6 - June - 2008

AlanAragonsResearchReviewJune,2008[BacktoContents] Page1
Copyright June 1st, 2008 by Alan Aragon

Home: www.alanaragon.com/researchreview
Correspondence: aarrsupport@gmail.com

2 Whats the deal with egg consumption and
cardiovascular disease? By Alan Aragon

7 Moderate protein intake improves total and regional
body composition and insulin sensitivity in
overweight adults.

Arciero PJ , et al. Metabolism. 2008 J un;57(6):757-65.
[Medline]

8 Effects of dietary protein content on IGF-I,
testosterone, and body composition during eight
days severe energy deficit and arduous physical
activity.
Alemany J A, et al. J Appl Physiol. 2008 May 1. [Epub
ahead of print] [Medline]

9 Effect of Preexercise Meals With Different
Glycemic Indices and Loads on Metabolic
Responses and Endurance Running.

Chen YJ, et al. IJ SNEM. 2008:(18):281-300. [IJ SNEM]

10 High rates of muscle glycogen resynthesis after
exhaustive exercise when carbohydrate is co-
ingested with caffeine.

Pedersen DJ, et al. J Appl Physiol. 2008 May 8. [Epub
ahead of print] [Medline]

11 Effects of resistance vs. aerobic training combined
with an 800 calorie liquid diet on lean body mass
and resting metabolic rate.
Bryner RW, et al. J Am Coll Nutr. 1999 Apr;18(2):115-21.
[Medline]

12 The wisdom of pro bodybuilder Lane Norton.
Interviewed by Alan Aragon

14 The wisdom of pro figure competitor Pauline Nordin.
Interviewed by Alan Aragon


Whats the deal with egg consumption and
cardiovascular disease? By Alan Aragon

I

n this article
I find it humorous that whole eggs are a controversial food.
Ironically, a food that (quite literally) embodies the essence of
life has been portrayed by many as a stealthy dealer of death.
This article will first take a look at the structure and function.
Then well examine the research behind the dichotomous
reputation of the humble egg, and attempt to draw some
conclusions about whats bull and whats genuinely concerning.
Before we dive in, lets get to know the egg a little better by
starting with its chemical composition.

W

hats in an egg?
As much as I would love to fantasize about eating ostrich egg
omelettes, our discussion will be limited to chicken eggs. Heres
some of the relevant nutritional information:

Eggs are approximately 9.5% shell, 63% albumen (egg white),
and 27.5% yolk. Their predominant component is water (75%),
with proteins and fats evenly splitting the remainder. A little-
known fact is that eggs actually contain carbohydrate, but only
as a minor component, existing in free and conjugated forms,
attached to the fats and proteins. The majority of the proteins are
found in the yolk and the white, with a small proportion in the
shell and shell membrane. Fats (mainly in the form of
lipoproteins) are virtually all in the yolk. Most of the minerals in
eggs are in the shell.
Diverse Biological Functions

Aside from their well-known high protein quality, eggs have a
surprisingly wide range of beneficial biological effects. Both the
white and the yolk have anti-microbial, anti-adhesive (thus anti-
infective), protease-inhibitory (thus anti-cancer), anti-
inflammatory, and antioxidant properties.
1
Including egg yolk
phospholipids in infant formula increases its semblance to
mothers milk, and has been seen to decrease the incidence of
necrotizing enterocolitis (an intestinal disease).
2
Egg yolks
contain phosphatidyl choline, which plays a key role in brain
development and memory retention. To top things off, yolks are
a significant source of the carotenoids lutein and zeaxanthin. As
little as one egg per day has been seen to increase plasma and
macular levels of these antioxidant nutrients.
3,4
The significance
that increased blood levels of lutein and zeaxanthin are
associated with a lower risk of age-related macular
degeneration.
4
According to a review by Krinsky et al, lutein and
zeaxanthin in the macula of the eye absorb blue-light, and thus
protect the photoreceptor layer from light damage.
5
With a
multitude of benefits to human health, it would seem pretty easy
to position eggs as a stereotypical superfood. But due to the
focus on a singular aspect of its composition (cholesterol
content), a storm of debate has raged on for much of the last
half-century.
1 Large Egg (50 g): Selected Nutrient Content
Source: Hhttp://www.nutritiondata.com/facts-C00001-01c201t.html

Nutrient Amount % Daily Value

Kcal....................................... 77.5 4%
P

rotein................................... 6.3 g 13%
Total carbohydrate.................... 0.6 g --
Sugar.......................... 0.6 g --
Starch......................... 0.0 g --
Fiber....................

....... 0.0 g --
Total fat................................. 5.3 g 8%
Saturated............................ 1.6 g 8%
16:0 (palmitic acid)........ 1174 mg --
18:0 (stearic acid).......... 414 mg --
Other saturates.............. [trace]
Monounsaturated................... 2.0 g --
18:1 (oleic acid)............. 1862 mg --
16:1 (palmitoleic acid)..... 155 mg --
Other monounsaturates.... [trace]
Polyunsaturated.................... 0.7 g --
Omega-3 fatty acids....... 39 mg** --
Omega-6 fatty acids....... 594 mg --
Other fatty acids............ 67 mg
Trans fatty acids................... [unlisted,
but not likely a significant source]

C

holesterol.............................. 212 mg 71%
Lutein + Zeaxanthin.................. 176 mcg --

--No value established
* 3 *Omega- fortified eggs contain about 6-10 times as much as regular eggs

Cholesterol at the heart of controversy

Cholesterol is a component of all animal (including human) cell
membranes, a critical requirement of infant growth, and a
precursor to a range of hormones in the body. However, it has
been targeted as an enemy of cardiovascular health by much of
the medical mainstream. In one of their recently updated online
articles, the American Heart Association (AHA) recommends
that cholesterol intake should be limited to less than 300 mg per
day for most people.
6
Those with coronary heart disease or an
LDL level of 100 mg/dl or more should consume less than 200
mg of cholesterol per day. Taking a look at the chart on the left,
cholesterol per egg is 212 mg. Thats about two-thirds of the
recommended intake down the hatch for normal individuals, and
it completely takes care of the daily limit (and then some) for
those with CHD or high LDL readings. I eat three whole eggs
almost every day of the week, so as far as AHA limits are
concerned, Im blowing past them like Stevie Wonder through a
stop sign. Yet, my blood lipids are all within normal ranges. This
is a personal example, and individual case studies hold very little
weight since they involve many uncontrolled variables. So, lets
ease into the literature for an objective look, beginning with the
roots of the issue.

O

rigins of indictment
As stubborn as large-scale health organizations are, theres
generally some degree of evolution in their recommendations.
Take for example, the Dietary Guidelines for Americans.
Theyve gone from having four food groups and relative
simplicity from 1950s-1970s, to a six-group Pyramid which
mainly succeeded in confusing the public from 1992-2000. This
was followed up by the current Pyramid an even more
abstract/symbolic rendering that requires either online access or
extensive literature for the lay public to vaguely understand; let
alone implement. In contrast, the AHA has maintained a rigid
stance despite substantial contrary evidence. A 1961 AHA report
published in the journal Circulation recommended a reduced
intake of total fat, saturated fat, and cholesterol, and an increased
proportion of polyunsaturated fat.
7
This particular set of
recommendations support whats now known as the diet-heart
hypothesis, which essentially states that dietary cholesterol
increases serum cholesterol, and elevated serum cholesterol
increases the risk for heart disease. Thus, it follows that
consuming whole eggs would directly violate these tenets.
However, based on accumulating research data, the AHAs
tenacious grip on the diet-heart hypothesis now resembles a
childish refusal to admit error. The kicker of it all is that the only
controlled intervention trials supporting the guidelines in the
original 1961 AHA report were on rabbits fed diets way out of
their natural pattern. Lets look at humans, shall we?

Epidemiological soup

Epidemiology is observational (also called exploratory) research
that attempts to identify disease risk factors by using
correlational methods. Whereas experimental (controlled
intervention) research may not always reflect the big picture or
the real world, epidemiological research can be confounded by
uncontrolled yet critical details. Unlike experimental research,
epidemiology can only establish potential associations between
variables, not causal relationships. Keeping those limitations in
mind, the plus-side of epidemiology is that it gives us hints and
hypotheses that can eventually be put to controlled trials.

Let it be known that the epidemiological data as a whole is an
ongoing convoluted mess. However, the majority of it does not
support the idea that increased egg or cholesterol consumption
increases the risk for cardiovascular disease.
8-12
In an interesting
example, Okayama et al examined J apans dietary habits from
1980-1989 and found a decline in mortality from coronary heart
disease while the prevalence of hypercholesterolemia in both
men and women increased nearly 100%.
13
Weird stuff, this
uncontrolled research. In another example of an inverse
relationship, Dawber et al found that in a population of 12,847
men with total cholesterol levels <200 mg/dL consumed more

eggs as a percent of calories than did participants with
cholesterol

levels 220mg/dL. Hu et al conducted one of the
largest studies of its kind (over 100,000 subjects), and found that
coronary heart disease risk was not associated with higher egg
consumption, with the exception of diabetic subjects.
14
A more
recent comparably-sized study of the J apanese population found
no association between higher egg consumption and increased
coronary heart disease incidence.
15
A more recent trial by than
the latter echoed the results of Hu et al. Qureshi et al found that
one egg per day did not increase the risk for cardiovascular
diseases and mortality, except in diabetics.
16

In the most recent set of reports to date, the Physicians Health
Study found that egg consumption of one or more per day was
associated with the risk of heart failure.
17
In addition, egg
consumption was positively correlated with mortality, especially
in diabetic subjects.
18
Its noteworthy that this particular trial
examined the health of physicians, who at least from an
anecdotal standpoint are no better off than the lay public. In fact,
many of them lead less balanced lives in terms of health and
fitness behaviors compared to the average Joe whose career
demands and general barometer of life stress may be
considerably less. Okay, lets forget about anecdote for a second.
This study has a few important limitations to bear in mind. First
of all, its epidemiology, in all of its uncontrolled, self-reported,
survey-based glory. There was a clear lack of complete, detailed
dietary information,

such as intake of saturated and trans fats,

fruit and vegetables, whole grains and other fiber-containing
foods, and fish/fish oil. Secondly, egg intake as assessed every 2
years for a 10 year period. A time-dependent Cox model was
used to determine event history. Cox regression does not require
researchers to specify a baseline hazard rate or estimate absolute
risk. As such, since egg intake at 2 years wassimilar to baseline,
these values were substituted for

baseline data in the 113
participants with missing baseline data. To quote an editorial by
Eckel regarding this particular trial,
19

One would assume that the overall lifestyle of subjects with

higher egg consumption would have predicted more CVD. That
is,

the physicians with higher egg intake were older, smoked
more

cigarettes, were less physically active, ate breakfast cereal

less often, and had a higher prevalence of hypertension and

diabetes than did those with lower egg intake.

As illustrated by the above point, large-scale observational
studies are much like an attempt to find diamonds in the snow
when it comes to hinting toward causality. There are far too
many variables that might confound the data. So, this brings us
to the next and last leg of the trip, the controlled experiments.
Although by nature, lab-supervised controlled interventions
dont necessarily reflect free-living conditions, they can at least
suppress the frustrating floating variables. Lets take a look.

Controlled interventions: revenge of the yolk

For those unfamiliar with the jargon, HDL-C is often tagged as
good cholesterol. In a very recent trial by Mutungi et al on
overweight men on a carbohydrate-restricted diet (10-15% of
total kcal), 3 eggs per day raised HDL-C without raising LDL-
C.
20
Notably, this was despite an additional daily dose of 640 mg
cholesterol for 12-weeks. Both groups reduced bodyweight,
waist circumference, and triacylglycerol levels. Since there was
no HDL-C increase in the control group, the egg group actually
proved to receive the more cardioprotective treatment. In other
carb-restriction research, Ratliff et al found 3 eggs per day to
reduce markers of inflammation after 12 weeks compared to an
eggless carb-restricted diet.
21
In fact, the authors directly credit
the higher cholesterol content of the diet as a key contributor to
the overall beneficial effect since it led to increased HDL-C.
They also suspect that the lutein content of the egg group also
played a key role in the favorable outcomes.

Speaking of antioxidant carotenoids in the yolk, Goodrow et al
demonstrated that one egg per day for 5 weeks can significantly
increase serum lutein and zeaxanthin levels without elevating
total cholesterol or LDL-C concentrations.
22
In yet another
example, Greene et al found that 2 eggs per day raised LDL-C,
but also raised HDL-C to a degree that did not alter the ratio of
the two types thus neutralizing any potential atherogenic


concerns.
23
This brings us to our next area of controlled
research: dietary cholesterol response variability.

Response classification

Blood cholesterol levels are the result of feedback control
between dietary intake and endogenous production within the
liver. In other words, the more cholesterol you consume through
dietary sources, the less cholesterol your liver produces.
Conversely, the less you consume, the more you biosynthesize.
However, this feedback mechanism is not 100% efficient.
Although the effects of elevated blood cholesterol on heart
disease are unclear, meta-analyses of controlled trials indicate
that dietary cholesterol indeed causes a small yet measurable
increase in blood cholesterol.
24,25
According to the cumulative
data in these reports, a plasma total cholesterol increase of 0.05
0.06 mmol/L (22.2 mg/dL) can bepredicted for every 100 mg
increase in dietary cholesterol. Response to dietary cholesterol
varies among individuals, and those whose plasma cholesterol
increases exceed 2.2 mg/dL per every 100 mg increase in dietary
cholesterol are generally considered hyperresponders. Those
whose plasma increases are under that threshold are considered
hyporesponders.

This variability of response has prompted researchers to
investigate its clinical relevance, and some interesting results
have surfaced. In perhaps the first study to examine metabolic
responses to feedings in the two types of responders, Herron et
al found that the 3 egg/day experimental groups LDL:HDL ratio
increased slightly in hyperresponders but not hyporesponders.
26

Despite the increase, levels were still within National
Cholesterol Education Program guidelines. Whats pivotal is that
the hyperresponders had increased levels of lecithin cholesterol
acyltransferase and cholesteryl ester transfer protein activities
during the egg treatment. This indicates that hyperresponders
metabolize excess plasma cholesterol via an acceleration of the
reverse cholesterol transport pathway. The authors thus
concluded that additional dietary cholesterol does not adversely
impact lipid profiles in healthy men, regardless of response
classification. A subsequent study also led by Herron yielded
similar outcomes to the previous trial, but also demonstrated that
LDL peak diameter was not decreased, and the larger (less
atherogenic) LDL-1 subclass was greater in hyperresponders.
27

The investigators concluded that a high-cholesterol diet from the
equivalent of 3 eggs per day does not increase the atherogenicity
of the LDL particle, regardless of response category. Put in more
plain English, consumption of 3 eggs per day does not appear to
promote indicators of heart disease.

In related research, Clark et al found a potential hidden blessing
in hyperresponders regarding carotenoid response.
28
Plasma
concentrations of lutein and beta-carotene were significantly
greater in hyperresponders than in hyporesponders as a result of
the same chronic 3-egg protocol in previous trials. Another
veiled benefit mentioned in a review by Hernandez is the ability
of increased egg intake in addition to promoting the formation of
large LDL, is the shifting of the LDL pattern B to the less
atherogenic pattern A.
29

Omega-3 eggs: an expensive attempt to improve nature?
Theres been a growing interest in the benefits of omega-3
(commonly denoted as n-3) fatty acid intake, which has received
a lot of positive hype and press in the literature for a myriad of
health benefits ranging from cardiovascular protection, fat loss
(note that this is highly debatable), anti-depression, and even
bone health.
30-33
So, a logical direction in food technology was
the enrichment (technically, in the case of eggs its
fortification) of eggs with omega-3s. In an interesting yet
unreplicated example by Ferrier et al,
34
normolipidemic subjects
who consumed four n-3 eggs per day experienced a significant
increase in n-3 status of blood platelet phospholipids (a good
thing), yet no significant changes in overall blood cholesterol
and its subtypes. In agreement with these findings, a review by
Lewis et al states,
35
Overall results of studies to date
demonstrate positive effects and no negative effects from
consumption of n-3-enriched eggs.

So how can n-3 fortification of eggs at all be a bad thing? Its
known that n-3 eggs can lower triacylglycerol levels and boost
the n-3 status of the body, these effects are obviously beneficial.
However, my (perhaps nit-picky) concern is the idea of
increasing the proportion of long-chain polyunsaturated fatty
acids (PUFAs) in a food thats typically cooked under high heat,
especially if yolks are broken and scrambled. The problem with
this is the greater potential of the long-chain PUFAs to form
genotoxic oxidation products that can adversely alter cell
DNA.
36
Its fairly well known that cooking with polyunsaturated
fats is generally a bad idea compared to cooking with more heat-
stable fats such as saturates and monounsaturates. The actual
degree to which adverse effects can occur via normal cooking
practices of n-3 eggs compared to regular eggs is unknown, and
its not likely something to lose sleep over if only a small
amount of eggs is consumed. However, it makes more sense to
me to stick with the more economical regular eggs, and get the
bulk of the n-3s elsewhere in the diet, or through
supplementation. This is yet another reason to avoid the line of
thinking that more n-3 is better, and that eggs need some sort of
compensatory crutch for their cholesterol content which hasnt
been proven harmful in the first place.

S

ummary points
Eggs are a high-quality source of protein, fat, and various
micronutrients.
Egg yolks possess a surprisingly diverse range of protective
biological functions, including the potential to prevent vision
degeneration.
The AHAs guidelines restrictive guidelines on cholesterol
consumption are amazingly enough not rooted in a
complete data set that includes controlled human
experiments, and thus should be viewed with considerable
caution.
Because of their cholesterol content, eggs yolks have
historically, yet mistakenly been pegged as a food to either
minimize or avoid altogether.
Epidemiological evidence is mixed, but the majority of it
does not support the hypothesis that increased egg or
cholesterol consumption increases the risk for cardiovascular
disease. Some of it even correlates a higher risk of heart
disease with lower cholesterol consumption.
Recent research has credited the cholesterol content of the
egg as being inherently beneficial since it allows the
production of HDL-C.
Whole egg consumption can raise total cholesterol, but it
does not negatively alter the ratio of HDL-C to LDL-C.
Furthermore, it does not increase the LDL-C subtypes
considered to be atherogenic (artery-clogging).
The majority of controlled trials on the whole egg
consumption find either neutral or beneficial changes in
blood lipid profiles.
Recent research found eggs to reduce markers of
inflammation under hypocaloric conditions, thus proving to
actually have cardioprotective properties.
Although increases in dietary cholesterol can produce small
increases in blood cholesterol, the link between increased
blood cholesterol and cardiovascular risk is far from clearly
established. Its an outdated hypothesis that does not have a
consistent base of evidence.
Hyperresponders (those whose blood cholesterol increases to
a greater degree as a result of increases in dietary cholesterol)
show blood elevations of enzymes that deal with elevated
cholesterol through non-atherogenic means.
Fortifying eggs with n-3 fatty acids has been demonstrated to
increase n-3 levels in tissues, and lower plasma
triacylglycerol.
However remote or insignificant it might be, increasing the
proportion of long-chain PUFA in designer eggs has the
potential drawback of a greater formation of harmful
oxidation products from cooking.


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APPLICATION
Since neither the bulk of the epidemiological nor the
experimental research supports the hypothesis that whole
eggs are cardiovascular threats, they may be eaten freely
within the confines of the diets macronutrient targets. For
example, while eating a dozen eggs in one sitting is not an
inherently bad thing to do, it might fulfill your entire fat
allotment for the day, and any more fat on top of that will
contribute to an excessive caloric surplus. As long as they
fit in the daily macronutrient target, actual amount of eggs
consumed should be left to individual preference keeping
in mind that the average-size whole egg contains roughly 6
grams of protein and 5 grams of fat. Since fat consumption
occurs from several different sources per day, it simply
wouldnt be practical in most cases to exceed an upper
range of 4-6 eggs per day unless caloric demands are
xceptionally high. e

A

word about research funding source
The majority of egg research is funded by the egg industry.
As such, its no surprise that eggs can come off as some
sort of a superfood, which is not the case. Theyre simply
a viable, non-threatening option for those seeking a high-
quality balanced source of protein and fat. Regardless of
potential sponsorship bias, eggs and cholesterol intake have
received a bad rap despite numerous controlled experiments
that are yet to be refuted by non-industry sources.
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Moderate protein intake improves total and regional
body composition and insulin sensitivity in overweight
adults.

Arciero PJ , et al. Metabolism. 2008 J un;57(6):757-65. [Medline]

PURPOSE: To test the hypothesis that moderate protein intake
(~25% of energy intake) would elicit similar benefits on body
composition and metabolic profile as high protein intake.
METHODS: 24 overweight/obese men and women (BMI =
32.2, %BF =37.3) were randomly assigned to one of 3 groups
for a 3-month nutrition/exercise training intervention: (1) high-
protein diet (~40% of energy intake) and combined high-
intensity resistance and cardiovascular training (HPEx), (2)
moderate-protein diet (~25% of energy intake) and combined
high-intensity resistance and cardiovascular training (MPEx), or
(3) high-protein diet only (HPNx). Total and regional body
composition (via DEXA), insulin sensitivity, insulin-like growth
factor-1 (IGF-1), IGF binding protein-1 (IGFBP-1), IGF binding
protein-3 (IGFBP-3), and blood lipids were measured.
RESULTS: All groups had similar losses of body weight, BMI,
and total and abdominal %BF, and similar improvements in
insulin sensitivity and leptin levels. HPEx had decreases in total
cholesterol (TC) and triacylglycerol, and increases in IGF-1 and
IGFBP-1. MPEx decreased TC, whereas the HPNx group had
increases in high-density lipoprotein cholesterol (HDL-C), ratio
of TC:HDL-C, IGF-1, and IGFBP-1. CONCLUSION:
Moderate protein intake elicits similar benefits in body
composition and insulin sensitivity as a high-protein diet. These
findings. SPONSORSHIP: Abbott Laboratories, EAS division.

S

tudy strengths
Its always nice to see DEXA (the gold standard) used for
assessing body composition. Time of assessment was
normalized (after a 12-hr fast), as was the restriction of alcohol,
caffeine, and exercise 48 hours prior to testing. Another plus was
the comparison of mixed exercise treatments in addition to the
different dietary treatments. Exercise was supervised by a
certified strength and conditioning specialist and a member of
the research team. Compliance to the exercise protocol was
enforced via daily exercise monitoring and subject-researcher
contact. The exercise protocol contained a higher frequency of
work than whats typically seen in research of this type. Six days
total per week consisted of 3 resistance training days (35-40
minutes per session) alternated with 3 high-intensity interval
cardio (20 minutes per session). Diets were set at 2000 kcals,
making them relevant to populations involved with moderate
rather than extreme calorie reduction. Dietary compliance was
bolstered by weekly meetings with a registered dietitian as well
as daily subject-researcher contact.

Study limitations
The allowance of up to 3 alcoholic beverages and 1 free day
per week was implemented for the purpose of decreasing
boredom and improving compliance. However, all this really
does ultimately is decrease the level of experimental control. A
better move would have been to either fix (absolutely or
proportionately) the allotment of alcoholic beverages, and either
provide or specifically define the free day in order to minimize
variation across individuals. Those who are familiar with EAS
and the Body-for-Life program would immediately recognize the
exercise protocol, as well as the dietary protocol of 3 protein-
rich meal replacement products plus 3 real food meals. As
mentioned by the authors themselves, questions remain about
whether this 6 meals/day frequency is applicable to free living
conditions. In other words, 6 meals per day might be a pain in
the ass for many dieters to sustain long-term.

C

omment/application.
Here are the key nutritional variables of exercising groups at
baseline and at the end of the trial, including the degree of
change:

Variable High-Protein Moderate-Protein

Pre Post Change Pre Post Change

Kcals 2180 1855 -15% 2043 1890 -7%
Protein (g) 80.2 187.0 +137% 86.8 109.8 +31.1%
Carbohydrate (g) 266.2 113.5 -56.8% 242.6 183.1 -19.3%
Fat (g) 85.6 59.6 -26.5% 80.3 53.0 -16.6
Since there were no significant differences between the
exercising groups regarding body composition and insulin
sensitivity. This serves to illustrate a point I often make that
exercise is the great equalizer. In other words, with a sufficient
exercise program in place, dietary differences tend to make less
of an impact on body composition. This is especially the case
when protein intake is sufficient across the groups. But as you
can see in the above chart, this equalizing effect can also occur
when protein intake is low-balled (as in the case of the
moderate-protein group at 109.8g/d). I found it interesting that
this group not only kept its lean mass despite the lower protein
intake, but it actually appeared to gain a bit of lean weight (+0.2
kg) while the high-protein group lost a bit of it (-0.1 kg). This
can be attributed to either greater glycogen stores, or inaccurate
self-reporting.

The differences between the exercising groups boiled down to
certain aspects of blood lipid profile. Triacylglycerol levels
decreased significantly in the high-protein group, but not in the
moderate-protein group. This is consistent with other research
showing the plasma triacylglycerol-retentive ability of a higher-
carbohydrate diet.
1
Improvements in cholesterol occurred in both
groups, but differed slightly in nature. The high-protein group
decreased total cholesterol (TC), while the moderate-protein
group displayed a significant reduction in TC to HDL ratio but
no change in TC. This discrepant outcome, once again, is likely
a result of the inaccuracies of self-reported dietary intake.

The authors conclude that its possible to get the same benefits
of a high protein (40%) diet on a moderate protein (25%) diet.
Given the substantive exercise protocol, this didnt surprise me.
However, I am surprised that the studys sponsor (EAS a
sports supplement company) didnt tweak all of the outcomes in
favor of the high-protein group, since this would benefit protein
supplement sales. Either there still is a shred of integrity in
science, or theyre working on a carb supplement.
Effects of dietary protein content on IGF-I,
testosterone, and body composition during eight days
severe energy deficit and arduous physical activity.

Alemany J A, et al. J Appl Physiol. 2008 May 1. [Epub ahead of
print] [Medline]

PURPOSE: To determine the effects of two levels of dietary
protein content and its effects on IGF-I, androgens, and losses of
fat free mass accompanying energy deficit. METHODS: 34
men (24 yrs old, 180.1 cm, 83.0 kg) underwent an 8-day military
exercise characterized by high energy expenditure (16.5 MJ /d;
3940.9 kcal), low energy intake (6.5 MJ /d; 1552.5 kcal), and
sleep deprivation (4 h/24 h) were divided into two groups of 0.9
g/kg or 0.5 g/kg dietary protein. IGF-I system analytes,
androgens and body composition were assessed throughout the
intervention. RESULTS: Total, free and non-ternary IGF-I as
well as testosterone declined 50%, 64%, 55% and 45%,
respectively, with similar reductions both groups, except that
there was a diet x time interaction on day 8 for total IGF-I and
sex-hormone binding globulin. Decreases in body mass (3.2 kg),
fat-free mass (1.2 kg), fat mass (2.0 kg) and & body fat (1.5 %)
were similar in both groups. CONCLUSION: Protein intake of
0.5 or 0.9 g/kg had minimal effects in attenuating the decline in
the IGF-I and androgenic systems and fat-free mass during eight
days of negative energy balance associated with high energy
expenditure and low energy intake SPONSORSHIP: Army
Medical Research and Materiel [thats the actual spelling]
Command

Study strengths

The general concept here is interesting, and it was a reality-
based progression; the study occurred during the U.S. Marine
Corps Infantry Officer Candidate (IOC) 17 school eight-day
military field exercise in Quantico, VA. Its basically the
assessment of a catabolic blitz that would closely mimic certain
periods of military combat characterized by the deprivation of
sleep and food under a massive energy expenditure. The low
protein amounts were purposely chosen to reflect the protein
content in MREs (meals ready to eat) currently available to the
military, which typically provide less than 0.9g/kg/day. Body
composition was assessed by DEXA. An actigraph as well as
doubly-labeled water was used to objectively assess physical
activity. All food was prepackaged and provided by the lab.

Study limitations

Since this intervention has the characteristics of a matter-of-fact
case observation, the only real limitation was the absence of a
genuinely adequate or high-protein group. Ideally, this group
would consume at least in the neighborhood of 2.0g/day, which
is within the range considered not just protective, but capable of
improving anabolism and other training adaptations.
2
Perhaps
this wasnt necessarily the point of the study, but it might
certainly help in the campaign for better-designed MREs.
Another minor limitation was the short length of the study, but
the extreme rigorousness of the protocol might understandably
be self-limiting. For example, one of the participants in the
original sample didnt complete the trial due to injury.
Comment/application

Here are the body composition changes from the two levels of
insufficient protein intake over 8 days in a severe deficit:

Variable 0.8g/kg 0.5g/kg

Pre Post Pre Post
Total mass (kg) 83.0 79.0 81.6 79.5
Fat-free mass (kg) 69.2 67.5 69.1 67.8
Fat mass (kg) 13.9 12.5 12.5 11.0
Bodyfat % 16.6 15.3 15.1 13.3
Given that both groups consumed the same amount of total
calories (1552.5 kcal) with the only difference being protein
intake (82g/day or 38g/day), these results are intriguing indeed.
Although the differences in body composition change didnt
rech statistical significance, the lower protein group lost a touch
less lean mass (0.4 kg), and also lost a smidge more fat mass
(0.1 kg). Comparing those numbers at their absolute value, the
lower protein group actually had a more favorable outcome.
Thats pretty weird. This indicates that below a certain level of
insufficient protein intake, there appears to be no further
detriment, much like it might be in the opposite context. That is
to say, above a certain level sufficient protein intake, theres no
further benefit.

Another interesting finding was that there was very little
difference in the effect of the two protein treatments on
bioavailable IGF-I, since presumably the higher protein
treatment would have had at least a little preventive effect, but it
didnt. The authors presume that the energy deficit of 2149.6
kcal/day was too massive to allow for any preventive effects of
the increased protein intake compared to the low intake.

One thing that the higher protein intake did effect was sex
hormone binding globulin (SHBG). SHBG levels increased 23%
above baseline levels in the higher protein group, but increased
66% above baseline in the lower protein group. The significance
here is that SHBG controls the majority of the pool of
testosterone in circulation. Thus, when SHBG is suppressed,
more testosterone is available for use by the body. Inspite of the
blunting of SHBG by the higher protein treatment, no significant
differences were seen in free testosterone levels between the
groups. Once again, there seems to be a threshold of nutrient or
calorie-mediated sufficiency that simply was not met.

A disturbing fact mentioned by the authors was the protein
amounts in several of the MRE menus available to the military
personnel. Specifically, 7 of the MRE menus contained an
average of 32 g protein while seven other menus contained an
average of 53 g protein. This means that the population with the
most critical need for utmost physical performance is subsisting
in the dark ages of the RDA and below. Thats a sad state of
current affairs, but it provides an excellent opportunity for
protein supplement and prepackaged food manufacturers to
spearhead a market in desperate need of re-designing their
MREs for the troops. My guess is that trials like this will serve
as a step in the right direction. GET THEM BOYS SOME
DAMN PROTEIN & CALORIES!

Effect of Preexercise Meals With Different Glycemic
Indices and Loads on Metabolic Responses and
Endurance Running
Chen YJ, et al. IJ SNEM. 2008:(18):281-300. [IJ SNEM]

PURPOSE: To examine the effect of ingesting 3 isocaloric
meals (roughly 630 kcals each) with different glycemic indices
(GI) and glycemic loads (GL) 2 hr before exercise on metabolic
responses and endurance running performance. METHODS:
Eight male runners completed 3 trials in a randomized order,
separated by at least 7 days. Carbohydrate (CHO) content (%),
GI, and GL were, respectively, 66%, 79, and 82 for the high-
GI/high-GL meal (H-H); 66%, 40, and 42 for the low-GI/low-
GL meal (L-L); and 36%, 78, and 44 for the high-GI/low-GL
meal (H-L). Each trial consisted of a 1-hr run at 70% VO
2max
,
followed by a 10-km performance run. RESULTS: Low-GL
diets (H-L and L-L) were found to induce smaller metabolic
changes during the postprandial period and during exercise,
which were characterized by a lower CHO oxidation in the 2
trials (p <.05) and a concomitant, higher glycerol and free-fatty-
acid concentration in the H-L trial (p <.05). There was no
difference, however, in time to complete the preloaded 10-km
performance run between trials. CONCLUSION: This suggests
that the GL of the preexercise meal has an important role in
determining subsequent metabolic responses. SPONSORSHIP:
None listed.

Study strengths

To control dietary intake prior to each main trial, the participants
completed 3-day weighed food records that were analyzed via
nutritional software. The treatment variations were thoroughly
executed (no permutation was left out). The procedure was
relatively cut-and-dried with little room to mess things up. This
study is the first one yet to directly examine the effect of
glycemic load (GL) of the pre-exercise meal on endurance
exercise performance.

S

tudy limitations
Sample size was small (8 subjects), and they were described as
healthy volunteers. This means that they werent necessarily
trained athletes. Its generally more meaningful in these types of
trials to use highly trained subjects, since newbies tend to be
more responsive to variations in protocol. One of the unknown
yet critical aspects of this trial was an absence of muscle
glycogen status measurements preceding the tests. Other missing
data were glucose kinetics during exercise. Thus, its impossible
to be certain whether or not variations in glycogen status might
have influenced the outcomes in this study.

Comment/Application

Historically, various carbohydrate manipulations have been
made in attempts to maximize endurance capacity, as well as
exercise performance. Glycemic index (GI), has thus far the
longest history of research in this vein. As the authors of the
present study point out, the majority of research shows that pre-
exercise meal GI manipulation doesnt make a difference in
performance. Untapped ground, however, is the effect of GL.
First off, lets clear up some definitions. GI is a measure of a
fixed amount of carbohydrates ability to raise blood glucose,
expressed as the glucose area under the curve (AUC) in the
post-ingestion period typically spanning a couple of hours. GL is
a more recent classification system that takes into account the
amount of carbohydrate per serving. GL takes GI a step further
by indicating a foods carbohydrate concentration in addition to
the glycemic response of the carbohydrates it contains.
However, the bottom-line clinical value of GL, much like GI, is
highly questionable. A prime example of the insignificance of
GI and GL is their effect on body composition. In perhaps the
most tightly controlled trial on this subject, Das et al compared
effects of 2 macronutrient patterns with different GL on
adherence to calorie restriction, weight and fat loss, and related
variables.
3
No differences in the changes in energy intake, body
weight, body fat, and resting metabolic rate were seen between
groups.

Back to the present study... The 3 experimental whole-food
meals were consumed 2 hours prior to the exercise trials. The
high-GI/high-GL and low-GI/low-GL both had 66%
carbohydrate, 15% protein, and 20% fat. The high-GI/low-GL
had 36% carbohydrate, 15% protein, and 49% fat, a breakdown
achieved mainly by increasing the corn oil and reducing the
portion of carbohydrate. Unsurprisingly, stomach distress was
reported in the later stage of the 10 km performance trial in the
high-GI/low-GL group. Gastric disturbance has been seen in
other research when medium-chain triacylglycerol was used pre-
and during exercise.
4
Its likely that the delayed gastric emptying
via the high fat content was the culprit. Nevertheless, no
performance differences were seen in the present study. An
unexpected finding to the authors was a lack of difference in
ubstrate oxidation. To quote the text, s

This might be the most interesting finding of the current study:
Despite the big difference in micronutrients in the two equally
low-GL meals (L-L and H-L), achieved by changing either the
GI or the amount of the CHO by replacing CHO with fat, they
oth produced similar fat oxidation during exercise. b

The authors dont speculate over a possible mechanism for this,
but instead mention previous research by that showed similar
effects.
5
This effect reminds me of work by Febbraio et al, who
saw no difference in fat oxidation during exercise between fasted
and carbohydrate-fed subjects.
6

An interesting issue raised by the authors of the present trial is
the controversial nature of GL. Currently, GL is not a recognized
index by any major professional or governmental entity in the
world. It might remain this way, since GL is based partially on
GI, which has its own set of problems. A memorable point made
by Pi-Sunyer in a nearly decade-old review is that a great
number of factors can affect the reproducibility (and thus
reliability) of GI values.
7
An abbreviated list of factors include
ripeness of fruit, physical form of food, variability within food
classes, processing, preparation, and previous meal influence. As
I mentioned previously, the manipulation of pre-exercise GI has
an inconsistent track record, with most of the data in favor of
abandoning the idea that it makes any difference. This trial is yet
another one to add to the list, except you can also include the
possibility that GL might not matter either.


High rates of muscle glycogen resynthesis after
exhaustive exercise when carbohydrate is co-ingested
with caffeine.

Pedersen DJ , et al. J Appl Physiol. 2008 May 8. [Epub ahead of
rint] [ p Medline]

PURPOSE: To determine the effects of the co-ingestion of
caffeine with carbohydrate on rates of muscle glycogen
resynthesis during recovery from exhaustive exercise.
METHODS: 7 trained subjects completed 2 experimental trials
in a randomized, double-blind crossover design. Prior to testing,
subjects performed exhaustive cycling and consumed a low-
carbohydrate diet. The following morning subjects reported to
the lab and rode until volitional fatigue. Upon completion,
subjects consumed either carbohydrate (CHO; 4g/kg) or
carbohydrate +caffeine (CAFF, 8mg/kg) during 4 h of passive
recovery. Muscle and blood samples were taken throughout
recovery. RESULTS: Muscle glycogen levels were similar at
exhaustion and increased by a similar amount after 1 h of
recovery. After 4 h of recovery CAFF resulted in higher
glycogen accumulation (313 vs. 234 mmol/kg d.w). The overall
rate of resynthesis for the 4 h recovery period was 66% higher in
CAFF compared to CHO (57.7 vs. 38.0 mmol/kg).
Phosphorylation of CAMKThr286 was similar post-exercise and
after 1 h of recovery but after 4 h CAMKThr286
phosphorylation was higher in CAFF than CHO.
Phosphorylation of AMPKThr172 and AktSer473 was similar
for both treatments at all time points. CONCLUSION: In
trained subjects, coingestion of large amounts of caffeine with
carbohydrate has an additive effect on rates on post-exercise
muscle glycogen accumulation compared to carbohydrate alone.
SPONSORSHIP: GlaxoSmithKline (U.K.)

S

tudy strengths
Subjects were trained, so this removes the beginner/newbie
effect of anything working beyond nothing. Diet and exercise
records were used to standardize food intake and physical
activity for 48 hours prior to testing. All diets were constructed
by a dietitian, and were individualized to the body mass of each
subject. All food and drinks were pre-packaged and supplied by
the lab. This trial gets minor innovation points for being the first
to test post-glycogen depletion caffeine dosing. Finally,
something Im beginning to appreciate is when authors explicitly
report what they feel are the limitations of the research they
conducted. This is coming up next, along with some other
limitations I spot.

S

tudy limitations
As mentioned by the authors, this trial lacked the measurement
of glycogen synthase (GS) levels. However, this is a minor
limitation since measuring the actual concentration of
resynthesized glycogen makes GS measurement somewhat
trivial and redundant. Furthermore, GS might not be the most
accurate indicator of glycogenic potential in the first place. In
research by Thong et al, a caffeine-induced suppression of GS
and glucose disposal did not impede the rate of glycogen
resynthesis in the leg after exercise
8

C

omment/Application
One thing I found to be an odd recurring theme throughout this
paper was the mentioning of caffeine having a negative effect on
glucose metabolism. This is qualified somewhat by mentioning
that this occurs in the resting state rather than the trained state.
The potential extrapolation here is that caffeine poses some sort
of threat to those with compromised glucose metabolisms and
should be avoided. However, heres the catch: caffeine has been
seen to acutely impair insulin sensitivity and glucose tolerance,
but chronic studies show a decreased risk for diabetes in
caffeinated coffee drinkers. A recent trial by Battram et al found
a potential explanation for this disparity. They found that
chronic coffee intake did not result in the same impairment of
glucose tolerance as isolated caffeine. It was speculated that the
additional biological compounds in coffee (chlorogens and
quinides) in large part neutralize any adverse effect on resting
glucose metabolism that isolated caffeine might cause.
9
10

Back to our study... The subjects were endurance-trained cyclists
and triathletes. Miraculously, they werent habitual caffeine
users (most recreational and competitive endurance athletes I
know live on the stuff). The non-use of caffeine-containing
foods/products by the subjects is both a good and a bad thing;
good in the sense that we get to isolate the effect of a novel
substance, but bad in the sense that we dont get to see whether
or not these effects are diminished in regular users who comprise
a large proportion of the endurance athlete population.

Carbohydrate dosing was a total of 4g/kg by the end of the 4-
hour recovery period. This dosing scheme towards the
conservative side, since a maximal rate of glycogen resynthesis
has been fairly well established in the neighborhood of 1.0-
1.85g/kg/hr The carbohydrate consumed was in the form of
sports bars, gels, and sports drinks. Interestingly, a record-setting
rate of glycogen resynthesis was achieved without the use of
special carbohydrate sources such as waxy maize starch.
11

Caffeine dosing was 8mg/kg immediately post-depletion, and
then a 2 time 2 hours afterward. This dose is higher than that
used in similar research, which averages roughly a single dose of
5mg/kg. As mentioned by the authors, questions remain as to
how comparatively effective a lower dose would be. All said, the
present study generated the highest overall rate of glycogen
synthesis (60 mmol/kg) thus seen in orally administered
conditions in humans, with the second highest range being
roughly 40-45 mmol/kg. Several signalling proteins were
measured in attempt to pinpoint a possible mechanism for the
increased rate of glycogenesis, and only the phosphorylation of
CAMK
nd
Thr286
was higher as result of the caffeine treatment.
However, additional biopsies would be necessary to determine
whether this can be linked to increased glucose transport
signalling. Future research on post-depletion coffee intake
(versus isolated caffeine) would very interesting to see.


Effects of resistance vs. aerobic training combined with
an 800 calorie liquid diet on lean body mass and resting
metabolic rate.

Bryner RW, et al. J Am Coll Nutr. 1999 Apr;18(2):115-21.
[Medline]

PURPOSE: To examine the effect of intensive, high volume
resistance training combined with a very-low-calorie diet
(VLCD) on these parameters. METHODS: Twenty subjects (17
women, three men), mean age 38 years, were randomly assigned
to either standard treatment control plus diet (C+D), or
resistance exercise plus diet (R+D). Both groups consumed 800
kcal/day liquid formula diets for 12 weeks. C+D exercised 1
hour, 4 days/week by walking, biking or stair climbing. R+D
performed resistance training 3 days/week at 10 stations
increasing from two sets of 8 to 15 repetitions to four sets of 8 to
15 repetitions by 12 weeks. Groups were similar at baseline with
respect to weight, body composition, aerobic capacity, and
resting metabolic rate. RESULTS: Maximum oxygen
consumption (VO2max) increased significantly but equally in
both groups. Body weight decreased significantly more in C+D
than R+D. The C+D group lost a significant amount of LBW (51
to 47 kg). No decrease in LBW was observed in R+D. In
addition, R+D had an increase in RMR. The 24 hour RMR
decreased in the C+D group. CONCLUSION: The addition of
an intensive, high volume resistance training program resulted in
preservation of LBW and RMR during weight loss with a
LCD. SPONSORSHIP: None listed. V

S

tudy strengths
Hydrostatic weighing (hydrodensitiometry) was used to assess
body composition. This is generally regarded as reliable and
valid, with a small notch up being DEXA a method thats
much more common in studies conducted within the past few
years. It seems the standard of accuracy is steadily but surely
being raised, since Im seeing hydrodensitiometry being used
less and less in the literature. In my observations, however,
hydrodensitiometry has been more reliable than bioimpedance
analysis (BIA). Diet was strictly controlled by virtue of being
liquid formulas provided by the lab. Meals were administered in
bulk once per week at the meetings with an investigator, and
compliance was questioned whenever less than 2 lbs per week
was lost. Self-reported dietary compliance was reported by the
nvestigators as excellent. i

S

tudy limitations
The aerobic training protocol was somewhat nebulous; it didnt
have clearly-defined parameters as did the resistance training
protocol. The aerobic group did 4 days per week of walking,
biking, or stair climbing. Duration began at 20 minutes per day
and increased 10 minutes per day every week, until each session
was 50 to 60 minutes. This program was described as self-paced,
and as such, specific intensity parameters were not met. As a finl
nit-pick, the number of women exceeded the men by more than
5 to 1, opening up the possibility for the outcomes to have sex-
specific bias.
Comment/application

This is one of the most commonly cited trials in support of the
idea that its in fact possible to gain muscle under a caloric
deficit. And in this case, it was quite a severe caloric deficit,
since the participants were training in addition to consuming a
mere 800 calories per day. However, its critically important to
remember that these subjects are unconditioned and overweight.
These characteristics lend themselves to a simultaneous muscle
gain and fat loss to a much higher magnitude than what would
occur in lean, highly conditioned subjects who are more prone
o muscle loss exclusively under the present conditions. t

The macronutrient breakdown of was 80 g protein, 98 g
carbohydrate, and 10 g fat. At baseline, the bodyweight of the
subjects in both groups averaged 97.7 kg, which set their protein
intake at roughly 1.2g/kg. While this amount exceeds the RDA
of 0.8g/kg, it still barely makes it into the range recommended
for athletes and individuals involved in an exercise program,
which according to whose philosophy in the literature you want
to believe, is a range of 1.2-2.0g/kg.
12,13
Keep in mind, with this
protein recommendation, its assumed that total calories are
sufficient. In the present trial, subjects were severely
hypocaloric, which astounds me that any of the groups held on
to its lean mass. But according to the instruments used, this
indeed was the case. The aerobic group lost 4 kg lean mass
while the resistance groups loss was too small to reach
statistical significance. By the trials end, the resistance group
lost 1.2% more body fat than the aerobic group. Would DEXA
eadings be different? We can only speculate. r

Perhaps the most clinically significant finding of this study was
a 4% increase in resting metabolic rate (RMR) in the resistance
group while the aerobic groups RMR dropped 13.4%. An
interesting outcome is that the resistance group lost less total
bodyweight due to the retention of lean mass and this
happened despite having a similar energy output as the aerobic
group. Its tempting to assume that at least a subset of the
resistance group expended more energy than the aerobic controls
ue to the continual progression of load and training intensity. d

One of the most useful aspects of this study is that it gives us
some reference data for judging the relative speed and
effectiveness of a given crash fat/weight loss program compared
to whats been observed under controlled conditions in research.
Here are the 12-week stats:

Variable Aerobic Training Resistance Training

Pre Post Change Pre Post Change
Total mass (kg) 93.8 75.7 -18.1 97.7 83.3 -14.4
Lean mass (kg) 51.4 47.3 -4.1 51.6 50.8 -0.8
Fat mass (kg) 40.8 28.0 -12.8 44.9 30.4 -14.5
Body fat % 44.5 37.1 -7.4 46.2 37.6 -8.6
This trial doesnt necessarily have a moral to the story, mainly
because the protocol was too extreme to apply to most free-
living non-medically supervised populations. If theres anything
solid to glean from this data, its that resistance/strength training
rather than aerobic training should comprise the bulk of the
training in a severe caloric deficit.


The Wisdom of Layne Norton By Alan Aragon

Layne is a natural pro bodybuilder who (amazingly enough) is
interested in the science behind bodybuilding. Hes currently
working on his PhD at the University of Illinois, specializing in
skeletal muscle protein metabolism. I specifically sought him out
for this interview because for one thing, I knew that hed be kind
enough to take the time to do it (he doesnt have a big ego yet),
and secondly, Layne is one of those guys that many of us would
model our work ethic after if we had enough nerve. Hes one
heck of an overachiever who has accomplished quite a bit for
being only in his mid-20s. Perhaps most importantly, Layne
recognizes the value of science and research, and is destined to
be cited many times over by secondary sources like myself.

AA: How did you get interested in bodybuilding, and who
are your main mentors/influences?

LN: I started lifting in high school because, quite frankly, I was
picked on by my peers and didn't get much attention from girls.
Over the years I grew to love lifting for the sake of pushing
myself and trying to ascend to the next level. Once I got to
college, I decided it was time to take it to the next level &
compete. I always read magazines like FLEX and looked up to
the guys in there, but somehow I never could relate them to
myself. Then I started reading about natural bodybuilding and
guys like Dave Goodin and Dr. J oe Klemczewski. J oe is as
close to a guru of natural bodybuilding as their is and he really
went out of his way to take me under his wing when I was
getting into competitive bodybuilding and that made a big
difference for me. Now Joe I'm proud to call J oe a friend of
mine.
AA: What are your proudest personal or career
accomplishments?

In terms of competing I am probably most proud of my very first
contest win at the 2001 INBF Mid America Muscle Classic. I
won the teen class and the men's novice tall class. Although I
later turned pro at a different show; my first show really stuck
with me, I can never get that feeling out of my head and my
heart of the way it felt to hoist that trophy for the first time, and
the first sensation I ever got from being onstage. Nothing
compares to it. Overall though, I am most proud of the way I've
been able to integrate competitive bodybuilding into my daily
life. I enjoy bodybuilding but I don't let it prevent me from
enjoying my life like I see it do to so many others.

AA: What are the biggest precontest training and dieting
mistakes you've made in the past?

Not giving oneself enough time to get lean. I see too many
people who are not honest with themselves about their bodyfat
level and think they can get shredded in 12 weeks when it's
obvious they have around 40 lbs to lose.

Going on extreme diets. Super high protein (>400g) with the
notion that protein cannot be stored as fat, or going super super
super low carb with the belief that all carbs are evil. Honestly,
any type of extreme diet is usually not a good idea.

Cutting water. This could possibly be #1. People think that water
is what causes you to retain water. This is nonsense, the more
water you drink, the more your body expels. Your body
regulates water balance by the MINUTE. The notion that you
can cut water out days in advance and trick your body is
nonsense. People cut water totally out and then they wonder why
they can't fill out or get a pump on contest day and always look
better the day after the show. You can carb up all you want, but
if you don't drink water, the muscle cells will simply not fill out,
period. Additionally, depriving the body of water will reduce the
amount of carbs that the muscle cells can store as there will not
be enough solute to retain them in the muscle cells. The reason
you always hear competitors say I looked better the next day is
because they drink a bunch of water after their show is done and
finally fill out. All my clients tell me they look like crap the day
after the show... that's because they kept water in on contest day
and filled out & peaked properly.

AA: Give us a workday in the life of Layne Norton.

7:00am-7:15- wake up and grab a shower while starting
breakfast
7:15-8:15- eat breakfast while answering emails
8:15-8:30- walk dog
8:30-8:45- prep food & pack bags for lab/school
8:45-9:15- catch bus to campus
9:15-4:30pm- work in lab
4:30-5:00- catch bus back to home
5:00-6:00- eat preworkout meal
6:00-8:00- workout
8:00-8:30 fix dinner & shower
8:30-9:30-eat dinner with Isabel and catch a show on TV
9:30-11:30- answer emails and work on anything I brought home
from lab
11:30-12:00am walk dog & prepare meals for following day
12:00- sleep


AA: What are your biggest rants about any aspect of the
fitness & bodybuilding industry?

It's such an extreme industry filed with people who fly off one
handle or the other on extremes. Moreso than any industry it is
filled with 'guru's' most of which couldn't find their ass if their
finger was stuck up it, yet people blindly follow them around
without thinking for themselves.

AA: What are the biggest challenges you personally face in
the field of scientific research?

Timing is always difficult. Many of the assays I run can take up
to several days including incubation periods, so making sure I
time everything properly can be difficult. Research in general is
very difficult. Sometimes you will work on an experiment or
working up data for an experiment for literally months only to
find out the experiment didn't work or their was something
flawed with it and you have to go back and re-do it or start from
scratch. There is no "E" for effort. Either you get results or you
don't.

AA: What's your take on precontest cardio in terms of
intensity, frequency & duration?

Like everything else it really depends on the individual. For
people who specifically have difficulty losing fat from their legs
or abdominal region I really recommend more high intensity
cardio. High intensity cardio will activate the sympathetic
nervous system to a greater extent than steady state cardio and
will help target the receptors largely responsible for initiating
lipolysis in adipose. Additionally, high intensity cardio will also
increase mitochondrial density and activity of the area being
worked. Mitochondria are the organelles of the cell responsible
for energy production and this includes fat oxidation. So
increasing the number and activity of the mitochondria will give
an individual a greater capacity to oxidize fat. That said I still
think steady state cardio is good to use as well, since doing more
than 3-4 high intensity sessions per week can make weight
training difficult due to soreness and stiffness from high
intensity sessions.

AA: Can give us your typical offseason day's diet &
supplement intake as well as your typical precontest diet &
supplement intake? You can leave out the drug protocol (just
kidding).

My diet during the offseason is a cyclical diet: 4-8 weeks in a
500 kcal surplus followed by 4-8 weeks in a 500 kcal deficit.
Typically during bulking phases I will eat around 225g protein,
400-500g carbohydrates, and 60-70g fat depending upon what
bodypart I am working on a particular day and how much energy
I expend. During the cutting phases I usually consume 250g
protein, 200-225g carbohydrates, and 50-60g fat. My precontest
diet will look similar to that, though I reduce calories when fat
loss progress slows.

S

upplentation in the offseason includes:
5g of BCAA (Xtend) between meals and 10g post workout
(total of 25-30g Xtend/day)
5g creatine monohydrate post workout
3-4g beta-alanine per day
Citrulline malate (this is in Xtend so I do not add extra)
3 fish oil caps per day
300mg lipoic acid post workout
1000mg glucosamine per day
Multivitamin

D

uring cutting phases I will add:
Sesamin: 3 caps/day
Scivation Dialene 4: 3 caps 3x/day

AA: Any general or specific words of wisdom to those
considering competitive bodybuilding?

Be patient. Everyone wants to gain 10 lbs of shredded muscle in
2 weeks but it just takes time to put on quality muscle. Be
consistent with your diet and training and things will fall into
place. Even if you only gain 5-10 lbs of muscle in a year, that is
good progress, it may not sound like much but think of it this
way; go to the supermarket and look at 5 lbs of beef. THAT'S A
WHOLE LOT OF TISSUE! Think about slapping that on
yourself... that's a lot of muscle. Always remember that it is very
hard work and that no one really cares about excuses in the end.
Everyone has their own challenges when competing, no one
wants to hear a sob story, get it done or don't get it done. J ust
remember, if you want to win, you need to ask yourself: am I
working harder than the person I'll be standing next to onstage?

AA: Any personal or career goals you're currently pursuing
that youd like to share?

Right now I'm one week out from marrying the love of my life,
my longtime girlfriend Isabel. Then we take a cruise for our
honeymoon. I've never been on one so I'm really excited. The
week after we get back I'm presenting at the ISSN (International
Society of Sports Nutrition) symposium as a guest speaker so
I'm excited about that. Additionally, my first DVD, Layne
Norton Unleashed will be released shortly after that and I really
think that the people who buy it will get a good combination of
science based advice as well as 'in the trenches' type scenes that
every hardcore lifter can relate to. Should be a busy summer, but
I'm really looking forward to it!

Thanks Alan.
-Layne

AA: Nah man, thank YOU. Congrats on getting married,
and beware of unforeseeable honeymoon injuries.

[Editors note: Laynes personal website is www.biolayne.com.]

The Wisdom of Pauline Nordin By Alan Aragon


Its safe to say that the above picture of The Squat Girl is
legendary on the internet; its one of the most recognizable,
iconic shots online. Little did I know that it would end up in
AARR as a legitimate example of the hard work of my
interviewee rather than merely a gratuitous distraction (eat your
heart out T-Nation)!

Enter Pauline Nordin. She has achieved a level of physical
development and refinement that most of our subculture would
donate a nut or two to get. Initially, I assumed Pauline must be
pretty well-informed ever since she contacted me about re-
printing an article of mine. What I came to find out was that
shes not only an avid student of the fitness game, but also highly
accomplished professional in several arenas. Shes a
professional figure competitor and AST-sponsored athlete whos
been on several major magazine covers. She also has national
TV exposure, gaining bona fide celebrity status in her original
home country of Sweden (shes now a Californian). Im pleased
to have had the chance to pick her brain, so lets get to it.

AA: Hello Pauline, Im excited that you agreed to let me
interrogate you for my readership. What are your biggest
career accomplishments, as well as your biggest mistakes or
regrets?

Thank you Alan. My biggest career accomplishments are not as
a competitor but as a model and TV personality. I was the
Biggest Loser Shows Swedish trainer which was a great career
move, and I have made the cover of Ironman Magazine and
lately got 18 pages featured in the HARDBODZ Magazine. As
an athlete I am proud I obtained pro status and went from
Sweden to America to compete as a pro.

AA: I'm sure many of my readers would be curious to know
what your typical workday looks like. That's okay if it's
boring, at least our curiosity will be satisfied.

Wake up at 4 am, drive to Hollywood where I have three clients.
7 am cardio. Drive home in traffic. Computer work (I work as a
journalist too) or photo shoots (as a creative director and some
times as technical advisor), in the afternoon clients, then me
training. Then home, prep for next day. Eat. Sleep. Repeat.

AA: When prepping for a show, how many days a week do
you weight train, and how many days a week do you do
cardio? How much time do you spend on each activity?

I weight train year round 5 days a week. I do cardio year round
10-28 minutes a day for 5-9 sessions per week. This does not
change.

AA: How do your off-season and pre-contest training
regimes differ? Do you have any unique pre-contest training
philosophies that others might benefit from trying?

They dont change at all. I do the same thing year round. I try to
take some days off at times but its hard. I always have one full
day off when I almost cannot make it out of my house. I
recuperate very fast and have a patient work horse body wise! It
can take a lot of punishment...

AA: Much ado has been made over bodybuilding-type
bodypart split training versus functional or movement plane-
type training. The two camps seem to love to bash each
other. What have you found works best for you regarding
training splits?

Since I train too much in general I always work on some
weaknesses that I find out about throughout my training.
Sometimes I feel a knee is starting to tell me something so I then
incorporate more coordination work or pay more attention to
unilateral training. I always prehab with strengthening lower
trapezius, I do hand stands, I work rotator cuff and work on my
medial gluteus mind/muscle connection so I stop or prevent any
injuries. I make sure I dont train upper body two days in a row
and I have one day dedicated to hamstrings, deadlifts. I am very
meticulous and dont do many sets or reps. Pretty much do 1-6
reps on most exercises and only leg press, hamstring leg curl and
calf raise are machines I use.


AA: I know that you stay in great shape year-round. So, my
hunch is that your offseason and pre-contest diet are not
drastically different, although I could be wrong on that.
Could you give us a sample of your off-season day's eating as
well as a pre-contest day's meal schedule?

It does not change at all. I never cheat or eat too many calories.
Well, thats a lie, I have a cheat day about once every six
months... I can count them on one hand since I moved to the US
on March 31
st
, 2006. I dont have a set diet, but I always have at
least 5 lbs of broccoli coleslaw a day, I eat pink salmon in a
pouch and lots of egg whites. I dont eat any starches what so
ever. I supplement with fish oil and since I am endorsed by AST
sports science I use most of their products. For instance, the
whey protein VP2.

AA: What are your thoughts on sodium and water
manipulation in the final days before a show? I feel like this
is where many competitors screw everything up thinking it's
gonna make all the difference. Is there any strategy you've
found works consistently well for you?

This is what I do change before a photo shoot or a contest. I
always eat lots of sodium and drink lots of water. Before a shoot
I just stop drinking the very same day and I cut out all additional
sodium from mustard and spices the day before the
shoot/contest. Thats all. I also dont have the veggies the day
before since it makes my stomach too full!

AA: What supplements do you feel have helped you get
contest-ready? I personally feel that they mainly serve as a
motivational/placebo tool whose actual effects on their own
are miniscule. You may have a different opinion on this, and
I'd love to hear about specific compounds (if any) that you
find useful.

I am a BCAA addict. I superdose it. I use about 40 grams a day.
Other than that glutaminaholic and time nutrients around my
training. Pretty much I fast throughout the day like in taking
mini meals and then I eat about 60% of my calories for the day
in the two hours post workout (weights).

AA: This is a touchy subject for some people, but in your
observations, how common is drug use amongst figure
competitors, and do you have any personal philosophies or
opinions about drug use in figure competition?

I am a 100% drug-free athlete myself and always will be. Yes,
there are many competitors that go the druggie road, but I dont
see a reason why. There is no money in figure in general and if
you screw up your looks it wont be nice to see after a few years.
I think most people are impatient and want to build a pro body in
one or two years. That does not happen if you stay natural.... It
took me many years before I finally got it in a way I
think is good-looking.

Having achieved a world-class physique, are there any gems
of advice you'd like to give those who have dumpster-class
physique but are intent on changing that?
Yes work hard, be very meticulous and patient. It takes
time!!!!!

AA: What are some of your goals - career, or other - that
you'd like to share with the readers? Any up-coming projects
you'd like to let us in on?

I want to get back on TV but in America this time. I also want to
keep on working as a model. I want to write books about fitness
and keep working my production company Conforce Inc. I am a
multi tasker and right now I am also working on a coffee shop
book! I need different project in order to not wear out.

What do you say to guys who try to hit on you at the gym
besides, I'm taken bro, go choke on a dumbbell.

I am pretty unapproachable. I dont talk that much and usually
people find me too serious. I am at the gym either working or
working out. So, I send out those signals I am not there to get hit
on.

AA: Ah, oh well. Thanks very much Pauline, all the best to
you.

[Editors note: check out this video in order to get a feel for
what she really means by an absence of dating signals while
shes in the midst of a workout. Paulines personal website is
www.paulinefitness.com. Heres a link to the page containing
the details of her online personal diet & training consulting. ]

1. Noakes, et al. Effect of an energy-restricted, high-protein,
low-fat diet relative to a conventional high-carbohydrate,
low-fat diet on weight loss, body composition, nutritional
status, and markers of cardiovascular health in obese women.
Am J Clin Nutr. 2005 Jun;81(6):1298-306. [Medline]

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. [Medline]

3. Das SK, et al. Long-term effects of 2 energy-restricted diets
differing in glycemic load on dietary adherence, body
composition, and metabolism in CALERIE: a 1-y
randomized controlled trial. Am J Clin Nutr. 2007
Apr;85(4):1023-30. [Medline]

4. J eukendrup AE, Adred S. Fat supplementation, health, and
endurance performance. Nutrition. 2004 J ul-Aug;20(7-
8):678-88. [Medline]

5. Bosher KJ, et al. Effects of different macronutrient
consumption following a resistance-training session on fat
and carbohydrate metabolism. J Strength Cond Res. 2004
May;18(2):212-9. [Medline]

6. 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. [Medline]

7. Pi-Sunyer FX. Glycemic index and disease. Am J Clin Nutr.
2002 J ul;76(1):290S-8S. [Medline]

8. Thong et al. Caffeine-induced impairment of insulin action
but not insulin signaling in human skeletal muscle is reduced
by exercise. Diabetes. 2002 Mar;51(3):583-90. [Medline]

9. Greenberg JA, et al. Coffee, diabetes, and weight control.
Am J Clin Nutr. 2006 Oct;84(4):682-93. [Medline]

10. Battram DS, et al. The glucose intolerance induced by
caffeinated coffee ingestion is less pronounced than that due
to alkaloid caffeine in men. J Nutr. 2006 May;136(5):1276-
80. [Medline]


11. J entjens R, J eukendrup A. Determinants of postexercise
glycogen synthesis during short-term recovery. Sports Med.
2003;33(2):117-44. Review. [Medline]

Over this past weekend, I lectured at the annual J P Fitness
Summit in Little Rock, AR. I covered the nutrition section, and
Steve Cotter did an amazing job teaching the class about his
approach to training with kettlebells. The unique thing about the
J P Fitness Summit is that as intensely interested as everyone is
in training, theyre just as interested in, um, lets call it
recovery. I had a hell of a good time with a great bunch of
folks, and it all culminated in my Youtube debut: a cheesy
karaoke duet. Enjoy this clip but be warned that its NOT for
the faint of heart or weak of spirit.
12. Tipton KD, Wolfe RR. Protein and amino acids for athletes.
J Sports Sci. 2004 J an;22(1):65-79. [Medline]
13. Campbell B, et al. International Society of Sports Nutrition
position stand: protein and exercise. J Int Soc Sports Nutr.
2007 Sep 26;4:8. [Medline]

Thanks once again for getting your wits filled with another
AARR issue. If you have any questions, comments, suggestions,
bones of contention, cheers, jeers, any feedback at all, send it
over to aarrsupport@gmail.com. All suggestions are taken very
seriously. I want to make sure this publication continues to stand
alone in its excellence.

6 - June - 2008

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AlanAragonsResearchReviewJune,2008[BacktoContents] Page1

Copyright June 1st, 2008 by Alan Aragon

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