11 Charles Poliquin’s 10 tips for staying healthy and

fit at age 51.

By Alan Aragon

14 Caffeine + creatine = conflict?

By Alan Aragon

15 An update has been made in the previous issue.

Copyright © April 1st, 2012 by Alan Aragon
Home: www.alanaragon.com/researchreview
Correspondence: aarrsupport@gmail.com

2 Silk amino acids: spinning science to sell

supplements.
By Dylan Klein

5 Aerobic and resistance training effects on energy

Intake: The STRRIDE AT/RT Study: (exercise
training effects on energy intake).
Bales CW, et al. J Med Sci Sports Exerc. 2012 Apr 19.
[Epub ahead of print] [Pubmed]

6 Preexercise aminoacidemia and muscle protein

synthesis after resistance exercise.
Burke LM, et al. Med Sci Sports Exerc. 2012 May 22.
[Epub ahead of print] [Pubmed]

7 Effect of alginate supplementation on weight loss

in obese subjects completing a 12-wk energy-
restricted diet: a randomized controlled trial.
Georg Jensen M, et al. Am J Clin Nutr. 2012 May 30. [Epub
ahead of print] [Pubmed]

8 Preexercise galactose and glucose ingestion on

fuel utilization during exercise.
O'Hara JP, et al. Med Sci Sports Exerc. 2012 Apr 19. [Epub
ahead of print] [Pubmed]

9 The acute effects of twenty-four hours of sleep

loss on the performance of national-caliber male
collegiate weightlifters.
Blumert PA, et al. Strength Cond Res. 2007
Nov;21(4):1146-54. [Pubmed]

Alan Aragon’s Research Review – April 2012 [Back to Contents] Page 1


Silk amino acids: spinning science to sell
supplements.
By Dylan Klein
Editor’s note: Special thanks is due to Dylan for contributing
his insight. A bounty of excellent information can be found at his
website, nutridylan.com.
_________________________________________________________________
Opening comments
It wasn’t until recently that I discovered (well, more like
regrettably stumbled upon) silk amino acids (SAA). Among
other things, they claim to be the amino acids of the future while
dismissing the ever-so-popular branched-chain amino acids
(BCAA) as “yesterday’s science.” Without completely
exhausting the desires of every muscle-hungry meat-head, SAAs
are claimed to; increase muscle hypertrophy; increase muscle
endurance; improve body composition; promote natural
testosterone (whatever that means); maintain healthy cortisol
levels; provide antioxidant support; and provide enhanced
performance – which I’m assuming is sports-related
performance, although you could just as easily make the case for
enhanced sexual performance; but more on that later. Now, I
have always jokingly said – although somewhat half-serious –
that bodybuilders would eat their own feces if it meant gaining
more muscle. And although SAAs are a long shot from eating
your own excrement, the point remains the same; people are
willing to take just about anything in order to build more muscle,
especially when it’s supposedly “backed by science.”
Supplement companies prey at this weakness time and time
again, and it’s only a matter of time before they completely jump
the shark; right now they’re just merely curling their toes over
the edge. So before people go rushing to the mountain tops with
stuff, and before SAAs are a staple in every “proprietary blend,”
I would like to provide a little background on silk proteins, touch
upon the limited (ir)relevant research behind them, and then
wrap things up with my own comments and conclusions. So
without much further ado, let’s begin.
Silk proteins: history, usage and structure
Silk amino acids are derived from silk polymers, specifically
polymers from Bombyx mori, otherwise known as the silkworm.
This is opposed to deriving them from silk polymers from
spiders, mites, and even scorpions which also produce silk. This
is an important distinction because silks differ in their
composition, structure and other properties based on the source
of the silk.1 Historically, silkworm silk has been used in
biomedical sutures for decades and in textile manufacturing for
centuries.1,2 Even more recently, silk protein has been used in
various cosmetic products such as lotions, creams and
ointments.2 The structure of silk is comprised of two double-
stranded filaments; fibroin and sericin. Fibroin is a glycoprotein
and forms the structure of the filament and is responsible for
some of the chemical properties associated with silk.2 Fibroin
primarily contains the amino acids alanine, glycine and serine
(12, 30 and 44 percent, respectively). Sericin, on the other hand,
Alan Aragon’s Research Review – April 2012
is sticky and is meant to encase the fibroin filaments, making the
finalized cocoon hard and tough. Sericin is comprised of roughly
18 amino acids and is about 30-33 percent serine.2 Based on
what little information I could gather, it appears that silk amino
acid supplements derive their aminos from sericin rather than
fibroin. I cannot speculate as to why. Nevertheless, the use of
silk amino acids as a muscle-building supplement is extremely
novel. Not until recently has there been any scientific evidence
to even suggest the consumption of SAAs in terms of sports-
related/body compositional outcomes; and I say this with
extreme hesitation. There are, however, numerous studies – both
in vitro and animal – with clinical implications involving SAAs
that do warrant some discussion despite their virtually non-
existent application in terms of muscle gain, body composition
and sports performance.
Clinical implications of silk proteins
In brief, both fibroin and sericin have been shown – in vitro – to
enhance insulin sensitivity3 and to possess anti-HIV,4 anti-
oxidant,5 and anti-cancer properties.6 Moreover, in mice, silk
proteins – specifically sericin – have been shown to possess anti-
diabetic properties7,8 and cholesterol-lowering properties9 by
improving blood glucose and lipid profiles. Sericin has even
been shown to have a protective effect on alcohol-induced liver
damage in mice.10 Furthermore, there is even some data that
suggests that sericin enhances the intestinal absorption and
bioavailability of zinc, iron, magnesium and calcium.11
Collectively, you could make a good case for mice to
incorporate silk proteins into their diet – that is if they consume
outrageous quantities of fat and drink like Lindsey Lohan.
Unfortunately, sericin has yet to be studied in this capacity using
human models, so the jury is still out on whether or not the
consumption of silk proteins will have any beneficial effects in a
human diet. I am, however, inclined to think not given that – in
some instances – the dosages of silk proteins administered were
in the range of 0.375-1.5g/kg body weight. I don’t know about
you, but I don’t think anyone is willing (or fiscally stupid
enough) to consume that much silk protein on a daily basis.
Stranger things have been known to happen, however.
Special amino acid “sequence”
Before we get into whether or not SAAs are beneficial for
muscle gain and body comp, let’s first take a look at what is
actually in the product. Earlier I briefly touched upon the serine
content of sericin and mentioned that it was the source of amino
acids for SAA supplementation. As far as I know, there is only
one U.S. Company that
sells SAAs (there are
many in Korea and
Asia), so we will use
their nutrition fact label
as the proxy.
As you can see to the
left, their product
contains “sequenced
proteins” comprised of
the amino acids
alanine, glycine, serine,
[Back to Contents] Page 2
valine, and threonine. Having even a basic understanding of
biochemistry, one can easily establish that two out of the five
amino acids are essential (valine and threonine), with the rest
being non-essential (NEAA). This is important because the
stimulation of muscle protein synthesis (MPS) seems to be
dependent upon EAAs, most notably leucine.12-14 In fact, there is
neither a role nor a benefit of having NEAAs added, even at very
high doses [14]. Therefore, it does not make sense – at least
from an anabolic point of view – to even supplement with
glycine, serine, or alanine. Furthermore, you will notice that
leucine is completely absent. It is well established that leucine
plays a pivotal role in stimulating MPS, if not THE role.15
However, even if leucine were added, there’s no research to
suggest that extra leucine would further increase MPS when
combined with the appropriate post-workout meal and therefore
lead to increases in muscle mass. Case in point, multiple studies
by Koopman et al. specifically showed that there was no additive
benefit from consuming free leucine when a sufficient amount of
casein hydrolysate was ingested post-workout.16-18 Simply
looking at the label has to make one wonder. But then again,
I’ve seen crazier things on a supplement label. Perhaps the
research looking specifically at SAAs and muscle-building/body
comp outcomes will prove to be more promising?
SAAs for muscle gain, body composition & performance
Unfortunately, there are only two studies that even attempted to
look at sport-related parameters using silk amino acid
supplementation. Even more unfortunate, and all the while not
surprising, is that they were both done in mice. Lastly, and most
importantly, neither study used any measure indicating either an
increase in muscle mass or an improvement in body composition
over the duration of the study; not one. Therefore, any claim
about increased muscle hypertrophy or better body comp from
ingestion of SAA is complete BS. So before you read one more
sentence, know this: any SAA supplement – for now – is basing
its claims off of two (poorly controlled) rodent studies, with
limited – even borderline irrelevant – applicability. That being
said, let’s dissect these papers.
In the first study,19 researchers from Chungbuk University,
Korea examined the effects of 800mg/kg body weight SAA
preparations on stamina and male reproductive function in
forced-swimming mice. They noticed increased stamina despite
reductions in body weight and increased testes weight due to
increased sperm counts; most likely because of increased
testosterone production. Furthermore, they saw that SAAs
reduced the effects of swimming on muscular tissue damage,
liver damage, and glycogen depletion. Unfortunately, the article
was published in an obscure Korean journal and therefore I
cannot access the entire article to get into specifics. The good
news, however, is that the second study (which I could access)
was conducted by the same group of researchers a year later.
Therefore, I will draw most of my conclusions and comments
from this single study. I should also note that this second study is
the paper that most advocates for SAAs usually draw upon.
20
In the second study, the same group of researchers looked to
examine the effects of SAAs on physical stamina and male
reproductive function in mice. This time, however, the mice
were divided into four different groups: control (water only),
Alan Aragon’s Research Review – April 2012
50mg SAA/kg body weight, 160mg SAA/kg body weight, and
500mg SAA/kg body weight. Each group received the treatment
30 minutes before undergoing a 30-minute swim test. The mice
completed this 30-minute swim every day for 42 days. In
addition, every 2 weeks the mice underwent a weight-loaded
(5% of body weight), forced swim in order to establish
maximum swimming time.
Consistent with their previous results, the researchers noticed a
marked increase in stamina (~60-120%) despite reduced body
weight, and increases in blood testosterone levels and sperm
counts (~38-55%) across all test conditions. Moreover, SAAs
were said to decrease the effects of swimming on tissue damage
and attenuate the levels of cortisol during swimming as well
weight gain over the 42-day study period (I assume this is where
the reports of improved body comp come from). Lastly, SAA
consumption attenuated the loss of muscle glycogen in a dose-
dependent manner, which possibly explains the increase in
stamina in a similar manner with the highest dosage (500mg/kg)
resulting in the longest swim time.
Now, despite the glaringly obvious fact that this study was done
in mice, there are some other serious limitations that weaken the
results of this study that, had the study been done in humans,
would have still made the results tenuous at best. The biggest
flaw in the study design was the diet protocol. Researchers
allowed for an ad libitum diet, meaning that the mice ate at their
leisure. In fact, there was no mention of diet apart from the
researchers saying that the mice ate “standard rodent chow.”
Theoretically, this allows for highly variable caloric intake and
macronutrient composition between the mice. Secondly, the
researchers had varying dosages of SAA for each group.
Therefore, not controlling for calories or protein in the rat’s diets
dismisses the results altogether. Put another way, we could
simply be witnessing the effects of consuming a diet with
sufficient protein and or calories; something most lifters and
athletes already consume. A much better study protocol would
have had isocaloric and isonitrogenous diets to eliminate any
confounding elements of the diet. As far as I can see, these
results tell us nothing other than those who ate more protein,
swam better. It could have just as easily been BCAAs or any
other protein/amino acid supplement as far as I’m concerned.
Future studies should aim to correct this huge oversight so that’s
the effects of SAAs can be accurately isolated.
Lastly, with respects to increased testosterone production, one
should not get too carried away with the results. Even the
highest increase in testosterone (~160% above resting
condition), which was actually seen at the lowest dosage
(50mg/kg), is nowhere near what is seen with
supraphysiological doses of Test.21 Not only is the overall effect
negligible in the big scheme of things, but the effects are only
relevant to mice! One cannot go assuming that the same effects
would hold true for a human following a resistance training
program.
Conclusions
So, to wraps things up, it appears that SAAs are nothing more
than a novelty amino acid supplement with outrageous claims
backed by either non-existent or poorly controlled animal
research. But then again, what supplement hasn’t walked down
[Back to Contents] Page 3
that road before? Until more research is done, especially studies 12. Volpi E, Kobayashi H, Sheffield-Moore M, Mittendorfer B,
done in humans, there isn’t one shred of convincing evidence to Wolfe RR. Essential amino acids are primarily responsible
suggest the consumption of SAAs in addition to a proper diet for the amino acid stimulation of muscle protein anabolism
and training protocol. Although I may be preaching to choir in healthy older adults. Am J Clin Nutr. 2003;78:250-258.
here, the fact still remains that idiots abound, and no matter [Pubmed]
where you go someone is always going to fall for the seducing 13. Smith K, Barua JM, Watt PW, Scrimgeour CM, Rennie MJ.
claims on the side of a bottle, especially when it means the Flooding with [1-13C]leucine stimulates human muscle
potential for more muscle. Also, it goes without saying, but I protein incorporation of continuously infused 1-[1-
13
probably should mention that the safety of habitual SAA C]valine. Am J Physiol. 1992;262:E372-6. [Pubmed]
ingestion has never been studied in humans… at any dosage. 14. Smith K, Reynolds N, Downie S, Patel A, Rennie MJ.
Therefore, given the available data, clearly showing a lack of Effects of flooding amino acids on incorporation of labeled
safety and efficacy in humans, I wouldn’t waste my money on amino acids into human muscle protein. Am J Physiol.
novel silk amino acids, no matter how attractive supplements 1998;275:E73-8. [Pubmed]
companies make them appear. 15. Drummond MJ, Rasmussen BB. Leucine-enriched nutrients
and the regulation of mammalian target of rapamycin
References signaling and human skeletal muscle protein synthesis. Curr
Opin Clin Nutr Metab Care 2008;11(3):222-6. [Pubmed]
1. Altman GH, Diaz F, Jakuba C, Calabro T, Horan RL, Chen
16. Koopman R, Wagenmakers AJ, Manders RJ, Zorenc AH,
J, Lu H, Richmond J, Kaplan DL. Silk-based biomaterials.
Senden JM, Gerselink M, Keizer HA, van Loon LJ.
Biomaterials 2003;24:401-416. [Pubmed]
Combined ingestion of protein and free leucine with
2. Padamwar MN, Pawar AP. Silk sericin and its application: a
carbohydrate increases postexercise muscle protein
review. J Sci Indust Res. 2004;63:323-329. [NISCAIR]
synthesis in vivo in male subjects. Am J Physiol Endocrinol
3. Hyun CK, Kim IY, Frost SC. Soluble fibroin enhances
Metab. 2005;288:E645-E653. [Pubmed]
insulin sensitivity and glucose metabolism in 3T3-L1
17. Koopman R, Verdijk L, Manders RJ, Gijsen AP, Gorselink
adipocytes. J Nutr. 2004;134(12):3257-3263. [Pubmed]
M, Pijpers E, Wagenmakers AJ, van Loon LJ. Co-ingestion
4. Gotoh K, Izumi H, Kanamoto T, Tamada Y, Nakashima H.
of protein and leucine stimulate muscle protein synthesis
Sulfated fibroin, a novel sulfated peptide derived from silk,
rates to the same extent in young and elderly men. Am J
inhibits human immunodeficiency virus replication in vitro.
Clin Nutr. 2006;84(3):623-32. [Pubmed]
Biosci Biotechnol Biochem. 2000;64(8):1664-1670.
18. Koopman R, Verdijk LB, Beelen M, Gorselink M,
[Pubmed]
Kruseman AN, Wagenmakers AJ, Kuipers H, van Loon LJ.
5. Kato N, Sato S, Yamanaka A, Yamada H, Fuwa M, Nomura
Co-ingestion of leucine with protein does not further
M. Silk protein, sericin, inhibits lipid peroxidation and
augment post-exercise muscle protein synthesis rates in
tyrosinase activity. Biosci Biotechnol Biochem.
elderly men. Br J Nutr. 2008;99(3):571-80. [Pubmed]
1998;62(1):145-147. [Pubmed]
19. Shin S, Park D, Yeon S, Jeon JH, Kim TK, Joo SS, Lim
6. Zhaorigetu S, Yanaka N, Sasaki M, Watanabe H, Kato N.
WT, Lee JY, Kim YB. Stamina-enhancing effects of silk
Silk protein, sericin, suppresses DMBA-TPA-induced
amino acid preparations in mice. Laboratory Animal
mouse skin tumorigenesis by reducing oxidative stress,
Research. 2009;25(2):87-96. [ARGIS]
inflammatory responses and endogenous tumor promoter
20. Shin S, Yeon S, Park D, Oh J, Kang H, Kim S, Joo SS, Lim
TNF-α. Oncology Reports 2003;10:537-543. [Pubmed]
WT, Lee JY, Choi KC, Kim KY, Kim SU, Kim JC, Kim
7. Okazaki Y, Kakehi S, Xu Y, Tsujimoto K, Sasaki M,
YB. Silk amino acids improve physical stamina and male
Ogawa H, Kato N. Consumption of sericin reduces serum
reproductive function in mice. Biol Pharm Bull.
lipids, ameliorates glucose tolerance and elevates serum
2010;33(2):273-278. [Pubmed]
adiponectin in rats fed a high-fat diet. Biosci Biotechnol
21. Bhasin S, Storer TW, Berman N, Callegari C, Clevenger B,
Biochem. 2010;74(8):1534-38. [Pubmed]
Phillips J, Bunnell TJ, Tricker R, Shirazi A, Casaburi R.
8. Jung EY, Lee HS, Lee HJ, Kim JM, Lee KW, Suh HJ.
The effects of supraphysiologic doses of testosterone on
Feeding silk protein hydrolysates to C57BL/KsJ-db/db mice
muscle size and strength in normal men. N Engl J Med.
improves blood glucose and lipid profiles. Nutr Res.
1996;335(1):1-7. [Pubmed]
2010;30:783-790. [Pubmed]
9. Limpeanchob N, Trisat K, Duangjai A, Tiyaboonchai W,
Pongcharoen S, Sutheerawattananonda M. Sericin reduces
serum cholesterol in rats and cholesterol uptake in Caco-2
cells. J Agric Food Chem. 2010;58(23):12519-12522.
[Pubmed]
10. Li YG, Ji DF, Chen S, Hu GY. Protective effects of sericin
protein on alcohol-mediated liver damage in mice. Alcohol
& Alcoholism 2008;43(3):246-253. [Pubmed]
11. Sasaki M, Yamada H, Kato N. Composition of silk protein,
sericin elevates intestinal absorption of Zn, Fe, Mg, and Ca
in rats. Nutr Res. 2000;20(10):1505-1511. [NR-Journal]

Alan Aragon’s Research Review – April 2012 [Back to Contents] Page 4


Aerobic and resistance training effects on energy
Intake: The STRRIDE AT/RT Study: (exercise training
effects on energy intake).
Bales CW, et al. J Med Sci Sports Exerc. 2012 Apr 19. [Epub
ahead of print] [Pubmed]
PURPOSE: Our study characterizes food and energy intake
responses to long-term aerobic (AT) and resistance training (RT)
during a controlled 8-month trial. METHODS: In the STRRIDE
AT/RT trial, overweight/obese sedentary dyslipidemic men and
women were randomized to AT (n = 39), RT (n = 38), or a
combined treatment (AT/RT; n = 40) without any advice to
change their food intakes. Quantitative food intake assessments
(QDI) and food frequency questionnaires (FFQ) were collected
at baseline (BEF) and after 8 mo. training (END); body mass
(BM) and fat free mass (FFM) were also assessed. RESULTS:
In AT and AT/RT, respectively, meaningful decreases in
reported energy intake (REI) (-217 and -202 kcal; p < 0.001) and
in intakes of fat (-.9 and -14.9 g; p < 0.001, p = 0.004), protein (-
3 and -10.7 g; p = 0.002, p < 0.001), and carbohydrate (-28.1 and
-14.7 g; p = 0.001, p = 0.030) were found by FFQ. REI relative
to FFM decreased (p < 0.001 and p=0.002) as did intakes of fat
(-0.2 and -0.3 g; p = 0.003 and p = 0.014) and protein (-0.1 and -
0.2 g; p = 0.005 and p < 0.001) in AT and AT/RT and
carbohydrate (-0.5 g; p<0.003) in AT only. For RT, REI by QDI
decreased (-3.0 kcal/kg FFM; p=0.046), as did fat intake (-0.2 g;
p = 0.033). BM decreased in AT (-1.3 kg, p=0.006) and AT/RT
(-1.5 kg, p = 0.001) but was unchanged (0.6 kg, p = 0.176) in
RT. CONCLUSIONS: Previously sedentary subjects
completing 8 months of AT or AT/RT reduced their intakes of
kcal and macronutrients and BM. In RT, fat intakes and REI
(when expressed per FFM) decreased, BM was unchanged, and
FFM increased. SPONSORSHIP: This work was supported in
part by a grant from the NHLBI, 2R01HL57354.
Study strengths
In light of the current obesity problem, this study asks the
important question of which mode of exercise has the greatest
influence on energy intake. The sample size (196 subjects, 3
conditions) was relatively large for this type of research. The
trial duration was lengthy as well (8 months). Exercise was
supervised. A multiple-pass approach was used to assess dietary
intake. This involves five steps in the interviewing process
designed to limit underreporting. Dietary intake was software-
analyzed.
Study limitations
Despite added measures to track dietary intake (averaging 3-day
records with 24-hour recalls), food frequency questionnaires
(FFQs) have a questionable track record of accuracy.1,2 The
authors acknowledge the limitation of self-reported intake and
its tendency to selectively under-report. However, they
disclaimed this possibility by stating the following: “And, even if
underreporting occurred, there is no reason to think it would
worsen over time; if anything, one would expect reporting to be
more complete over time as subjects become more familiar with
Alan Aragon’s Research Review – April 2012
the assessment methods and offer more details about their food
intakes.” Another limitation acknowledged by the authors was
the intensity of the aerobic training protocol. Oddly, they
described the intensity range as moderate. At 65-80% of
VO2max (roughly 79-89% of max heart rate), this is more
accurately described as high-intensity (or at least high-moderate
to high). The aerobic + resistance training (AT/RT) condition
was not matched with the others in terms of energy expenditure;
the two protocols were merely stacked on top of each other. A
final limitation was the use of overweight/obese, sedentary,
dyslipidemic men and women. The outcomes in this population
might not reflect what might happen in the active or athletic
population. Note that the use of these subjects can also be
viewed as a strength since the overweight/dyslipidemic
population is more urgently in need of interventions that
improve health and/or prevent the progression of disease.
Comment/application
The main findings of this study were 3-fold: 1) Both groups that
included aerobic training significantly decreased absolute caloric
intake, although the decreases weren’t exactly staggering at -217
& -202 kcal for the aerobic training (AT) & AT/RT groups,
respectively. When caloric intake is expressed as a proportion of
fat-free mass, all groups showed a reduction according to one or
both of the measurement methods. 2) No significant change in
total bodyweight was seen in the RT group, although this was
due to a decrease in fat mass and increase in lean mass. On the
other hand, the other groups both lost net bodyweight, mainly
from body fat reductions, with statistically significant fat loss
occurring in AT/RT. 3) A final set of notable findings were the
changes in macronutrient intake relative to the protocols, which
overall were minor. AT & RT/AT showed small reductions in all
of the macronutrients, whereas RT only showed a reduction in
fat intake. To quote the investigators, “…the lack of any clear
trend is loosely in agreement with our observation that the
proportions of energy-yielding macronutrients were largely
unchanged.”
It’s somewhat predictable that the resistance-only group gained
lean mass while the other groups’ body composition change was
primarily from fat loss. All groups lost fat mass, but the AT
group was the only one to lose a small/statistically insignificant
amount of lean mass. It’s also predictable that the greatest
amount of fat loss occurred in the combination group, whose
training energy expenditure was greatest. However, the most
important finding was that energy intake did not increase in any
of the groups as a result of implementing an exercise program.
Although dietary intake was tracked, the subjects were not
instructed to alter their normal eating habits in any way since the
primary aim of the study was to see how the addition of various
training modes on energy intake. The lack of increased energy
intake despite training is in line with previous research, which
has not directly shown an increased energy intake caused by
training.3 The authors specifically state that they are unaware of
any long-term research showing that exercise increases energy
intake in previously sedentary subjects. This is an interesting
contrast with popular diet author Gary Taubes’ infamous
preaching that exercise antagonizes weight loss by increasing
appetite & thus food consumption. The present study throws a
bit of a wrench into that idea.
[Back to Contents] Page 5

Preexercise aminoacidemia and muscle protein
synthesis after resistance exercise.
Burke LM, et al. Med Sci Sports Exerc. 2012 May 22. [Epub
ahead of print] [Pubmed]
PURPOSE: We have previously shown that the aminoacidemia
caused by the consumption of a rapidly digested protein after
resistance exercise enhances muscle protein synthesis (MPS)
more than the amino acid (AA) profile associated with a slowly
digested protein. Here, we investigated whether differential
feeding patterns of a whey protein mixture commencing prior to
exercise affect post-exercise intracellular signaling and muscle
protein synthesis (MPS). METHODS: Twelve resistance-
trained males performed leg resistance exercise 45 min after
commencing each of three volume-matched nutrition protocols:
placebo (PLAC; artificially sweetened water); BOLUS (25 g
whey protein + 5 g leucine dissolved in artificially sweetened
water; 1 × 500 mL); or PULSE (15 × 33 mL aliquots of BOLUS
drink every 15 min). RESULTS: The pre-exercise rise in
plasma AA concentration with PULSE was attenuated compared
with BOLUS (P<0.05); this effect was reversed following
exercise, with two-fold greater leucine concentrations in PULSE
compared to BOLUS (P<0.05). One-hour post-exercise,
phosphorylation of p70 S6K and rpS6 was increased above
baseline with BOLUS and PULSE, but not PLAC (P<0.05);
furthermore, PULSE > BOLUS (P<0.05). MPS throughout 5 h
of recovery was higher with protein ingestion compared with
PLAC (0.037 ±0.007) with no differences between BOLUS or
PULSE (0.085 ±0.013 vs 0.095 ±0.010 %·h respectively, P =
0.56). CONCLUSIONS: Manipulation of aminoacidemia prior
to resistance exercise via different patterns of intake of protein,
altered plasma AA profiles and post-exercise intracellular
signaling. However, there was no difference in the enhancement
of the muscle protein synthetic response after exercise. Protein
sources producing a slow AA release, when consumed before
resistance exercise in sufficient amounts, are as effective as
rapidly digested proteins in promoting post-exercise muscle
protein synthesis. SPONSORSHIP: This study was supported
by a grant from Nestec Ltd., Vevey, Switzerland, and authors
Moore and Stellingwerff were employees of Nestec Ltd during
the period in which the study was conducted.
Study strengths
This study is innovative since it’s the first to ever examine the
effect of different protein dosing manipulations (single large
bolus vs spread small doses) prior to the resistance training bout
on measures of muscle anabolism. Resistance-trained subjects
were used, which minimized the tendency for newbie effects to
mask the effects of the nutritional protocols. 24 hours prior to
each trial, subjects were provided a pre-packaged diet
standardized proportionally to individual body mass.
Study limitations
As with all acute studies, the 5-hour effects examined here
remain speculative in the long-term. Another limitation easy to
overlook is that the authors aimed to compare the blood amino
acid profile associated with a fast versus a slowly digested
Alan Aragon’s Research Review – April 2012
protein, so it begs the question of why they did not simply
compare the effects of whey versus a slowly digested protein
such as egg or casein. The authors aimed at eliminating the
amino acid content of a protein as a confounding factor, thus
focusing on the pattern of aminoacidemia’s effects on muscle
protein synthesis (MPS). But in doing so, the study’s practical
application is heavily compromised. The simulated slow protein
profile was achieved by consuming 15 separate small doses
every 15 minutes of the same treatment that was consumed in a
single bolus. This obviously has limited applicability to real-
world feeding/dosing patterns.
Comment/application
The main findings of this study were two-fold: First off, the
spread-out/multi-dose “pulse” protocol designed to simulate a
slowly digested protein caused higher amino acid & insulin
elevations after the training bout than a single bolus of the same
total amount of protein. Specifically, the elevated post-exercise
blood nutrient profile enhanced signal transduction of the Akt-
mTORp70S6K pathway at 1 hour postexercise to a greater
degree than the bolus protocol. Expectedly, there was only
modest anabolic signaling with a placebo treatment. The second,
and most important finding was that by the 5-hour mark
postexercise, no significant differences in markers of muscle
protein synthesis were detected between the two protein dosing
protocols (below depicts fractional synthetic rate, with no
significant difference between the pulse & bolus treatments).
The authors note that the present study’s results differed from
their recent previous study comparing protein dosing
manipulations after resistance training.3 The same bolus dose
used in this study (25 g) outperformed a pulsed pattern (ten 2.5 g
doses every 20 minutes) for enhancing MPS. Thus, they
concluded that the present study supports the idea that a
substantial, fast-acting protein dose in the resistance-trained state
has an additive effect on anabolism, whereas pre-exercise
protein dosing manipulation does not have the same anabolic
effect – regardless of whether or not the amino acid pattern
resembles a fast (bolus) or slow (pulse) protein. They
specifically state that there’s no disadvantage to consuming a
protein source with a slow amino acid response as long as the
serving is large enough to have a high leucine content (in this
case, 5 g leucine was added to 25 g whey).
This data is interesting, and will likely be used to give credence
to the “postexercise anabolic window” concept. However, the
fact remains that while a minority of longer-term research
supports differential protein placement relative to resistance
training,4,5 the majority has thus far failed to do so.6-8
[Back to Contents] Page 6
Effect of alginate supplementation on weight loss in
obese subjects completing a 12-wk energy-restricted
diet: a randomized controlled trial.
Georg Jensen M, et al. Am J Clin Nutr. 2012 May 30. [Epub
ahead of print] [Pubmed]
BACKGROUND: Acute studies with alginate-based preloads
suggested that these strong gelling fibers may induce increased
feelings of satiety and reduce energy intakes. However, the long-
term efficacy and safety of alginate supplementation on body
weight regulation are lacking. OBJECTIVE: The primary aim
of the study was to investigate the effects in subjects of alginate
supplementation in conjunction with energy restriction (-300
kcal/d) on loss of body weight and fat and, second, on metabolic
risk markers in comparison with in a placebo group. DESIGN:
In a parallel, double-blind, placebo-controlled study, we
randomly assigned 96 obese subjects to either an energy-
restricted diet plus a placebo preload supplement or an energy-
restricted diet plus an alginate-based preload supplement (15 g
fiber). The preload was administered as a beverage 3 times/d
before main meals for a period of 12 wk. RESULTS: No
differences in loss of body weight and fat between groups were
shown in the intension-to-treat (ITT) analysis (P > 0.1).
However, in the completer analysis (n = 80), we showed a
greater weight loss with alginate (6.78 ± 3.67 kg) than with the
placebo (5.04 ± 3.40 kg) (P = 0.03), which was mainly attributed
to a reduction in the percentage of body fat (P = 0.03). In the
ITT analysis, a larger decrease in systolic and diastolic blood
pressure was shown in the placebo group than in the alginate
group (P < 0.05). Plasma concentrations of glucose, insulin,
HOMA-IR, C-reactive protein, ghrelin, and lipid metabolism did
not differ between treatment groups in the ITT analysis (P >
0.1). CONCLUSIONS: These results suggest that alginate
supplementation as an adjunct to energy restriction may improve
weight loss in obese subjects who complete a 12-wk dietary
intervention. This trial was registered at clinicaltrials.gov as
NCT01231178. SPONSORSHIP: Supported by grants from S-
Biotek Holdings ApS and FOOD Research School/SCIENCE,
University of Copenhagen.
Study strengths
This study is novel since it’s the first to ever investigate the
long-term effects of sodium alginate supplementation in dieters.
Dual X-ray absorptiomerty (DXA) was used to assess body
composition. A range of useful blood markers of health were
assessed, including insulin sensitivity. Compliance to the
supplement & diet protocol was bolstered by subjects returning
all opened & unopened supplement packages each meeting. All
subjects kept diet records and met individually with a dietitian 4
times through the 12-week trial period. The sample size (96
subjects) was relatively large for this type of research.
Study limitations
The authors acknowledge two methodological limitations. First
off, the use of a maltodextrin placebo control instead of an
insoluble fiber prevented the investigation of whether or not
gelling in the stomach was a potential contributor to the
supplement’s effects. The second limitation they mentioned was
the use of automated blood pressure readings, which could have
Alan Aragon’s Research Review – April 2012
been more accurate with manual readings. Another limitation I’d
add is that there was no formal exercise program imposed upon
the subjects. A weight loss program minus a training element is
obviously not optimal. Also, questions remain about whether or
not a training program would have overrode any of the
detectable effects of sodium alginate supplementation. A final
limitation was that diet was not necessarily optimized in terms of
macronutrition. A minimum of 60 g daily protein intake was set,
and unfortunately, no other intake specifics were reported in the
text. This tells us very little about how good, bad, or ugly the
diet was. We do know that a relatively subtle energy deficit
(appx 300 kcal) was imposed, and that subjects were not allowed
to dip below 1200 kcal/day, but this only provides limited data.
Only 50 of the 96 subjects kept food records that were eligible
for analysis.
Comment/application
The main finding was better weight & fat loss in the sodium
alginate-supplemented group compared to the control group in a
post hoc analysis involving only the 80 subjects who completed
the study. It’s notable that the absolute differences between
groups were small. Total bodyweight decrease in the alginate
group surpassed the control by only 1.74 kg over the 12-week
period. The alginate group’s fat mass reduction was 1.34 kg
greater than the control. Both groups lost a similar, insignificant
amount of lean mass (1.08 kg in the alginate group, 0.81 kg in
the control). Waist circumference reduction in the alginate group
was 1.3 cm greater than the control. As you can see, these
numbers are not staggeringly impressive. It also should be noted
that the control group reported a nonsignificantly greater daily
energy intake (roughly 30 kcal) than the alginate group, which if
underestimated (a likely possibility), could have accounted for a
significant amount of the weight/fat loss differences between the
groups. Another notable tidbit is that more subjects dropped out
of the alginate than the control group, which suggests less
tolerance for the taste of the supplement.
The authors speculated that the alginate exerted its effect via its
gelling action in the gut, which altered hormones that influence
hunger. Specifically, they observed a greater (although
statistically insignificant) suppression of plasma ghrelin in the
supplemented group compared to the control. Given the
unremarkable effects on body composition and greater decrease
in blood pressure in the control group, sodium alginate is thus
far a mediocre performer not worth the investment.
[Back to Contents] Page 7
Preexercise galactose and glucose ingestion on fuel
utilization during exercise.
O'Hara JP, et al. Med Sci Sports Exerc. 2012 Apr 19. [Epub
ahead of print] [Pubmed]
PURPOSE: This study determined the effect of ingesting galactose
and glucose 30 minutes prior to exercise on exogenous and
endogenous fuel utilization during exercise. METHODS: Nine
trained male cyclists completed three bouts of cycling at 60%
Wmax for 120 minutes, following an overnight fast. Thirty minutes
prior to exercise the cyclists ingested either a fluid formulation
containing placebo, 75g of galactose (Gal) or 75g of glucose (Glu)
to which C tracers had been added, in a double blind randomized
manner. Indirect calorimetry and isotope ratio mass spectrometry
were used to calculate fat oxidation, total carbohydrate (CHO)
oxidation, exogenous CHO oxidation, plasma glucose oxidation and
endogenous liver and muscle CHO oxidation rates. RESULTS:
Peak exogenous CHO oxidation was significantly higher following
Glu (0.68 ± 0.08g·min, P<0.05) compared to Gal (0.44 ± 0.02
g·min), however mean rates were not significantly different (0.40 ±
0.03 vs. 0.36 ± 0.02 g·min, respectively). Glu produced significantly
higher exogenous CHO oxidation rates during the initial hour of
exercise (P<0.01), while glucose rates derived from Gal were
significantly higher during the last hour (P<0.01). Plasma glucose
and liver glucose oxidation at 60 minutes of exercise were
significantly higher for Glu (1.07 ± 0.1 g·min, P<0.05 and 0.57 ±
0.08 g·min, P<0.01) compared with Gal (0.64 ± 0.05 g·min and 0.29
± 0.03 g·min, respectively). There were no significant differences in
total CHO, whole body endogenous CHO, muscle glycogen or fat
oxidation between conditions. CONCLUSIONS: The pre-exercise
consumption of Glu provides a higher exogenous source of CHO
during the initial stages of exercise, but Gal provides the
predominant exogenous source of fuel during the latter stages of
exercise and reduces the reliance on liver glucose.
SPONSORSHIP: No funding was received for this research.
Study strengths
This study is innovative since it’s the first study to compare the
effects of the pre-exercise galactose with glucose ingestion on
plasma glucose oxidation and endogenous glucose contributions
from the oxidation of glucose released from liver and muscle
glycogenolysis (including the lactate shuttle). You can read that
again if you want. Trained cyclists were used, which minimizes
the chance of confounding variability seen in novices. A
crossover design (all subjects completed a glucose, galactose,
and water trial – separated by 1 week wash-out periods) reduced
the potential for inter-subject variability from the small sample
size. The evening meal before each test was standardized in
terms of the time consumed and composition.
Study limitations
This study was pretty straight-forward in its design and purpose,
so limitations are somewhat of a grope. One nit-pick at the
design was that pre-training or pre-competition meals are
typically not made of a single macronutrient. At minimum; they
typically include a certain amount of protein & fat – not just
carbohydrate as in the present study’s case. Furthermore, the
results may be limited to the exercise protocol used (60% Wmax
for 120 minutes, which translates in this case to roughly 70% of
VO2max). A final limitation I’d note is that the testing did not
Alan Aragon’s Research Review – April 2012
involve a performance aspect, such as a time trial where the
greatest amount of work had to be done in a fixed amount of
time. To me, this is the biggest limitation, since the study
neglects the outcome that ultimately matters most.
Comment/application
The chart above captures the different metabolic profiles of a
75g galactose vs. a 75g glucose preload’s effect on exogenous
carbohydrate (CHO) oxidation during a bout of endurance
training. The exogenous CHO oxidation via glucose ingestion
was significantly higher during the first hour of exercise, while
the CHO oxidation via galactose ingestion was significantly
higher during the second hour. In addition, plasma CHO & liver
CHO oxidation in the first hour were significantly higher in the
glucose preload condition. Despite these temporal differences in
exogenous CHO oxidation, there were no significant differences
in liver and muscle glycogen-derived glucose oxidation
throughout the 2-hour bout. There also was no significant
difference between the two conditions in terms of both absolute
& relative whole-body endogenous CHO oxidation rates.
Interestingly, despite the higher serum insulin elevations via the
glucose preload, there were no significant differences in total fat
oxidation between the treatments. This occurrence immediately
reminds me of a study by Febbraio et al, who found no
difference in total fat oxidation during endurance exercise
between fasted and fed subjects despite higher insulin
concentrations in the latter condition.9 Another similar example
that comes to mind is Horowitz et al, who found that despite the
suppression of lipolysis in fed subjects (in addition to mid-
training hyperglycemia & hyperinsulinemia), no difference in fat
oxidation was seen between fasted & fed conditions.10 This
suggests that liploysis is not a rate-limiting step to fat oxidation,
and insulin elevations are not reliably preventive of fat oxidation
either – especially in trained subjects.
The practical application of the present study’s outcome is
speculative in nature since no performance endpoints were
assessed, but it’s tempting to hypothesize that an even
combination of glucose and galactose would be a highly
favorable pre-exercise carbohydrate mix. Incidentally, lactose
(the primary sugar in milk), is comprised of an even ratio of
glucose and galactose. So, those who can tolerate milk might
well be getting the best of both worlds when it comes to a pre-
exercise carbohydrate for endurance purposes.
[Back to Contents] Page 8

The acute effects of twenty-four hours of sleep loss on
the performance of national-caliber male collegiate
weightlifters.
Blumert PA, et al. Strength Cond Res. 2007 Nov;21(4):1146-54.
[Pubmed]
BACKGROUND/PURPOSE: Currently, the degree to which sleep
loss influences weightlifting performance is unknown. This study
compared the effects of 24 hours of sleep loss on weightlifting
performance and subjective ratings of psychological states pre-
exercise and postexercise in national-caliber male collegiate
weightlifters. METHODS: Nine males performed a maximal
weightlifting protocol following 24 hours of sleep loss and a night
of normal sleep. The subjects participated in a randomized,
counterbalanced design with each sleep condition separated by 7
days. Testosterone and cortisol levels were quantified prior to,
immediately after, and 1 hour after the resistance training session.
Additionally, profile of mood states and subjective sleepiness were
evaluated at the same time points. The resistance training protocol
consisted of several sets of snatches, clean and jerks, and front
squats. Performance was evaluated as individual exercise volume
load, training intensity and overall workout volume load, and
training intensity. During each training session the maximum weight
lifted for the snatch, clean and jerk, and front squat were noted.
RESULTS: No significant differences were found for any of the
performance variables. A significant decrease following the sleep
condition was noted for cortisol concentration immediately after and
1 hour postexercise. Vigor, fatigue, confusion, total mood
disturbance, and sleepiness were all significantly altered by sleep
loss. CONCLUSION: hese data suggest that 24 hours of sleep loss
has no adverse effects on weightlifting performance. If an athlete is
in an acute period of sleep loss, as noticed by negative mood
disturbances, it may be more beneficial to focus on the
psychological (motivation) rather than the physiological aspect of
the sport. SPONSORSHIP: This study was funded by a National
Strength and Conditioning Association Student research award.
compromises the generalizability of the outcomes. The outcomes
of this study might potentially be limited to the type of training
done, which consisted of the snatch, clean & jerk, and front
squat. It’s not likely that bodybuilding-type training or strength-
training of the upper body would incur huge differences from the
present conditions under acute sleep loss, but it’s still open to
question nonetheless. Ironically, one of the design strengths (the
use of highly trained athletes) could potentially be a limitation
since the outcomes might not apply to novices, who might be
more susceptible to performance decrements from challenges
such as sleep deprivation. A final limitation is the chosen
duration of sleep deprivation (24 hours). Significantly more or
less than this might have imparted different effects. I would also
mention that based on personal observations, sleep deprivation is
often a subtle/chronic/cumulative phenomemon (e.g., 3-4 hours
per night for several nights in a row) rather than a substantial,
singular event such as a 24-hour bout without sleep.
Comment/application
The main findings of this study were 3-fold. First off, there were
no significant differences in any lifting performance parameter
between the slept & non-slept conditions. Secondly, despite the
lack of performance differences, the non-slept group showed
significantly greater disturbances in several psychological
measures (as measured by profile of mood states – POMS) than
the slept group. Interestingly, there was a lack of between-group
differences in subjective ratings of sleepiness and rate of
perceived exertion. The third major finding was a difference in
hormonal profile. Specifically, although no significant
differences were seen in testosterone flux, postexercise cortisol
levels (both immediately & 1 hour post) in the slept condition
were significantly lower than pre-exercise, as seen below.

Study strengths
This study was conceptually strong since it was the first to ever
examine the physiological & psychological effects of an acute
bout of sleep loss on the high-velocity & high-intensity exercises
performed with multiple sets and repetitions. In fact, this was the
first study to ever investigate how acute sleep loss affects a
rigorous weight-training session, let alone Olympic-style
weightlifting. Collegiate national-level weightlifters were used,
eliminating the confounding effects of a learning curve to gain
proficiency with the lifts. Subjects habitually slept 8 hours per
night, and all subjects had a similar chronotype/sleep schedule.
This minimized confounding variability across the small sample
of subjects. During the testing procedure, all subjects were
quarantined in the lab and supervised by trained staff who
enforced compliance. Sleep, physical activity, and dietary intake
were tracked & verified for 3 days prior to testing. Subjects were The authors conclude that since acute sleep loss did not
instructed to duplicate their normal diets (indicated in their adversely affect short-term maximal training efforts in athletes,
journals) on the day prior to testing. an emphasis should be placed on bolstering their
mental/psychological state in the case of sleep deprivation. I
Study limitations
would add that athletes should practice good time management
Although the subject profiles were homogeneous, the sample in order to avoid sleep debt, which on a frequently recurring
size was small (9 subjects), which reduces statistical power and basis is likely to affect performance, regardless of training status.

Alan Aragon’s Research Review – April 2012 [Back to Contents] Page 9

1. Mahabir S, et al. Calorie intake misreporting by diet record
and food frequency questionnaire compared to doubly
labeled water among postmenopausal women. Eur J Clin
Nutr. 2006 Apr;60(4):561-5. [Pubmed]
2. Schatzkin A, et al. A comparison of a food frequency
questionnaire with a 24-hour recall for use in an
epidemiological cohort study: results from the biomarker-
based Observing Protein and Energy Nutrition (OPEN)
study. Int J Epidemiol. 2003 Dec;32(6):1054-62. [Pubmed]
3. West DW, et al. Rapid aminoacidemia enhances
myofibrillar protein synthesis and anabolic intramuscular
signaling responses after resistance exercise. Am J Clin
Nutr. 2011 Sep;94(3):795-803. Epub 2011 Jul 27.
[Pubmed]
4. Cribb PJ, Hayes A. ffects of supplement timing and
resistance exercise on skeletal muscle hypertrophy. Med Sci
Sports Exerc. 2006 Nov;38(11):1918-25. [Pubmed]
5. Esmarck B, Andersen JL, Olsen S, Richter EA, Mizuno M,
Kjaer M. 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]
6. Wycherley TP, et al. Timing of protein ingestion relative to
resistance exercise training does not influence body
composition, energy expenditure, glycaemic control or
cardiometabolic risk factors in a hypocaloric, high protein
diet in patients with type 2 diabetes. Diabetes Obes Metab.
2010 Dec;12(12):1097-105. [Pubmed]
7. Burk A, et al. Time-divided ingestion pattern of casein-
based protein supplement stimulates an increase in fat-free
body mass during resistance training in young untrained
men. Nutr Res. 2009 Jun;29(6):405-13. [Pubmed]
8. Hoffman JR, et al. Effect of protein supplement timing on
strength, power and body compositional changes in
experienced resistance trained men. Int J Sport Nutr Exerc
Metab. 2009 Apr;19(2):172-85. [Pubmed]
9. Febbraio MA, et al. Effects of carbohydrate ingestion before
and during exercise on glucose kinetics and performance. J
Appl Physiol. 2000 Dec;89(6):2220-6. [Pubmed]
10. Horowitz JF, et al. Substrate metabolism when subjects are
fed carbohydrate during exercise. Am J Physiol. 1999
May;276(5 Pt 1):E828-35. [Pubmed]

Alan Aragon’s Research Review – April 2012 [Back to Contents] Page 10


Charles Poliquin’s 10 tips for staying healthy and fit at
age 51.
By Alan Aragon
_________________________________________________________________
Introduction
From my perspective, Charles Poliquin has had a 2-part career. I
first became aware of him as a strength coach back in the late
1990’s when he had a monthly column called “A Question of
Strength.” I felt that he genuinely made some valuable
contributions – at least to the generally crappy print magazine
landscape. Fast-forward about a decade, and now we’re deep in
the second phase of Poliquin’s career, where he’s more easily
recognized as a nutrition guru & supplement marketer. He also
offers a $1500 “Biosignature” certification that’s heavy on the
nutrition & supplementation programming.
The problem is, much of his bold claims are not scientifically
supported. A perfect example of this is this video outlining his
10 tips for staying healthy & fit at age 51. This video has caused
quite a stir in fitness-oriented social media circles, so I thought it
might be fun & educational to give my take on each tip. For
those who find Poliquin’s shortness of breath disconcerting, I’m
sure he’s just fine; he probably just got a nice biceps pump
seconds before filming each tip. After all, big muscles equal
instant credibility, and that’s just how it is.
Tip #1: Meat & nut breakfast.
Poliquin claims that the first thing you eat for the day “will
dictate all your neurotransmitters for the day.” He chooses a
meat & nut breakfast to maximize levels of dopamine & acetyl
choline so that his day is “driven with mental clarity, drive,
energy.” This purely and simply strikes me as humorous. I
looked up his article on the meat & nut breakfast on his website
in hopes to find scientific references that at least hint toward a
hypothetical basis for this, but came up dry. This makes his
vehemence toward this breakfast particularly strange.
Alan Aragon’s Research Review – April 2012
Tip #2: Wild meats
“Elk, buffalo, ostrich, and so on.” Poliquin thinks that farm-
raised meat is inferior to wild meat due to its lower omega-3 to
omega-6 fatty acid profile. This is fine and wonderful if for
some odd reason your objective is to obtain the bulk of your
omega-3 fatty acid intake from land animals. This is also a rather
redundant policy, since Poliquin is notorious for promoting the
mega-dosing of fish oil supplements. Given this, the pursuit of
exotic meat consumption doesn’t make sense from a logical,
practical, or economic standpoint.
Tip #3: Frequent eating
Poliquin claims that you need to eat every 2.5-3 hours in order to
be as productive as possible, skipping meals adversely raises
cortisol, and eating “far too late” raises insulin too much. There
indeed is research indicating that a regular meal pattern, as
opposed to a hap-hazard one, has beneficial effects on insulin
sensitivity, blood, lipids, and thermogenesis.1 However, this
research did not specifically demonstrate the superiority of
higher meal frequency. It’s also notable that this research
involved sedentary subjects.
The real kicker is when Poliquin said, “I’m not a believer at all
in that so-called intermittent fasting. In my opinion, intermittent
fasting is how to become diabetic scientifically.” It’s rare that I
hear a claim that makes my jaw drop onto my desk, but this was
one of them. First of all, intermittent fasting is typically done to
reduce bodyweight, and as such, a net caloric deficit is sustained.
I do not know of any research where subjects under sustained
hypocaloric conditions have experienced adverse effects on
glucose control. This simply doesn’t make physiological sense.
One of the earlier studies examining this question was by
Halberg et al, who found that over a 15-day period, alternate-day
fasting (20-hr fasting cycles) improved insulin-mediated glucose
uptake.2 This is actually the opposite of what Poliquin is worried
about. Notably, this was not a hypocaloric regimen; the diet was
specifically designed to maintain weight. Subsequent research
by Soeters et al compared an intermittent fasting regimen similar
to Halberg’s with a conventional diet.3 Despite that neither
condition was hypocaloric, no differences in whole-body
glucose, lipid, or protein metabolism were seen.
As far as hypocaloric conditions go, recent research by Harvie et
al found that 6 months of intermittent energy restriction (75%
reduction 2 days per week) was as effective as continuous
energy restriction (25% reduction 7 days/week) for decreasing
bodyweight and increasing insulin sensitivity.4 Further refuting
Poliquin’s claim is recent work by Holmstrup et al, who found
that in the course of a day, 6 meals actually caused a higher
overall glucose elevation than 3 meals, without any difference in
insulin levels between conditions. Given the evidence, saying
that intermittent fasting is “how to become diabetic
scientifically” is patently ludicrous.
Tip #4: Thin-skinned fruits
Poliquin says that thin-skinned fruits such as blueberries &
raspberries have a higher antioxidant content, lower insulin load,
and lower glycemic index than thick-skinned fruits like bananas.
[Back to Contents] Page 11
My response to this is a big so what? First off, fruit intake of
most individuals is not likely to comprise a large proportion of
their total calories – perhaps roughly 10-15% if the person is a
regular fruit eater. This alone is insufficient grounds for the nit-
picky/neurotic guideline to shun thick-skinned fruits. If someone
enjoys bananas, then there’s no good reason on Earth to
discourage their consumption on the grounds of glycemic or
insulinemic effect, given their insignificant proportion of the
diet. Furthermore, focusing on just the antioxidant content of
fruit is missing the big picture. All species of fruit have unique
nutritional benefits, so being discriminatory can only narrow the
spectrum of beneficial compounds consumed.
If we were to take the examples Poliquin gave, deeming bananas
as a nutritionally inferior choice to blueberries is ridiculous. On
a calorie-matched basis (1 small banana vs. 1 cup of
blueberries), although blueberries have more vitamin K, bananas
have 2 times more folate, 7 times more magnesium, and 3 times
more potassium. The latter nutrients tend to run low in Western
diets, so that’s all the more reason to eat bananas if they suit
your personal taste.
Tip #5: Refuel day
This is designed to replenish low glycogen stores from a high
training volume. It’s implied here that Poliquin’s regular daily
diet is carb-restricted to a certain degree, otherwise this refueling
(occurring every 5th day) would not be needed. The refuel day
involves 50% more calories than the other days, and more
simple carbs. I find Poliquin’s scheme to be rather arbitrary, and
also ironic in light of his disdain for non-linear dieting patterns
such as intermittent fasting. He simply is doing a variation on
this theme, since he is interspersing carb-restrictive periods with
carb-feasting. There’s nothing inherently wrong or unhealthy
with non-linear dieting setups, but there’s also a lack of evidence
indicating their universal superiority over linear diets. Personal
preference should dictate which type of diet structure to adopt.
Tip #6: Nap day
Poliquin takes 2 naps on either Saturday or Sunday. His
objective is to recharge his body & mind. Good for him, sounds
relaxing. I personally never have taken more than one nap in a
single day, and I rarely take naps at all. This is likely because I
don’t lack sleep throughout the week. It’s entirely possible that
Poliquin’s hectic schedule with tons of traveling puts him in
sleep debt during the week, so this must be compensated for on
the weekend.
Tip #7: Alcohol
He rarely drinks alcoholic beverages, but when he does, it’s
wine – and he’s very particular about which type. Funny enough,
it’s not about taste, it’s about choosing wines with a high
antioxidant content! To me, this is fundamentally wacky. If you
don’t drink much at all in the first place, getting nitpicky about
the nutrient content of your drinks is an exercise in neurotic
dietary perfectionism. Poliquin limits his intake to 1-2 glasses on
rare occasion, but he also gives the vibe that it’s a very forced
thing in order to avoid being a “party pooper” in a social
situation where drinking is encouraged & expected. In my view,
Alan Aragon’s Research Review – April 2012
if you don’t particularly like drinking, it’s perfectly fine to forgo
it completely. I’ve never been to a party where anyone was
ostracized or berated for not drinking. I’m sure such parties
exist, but then I’d imagine that the people in those parties are a
bigger problem than the drinks themselves.
Tip #8: Microcurrent unit
In order to combat jet lag or overtraining, Poliquin uses
Frequency-Specific Microcurrent therapy (FSM). This involves
the topical application of electrode pads that induce a mild
electrical current. FSM was developed by a chiropractor named
Carolyn McMakin in 1996, but FSM research has only recently
surfaced in a major publication. Although Poliquin gives FSM a
spirited endorsement, its evidence basis in the peer-reviewed
literature is still sparse.
The first big break for FSM in a mainstream publication was in
2004 in the Journal of Bodywork and Movement Therapies
(JBMT), an alternative medicine-oriented journal, where
McMakin reported that in a case study of 22 patients with
chronic low back pain, microcurrent therapy was “the single
most consistent difference in patient-reported pain relief.”6 A
subsequent study headed by McMakin in JBMT reported that
symptoms of fibromyalgia following cervical spine trauma were
successfully treated with microcurrent therapy.7 The results of
these studies should be viewed with caution since their
observational designs can only draw associations; they cannot
establish causation.
The most recent FSM study (again, published in JBMT) lends
further support to its potential effectiveness. Unlike previous
research which as not controlled at all, Curtis et al compared
FSM with a sham (fake) treatment.8 FSM reduced delayed onset
muscle soreness (DOMS) from to a significantly greater degree
than the sham therapy at all points tested (24, 48, & 72 hours
post-exercise). Unfortunately, this was not a double-blind
experiment, and only perceived muscle soreness was assessed. A
stronger design would have included objective measures of
muscle damage, such as biochemical markers (e.g., creatine
kinase levels) and/or exercise performance. Until more
methodologically sound research surfaces, the current FSM data
should be viewed cautiously.
Tip #9: Sleep
Poliquin recalls & renounces his former belief that sleep wasn’t
important. Being obsessed with work & succeeding, he got about
3-3.5 hours of sleep per night. Now he feels that this was a
damaging habit; a huge mistake. He now strives to maintain an
increased quality & quantity of sleep but still maintain work
productivity by going to bed early (8 pm), and waking up early
(4 am). I don’t have any major disagreement with this, and if this
routine suits his lifestyle & personal preference – great.
Judging from his current routine, Poliquin has approximately
doubled his sleep duration from his former sleep-deficient
routine. Unless he’s exaggerating, this is quite a substantial
increase. Still, sleeping from 8 pm to 4 am amounts to 8 hours
per night, which is not a particularly extravagant duration. In
fact, 8 hours might better be described as adequate. To
quote a review by Banks & Dinges,9 “Recent experiments reveal
[Back to Contents] Page 12
that following days of chronic restriction of sleep duration below 5. Holmstrup ME, et al. Effect of meal frequency on glucose
7 hours per night, significant daytime cognitive dysfunction and insulin excursions over the course of a day. e-SPEN,
accumulates to levels comparable to that found after severe The European e-Journal of Clinical Nutrition and
acute total sleep deprivation.” Metabolism. 2010;5(6):e277-80. [e-SPEN]
6. McMakin CR. Microcurrenttherapy: a novel treatment
Given the details of the aforementioned review, Poliquin’s method for chronic low back myofascial pain. Journal of
double-nap day might be doing him even more good than he Bodywork and Movement Therapies. 2004;8(2):143-53
realizes. A more recent review by Goel & Dinges reports that an [JBMT]
estimated 20-40% of the adult US population sleeps less than 7 7. McMakin CR, et al. Cytokine changes with microcurrent
hours per night.10 These authors harbor a similar degree of treatment of fibromyalgia associated with cervical
concern over sleep deficiency, including chronic partial sleep spinetrauma. Journal of Bodywork and Movement
deprivation (PSD). This sounds just like what Poliquin describes Therapies. 2005;9(3):143-53 [JBMT]
putting himself through before he embraced the benefits of 8. Curtis D, et al. The efficacy of frequency specific
adequate sleep. Here’s a passage from Goal & Dinges worth microcurrent therapy on delayed onset muscle soreness. J
quoting directly:10 “Moreover, sleep loss has become a Bodyw Mov Ther. 2010 Jul;14(3):272-9. [Pubmed]
significant public health concern as population studies have 9. Banks S, Dinges DF. Behavioral and physiological
found reduced sleep duration (less than 7 hours) associated with consequences of sleep restriction. J Clin Sleep Med. 2007
increased risks of obesity, morbidity, and mortality.” Aug 15;3(5):519-28. [Pubmed]
10. Goel N, Dinges DF. Behavioral and genetic markers of
Tip #10: Weekly “fun day” sleepiness. J Clin Sleep Med. 2011 Oct 15;7(5 Suppl):S19-
Poliquin makes a couple of points here, but the major one is that 21. [Pubmed]
it’s important to schedule in a “fun day” every week. The
secondary point he makes is that you should hire someone (e.g.,
a personal assistant) to do the mundane tasks that you don’t
enjoy. This will free up the time for recreation, such as family
time, playing around, etc. While it’s obvious that not everyone
has the financial capacity to hire someone to do menial jobs, I
agree that it’s important to block out recreational time in your
weekly schedule, whether it’s a whole day per week, or some
other variation such as a certain amount of time per day. All
work & no play eventually leads to sub-optimal work
productivity and eventually, burnout. Again, I have no
disagreement with Poliquin here.
Aside from his nutrition & supplementation recommendations,
everything is wonderful. Well, almost everything. The use of
microcurrent therapy can be seen as either cutting-edge, or a
waste of time & energy. Since I don’t constantly overtrain &
undersleep while traveling the globe all year, I doubt I’d benefit
from that technology in this lifetime. For those of you high-
rollers who feel like your Poliquin-esque lifestyle is wearing you
down, it might be worth a try.

References
1. Farshchi HR, et al. Beneficial metabolic effects of regular
meal frequency on dietary thermogenesis, insulin
sensitivity, and fasting lipid profiles in healthy obese
women. Am J Clin Nutr. 2005 Jan;81(1):16-24. [Pubmed]
2. Halberg N, et al. Effect of intermittent fasting and refeeding
on insulin action in healthy men. J Appl Physiol. 2005
Dec;99(6):2128-36. Epub 2005 Jul 28. [Pubmed]
3. Soeters MR, et al. Intermittent fasting does not affect whole-
body glucose, lipid, or protein metabolism. Am J Clin Nutr.
2009 Nov;90(5):1244-51. Epub 2009 Sep 23. [Pubmed]
4. Harvie MN, et al. The effects of intermittent or continuous
energy restriction on weight loss and metabolic disease risk
markers: a randomized trial in young overweight women.
Int J Obes (Lond). 2011 May;35(5):714-27. [Pubmed]

Alan Aragon’s Research Review – April 2012 [Back to Contents] Page 13


Caffeine + creatine = conflict?
By Alan Aragon
             I’ve  read  on  the  forums  that you’ve recommended    baseline. The authors concluded that an acute dose of caffeine
              creatine,  but  also  drink  coffee.  Does  caffeine  not  was ergogenic despite prior creatine loading, perhaps because
negate  the  effects  of  creatine,  or  is  that  also  controversial?  I  caffeinated beverages were avoided during the creatine loading
love coffee but haven't been taking it when taking creatine.  phase.
This is a good question that doesn’t have a simple answer. I’ll
chronologically review the body of research involved, discuss
the key limitations, and wrap it up with field observations.
A rough start
The very first study to examine this question was done in 1996
by Vandenberghe et al.1 Although they hypothesized that
combining caffeine & creatine would enhance performance, they
observed just the opposite. A daily dose of caffeine (5 mg/kg)
negated the ergogenic effect that creatine loading had on
isokinetic performance, including isometric and dynamic
strength and fatigability of the knee extensors. Interestingly, the
yet-unknown mechanism of caffeine’s interference with
creatine’s ergogenic action did not appear to be directly involved
with muscle phosphocreatine availability.
A 1998 study by Vanakoski et al examined the effect of high-
dose caffeine (7 mg/kg) ingested during creatine loading.
Creatine or caffeine - alone or combined - failed to improve
maximal pedalling speed, maintenance of maximal speed or total
work output during the 1-minute cycling ergometer bouts, when
compared to placebo. Thus, neither aerobic nor anaerobic
performance was affected by either treatment. Given the lack of
effect of anything beyond placebo, it’s not necessarily valid to
conclude that caffeine interfered with creatine’s actions or vice
versa. Also, it’s notable that the subjects were trained athletes.
Creatine's performance failure was also seen in research by
Delecluse et al, examining its effect on repeated 40-meter sprint
running performance in highly trained sprinters.3
A 2002 study by Hespel et al found that 3 days of caffeine dosed
at 5 mg/kg increased muscle relaxation time (RT).4 This
occurrence counteracted the decrease in RT caused by creatine
loading. The significance here is that a shorter RT is important
for power production, and lengthening RT can potentially
indicate an increase in fatigue. It’s important to note that even
the authors acknowledge the mechanistic nature of the study.
They admitted that the exercise protocol used (a series of 30
isometric muscle contractions induced by intermittent electrical
stimulation) is not suitable for evaluating the ergogenic effect of
creatine supplementation. Nevertheless, they concluded that they
may have found a potential mechanism for caffeine’s
counteraction of creatine’s ergogenic effect.
Glimmers of hope
A twist in the saga occurred the same year (2002) as Hespel et
al’s study. Doherty et al examined the effect of a single caffeine
dose (5 mg/kg) after creatine supplementation in trained
subjects.5 They hypothesized that abstaining from caffeine
Alan Aragon’s Research Review – April 2012
dosing during the 6-day creatine loading phase would prevent
the performance interference seen in previous studies. They were
correct. Time to exhaustion at 125% VO2max was greater than
baseline and the placebo (creatine-only) treatment. Rating of
perceived exertion was also lower at 90 seconds compared to
Nearly a decade elapsed before the latest study in the
creatine/caffeine saga was published. In 2011, Lee et al
conducted a similar study to Doherty et al’s, except the
performance testing involved intermittent high-intensity
sprinting (six 10-second intermittent high-intensity sprints on a
cycling ergometer, with 60-second rest intervals).6 As in
Dogherty et al’s study, the subjects abstained from caffeinated
beverages during the creatine loading phase. No differences in
RPE were seen between the 3 trials. However, mean & peak
power in the creatine + caffeine (a single dose of 6 mg/kg taken
1 hour before testing) condition were significantly higher than
the control during sprints 1 & 3, and higher than creatine +
placebo in sprints 1 & 2. Mean & peak power during sprint 3 in
creatine + placebo was was significantly greater than that in the
control condition. This study echoed the results of Doherty et al,
suggesting that caffeine does not inhibit the ergogenic effect
of creatine if it’s acutely dosed after, rather than during creatine
loading.
Collectively, the designs investigate short-term effects of
creatine loading with or without caffeine on mostly anaerobic
exercise performance. As the scant evidence illustrates,
creatine’s ergogenic effect is still intact right after a loading
phase despite a single dose of caffeine before an event. In fact, in
the latest study by Lee et al, caffeine has been seen to additively
enhance performance to when combined with creatine. But
again, this was under the condition that the single caffeine dose
was administered after the creatine loading phase.
Elusive conclusions
As you can see, the available research has not investigated the
specific questions physique athletes, strength/power athletes, and
even endurance athletes are pondering – which mainly involve
the long-term effects of concurrent caffeine and creatine
consumption. It’s currently not known whether or not creatine’s
effectiveness is reduced in habitual coffee drinkers. As a
corollary, it’s not known whether these effects in habitual
caffeine users can be altered by manipulating the timing of
creatine relative to caffeine intake within the day or week.
Currently, the body of research on this topic leaves more
questions than answers. Whenever there’s a major gap in the
research, we have to turn to personal observations and anecdotal
data. As far as field observations go, I haven’t personally seen or
received reports of habitual caffeine use interfering with
creatine’s ergogenic effects – regardless of the timing of either
compound within a day. I also have not experienced or heard of
habitual caffeine intake inhibiting creatine-induced weight gain.
Conversely, I haven’t experienced or heard of any increases in
creatine’s effects upon the cessation of chronic caffeine
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consumption. These observations are admittedly subjective, but
they’re the necessary evil in light of the data shortage. Until
research demonstrates otherwise, I don’t think habitual
consumers of caffeinated beverages need to worry about
concurrent creatine consumption.

References
1. Vandenberghe K, et al. Caffeine counteracts the ergogenic
action of muscle creatine loading. J Appl Physiol. 1996
Feb;80(2):452-7. [Pubmed]
2. Vanakoski J, et al. Creatine and caffeine in anaerobic and
aerobic exercise: effects on physical performance and
pharmacokinetic considerations. Int J Clin Pharmacol Ther.
1998 May;36(5):258-62. [Pubmed]
3. Delecluse C, et al. Effect of creatine supplementation on
intermittent sprint running performance in highly trained
athletes. J Strength Cond Res. 2003 Aug;17(3):446-54.
[Pubmed]
4. Hespel P, et al. Opposite actions of caffeine and creatine on
muscle relaxation time in humans. J Appl Physiol. 2002
Feb;92(2):513-8. [Pubmed]
5. Doherty M, et al. Caffeine is ergogenic after supplementation
of oral creatine monohydrate. Med Sci Sports Exerc. 2002
Nov;34(11):1785-92. [Pubmed]
6. Lee CL, et al. Effect of caffeine ingestion after creatine
supplementation on intermittent high-intensity sprint
performance. Eur J Appl Physiol. 2011 Aug;111(8):1669-77.
[Pubmed]

An update has been made in the March 2011 AARR.

On page 12, the initial portion of “Study Strengths” has been
updated. I changed it to clarify that Cribb & Hayes were the first
to examine nutrient timing on both sides of the resistance
training bout, while Esmarck et al were the first to examine
nutrient timing on one side of the resistance training bout
(postexercise). Please re-download the updated issue here:
http://alanaragon.com/members-page.html

This clip (9 minutes, 22 seconds) is a fascinating study of lion

behavior – at the potential expense of life & limb.

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 – April 2012 [Back to Contents] Page 15