece of cake (no pun intended).
My career is in the field of Information Technology. I'm a
project manager at a software company that develops and sells
data protection and disaster recovery products. Unfortunately,
that involves sitting at a desk from 9-5, so I'm mostly inactive
during the day. However, I'm able to go to the gym after work
and on the weekends, and usually train 6 times per week. I take
advantage of the weekends to be more active, which is not only
good for health, but allows me to eat more as well!
Since my work hours are always the same, my eating pattern is
usually very consistent during the week. I prepare lunch in the
morning which I bring to work. Along with various snacks I
keep at my desk, it holds me over until I get home and have
dinner, which is by far my biggest meal of the day. The main
challenge at work is keeping my hands off all cookies, muffins,
and bagels laying around! I often spend my lunch breaks on the
internet reading about nutrition. If I’m going out to lunch with
co-workers or customers, I'll approximate the calories in my
food to ensure that I'm eating the right amount for my goal,
whether it be gaining lean mass or dieting for a show.
What was your starting/off-season BF% & total weight, as
well as your contest BF% & weight? I realize these questions
might be moot if you did not take quantitative measures of
these parameters. How many weeks did you allot to get
dialed into contest shape?
I don't take precise measurements of my BF%, focusing instead
on the trend of my weight gain or weight loss and what I see in
the mirror. My highest total weight during my last off-season
was about 182 pounds, at an estimated 16% bodyfat. I began
dieting 23 weeks out to give myself ample time for slow and
steady weight loss and be ready several weeks out from the
show. My contest weight was 151 pounds.
What was your weight training split each week? Please
include sets, & reps. About how many average weekly hours
of weight training did you do?
I had been training one body part per night for several years and
saw good results, so I continued to train this way up until I
started competing. Four to six exercises per body part, three to
five sets per exercise, six to ten reps per set. About an hour and
a half of weight training for six days works out to an average of
9 hours per week. I currently still lift for a similar amount of
time, however I've since switched to training two body parts per
night (training everything but arms twice a week) in an effort to
continue making progress.
[Back to Contents] Page 14
What was your weekly cardio regimen? Please include
exercises & intensities. About how many average weekly
hours of cardio did you do?
Prior to competing, I was doing cardio daily after lifting in an
effort to become leaner, sometimes for as long as an hour.
When I learned how to diet, cardio became less important as a
means of losing weight. It was never something I enjoyed, and
therefore I did minimal (if any) cardio in the off-season. At
about 6 weeks out from a competition, I would begin cardio
every day. The majority would be moderate intensity on the
StepMill, with a few days per week of high intensity interval
training (HIIT) on the treadmill. About a half hour of weight
training for six days works out to an average of 3 hours per
week. Understanding the importance of good cardiovascular
health, however, I am now trying to do a half hour of cardio at
least three times per week in the off season.
What were the specifics of your diet in terms of carbs,
protein & fat? Were any of the macros cycled, if so, what
was your approach, or was intake linear (doubt it)?
I focus on ensuring adequate protein (at least 1 gram per pound
of lean mass), and plenty of fat. I do better on higher fat than
carbs, so during the off-season I'll often eat over 150 grams of
fat per day with carbs ending up less than 400 grams. I do not
cycle any macros and, when dieting, decrease intake in a linear
fashion. Before I began dieting for my shows last year I was at
about 3800 calories and dropped them gradually to maintain a
500 calorie deficit, with the goal being a one pound per week
weight loss. I incorporated a refeed day (to slightly above
maintenance calories) every few weeks at the beginning of
contest prep, and increased the refeed frequency to once per
week toward the latter stages.
Could you give us a typical day's menu during prep - on both
lower & higher-carb days (if applicable)?
A typical day's menu would consist of fish or chicken, eggs,
beef, dairy, nuts, and vegetables. My favorite sources of carbs
are bread, oats, and cereal. I sneak in fun foods like ice cream,
pizza, and pancakes to keep me sane. This becomes more
difficult as calories plummet, of course. When dieting, I reduce
calories by gradually reducing carbs and fats and, being a
volume eater, it's important for me to choose foods which are
satiating. I look forward to and take advantage of refeed days to
satisfy any cravings I may have.
There are plenty of horror stories of guys going on a week-
long bender & slamming 20 or more pounds of fat back on,
along with a number of accompanying emotional
disturbances. Do you have any specific tactics for
transitioning back to 'normal' eating after contest dieting
without going through the typical problems competitors do?
The main contributing factor to having a bad rebound after a
show, in my opinion, is when guys completely deprive
themselves of food they love [during prep]. I made this mistake
when I dieted for my first competition and gained over twenty
pounds in the days following the show. Luckily, it was mostly
waterweight. Now I incorporate my favorite foods and satisfy
any cravings I have, even while dieting. Accounting for some of
Alan Aragon’s Research Review – December 2011
your "comfort foods" in your daily calorie and macronutrient
allotment will not hurt your progress and you won't have the
urge to go crazy on them after the show.
I recommend drinking a ton of fluid immediately after the
competition, since you may actually be confusing thirst for
hunger, and easing up on the diet gradually instead of
immediately going out to an all you can eat buffet. Avoid
stuffing your face in the hours after the show, go the gym the
next day and get back into your normal routine. If you
temporarily exercise control during this critical time, you'll much
more likely be able to reverse your diet in a smooth fashion.
Could you describe in detail what your post-contest blood
test revealed in terms of androgen levels (ie, total & free T,
etc, etc)? Did you have any prior test done to compare these
values to? I'd also like to get an update on whether you were
able to normalize these lab values & the specifics of how you
did it.
Reduced calories, fats, and carbs all contribute to lower
androgen levels during prolonged dieting. This year's post-
contest blood tests revealed total testosterone levels of 306 ng/dl
(half that of the average 25 year old) and free testosterone levels
of 3 ng/dl (one quarter that of the average 25 year old!).
Unfortunately I don't have any prior data to compare it to (I
never requested androgen levels during previous blood tests).
Since these results, I've been reverse dieting for several months,
continuously increasing my fats and carbs. Total calories are
almost double what they were leading up to the show and I feel
significantly better. I've not yet gotten bloodwork done since
then (I hate going to the doctor), but if I had to guess, I'd say that
my hormonal state has made a significant rebound and I plan to
verify that soon.
What supplements do you take offseason & precontest
(dosages too)?
In both the offseason and precontest, the only supplements I take
are whey protein (one scoop a day), creatine (5 grams per day),
fish oil (3 grams per day high in EPA/DHA), and a multivitamin.
Occasionally I also take a pre-workout energy drink if I'm
feeling tired before a workout. This happens much more often
pre-contest!
What are the details of your showtime peaking strategy? Do
you employ any sort of water, sodium, or carb manipulation
within the week leading into the show? If so, please specify
the details.
I increase water intake a week out from the competition and drop
sodium and carbs out of my diet. When I'm three days out, I
begin to decrease water intake and stop all fluids a day before
the show. Once I'm happy with the amount of water I've lost, I
re-introduce carbs 24-36 hours before stepping on stage to
replenish muscle glycogen. The night prior to and the morning
of the show, I continue to eat carbs while adding more fats and
re-introducing sodium. Many competitors employ water
manipulation and carb up strategies similar to this, while others
do not. I found that for my body, water depletion is necessary to
reach a high level of conditioning.
[Back to Contents] Page 15
What are your future plans in competitive bodybuilding, and Home & stage shots from the latest round of competitions:
what are some of the key tips you would give to aspiring
competitors - especially in terms of the common pre-contest
diet or training mistakes that can easily be avoided?
I plan to take some time off to build more lean mass and
improve several areas of my physique. I haven't picked a
timeframe for my next show yet because I want to wait until I'm
happy with my improvements, at which time I'll pick my next
show and begin dieting. I'm also working with my girlfriend on
her contest prep and coaching her as she gets ready for her
competitive debut this year in the women's figure division.
Nutrition has become a passion of mine and it needs to be a
primary focus for aspiring bodybuilding competitors. Losing
weight for a show should be done slowly to minimize muscle
loss, and the pre-contest diet should still incorporate comfort
foods to satisfy or prevent cravings. Dieting for a show isn't
easy; it requires commitment, dedication, and plenty of will
power, but it shouldn't be more painful than it has to be.
Sufficient calories and protein are necessary in the off-season for
muscle gains, regardless of how hard or how often one trains.
However, a common mistake I see is guys overeating in the off-
season and gaining too much bodyfat. Unless someone only
recently began lifting, muscle gains will come slowly even with
proper nutrition and training. Just like I learned myself, much of
that weight will just be unnecessary bodyfat, and you'll need to
diet that much longer to lose it all before the show. A key piece
of advice is to eat only slightly above maintenance, train hard,
and get plenty of sleep!

Thanks again for doing the interview, Mike. Without further

ado... Here comes the inspiration!
__________________________________________________

Age 9, cuddly as heck, 10 years before joining a gym:

Alan Aragon’s Research Review – December 2011 [Back to Contents] Page 16

 amounts of detail with the evidence and my recommendations –
which have nothing to do with timing being “bogus.” The
Nutrient timing – lingering controversy & confusion. precision of nutrient timing lies on a continuum of importance
By Alan Aragon according to the goal. With certain activities such as competitive
endurance events, it’s critically important. On the other end of
  the spectrum, the casual trainee seeking to lose enough weight to
            So,  reading  some  of  the latest stuff showing how the 
             anabolic response to feeding post workout is extended  escape obesity needs to worry about little else than burning more
for  a  long  while,  and  considering  that  most  of  the  studies  on  calories than he takes in each day – or for folks who prefer a
around  workout  nutrition  were  not  done  in  the  post  prandial  non-linear approach, each week. And of course other important
state  which  most  bodybuilders  (even  those  dieting)  tend  to  details like getting enough protein comes into play, but the
operate  in,  I've  seen  you  and  a  few  others  come  to  the  timing of this for the vast majority of casual dieters and
conclusion that peri‐workout nutrition is really non‐existent or  recreational trainees is a matter of making sure it all gets in
vastly  overstated  in  importance.  But,  do  you  really  think  it’s  between waking & sleeping.
prudent at this point to kind of say the whole idea of nutrient  So, what about the folks who want to push the limits of muscle
timing  is  bogus?  I  mean  sure  the  body  is  fantastic  at 
gain and/or fat loss – or both? I realize that these are probably
compensating  for  things,  but  over  the  long  term  are  we  sure 
the populations you have in mind when referencing acute
that it all "evens out?". For instance, yes maybe not eating for 
research showing the anabolic benefits of timing protein and/or
20 hours post workout, and then eating would greatly increase 
the  anabolic  stimulus  of  said  meal,  but  would  it  effectively  carbohydrate around the training bout in order to maximize
compensate to the same level as to compare to a meal within a  anabolism. Wouldn’t these acute benefits be additive over time,
shorter time frame? And if it did not even out, and even if only  you ask? That’s a good question, and thus far, the answer is that
slightly  being  more  superior,  wouldn't  this  have  an  additive  these acute benefits have largely failed to accumulate & result in
effect over time on progress?   significant differences in studies lasting several weeks.
  In order to level the playing field, the chronic effect studies that
Lastly, I've seen some stuff on there not being an added benefit  truly show timing benefit must be macronutrient-matched, and
to  combining  CHO/EAA  post  workout,  or  preworkout,  so  long 
this includes protein &/or carb supplements. What we’re looking
as  glycogen  levels  aren't  depleted,  but  in  short  term  studies 
for are the special effects of specific placement of things. We’re
hasn't  post  workout  CHO+EAA  been  shown  to  be  superior? 
Sure  they  are  acute,  but  I  haven't  seen  any  long  term  studies 
not looking for the benefits of adding things – as in the case of a
where  these  things  are  actually  compared  on  a  more  applied  commonly cited trial by Willoughby et al, whose experimental
basis,  like  matching  two  isocaloric  diets,  one  with  a  greater  group ended up with 40 grams more daily protein than the
proportion  of  protein  and  carbs  post  workout  vs  one  with  a  control group, thanks to the timed supplement.1 In similar
normal distribution of CHO and EAA and the effects on LBM, fat  principle but contrasting results, Verdijk et al found no effect of
loss  and  performance  over  time.  Isn't  it  a  bit  premature  to  protein supplementation (20 grams total) split immediately
dismiss  the  acute  short  term,  around‐workout  nutrition  before and after resistance training over a 12-week period.2
studies? Or am I just missing some data here?  With that out of the way, of the chronic-effect investigations that
 
either purposely or by default examined the effect of protein
I  ask  because  again  and  again  and  again  and  again  in  my 
&/or carb timing around the resistance training bout, only two3,4
research of protein intake and optimal levels, researcher after 
researcher  from  the  late  80's  into  present  day  emphasize  the 
out of six3-8 studies have shown superior effects of nutrients
timing of protein intake relative to training as possibly having a  timed near training on strength &/or body composition. Granted,
greater influence than total protein intake on lbm, fat loss and  that’s not a very deep body of literature. But it certainly doesn’t
performance and the references seem solid. I kind of feel  like  lend much confidence in the promise that acute studies have
I'm  missing  something...even  with  the  few  recent  studies  I've  shown.
seen  they  don't  seem  to  conflict  with  prior  data  to  the  point  A detail that doesn’t help the protein timing cause is the fact that
where  it  seems  prudent  just  to  toss  all  the  peri‐workout  2 of the 4 studies showing no significant effect involved protein
nutrition data out the window... 
intakes that averaged a little over 1 g/kg. This is roughly half of
 
what’s typically consumed by the bodybuilding, sports, & fitness
Maybe I'm just reluctant to let go of something I thought had 
enthusiasts who are most concerned about nutrient timing. It’s
been rather definitively established because this seems to be a 
relatively new paradigm shift in the last few years. Would love 
reasonable to speculate that the closer the total daily protein
to hear your insight. Thanks Alan.  – EH intake comes to being optimal or abundant, the less impact that
special positioning of the constituent protein doses has.
Nutrient timing is a topic I’ve covered in-depth more than With all of that said, it’s unwise to be closed-minded about the
once in AARR (Jan-Mar 2008, update in Dec 2010), and possibility of the evidence eventually shifting in favor of timing
it’s a topic I’m bound to comb through again as enough new bits nutrients (protein in particular) in sufficient doses, closely
of evidence accumulate to discuss any notable directions or around the resistance training bout in order to maximize
confirmations. The first thing I’d like to address is the muscular size & strength. Furthermore, the current body of
misconception that “the whole idea of nutrient timing is bogus.” nutrient timing research is lacking in non-acute studies that
Anyone who feels that way has not read the aforementioned optimize both training and macronutrition for the goals of
issues, or has not read them carefully enough. I go into painful improving strength and body composition. However, it would

Alan Aragon’s Research Review – December 2011 [Back to Contents] Page 17

also be naive to deny or dismiss the current longer-term
evidence, most of which has betrayed the short-term data. Many
folks in both the public & academic domain are simply not
aware of this non-acute research because the majority of it was
published only recently (2009 & onward).
For those who are determined to scoot nutrients close to the
weight training bout in the spirit of covering all hypothetical
bases, more power to them. It won’t hurt, and according to 2 out
of 6 chronic effect studies, it might help. Depending on your
lean mass, it’s mind-numbingly simple to consume roughly 25-
55 grams of protein within about 1-2 hours on both sides of the
training bout. That’s as precise as the collective body of acute &
chronic evidence shows you need to be. For those who disregard
timing other than nailing your macronutrient totals for the day
without purposely skipping the meals that typically fall before &
after training, the precise timing benefits you’re missing out on
are likely to be miniscule, un-split hairs.

References
1. Willoughby DS, et al. Effects of resistance training and
protein plus amino acid supplementation on muscle
anabolism, mass, and strength. Willoughby DS, et al.
Amino Acids. 2007;32(4):467-77. [Pubmed]
2. Verdijk LB, et al. Protein supplementation before and after
exercise does not further augment skeletal muscle
hypertrophy after resistance training in elderly men. Am J
Clin Nutr. 2009 Feb;89(2):608-16. [Pubmed]
3. Esmarck B, Timing of postexercise protein intake is
important for muscle hypertrophy with resistance training in
elderly humans. J Physiol. 2001 Aug 15;535(Pt 1):301-11.
[Pubmed]
4. Cribb PJ, Hayes A. Effects of supplement timing and
resistance exercise on skeletal muscle hypertrophy. Med Sci
Sports Exerc. 2006 Nov;38(11):1918-25. [Pubmed]
5. Keim NL, et al. Weight loss is greater with consumption of
large morning meals and fat-free mass is preserved with Corrections have been made to the following errors in
large evening meals in women on a controlled weight previous issues.
reduction regimen. J Nutr. 1997 Jan;127(1):75-82.
[Pubmed] ƒ Sept 2008: Robinson et al should have been cited as Goto et
6. Burk A, et al. Time-divided ingestion pattern of casein- al in reference 13 on page 6.
based protein supplement stimulates an increase in fat-free ƒ Nov 2011: Robinson et al should have been cited as Goto et
body mass during resistance training in young untrained al in reference 15 on page 10.
men. Nutr Res. 2009 Jun;29(6):405-13. [Pubmed]
7. Hoffman JR, et al. Effect of protein supplement timing on These errors have been fixed, please re-download the updated
strength, power and body compositional changes in versions: http://alanaragon.com/members-page.html
experienced resistance trained men. Int J Sport Nutr Exerc
Metab. 2009 Apr;19(2):172-85. [Pubmed]
8. Wycherley TP, et al. Timing of protein ingestion relative to
resistance exercise training does not influence body Although he’s been active for at least a decade, I’ve just become
composition, energy expenditure, glycaemic control or aware of the reality-based comedian/troll-extraordinaire named
cardiometabolic risk factors in a hypocaloric, high protein Rémi Gaillard. According to his Wikipedia page, “The majority
diet in patients with type 2 diabetes. Diabetes Obes Metab. of Gaillard’s stunts have resulted in prison sentences for the
2010 Dec;12(12):1097-105. [Pubmed] comedian.” Now that’s true dedication to the art form! Here is a
clip of one of his fitness-based stunts.

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

contention, cheers, jeers, guest articles you’d like to submit, or
any feedback at all, send it over to aarrsupport@gmail.com.

Alan Aragon’s Research Review – December 2011 [Back to Contents] Page 18