1 - Jan - 2011

ean
Alan Aragons Research Review J anuary 2011 [Back to Contents] Page 1

Copyright January 1st, 2011 by Alan Aragon
Home: www.alanaragon.com/researchreview
Correspondence: aarrsupport@gmail.com

2 After over a half-century of study, were still
debating about protein requirements.
By Alan Aragon

5 Enhanced amino acid sensitivity of myofibrillar
protein synthesis persists for up to 24 h after
resistance exercise in young men.
Burd NA, et al. J Nutr. 2011 Feb 2. [Epub ahead of print]
[Medline]

6 Protein choices targeting thermogenesis and
metabolism.
Acheson KJ , et al. Am J Clin Nutr. 2011 J an 12. [Epub
head of print] [ a Medline]

7 Daily consumption of vitamin D- or vitamin D +
calcium-fortified yogurt drink improved glycemic
control in patients with type 2 diabetes: a
randomized clinical trial.
Nikooyeh B,, et al. Am J Clin Nutr. 2011 Feb 2. [Epub
head of print] [ a Medline]

8 Branched-chain amino acid supplementation
lowers perceived exertion but does not affect
performance in untrained males.
Greer BK. et al. J Strength Cond Res. 2011 Feb;25(2):539-
44. [Medline]

9 Excessive fructose intake induces the features of
metabolic syndrome in healthy adult men: role of
uric acid in the hypertensive response.
Perez-Pozo SE, et al. Int J Obes (Lond). 2010
Mar;34(3):454-61. [Medline]

11 Things I learned in 2010 (mostly serious edition).
B

y Alan Aragon

14 Interview with world record-holding competitive
eater Pete Czerwinski (AKA Furious Pete).
B

y Alan Aragon

15 An update has been made in the December 2010
issue.


After over a half-century of study, were still debating
bout protein requirements. a

By Alan Aragon
__________________________________________________

I

ntro & background
I spend a lot of time browsing fitness-related online message
boards (its a big part of my job, so I have a good excuse).
Though it may seem like a closed case, protein requirements for
the purpose of optimizing training adaptations are still debated
heatedly to this very day. This isnt without good reason to
fight, otherwise these debates would stop surfacing so
frequently. To state the obvious, one side argues in favor of
lesser amounts, while the other side argues for greater intakes.
Less obvious is the fact that different scenarios/goals create
different demands, and the current body of research has not
horoughly investigated all scenarios. t

Instead of discussing food sources or subtypes, it will be
assumed that were discussing high-quality protein. For a
thorough discussion of protein quality, see Millward et al.
1
Its
also assumed that were discussing the healthy population, since
the protein requirements of certain disease states may not
necessarily apply here. As much as possible, Ill avoid adjacent
topics such as effects on kidney & bone, which would warrant
their own article at best, and at worst just pull the current article
off-topic. Timing issues were covered last month, so this article
will be looking specifically at protein amount.

S

trength & endurance research versus the RDA
The current RDA for protein for adults is 0.8g/kg. This amount
is defined as sufficient ...to meet the known nutrient

needs for
practically all healthy people
2
According to the latest Dietary
Reference Intake (DRI) report, more than this is not necessary,
even for endurance or strength athletes. To quote them directly
(keep in mind that this is from a 2005 publication):
3

In view of the lack of compelling evidence to the contrary, no
additional dietary protein is suggested for healthy adults
undertaking resistance or endurance exercise.

Given such a recent authoritative dismissal of
recommendations above the RDA, its understandable that folks
who maintain a textbook knowledge of nutrition will fall on the
conservative side. Those who stay more current with the
scientific literature will definitely take issue with the claim that
the RDA is sufficient for all, including strength and endurance
athletes. The most recent scientific literature reviews and
position stands collectively list a range of 1.2-2.0g/kg,
4-7
with
one review pushing the upper end of its recommendation to
2.2g/kg.
8
These figures exceed the RDA by 50-175%. Given this
abundance of contrary research, its plainly false to claim that
the RDA is sufficient or optimal for most athletes and physically
ctive individuals. a

Non-athlete populations can also benefit from protein intakes
beyond the RDA. For example, in a tightly controlled 14-week
trial, Campbell et al observed that elderly subjects consuming
the RDA for protein (0.8g/kg) experienced a significant loss of
mid-thigh muscle area, despite consuming their projected
maintenance kcals.
9
Notably, these subjects age ranged 55-77
years, and the RDA for adults older than 70 remains at 0.8g/kg.
Keep in mind that this study & several others were published
years before the latest DRI report, so they had ample time to
make adjustments in their recommendations but failed to do
so. I, for one, am extremely curious about whether or not the
RDA for protein will be updated in the next edition. As long as
the RDA remains unchanged, the textbook worms (as opposed to
the Pubmed worms) have at the very least, a perceived
authoritative basis for their beliefs.

L

ower needs: energy maintenance & surplus
Certain circumstances decrease the demand for protein. When
overall kcals are adequate for maintaining or gaining
bodyweight, protein demands are lower compared to when a
kcal deficit is sustained chronically for weight loss.
7
A seldomly
discussed potential cause for reduced protein demand is habitual
or maintenance-level (as opposed to progressive) exercise over
time. Nearly 3 decades ago, Butterfield and Calloway found that
individuals subjected to chronic exercise actually showed an
increase in the efficiency of dietary protein utilization, despite
consuming only 0.57g/kg.
10
This adaptive protein economy was
indicated by an increase in nitrogen balance as the study
progressed. However, its important to note that this increased
efficiency was seen under caloric balance & surplus conditions,
with low-intensity exercise. Subsequent research using more
physically demanding protocols has yielded different results,
which Ill discuss in the forthcoming section.

Even for the goal of gaining muscular size (& strength), protein
demands decrease as athletes progress toward their potential. In
the earlier stages of an athletes development, dietary protein
surpluses are more prone to be used for muscle protein synthesis.
This is why I favor setting goals based on target bodyweight,
which is a surrogate measure of target lean mass. As the
athletes level of hypertrophy increases, so does the proximity to
the ceiling of growth for the given programming phase. The
curve of progress slows down and flattens out as equilibrium is
reached. In short, advanced athletes need (proportionally) less
protein to maintain their mass than they needed to attain it.
Bearing this in mind, some researchers can take their
conservative stance a bit too far. For example, Ill quote a review
y Phillips:
11
b

...in highly trained powerlifters and bodybuilders, in whom
muscle mass is high but stable, it is unlikely that their dietary
protein requirements are elevated much more than those of a
edentary person. s

In support of the above claim, Phillips cites research by
Tarnopolsky et al, who found that elite bodybuilders were able
to maintain their lean body mass at a protein intake of 1.05 g/kg,
which indeed was significantly less than their habitual intake of
2.7g/kg, yet only slightly more than the sedentary controls who
consumed 0.84 g/kg. However, Phillips neglected to mention the
short duration of the study period (10 days), the small sample
size (6 bodybuilders), and the fact that 2 of the 6 fell into
negative nitrogen balance by the 10th day. Furthermore,

Tarnopolsky et al noted that certain conditions such as levels of
very high training intensity, reduced energy intake, and reduced
proportion of carbohydrate can potentially drive up protein
equirements above what they observed in their study. r

On a related note, Phillips mentions that carbohydrate is
protein-sparing. In academic & sports nutrition circles, this is
another way of saying that carbs help the body retain muscle
protein. The support for this clich is research by Richardson et
al, who found that a diet with twice the proportion of carbs than
fat preserved nitrogen balance better than a diet with equal
proportions of carbs and fat.
13
This protein-sparing effect was
more pronounced in subjects who lost weight than those who
gained weight. However, the big confounder here is that protein
intake was set low (0.57 g/kg), which greatly compromises the
relevance of this data, which continues to be referenced by folks
on the carb-happy side of the fence. As well soon see, while
carbohydrate has a protein-sparing effect under certain
conditions, its actually dietary protein that has the most potent
protein-sparing effect.

H

igher needs: energy deficit (or increased training demand)
The benefits of increasing protein beyond the RDA become
concretely apparent when an energy deficit is imposed, and these
benefits are enhanced with the inclusion of training. For
example, in a 10-week trial, Layman et al compared the RDA
(0.8g/kg) with double that (1.6g/kg).
14
The high-protein group
lost less lean mass and more fat mass. Blood lipid profile and
glucose control improved to a greater degree in the high-protein
group as well. A subsequent study by Layman et al with the
same diet set-up included two extra treatments that had a
structured exercise regimen (5 days of walking, 2 days of
resistance training per week).
15
Only the training group
consuming double the RDA preserved lean mass. The high-
protein groups in each study reported greater satiety. Meckling
& Sherfey saw no lean mass losses in any groups when they
compared a 1:1 and 3:1 ratio of carbohydrate to protein
probably due to instrument error; BIA was used).
16
(

A notable detail is that both of the diets in Layman et als
research were 1700 kcal. As such, they were not severe in their
energy restriction; thus its unsurprising that only 1.6g/kg plus
exercise (including resistance training) was able to prevent lean
mass loss. Along these lines, Demling & Desantis subjects were
able to maintain and even gain lean mass & strength in a mild
energy deficit (20% below predicted maintenance) by
consuming 1.5g/kg and undergoing an exercise regimen that
ncluded resistance training.
17
i

Given the above, its not surprising that when Noakes et al put
non-exercising subjects on a 1377 kcal diet of either 34% protein
(1.3 g/kg) or half of that, neither treatment preserved lean
mass.
18
Oddly, there was no significant difference in body
composition change between groups. Predictably, the higher-
protein group showed a greater reduction in triacylglycerol
levels. In a study by Leidy et al comparing 30% protein diet
(1.4g/kg) versus 18% (0.8g/kg) within roughly 1530 kcals,
19
the
igh protein group lost less lean mass. h

Pikosky et al examined the effect differing protein intakes under
an exercise-induced energy deficit (1000 kcal was expended on
top of maintenance diet conditions).
21
The group consuming
1.8g/kg was able to maintain nitrogen balance while the
consuming 0.9g/kg fell into negative nitrogen balance. However,
this studys 1-week deficit period may have been too short to
raw any firm conclusions. d

As mentioned in the previous section, during a chronic energy
surplus or maintenance, the demand for protein to protect against
lean tissue loss decreases. However, if the nature of the training
(volume and/or intensity) is progressive, then protein needs can
remain high rather than progressively diminish as long as
ncreased demands are presented. i

Collectively, this body of research suggests that for individuals
who are not already well-trained or possessing a high level of
athletic conditioning, consuming protein at approximately
1.5g/kg is the minimum amount required to prevent loss of lean
mass in an energy deficit as long as a resistance training
program is in place. Without the training, preventing lean losses
would drive up the protein requirement.

I

ncreased needs for athletic subjects in an energy deficit
Unlike the abundance of studies on overweight, obese, and
deconditioned subjects, the literature specifically examining the
protein needs of already well-trained athletic subjects put in
hypocaloric conditions is surprisingly scarce. To my knowledge,
only 3 studies to-date fit these criteria.

The earliest is by Walberg et al, who compared the effect of
0.8g/kg with 1.6g/kg on weight lifters.
22
Although no significant
differences in body composition were seen, the higher-protein
treatment kept nitrogen balance positive while the lower-protein
treatment allowed it to fall into the negative, which would
indicate an increased risk for muscle loss over time. Regardless
of the positive nitrogen balance shown in the higher protein
group, both groups lost lean mass; just more was lost in the
ower-protein group. l

Next up, Mourier et al set out to test the effect of a BCAA-
enriched treatment, but also tested different protein levels under
hypocaloric conditions, and saw primarily a fat loss advantage in
the high-protein BCAA-enriched treatment.
23

Over two decades elapsed before the publication of the next
study on athletic subjects in hypoenergetic conditions. Mettler et
al compared 1.0 g/kg with 2.3 g/kg and saw significantly less
lean mass loss in the higher-protein group.
24
The fact that lean
mass loss occurred at all opens the possibility that even 2.3 g/kg
wasnt enough, and a higher proportion of protein may have
completely guarded against LBM loss. An alternate possibility is
that the deficit (60% of maintenance needs) is too aggressive for
lean mass retention in well-trained/athletic subjects regardless of
proportional intake of protein.

C

onclusions, applications, & future directions
Its gradually becoming apparent that optimal protein
requirements for athletes and physically active folks vary rather
widely, depending on a number of factors. The most recent
reviews and position papers collectively list a range of 1.2-
2.2g/kg. The demand for a surplus of protein intake diminishes
as the hypertrophy and/or strength goal draws closer, and

maintenance is approached, while an efficiency of utilization
occurs. However, the initiation of an increased level of
physiologic stress (ie, higher training intensity and/or volume)
can re-establish inefficiency, thus raising protein demand.

Theres a lack of solid or consistent justification for different
protein requirements between strength and endurance athletes.
The only thing thats relatively certain is that the RDA of 0.8
g/kg is often insufficient to prevent adverse effects on body
composition and various metabolic indexes when compared to
greater amounts (approximately 1.5 g/kg and up). In light of the
latest research indicating the anticatabolic benefit of intakes as
high as 2.3 g/kg, the academics need to swallow their pride and
admit that the cheesy physique media were not out of line in
their traditional recommendation of a gram per pound. This is
especially true, considering that physique sports involve periodic
phases of prolonged and often severe energy deficits.
In my practice, protein usually fluctuates somewhere between 2-
3g/kg (0.9-1.36g/lb) of target bodyweight, which is a proxy for
lean mass, with a small safety margin. Im not squeamish about
going as low as 1.2g/kg (0.54g/lb) for some individuals who
either are not in an energy deficit, or are simply not focused on
gaining or retaining muscle. As a trivial tidbit, anyone who
wants to balk at the higher end of what I work with (3.0g/kg), a
recent 3-week trial by J akobsen et al found this exact dose (but
applied to total bodyweight) to better improve reaction time
than 1.5 g/kg.
25
As for clinical concerns, no adverse effects were
seen on albuminuria or creatinine clearance.

Its worth mentioning that the assessment of protein
requirements is quite an art in itself, since much of it is based on
nitrogen balance, which has its fair share of limitations. The
most consistent error is an overestimation of nitrogen status. In
recognizing its shortcomings, the use of metabolic tracers
concurrently with nitrogen measurement is being done to narrow
he error margin. t

My personal preference would be to see more assessments of
performance & body composition endpoints, since nitrogen
balance and molecular data can often be immaterial. What would
hold more practical weight than nitrogen balance data or micro-
markers of proteolysis would be to test how well strength and/or
endurance can be maintained on various protein levels during
prolonged energy deficits. Such investigations are scarce at best.
Id also like to see the comparative effects of solid versus
powdered proteins, as well as isolated amino acids versus whole
proteins (in either powder or flesh form) on both body
composition and performance.

Another interesting line of investigation would be to compare
linear and nonlinear distributions of protein throughout the
week. For example, 3.0 g/kg on 3 days & 1.5 g/kg 4 days versus
2.14 g/kg each day of the week. Rounding out my wish list
would be studies examining the impact of varying protein
intakes while on versus off creatine (and other common
supplements or drugs), and how the outcomes might vary
depending on chronic energy balance.

Overall, its apparent to me that we have an abundance of data to
give sound practical recommendations for protein intake in
various conditions. However, due to a general disregard for
context when discussing protein requirements, I sense that the
debating is far from over.

References

1. Millward DJ , et al. Protein quality assessment: impact of expanding
understanding of protein and amino acid needs for optimal health. AmJ
Clin Nutr. 2008 May;87(5):1576S-1581S. [Medline]
2. National Research Council: "Recommended Dietary Allowances. Protein
and Amino Acids," 10th ed. Washington DC: National Academy Press,
pp.52 77,1989.
3. Institute of Medicine. Dietary Reference Intakes for energy, carbohydrate,
fiber, fat, fatty acids, cholesterol, protein, and amino acids. The National
Academies Press, Washington DC, 2005. [full report - PDF]
4. Kreider RB, Campbell B. Protein for exercise and recovery. Phys
Sportsmed. 2009 J un;37(2):13-21. [Medline]
5. Rodriguez NR, et al. Position of the American Dietetic Association,
Dietitians of Canada, and the American College of Sports Medicine:
Nutrition and athletic performance. J Am Diet Assoc. 2009
Mar;109(3):509-27. [Medline]
6. 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]
7. Tipton KD, Wolfe RR. Protein and amino acids for athletes. J Sports Sci.
2004 J an;22(1):65-79. [Medline]
8. Wilson J , Wilson GJ . Contemporary issues in protein requirements and
consumption for resistance trained athletes. J Int Soc Sports Nutr. 2006 J un
5;3:7-27. [Medline]
9. Campbell WW, et al. The recommended dietary allowance for protein may
not be adequate for older people to maintain skeletal muscle. J Gerontol A
Biol Sci Med Sci. 2001 J un;56(6):M373-80. [Medline]
10. Butterfield GE, Calloway DH. Physical activity improves protein
utilization in young men Br J Nutr. 1984 Mar;51(2):171-84. [Medline]
11. Phillips SM. Protein requirements and supplementation in strength sports.
Nutrition. 2004 J ul-Aug;20(7-8):689-95. [Medline]
12. Tarnopolsky MA, et al. Influence of protein intake and training status on
nitrogen balance and lean body mass. J Appl Physiol. 1988 J an;64(1):187-
93. [Medline]
13. Richardson DP, et al. Quantitative effect of an isoenergetic exchange of fat
for carbohydrate on dietary protein utilization in healthy young men. AmJ
Clin Nutr 1979;32:2217. [Medline]
14. Layman DK, et al. A reduced ratio of dietary carbohydrate to protein
improves body composition and blood lipid profiles during weight loss in
adult women. J Nutr. 2003;133:4117. [Medline]
15. Layman DK, et al. Dietary protein and exercise have additive effects on
body composition during weight loss in adult women. J Nutr.
2005;135:190310. [Medline]
16. Meckling KA, Sherfey R. A randomized trial of a hypocaloric high-protein
diet, with and without exercise, on weight loss, fitness, and markers of the
metabolic syndrome in overweight and obese women. Appl Physiol Nutr
Metab. 2007;32:74352. [Medline]
17. Demling RH, DeSanti L. Effect of a hypocaloric diet, increased protein
intake and resistance training on lean mass gains and fat mass loss in
overweight police officers. Ann Nutr Metab. 2000;44(1):21-9. [Medline]
18. Noakes M, 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. AmJ Clin Nutr. 2005;81:1298306. [Medline]
19. Leidy HJ , et al. Higher protein intake preserves lean mass and satiety with
weight loss in preobese and obese women. Obesity (Silver Spring). 2007
Feb;15(2):421-9. [Medline]
20. Walberg J L, Leidy MK, Sturgill DJ , Hinkle DE, Ritchey SJ , Sebolt DR.
Macronutrient content of a hypoenergy diet affects nitrogen retention and
muscle function in weight lifters. Int J Sports Med. 1988;9(4):2616.
[Medline]
21. Pikosky MA, et al. Increased protein maintains nitrogen balance during
exercise-induced energy deficit. Med Sci Sports Exerc. 2008
Mar;40(3):505-12. [Medline]
22. Walberg J L, Leidy MK, Sturgill DJ , Hinkle DE, Ritchey SJ , Sebolt DR.
Macronutrient content of a hypoenergy diet affects nitrogen retention and
muscle function in weight lifters. Int J Sports Med. 1988;9(4):2616.
[Medline]
23. Mourier A, et al. Combined effects of caloric restriction and branched-
chain amino acid supplementation on body composition and exercise
performance in elite wrestlers. Int J Sports Med. 1997 J an;18(1):47-55.
[Medline]
24. Mettler S, et al. Increased protein intake reduces lean body mass loss
during weight loss in athletes. Med Sci Sports Exerc. 2010 Feb;42(2):326-
37. [Medline]
25. J akobsen LH, et al. Effect of a high protein meat diet on muscle and
cognitive functions: A randomised controlled dietary intervention trial in
healthy men. Clin Nutr J an 2011 [in press] [Clin Nutr]


Enhanced amino acid sensitivity of myofibrillar protein
synthesis persists for up to 24 h after resistance
xercise in young men. e

Burd NA, et al. J Nutr. 2011 Feb 2. [Epub ahead of print]
[Medline]

BACKGROUND: We aimed to determine whether an exercise-
mediated enhancement of muscle protein synthesis to feeding
persisted 24 h after resistance exercise. We also determined the
impact of different exercise intensities (90% or 30% maximal
strength) or contraction volume (work-matched or to failure) on
the response at 24 h of recovery. METHODS: Fifteen men (21
1 y, BMI =24.1 0.8 kgm(-2)) received a primed, constant
infusion of l-[ring-(13)C(6)]phenylalanine to measure muscle
protein synthesis after protein feeding at rest (FED; 15 g whey
protein) and 24 h after resistance exercise (EX-FED).
Participants performed unilateral leg exercises: 1) 4 sets at 90%
of maximal strength to failure (90FAIL); 2) 30% work-matched
to 90FAIL (30WM); or 3) 30% to failure (30FAIL). RESULTS:
Regardless of condition, rates of mixed muscle protein and
sarcoplasmic protein synthesis were similarly stimulated at FED
and EX-FED. In contrast, protein ingestion stimulated rates of
myofibrillar protein synthesis above fasting rates by 0.016
0.002%/h and the response was enhanced 24 h after resistance
exercise, but only in the 90FAIL and 30FAIL conditions, by
0.038 0.012 and 0.041 0.010, respectively. Phosphorylation
of protein kinase B on Ser473 was greater than FED at EX-FED
only in 90FAIL, whereas phosphorylation of mammalian target
of rapamycin on Ser2448 was significantly increased at EX-FED
above FED only in the 30FAIL condition. CONCLUSION: Our
results suggest that resistance exercise performed until failure
confers a sensitizing effect on human skeletal muscle for at least
24 h that is specific to the myofibrillar protein fraction.
SPONSORSHIP: Supported by a grant from the Natural
Sciences and Engineering Research Council of Canada

S

tudy strengths
This study examined a number of understudied parameters
affecting muscle protein synthesis. While the combined effects
of exercise and feeding have often been studied in the
immediate-term (1-4 hours postexercise), a less studied effect is
protein feeding on muscle protein synthesis 24 hours later. Also,
a topic of great controversy is whether or not its optimal to take
sets to failure. This study adds to this body of knowledge by
comparing failure vs work-matched protocols of different
intensities (Ill touch upon the limitation here in a bit). Another
notable design strength was the measurement of varying types of
muscle protein synthesis (mixed, sarcoplasmic, and
myofibrillar). Recreationally active subjects with prior resistance
training experience were used, minimizing the variability of
response inherent with untrained subjects.

Study limitations

The most glaring limitation is the short-term nature of the trial.
Its not certain how any of the outcomes would manifest in terms
of size and strength gains over a period of weeks or months.
Another limitation was the choice of intensities compared (30%
vs 90% of 1RM). A relatively recent, exhaustive review by
Wernbom et al, found that the greatest rate of hypertrophy
tended to occur at 60-85% of 1RM.
1
Notably, the Wernbom
review examined the (admittedly limited) body of research that
measured concrete endpoints such as muscle cross-sectional
area. Given that this sweet spot lies between the intensities
compared in the present study, its puzzling why the authors did
not include or employ a moderate-intensity arm. This design
limitation was also seen in a previous study by Burd et al, which
oddly enough found that 30% of 1RM was more effective than
90% 1RM for stimulating acute measures of muscle anabolism.
2

C

omment/application
The primary finding of this study was that exercise-induced
increases in muscle protein synthesis and molecular signaling
via protein feeding persisted for at least 24 hours after the
resistance training bout. Furthermore, this sensitizing effect of
exercise was seen most prominently in the treatments where sets
were taken to failure, with no significant difference between the
30% & 90% of 1RM conditions. The authors stressed the
importance of measuring different protein fractions, since,
myofibrillar muscle protein synthesis was seen in both the 30%
& 90% of 1RM treatments, but no significant effects were seen
in mixed and sarcoplasmic muscle protein. This specificity
toward the myofibrillar fraction of muscle protein carries is
important since sarcoplasmic constituents might be more subject
to hydration flux. This carries the implication that research
neglecting to examine the changes in a range of muscle protein
ractions may be susceptible to false-negative results. f

The authors assert that regardless of intensity, the recruitment of
type II fibers during resistance training is critical for maximizing
muscle protein synthesis. They propose that this is achievable
through maximal fiber activation, which in this case was seen by
taking the sets to failure. To quote them directly, We speculate
that protocols eliciting maximal fiber recruitment (i.e. both type
I and type II fibers using manipulations of load and volume to
induce fatigue) during exercise are critical to optimize the
sensitivity of muscle to protein feeding for at least 24 h
ostexercise recovery. p

With the above said, the authors admit that given the current
studys methods, its not possible to definitively conclude that
the muscular receptivity to feeding after exercise is fiber type-
dependent. In support of the speculation that this is so, they cite
research by Robergs et al,
3
who found that resistance training at
35% of 1RM (work-matched with a comparative treatment of
70% of 1RM) indeed was able to recruit type II fibers. They
continue to speculate that the present studys protocol was able
to recruit type II fibers in the lower-intensity (30% of 1RM)
treatment due to a longer activation period, and not necessarily
ue to percentage of 1RM per se. d

These findings lend further refutation to the common idea of an
anabolic window typically described as a short period
postexercise wherein feeding of protein and/or carbohydrate has
special effects on anabolism. As discussed in last months
nutrient timing update, this window of opportunity is a non-issue
in most cases where daily macronutrient targets are hit. The
present study indicates a much wider window (at least 24 hours).
Protein choices targeting thermogenesis and
metabolism.
Acheson KJ , et al. Am J Clin Nutr. 2011 J an 12. [Epub ahead of
print] [Medline]

BACKGROUND: Dietary proteins stimulate thermogenesis and
satiety more than does carbohydrate or fat; however, less is
known about the differences between protein sources.
OBJECTIVE: The objective was to determine the differential
effects of 3 proteins on energy metabolism, satiety, and glucose
control. DESIGN: Energy metabolism, satiety, and glucose
control were measured in 23 lean, healthy subjects on separate
occasions, before and 5.5 h after consumption of 4 isocaloric test
meals in a randomized, double-blind, crossover design. Three
meals consisting of 50% protein (whey, casein, or soy), 40%
carbohydrate, and 10% fat and a fourth meal consisting of 95.5%
carbohydrate were compared with a glucose meal that provided
the same glucose load as the protein meals. RESULTS: The
thermic effect was greater after the whey (14.4 0.5%) than
after the casein (12.0 0.6%; P =0.002) and soy (11.6 0.5%;
P =0.0001) meals and was greater after the whey, casein, and
soy meals than after the high-carbohydrate meal (6.6 0.5%; P
<0.0001). Cumulative fat oxidation tended to be greater after
the whey meal (16.2 1.1 g) than after the soy meal (13.7 1.0
g; P =0.097) and was greater after the whey and soy meals than
after the high-carbohydrate meal (10.9 0.9 g; P <0.05). The
glycemic response to glucose was attenuated 32% by the
proteins (P <0.001) at the expense of a greater insulin response
after whey than after glucose (154%; P =0.02), casein (143%; P
= 0.07), and soy (151%; P = 0.03). Subjective appetite
sensations indicated that casein and soy were more satiating than
whey (P <0.01), but whey was more "liked" compared with
casein and soy (P = 0.025 and P = 0.09, respectively).
CONCLUSIONS: he results suggest that different protein
sources could be used to modulate metabolism and subsequently
energy balance. SPONSORSHIP: Supported by Nestec SA,
Vevey, Switzerland.

S

tudy strengths
This study addresses the interesting question of how different
protein types may affect thermogenesis, satiety, and fat
oxidation. This can have important implications for diet design
with the goal of weight/fat loss in mind (at least in theory). A
high degree of control was necessary to execute this study.
Subjects attended the Metabolic Unit on the day before each test
and consumed a lab-provided menu for breakfast, lunch, and
dinner. This was repeated with exactly the same ingredients on
the days before each of the other tests. After the evening meal,
subjects spent the night in the Metabolic Unit. Meals were
designed on the realistic side, although a bit low in fat. Each
meal was 20% of the projected daily kcal requirement, and
consisted of 50% protein, 40% carbohydrate, and 10% fat.

S

tudy limitations
This type of study just begs for a longer-term follow-up,
preferably one involving a structured training program. The
subjects used in this study were lean, but sedentary. The additive
or interactive effects of training and feeding would provide some
potentially valuable data. Although the 5.5 hr test period was
reasonably long; it wasnt quite long enough for the elevations
of each parameter to return to baseline. This criticism circles
back to the need for a follow-up trial lasting several weeks in
order to assess the impact on what really matters in this case -
body composition.

Comment/application

As shown above, the protein-containing meals predictably
stimulated more energy expenditure than the carbohydrate meal.
Importantly, the whey protein meal evoked more energy
expenditure than the casein or soy meal, whose responses did not
significantly differ. Fat oxidation was greatest in the whey group,
with casein, soy, and carbohydrate placing below it (respectively).
Although the tendency was in favor of whey, not statistically
significant differences in fat oxidation were seen among the 3
protein meals.
Glycemic effect was not significantly different among the
protein meals. When expressed as the glycemic index the 4
treatments measured as follows: glucose (100%), whey (33%),
casein (36%), soy (32%), isocaloric high-carbohydrate meal
(129%). Whey elicited a greater insulin response than the rest of
the protein-containing meals, and predictably more so than the
glucose treatment which had an equal amount of carbohydrate as
the protein meals (see below):

Its notable that the whey treatments effect on fat oxidation was
greater than the rest of the protein-containing meals despite its
greater stimulation of insulin. A potential explanation for this is
the whey treatments higher glucagon response following the
insulin response, but the authors cite work questioning the role
of glucagon in the regulation of adipose tissue lipolysis.
4
Casein
and soy were more satiating than whey, which is somewhat
unexpected, given past research finding whey more satiating
than casein.
5
Adding to the equivocal body of data, recent
research found casein to be more satiating than soy or whey, but
found soy to have the highest thermic effect, and whey to elicit
the lowest respiratory quotient (indicating greater fat oxidation).
6

While these results are interesting, theres a lack long-term trials
comparing these proteins specifically for weight/fat loss.


Daily consumption of vitamin D- or vitamin D +
calcium-fortified yogurt drink improved glycemic
control in patients with type 2 diabetes: a randomized
linical trial. c

Nikooyeh B,, et al. Am J Clin Nutr. 2011 Feb 2. [Epub ahead of
print] [Medline]
BACKGROUND: Low serum concentrations of 25-
hydroxyvitamin D [25(OH)D] have been associated with
impaired glucose tolerance and diabetes. DESIGN: Ninety
diabetic subjects were randomly allocated to 3 groups to
consume plain yogurt drink (PY; containing no vitamin D and
150 mg Ca/250 mL), vitamin D-fortified yogurt drink (DY;
containing 500 IU vitamin D(3) and 150 mg Ca/250 mL), or
vitamin D +calcium-fortified yogurt drink (DCY; containing
500 IU vitamin D(3) and 250 mg Ca/250 mL) twice per day for
12 wk. Fasting serum glucose (FSG), glycated hemoglobin (Hb
A(1c)), homeostasis model assessment of insulin resistance
(HOMA-IR), serum lipid profile, and percentage fat mass (FM)
were assessed before (baseline) and after the
intervention. RESULTS: RESULTS: In both the DY and
DCY groups, mean serum 25(OH)D(3) improved (+32.8 28.4
and +28.8 16.1 nmol/L, respectively; P <0.001 for both), but
FSG [-12.9 33.7 mg/dL (P =0.015) and -9.6 46.9 mg/dL (P
=0.035), respectively], Hb A(1c) [-0.4 1.2% (P <0.001) and -
0.4 1.9% (P <0.001), respectively], HOMA-IR [-0.6 1.4 (P
= 0.001) and -0.6 3.2 (P < 0.001), respectively], waist
circumference (-3.6 2.7 and -2.9 3.3, respectively; P <0.001
for both), and body mass index [in kg/m(2); -0.9 0.6 (P <
0.001) and -0.4 0.7 (P = 0.005), respectively] decreased
significantly more than in the PY group. An inverse correlation
was observed between changes in serum 25(OH)D(3) and FSG
(r =-0.208, P =0.049), FM (r =-0.219, P =0.038), and HOMA-
IR (r = -0.219, P = 0.005).
CONCLUSIONS: CONCLUSION: Daily intake of a vitamin
D-fortified yogurt drink, either with or without added calcium,
improved glycemic status in T2D patients. This trial was
registered at clinicaltrials.gov as NCT01229891.
SPONSORSHIP: Supported by the National Nutrition and Food
Technology Research Institute.

S

tudy Strengths
This study is conceptually strong because it simultaneously
examines two major health issues in the world today. According
to Holick,
7
an estimated 1 billion people on Earth have varying
degrees of vitamin D deficiency. Diabetes is considered the
worlds most widespread endocrinologic disorder. Aside from
being a randomized controlled trial & not merely observational,
an important design strength missing from previous studies was
a sufficiently large dose (500 IU) of a bioavailable form of
vitamin D (cholecalciferol). Compliance was bolstered by
checking consumption check-off charts, counting empty bottles,
and weekly phone communication with the research staff.

Study limitations

Bioelectrical impedance analysis (BIA) was used to assess body
composition. BIA has questionable accuracy compared to dual-
energy X-ray absorptiometry (DXA).
8
BIA may be adequate for
tracking differences in groups, but not individuals.
9
As
mentioned by the authors, intake of the yogurt drinks were self-
reported by the subjects, and no practical approach was used to
control the intakes. Dietary intake monitoring was minimal. A
24-hour recall questionnaire was used to assess dietary intake at
the start and end of the trial, and this has obvious reliability
limitations. Furthermore, although this trial was longer than
most of its predecessors, the authors considered 12 weeks a
potential limitation of what might be seen beyond that duration.

C

omment/application
Vitamin D status was suboptimal in 70% of the subjects at the
start, and this was reduced to 15% by the trials end. Expectedly,
no change in vitamin D status occurred in the non-fortified plain
yogurt (PY) group. A significant decrease in serum insulin,
glucose, HOMA-IR (indicating improved insulin sensitivity),
and HbA1c (indicating improved glucose tolerance) occurred in
the D-fortified yogurt group (DY) and the D+calcium-fortified
ogurt group (DCY), but not so with the PY group. y

No significant differences were seen among the groups with
respect to energy or macronutrition. On the outset of the trial, the
subjects were instructed to consume a weight-maintenance diet
based on the American Diabetes Association (ADA)
guidelines.
10
However, these guidelines are still stuck in the
aging carbohydrate-dominant paradigm. This is ironic, since
type 2 diabetes is essentially a malfunction of carbohydrate
metabolism. The ADA guidelines call for a protein intake of 15-
20% of total kcals. In the first place, protein recommendations
should be based on either lean body mass or a surrogate such as
ideal body weight). Secondly, this recommendation opens up the
possibility for deficiency, especially in the event of hypocaloric
regimes. Finally, the ADA doesnt issue a concrete
recommendation for total fat, but they call for a maximum of
10% of kcals from saturated fats, and roughly 10% from
polyunsaturated fats. No concrete recommendations for
carbohydrate are given, which again, is ironic. Assuming that
another 10% of total kcals might come from other fats, this still
leave carbohydrate as the dominant macronutrient. One of the
simplest, most reliable tactics for improving glycemic control in
iabetics is reducing the intake of usable carbohydrate.
11,12
d

Given the large proportion of vitamin D-deficient subjects
entering the trial, as well as the known positive association of
vitamin D with improved glycemic status, its not too surprising
that this correlation was confirmed in this controlled
intervention. However, whats intriguing is the decreased waist
circumference and bodyweight in the DY & DCY groups
compared to the PY group. Taking a closer look, although these
differences were statistically significant, the actual changes were
modest, especially for a 12-week duration. Specifically, the PYs
weight decrease was 0.1 kg, compared to the 2.1 kg & 1.1 kg
decreases in DY & DCY, respectively. As for waist
circumference, the differences were similarly unremarkable.
PYs decrease was 1.1 cm, compared to the 3.6 cm & 2.9 cm in
DY & DCY, respectively. Confidence in the reproducibility of
these results is difficult, given that dietary intake was self-
reported. Thus, correcting vitamin D deficiency appears to
improve glycemic control, and possibly body composition as
well, but Id like to see further confirmation of the latter
parameter in research with tighter dietary control.
Branched-chain amino acid supplementation lowers
perceived exertion but does not affect performance in
ed males.

untrain
Greer BK. et al. J Strength Cond Res. 2011 Feb;25(2):539-44.
[Medline]
BACKGROUND/ OBJECTIVE: The purpose of this study
was to determine whether branched-chain amino acid (BCAA)
supplementation affects aerobic performance, ratings of
perceived exertion (RPE), or substrate utilization as compared
with an isocaloric, carbohydrate (CHO) beverage or a noncaloric
placebo (PLAC) beverage. DESIGN: Nine untrained males
performed three 90-minute cycling bouts at 55% &OV0312;o2
peak followed by 15-minute time trials. Subjects, who were
blinded to beverage selection, ingested a total of 200 kcal via the
CHO or BCAA beverage before and at 60 minutes of exercise or
the PLAC beverage on the same time course. RPE and metabolic
measurements were taken every 15 minutes during steady-state
exercise, and each of the trials was separated by 8 weeks. Plasma
glucose and BCAA concentrations were measured pre- and post-
exercise. RESULTS: A greater distance (4.6 0.6 km) was
traveled in the time-trial during the CHO trial than the PLAC
trial (3.9 0.4 km) (p <0.05). There was no difference between
the BCAA (4.4 0.5 km) and PLAC trials. RPE was reduced at
the 75-minute and 90-minute mark during the BCAA trial as
compared with the PLAC trial. There were no significant
differences found for the trial vs. time interaction in regard to
respiratory exchange ratio. CONCLUSIONS: Thus, CHO
supplementation improves performance in a loaded time-trial as
compared with a PLAC beverage. BCAA supplementation,
although effective at increasing blood concentrations of BCAA,
did not influence aerobic performance but did attenuate RPE as
compared with a PLAC beverage. SPONSORSHIP: Not listed.

S

tudy strengths
After a redundancy of non-caloric placebos for comparison
against BCAA in previous research, this is perhaps the first
study to compare the effect of a BCAA beverage to an isocaloric
treatment on aerobic performance (a total of 200 kcal of each
treatment). A repeated measures design alleviated some of the
degree of compromise in statistical power inherent in a small
sample (9 subjects). Detailed dietary intake records were taken
3 days prior, and the day of each training session, and analyzed
with software. Subjects were instructed to maintain similar
dietary patterns throughout the study. As an extra measure of
control, dietary choices on exercise testing days were not
permitted to change. A final strength was the use of a time trial,
where after a 90 minute steady-state period, the subjects
completed as much distance as possible within a 15 minute
period. This is more reflective of actual race conditions than
merely measuring time-to-exhaustion.

S

tudy limitations
Subjects competed the exercised tests after a 4-hour fast. This
would have been fine if a standardized meal (preferably dosed
proportionally to individual lean mass) was consumed prior to
the fast. A lack of standardization here opens up the possibility
of variations in residual amino acid levels in circulation from the
previous meal. Thus, testing in an overnight-fasted state would
actually have been more appropriate in this case. The study
measured acute effects, so longer-term effects remain
speculative.
Comment/application

As shown above, the BCAA (lowest line) treatment lowered the
rating of perceived exertion (RPE) beyond placebo at the 75 &
90 minute mark, whereas this effect of carbohydrate (middle
line) did not reach statistical significance. The authors noted that
since this reduction in RPE via BCAA did not translate to
improved performance, ...the central fatigue hypothesis may
not be a relevant issue in humans when exercise duration is less
than 105 minutes at intensities of 55% VO2 peak or below.

The authors conceded that the idea of increased blood levels of
BCAA reducing tryptophan entry into the brain & inhibiting
central fatigue is not likely to occur, at least in the conditions
tested. To give a bit of background, brain levels of serotonin are
affected by blood tryptophan levels, and the hypothesis is that
large, neutral amino acids like BCAA can compete with
tryptophan to cross the blood-brain barrier. Tryptophan is
converted to 5-hydroxytryptophan, and finally to serotonin,
which is associated with fatigue and the onset of sleep.
Alas, BCAAs widely assumed inhibitory effect on central
fatigue was not apparent here, but according to a review by
Gleeson,
13
this shouldnt necessarily be expected to occur in the
first place. To quote him directly, The assumption that
increased fTRP uptake leads to increased serotonin synthesis
and activity of serotoninergic pathways (i.e., increased synaptic
serotonin release) is a rather large leap of faith. He goes on to
present the logical proposition that if this hypothesis is correct,
then the converse must be true for tryptophan supplementation.
That is, supplemental tryptophan should hypothetically increase
brain serotonin production and thus induce central fatigue, and
adversely affect endurance. However, the evidence thus far has
repeatedly shown tryptophan supplementation to have no
detrimental effect on training performance.
14,15

While its tempting to assume that BCAA is a perfect
replacement for carbohydrate due to its lower RER & RPE, the
carb group nevertheless covered a greater cycling distance in the
time trial than the BCAA group although not to a degree of
statistical significance. The take-home application of this studys
outcomes would be to combine carbohydrate and BCAA (or an
easily absorbed BCAA-rich protein source such as whey isolate)
pre- and/or during endurance training to maximize work output
and minimize muscle protein breakdown.


Excessive fructose intake induces the features of
metabolic syndrome in healthy adult men: role of uric
a

cid in the hypertensive response.
Perez-Pozo SE, et al. Int J Obes (Lond). 2010 Mar;34(3):454-61.
[Medline]

BACKGROUND: Excessive fructose intake causes metabolic
syndrome in animals and can be partially prevented by lowering
the uric acid level. We tested the hypothesis that fructose might
induce features of metabolic syndrome in adult men and whether
this is protected by allopurinol. METHODS: A randomized,
controlled trial of 74 adult men who were administered 200 g
fructose daily for 2 weeks with or without allopurinol. Primary
measures included changes in ambulatory blood pressure (BP),
fasting lipids, glucose and insulin, homeostatic model
assessment (HOMA) index, body mass index and criteria for
metabolic syndrome. RESULTS: The ingestion of fructose
resulted in an increase in ambulatory BP (7+/-2 and 5+/-2 mm
Hg for systolic (SBP) and diastolic BP (DBP), P<0.004 and
P<0.007, respectively). Mean fasting triglycerides increased by
0.62+/-0.23 mmol l(-1) (55+/-20 mg per 100 ml), whereas high-
density lipoprotein cholesterol decreased by 0.06+/-0.02 mmol
l(-1) (2.5+/-0.7 mg per 100 ml), P<0.002 and P<0.001,
respectively. Fasting insulin and HOMA indices increased
significantly, whereas plasma glucose level did not change. All
liver function tests showed an increase in values. The metabolic
syndrome increased by 25-33% depending on the criteria.
Allopurinol lowered the serum uric acid level (P<0.0001) and
prevented the increase in 24-h ambulatory DBP and daytime
SBP and DBP. Allopurinol treatment did not reduce HOMA or
fasting plasma triglyceride levels, but lowered low-density
lipoprotein cholesterol relative to control (P<0.02) and also
prevented the increase in newly diagnosed metabolic syndrome
(0-2%, P=0.009). CONCLUSIONS: High doses of fructose
raise the BP and cause the features of metabolic syndrome.
Lowering the uric acid level prevents the increase in mean
arterial blood pressure. Excessive intake of fructose may have a
role in the current epidemics of obesity and diabetes.
SPONSORSHIP: Support for this publication was provided by
generous funds from the Mateo Orfila Foundation.

Study strengths

With many current investigations concentrating their focus on
the potentially adverse health effects of fructose, this recent
study was (and still is) timely. This is perhaps the first study to
examine the effect of fructose-mediated increases in uric acid,
and whether this occurrence can be mitigated pharmacologically
(via allopurinol, a drug commonly used to treat gout). A
relatively large sample (74 subjects) was used. Subjects made 3
lab visits per week and were screened for side effects and
checked for compliance via submission of empty fructose
containers.

Study limitations

As acknowledged by the authors, the trial length was short (2
weeks). The experiment was not properly blinded. That is,
investigators and staff were aware of which participants were
receiving allopurinol. This opens up the possibility of
expectation bias from the investigators as well as the subjects.
Another limitation was the lack of a non-fructose carbohydrate
comparison treatment, which excludes the possibility of
claiming that fructose is uniquely adverse amidst the range of
commonly consumed carbohydrates. Furthermore, the subjects
randomized to allopurinol had higher baseline levels of uric acid
and BP, and also tended to have worse baseline measures of the
metabolic syndrome. This may have yielded a falsely low
herapeutic effect of the drug. t

Dietary intake was assessed via food frequency questionnaire
(FFQ), which is the standard tool for dietary intake assessment
in large epidemiological studies due to their relative ease of
administration & lack of expense. However, they are limited by
their retrospective nature and reliance on subjects
memory/perception of serving sizes and food types. Importantly,
FFQs often lack validation against objective reference methods
involving biomarkers that eliminate reporting bias. For example,
Schatzkin et al compared FFQ with doubly labeled water (DLW
the gold standard of assessing energy intake) during a 2 week
period and concluded the following:
16
Our results indicate that
the FFQ cannot be recommended as an instrument for
evaluating the absolute intakes of energy and protein in relation
to disease. In another example of its shortcomings, Schaefer et
al found that FFQs did not reliably estimate intakes of dietary fat
or cholesterol.
17
Notably, this assessment failure occurred in
subjects on diets containing foods of known composition. In
other words, the inaccuracy could not be blamed on exotic foods
or obscure recipes and combinations. In yet another example,
Kristal et al went as far as titling their critical review, Is it time
to abandon the Food Frequency Questionnaire?
18
They
definitely thought so.

Comment/application

The supplemental 200g dose of fructose evoked multiple
characteristics of the metabolic syndrome (increased fasting
triglycerides, decreased insulin sensitivity and decreased HDL).
Allopurinol was able to lower LDL-C, but was not able to
counteract the impairment in insulin sensitivity or increase in
triglyceride and fasting glucose. A novel finding of this study
was that the high intake of fructose was able to raise 24-hour
ambulatory blood pressure in humans. Interestingly, this effect is
only apparent in close proximity to the fructose ingestion (during
waking/ambulatory hours). Allopurinol blocked the increase in
both 24-hour ambulatory diastolic blood pressure and daytime
systolic & diastolic blood pressure brought on by the
xperimental fructose load. e

These outcomes may initially seem like a cause for panic, but
its important to maintain the proper perspective. A common
thread among fructose studies is the use of an artificially high
dose. In the present study, 200g fructose was imposed, adding to
a habitual daily intake of 55g. The total fructose intake of 255g
(34% of total kcal) is nearly four times the average intake in the
United States, which Marriott et al recently estimated to be 9.1%
of total kcal.
19
Those inclined to consume the extra 200g
fructose per day would be able to achieve it with 10 cans of non-
diet soda per day. Frankly, those who actually do that have far
greater problems than fructose per se.


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T

hings I learned in 2010 (mostly serious edition).
By Alan Aragon
____________________________________________________

I announced on Facebook that this issue would contain a review
of Tim Ferriss latest book, 4 Hour Body. Well, soon after that
announcement, I received an email from one of my ex-clients
and current AARR subscribers really hoping for a things I
learned in the previous year retrospective like Ive been doing
Since 2008. This pretty much stopped my plans in their tracks,
for a couple of reasons. First of all, its a potentially more
valuable & less frivolous writeup than a critique of some over-
the-top pop diet book. Secondly, based on some of the
responses, it became apparent that a fair amount of my readers
have already gotten their hands on Ferriss latest material, or
have already gotten a good whiff of it second-handedly from
other critiques. I still may give it a wringing-out at some point,
but I figured that can wait. Lets cover the important stuff first.
Here comes a random assortment of things (both on & off-topic)
that I learned in the past year. Some of it is video footage, and
ome of it may contain links that are not work-safe. s

1. In professional sports, you would assume that the health of
the athletes come first. This isnt always the case; in fact, it
often doesnt deviate far from the typical corporate churnm
& burnm routine. The longer an athletes career is, the
bigger pay he (or she) will potentially end up commanding.
So, theres not a huge incentive for the leagues powers-
that-be to do what they can to max-out the longevity of their
athletes. Why make sure that the athletes properly recover
from injury when theres always a new crop of talented,
injury-free rookies who will gladly play for a fraction of the
pay that the guys with seniority expect. This quote by my
friend & colleague Tom Vachet (trainer of more pro athletes
than anyone I know) captures the sentiment well:
At the end of the day, the process of healing an injury
requires a combination of smart medicine and patience.
Unfortunately, as I stated previously, patience is one of the
rarest commodities in the locker and training rooms of
collegiate and professional sports,

2. Paleos are very passionate, but many of them have a few
screws loose upstairs. Thats not a winning combination. A
perfect example is an unknown blogger named J ohn Berne,
vented to himself (since apparently no one reads his blog)
about my skepticism toward the Paleo diet. I mentioned in a
recent Fitcast podcast that the current research comparing
Paleo to other regimes does not match macronutrients
between treatments (Paleo groups either eat more protein or
less carbs). Unsurprisingly, he selectively listened, and
mistakenly thought that I claimed there was no research
comparing Paleo with an isocaloric treatment. Oh well, he
thinks he got me on that one, citing a study by Lindeberg et
al,
1
who found that the Paleo diet better improved glucose
tolerance in patients with ischemic heart disease than a
Mediterranean diet. But just like I mentioned, the Paleo diet
had 42% less carbohydrate than the Mediterranean diet, so
of-fawking-course glucose tolerance improvement would be
more pronounced in the lower-carb treatment. Alas, theres
nothing to stop the Paleos from attributing these effects to
their beloved diet-religion rather than the more logical
explanation that carbohydrate reduction has multiple
enefits for certain populations. b

But wait, heres the best part of his rant he actually
antasizes about killing me. Get a load of this: f

The only acceptable way I can see to deal with Alan for
viciously and callously attacking our dietary lifestyle is for
all Paleo adherents to immediately decide to, upon meeting
him, kill or maim him. One of us is bound to succeed
eventually. Like a jihad, only in English. Or maybe a good
old fashioned crucifixion. You don't see enough of those
anymore. No, I'm kidding. Seriously, I'm kidding.

3. The 1g of protein per pound of bodyweight guideline is still
viewed in most academic circles as a grossly excessive
artifact of bodybuilding lore. Even until the present, this
guideline is bashed as being unsubstantiated anecdote.
However, its finally beginning to gain legitimate scientific
support in scenarios where athletes are subjected to
prolonged hypocaloric conditions.
2

4. Nutrient timing around training has its place but that place
is more limited than I previously thought. Acute studies
have shown promise of timing protein or amino acids for the
goal of enhancing resistance training adaptations. But as far
as longer-term studies go, to my knowledge, only 2 studies
with matched total protein content (including supplemental
protein) have seen positive results,
3.4
while 5 have shown
zippo.
5-9
As things stand, its highly premature (& possibly
downright useless) to nitpick over perfect placement of
nutrients around the resistance training bout if youre
already nailing your macronutrient targets for the day.

5. Supplemental BCAA has been successfully used to
stimulate appetite in patients with anorexia.
11
Its a common
practice among certain athletes to supplement the diet with
BCAA while sustaining an energy deficit for weight loss.
The hope is that supplemental BCAA will minimize muscle
loss. For those with severe hunger issues, simply getting
enough whole intact protein (which contains BCAA
anyway) might better serve their goals than pouring fuel on
the fire of an already-raging appetite, regardless of the small
savings in kcals from isolated BCAA.

6. Rats are a poor model for human nutritional physiology,
especially when it comes to carbohydrate metabolism. De
novo lipogenesis (DNL) is the pathway by which
carbohydrate is converted to fat. Rodents are far more prone
to DNL than humans, which makes carbohydrate dosing
comparisons between humans and rats an exercise in
wishful speculation. To illustrate this quantitatively, heres a
quote a review by Sievenpiper et al:
12

Whereas DNL contributes 6070% TG in rodents, it only
contributes <5% TG in humans, under longer term,
isocaloric, high-carbohydrate feeding conditions.

7. Vitamin D deficiency is widespread,
13
but the state of panic
in the current slew of lay articles is not relayed as such in
recent systematic reviews.
14,15
For preserving normal
glucose control & insulin sensitivity and other measures of
cardiometabolic health, the research supports attempts to
guard against deficiency rather than mega-dosing. To
eiterate my own practical recommendations: r

A more logical/methodical approach would be to get the
test done first to see if youre within the normal range of
30.0-74.0 ng/mL This range translates to 74.8-184.7 nmol/L
(multiply the units listed in ng/mL by 2.496 if you need to
convert to nmol/L). If youre out of range, you can make
gradual adjustments (via diet, supplementation, or
increased sun exposure, or a combination). Either way, if
youre concerned enough, its wise to get your doctors
opinion.

A more subjective but simpler shotgun approach would be
to take supplemental vitamin D
3
(cholecalciferol) dosed at
1000-2000 IU per day.
16

8. Trans fatty acid (TFA) hysteria is generally overblown,
particularly in physically active populations whose diets
consist predominantly of whole and minimally processed
foods, and arent running unused caloric surpluses resulting
in over-fatness. While TFA in excess pose a host of health
concerns, theres no strong causal evidence indicating the
grave danger of moderate intakes.
17,18
This would especially
apply within the context of an overall healthy set of lifestyle
habits. Furthermore, it appears that ruminant-derived TFA
(from meat & dairy foods) poses less of a health threat than
industrially-derived TFA (from the hydrogenation of
vegetable oils).
19
Ultimately, these compounds have to be
put into the right perspective, and Meister & Kava do that
perfectly in this quote:
TFAs are not poison; they are simply one of several dietary
factors that affect blood lipid levels, and blood lipid levels
are only one of several major factors that influence the risk
of heart disease.

9. Resistance training is the confirmed champ of exercise
modes when it comes to the treatment & management of
type 2 diabetes. While the benefit of resistance training on
the markers of diabetes was seen as far back as the early
2000s, enough research has accumulated for us to conclude
that its indispensable in the optimization of treatment
particularly for patients with impaired glucose control.
20

This would undoubtedly translate positively for the
prevention of diabetes in those who are predisposed to the
disease.

10. At a protein dose (25g whey) known to maximally stimulate
muscle protein synthesis, additional carbohydrate (50g
maltodextrin) was unable to further enhance net muscle
protein balance after resistance training.
21
This finding
wasnt entirely too surprising given the work by Greenhaff
et al showing a rather modest upper threshold of insulin
elevation (15-30 mU/l) for maximally inhibiting muscle
protein breakdown.
21
The 25g protein dose raised insulin to
roughly 19 mU/l, so it was right within that range of this
appaently saturable response. r

Since the average bodyweight of the subjects used in this
study was 80 kg, the 25g protein dose works out to being
0.31g/kg. Of course, endurance goals can be a different
story from the goal of muscle anabolism. Its important to
note that this outcome may be limited to the training volume
used, which was relatively low (4 sets, 8-12 reps to failure
on the knee extension). Another caveat to this acute research
is that its still preliminary and thus far unconfirmed by
longer-term trials. Nevertheless, the practical message from
this data is that carbohydrate is not necessarily the
crucial/indispensable postexercise nutritional component
that its traditionally perceived to be, as long as sufficient
protein is consumed to max-out the anabolic response.

11. The infamous Shake Weight (official site here, warning:
video w/sound automatically plays) prompted one of the
funniest Saturday Night Live skits in the history of the show
(best quality version here, warning: strong sexual innuendo,
not safe for work). If you havent seen this before, prepare
to spit some coffee on your keyboard.

12. Apparently, the body is rather militant about survival and
driven toward homeostasis in ways we shouldnt be too
surprised about. For example, the body works extra hard to
make sure your muscle wont fly off of your bones if you
train in a fasted state. Deldicque et al found that at the
molecular level, the anabolic response to a
carb/protein/leucine postexercise meal was amplified to a
greater degree with fasted training rather than fed training
conditions.
22
Although this is likely a compensatory
response rather than a means to promote a greater net rate of
muscle anabolism, its a response that potentially neutralizes
the threat of muscle catabolism commonly presumed to
occur with fasted training. This is yet another bit of research
that just begs for a non-acute follow-up trial.

13. I can disappear from blogging for 3 months, really suck at
social networking, and still have a decent career in fitness.
Hallelujah & thank you all.

R

eferences
1. Lindeberg S, et al. A Palaeolithic diet improves glucose
tolerance more than a Mediterranean-like diet in individuals
with ischaemic heart disease. Diabetologia. 2007
Sep;50(9):1795-807. [Medline]
2. Mettler S, Mitchell N, Tipton KD. Increased protein intake
reduces lean body mass loss during weight loss in athletes.
Med Sci Sports Exerc. 2010 Feb;42(2):326-37. [Medline]
3. Esmarck B, Timing of postexercise protein intake is
important for muscle hypertrophy with resistance training in
elderly humans. J Physiol. 2001 Aug 15;535(Pt 1):301-11.
[Medline]
4. Cribb PJ , Hayes A. Effects of supplement timing and
resistance exercise on skeletal muscle hypertrophy. Med Sci
Sports Exerc. 2006 Nov;38(11):1918-25. [Medline]
5. Keim NL, et al. Weight loss is greater with consumption of
large morning meals and fat-free mass is preserved with
large evening meals in women on a controlled weight

reduction regimen. J Nutr. 1997 J an;127(1):75-82.
[Medline]
6. Verdijk LB, et al. Protein supplementation before and after
exercise does not further augment skeletal muscle
hypertrophy after resistance training in elderly men. m J
Clin Nutr. 2009 Feb;89(2):608-16. [Medline]
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 J un;29(6):405-13. [Medline]
8. Hoffman J R, 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. [Medline]
9. 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. [Medline]
10. Laviano A, et al. Branched-chain amino acids: the best
compromise to achieve anabolism? Curr Opin Clin Nutr
Metab Care. 2005 J ul;8(4):408-14. [Medline]
11. Sievenpiper JL, et al. Heterogeneous effects of fructose on
blood lipids in individuals with type 2 diabetes: systematic
review and meta-analysis of experimental trials in humans.
Diabetes Care. 2009 Oct;32(10):1930-7. [Medline]
12. Holick MF. Vitamin D deficiency. N Engl J Med. 2007 J ul
19;357(3):266-81. [Medline]
13. Alvarez J A, Ashraf A. Role of vitamin d in insulin secretion
and insulin sensitivity for glucose homeostasis. Int J
Endocrinol. 2010;2010:351385. [Medline]
14. Pittas AG, et al. Systematic review: Vitamin D and
cardiometabolic outcomes. Ann Intern Med. 2010 Mar
2;152(5):307-14. [Medline]
15. Thompson AK, et al. Trans fatty acids, insulin resistance
and diabetes. Eur J Clin Nutr. 2010 Oct 27. [Epub ahead of
print] [Medline]
16. Heaney RP. Vitamin D: criteria for safety and efficacy. Nutr
Rev. 2008 Oct;66(10 Suppl 2):S178-81. [Medline]
17. Odegaard AO, Pereira MA. Trans fatty acids, insulin
resistance, and type 2 diabetes. Nutr Rev. 2006
Aug;64(8):364-72. [Medline]
18. Motard-Belanger A, et al. Study of the effect of trans fatty
acids from ruminants on blood lipids and other risk factors
for cardiovascular disease. Am J Clin Nutr. 2008;87:593-
599. [Medline]
19. Strasser B, et al. Resistance training in the treatment of the
metabolic syndrome: a systematic review and meta-analysis
of the effect of resistance training on metabolic clustering in
patients with abnormal glucose metabolism. Sports Med.
2010 May 1;40(5):39. [Medline]
20. Staples AW, et al. Carbohydrate does not augment exercise-
induced protein accretion versus protein alone. Med Sci
Sports Exerc. 2010 Dec 1. [Epub ahead of print]. [Medline]
21. Greenhaff PL, et al. Disassociation between the effects of
amino acids and insulin on signaling, ubiquitin ligases, and
protein turnover in human muscle. Am J Physiol Endocrinol
Metab. 2008 Sep;295(3):E595-604. [Medline]
22. Deldicque L, et al. Increased p70 phosphorylation during
intake of a proteincarbohydrate drink following resistance
exercise in the fasted state Eur J Appl Physiol. 2009 Nov
18. [Epub ahead of print] [Medline]


Interview with world record-holding competitive eater
ete Czerwinski (AKA Furious Pete). P

By Alan Aragon
__________________________________________________

AA: First off, thanks for doing this interview. I've been a fan
of competitive eating for quite some time, ever since Takeru
Kobayashi first started owning the hotdog eating competition
way back. How did you get introduced to competitive eating,
and what actually was the turning point where you decided to
nter a formal competition? e

PC: I discovered competitive eating by accident really. I went
out for breakfast with some buddies after a night of drinking and
we all wanted something greasy to eat. Most of us ordered a dish
called the "Linebacker" which had two of every breakfast item
you could ever think of. I polished off my dish before anyone
got through a quarter of theirs, so my buddy Mike said he would
give me $40 to try and double the record, which was 2
plates...and so I did by eating 4.

After I got into doing more eating stuff I managed to break the
world record for a 72oz steak by eating it in 7 minutes. When I
posted that, I got asked to go down to California for the
Collegiate Nationals Eating Championships (where I won my
first contest).

AA: What accomplishments or milestones in competitive eating
re you most proud of, and why? a

I must say that getting the Guinness World Record for a 72oz
steak in 6:48 was a huge achievement. I made it official and it
feels good!

AA: Are you self-taught, or did you have some sort of coach or
mentor help you gain a high level of skill in competitive
eating?

PC: Self taught and to be honest I still don't know if I am doing
things right haha.

A

A: Who are your top 3 favorite eaters?
PC: Patrick "Deep Dish" Bertoletti, Takeru Kobayashi and Paul
"Porkslap" Arcaria.

AA: Do you have an off-season, and a formal in-season
preparation protocol? What tactics do you employ to get ready
or an event in the days leading up to it or the day of the event? f

I don't really have an on or off season, I just do competitions
when they appear, but most happen to be in the summer. My
prep is pretty simple, I drink a lot of water all the time and
before a contest I increase it to 12-15 liters the night before to
expand my stomach. Other than that there really isn't much other
rep. p

AA: Could you please fill us in on a typical day's eating for
you, when you're not doing a competition? If you can list
acros too, that would be great. m

PC: I couldn't give you an exact macro specification because I
never follow one. I eat 6-8 times a day and every meal contains
lean protein and healthy fats. I usually eat between 4000 - 5000
calories, mainly because my gym training is pretty intense all the
time. I stick mainly to foods like chicken, eggs, whey, nuts,
avocados, veggies and oats.

AA: How many days do you weight train per week, how many
ays cardio & how long? d

PC: I don't do much cardio as I incorporate CrossFit into my
workouts (yeah go ahead and laugh, I enjoy it and it keeps me
lean). I do strongman training most of the time in the gym and
then bodybuilding once a week or once every two weeks to keep
the physique in check (size). I try to stick to 5 days of training a
week. Each training session will be between 30 to 120 minutes
long.

AA: Haha, yeah, Crossfit can have its comic moments, thats
or sure. What training split are you currently following? f

PC: I deadlift very heavy once a week, squat heavy once a week
and do heavy chest once a week. All other workouts are kept
lighter and I do higher volume and do workouts for time.

AA: What goes on in your mind when you are in the midst of
competition? How do you stay motivated to keep going & finish
trong? s

PC: Well simply put I am doing these contests for MONEY. If I
don't win or finish strong I will be going home with no pay
check...which is a waste of a contest. I try to stick to a rhythm if
I can for the entire duration of the contest and make sure that I
am ahead of the other competitors all the time. But mainly its
the fact that I'm there for the money and that is a big enough
push to win.

AA: What was the most difficult eating challenge you've ever
one, and why was it so difficult? d

PC: A pound of butter in 3 minutes or a bottle of olive oil in 90
seconds...Do I really need to explain why these were so difficult!

AA: Interesting, it seems that perhaps taste or texture, and not
necessarily volume, can be key factors posing the challenge.
Speaking of volume, do you ever fear your stomach might
rupture in the midst of competition? What fears or concerns do
ou have to deal with in this sport - if any? y

PC: I try not to think of that. I mean I have done this for 4 years
now and I haven't had problems. I have had checkups and
doctors just simply call me a freak...haha. I have been on TV
shows where they show my stomach before and after and I
simply have a lot more folds in my stomach to allow for massive
expansion when I am eating a lot.

AA: What was the most embarrassing or strangest thing you've
itnessed while doing a competition? w

PC: Probably facing up against Kobayashi this past summer. I
went slice for slice with him for the first 7 minutes then I
couldn't keep up. I had a terrible technique of just stuffing my
AA: Please feel free to add anything you feel I should have
sked but left out.
mouth and meanwhile he had it down pat by eating two bites,
then drinking water and keeping that up for the entire contest.
But this is the contest that is making me a better eater today!
a

I'd really like to thank my main sponsor BodyBuilding.com
because without them things would have been a lot harder with
ating contests. I owe them a lot.
Editors note: Pete got 2nd Place behind winner Takeru
Kobayashi on in a pizza-eating contest on August 22. Heres a
photo blog of the highlights, and heres a video.
e

I would also like to say no one should ever TRAIN to become a
competitive eater. If you have the natural talent then go with it,
but don't practice eating all the time in an effort to become one
because it is really unhealthy to do, and you can easily choke
and die...which is obviously not good.

AA: I've always wondered why some of the top competitive
eaters are actually quite lean, when the normal expectation is
for them to be obese from practicing their craft. Why do you
hink this is so? t

AA: Thanks, Pete! Great food for thought (couldnt resist).
PC: Well there is some theory of something called the "fat belt"
which limits bigger eaters to be able to expand their stomachs
fast. As a lean eater I am able to breathe better and like I said my
stomach can expand much more easily.

AA: Please pardon this question, but I have to ask it.... Do
competitive eaters throw up their food afterwards, or do they
literally let it digest & eliminate normally? What do you do
ersonally?

p

PC: I don't know what everyone does. I know a lot do throw up.
I am 100% honest with this question always (I know a lot of
eaters aren't). My throw up ratio is 50-50. If I am eating a
straight meat product then I feel fine after and well I got my
protein in me for the day. However, If I am eating something
really saucy then I sure as hell am not feeling good after a
contest and I do whatever I need to do to make myself feel
better!

AA: Your candidness is appreciated on that. Shifting gears,
what sort of career & media opportunities have opened for you
ince you've started winning competitions?

s

PC: I've done a bunch of TV shows since I've started winning.
I've had a documentary made about my life which has been in a
ton of film festivals around the world. It's called "The Story of
Furious Pete" and people have been loving it! From Anorexia to
a Pro Eater. Very Ironic, I know...

AA: Is competitive eating something you plan to make a full-
time career out of, or do you see it more as a hobby?

PC: Well I have to keep things quiet but I have a BIG project
coming up which will make eating my career for awhile.
A

n update has been made in the December 2010 issue.
I recently added (& discussed) another study in last months
nutrient timing update. Please re-download it if you downloaded
it shortly after it was originally posted.

A

A: Do you have a regular day job?
PC: I just finished grad school (Master in Manufacturing
Engineering), and because of this project I have I don't have a
regular full time job.

Im not a theologian or a mathematician (both of whom could
probably tear apart this video) but I found it interesting
nonetheless.
AA: Congrats on completing your grad degree Can you
please provide my readers with any info on up-coming projects
or links you'd like them to check out?

PC: For sure! I upload crazy videos all the time on youtube:
http://www.youtube.com/user/furiouspete123
If you have any questions, comments, suggestions, bones of
contention, cheers, jeers, guest articles youd like to submit, or
any feedback at all, send it over to aarrsupport@gmail.com.
My website:
http://www.furiouspete.com

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