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February 2015
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The Reader’s Edition
Carbohydrate PeriodizationBy: Luke Harris
Burn Fat, Build Muscle?By: Brad Dieter, PhD
Meeting of the MindsBrad Dieter, Joakim Adzievski, Filipe Teixeira
Glutamine: Good for Muscle, or Good for the Gut?Brad Dieter
Driven By ScienceGuided By Evidence
Bridging the Gap Between Science and Industry, to Deliver you Evidence-Based Nutrition Information
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CONTENTS
Carbohydrate periodization
Meeting of the Minds
Burn Fat, Build Muscle
Main Articles
DepartmentsLetter from the Editor
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Glutamine: Gut or Muscles? 35
Letter From the Editor
This edition of Science Driven Nutrition is
unusual. We had several articles slated to go
out but decided to run with something
intriguing that happened. You will find a large
section of this edition is a conversation
between a reader, myself, and another
scientist/author.
There is a very important reason for the
lengthy discussion put forth in this issue, it
shows the importance of scientific discourse
and having conversations in which we leave our
biases at the door and are open to view points
that run orthogonal to our own.
I hope that you find the discussion
enlightening, productive, and civil as I believe it
was. I learned a lot from the discussion so I
figured it would be valuable to all of you!
In this issue we also have a really interesting
piece from Luke Harris, a reader of Science Driven
Nutrition. I was introduced to Luke through a
mutual friend and he proposed a really
interesting topic for the February issue,
carbohydrate periodization. I was unsure of what
exactly he meant by that, and curiosity got me so
I told him to take it and run with it. What we got
from Luke was a masterfully written article on a
pretty controversial topic, it is to date my favorite
piece in Science Driven Nutrition.
The quality of the readers (you) continues
to impress me. You are engaging, thoughtful,
and force me to grow and evolve, I am
sincerely thankful for that. So cheers to you,
the reader!
Brad Dieter, Director and Editor-in-Chief.
P.S. Next month’s issue is already lined up
and it is also going to be quite spectacular!
5
A tool for cyclists and other endurance athletes?
ince the gain in popularity of low
carbohydrate and ketogenic diets and other
trends that limit carbohydrate intake, many
athletes and performance driven individuals
have been manipulating their diet and
adopting a to low carbohydrate (CHO) diet.
These athletes are in the search of better
health, body composition changes, or
performance benefits. In a country where
diabetes will affect more than half of the
population by 2020, CHO are a
macronutrient that is more of a concern for
Americans than it’s ever been. In the realm
of sports nutrition, the role of CHO has
been well documented, and the role that
glycogen plays in endurance exercise has
also been well established.
It is now known that glycogen depletion
negatively impacts endurance exercise
performance, while glycogen content for
resistance exercise is less clear. For the
purposes of this article, let’s try to focus our
discussion on endurance exercise- though
that still includes high intensity work in the
form of HIT.
Carbohydrate manipulation for sports
has long been a tradition in endurance
sports, with carbo-loading a commonly
known term. Researchers, athletes and
coaches have been looking into ‘fat
adapting’ athletes for a long time (1985-
2005) in order to decrease glycogen
utilization, increase fatty acid oxidation and
improve performance. We know that a
habitually adapted athlete to a high CHO
diet will in turn utilize a higher percent of
CHO for fuel during exercise [1], when
compared to a fat adapted athlete.
7
S
Thus, there is a theory behind a potential
performance enhancement when an athlete
adapts a low CHO, high-fat (LCHF) diet. This
will then allow a fat adapted athlete to have
a nearly unlimited resource of energy
derived from fat (triglycerides) stores due to
the augmented and sensitized fatty acid
enzymes. If we train our bodies to need
CHO less, the hope is that we will not
limited by their depletion during exercise.
Thus far, very few studies have shown
that a LCHF will effectively improve
performance. A summary below
demonstrates what we know about LCHF
diets and some important physiological
changes that happen when glycogen is low:
• Low-glycogen availability causes a shift in
substrate metabolism, both during and
after exercise. It also induces an increase in
systemic release of amino acids and
increases fat oxidation – causing a drop in
exercise intensity and a rise in perceived
effort – important considerations for
athletes. [2]
•Expression of genes that stimulate fat
catabolism and mitochondrial biogenesis
are promoted – causing an improvement in
oxidative capacity and a rise in fat oxidation
at rest and during exercise by up to 3x. [3]
•It takes as few as 5 days to ‘retool’ muscles to
increase fat oxidation and reduce CHO oxidation
[4]
•Adaption or ‘retooling’ occurs by way of
changes in concentrations or activity of proteins
or metabolites that regulate fatty acid
availability (transport, storage, oxidation) and a
decrease in dependency on glucose for fuel [5].
•Because of this ‘retooling’, the ability to utilize
glycogen is severely limited – leading to a
reduction in CHO oxidation. Proponents
consider this a ‘sparing effect’, while critics may
consider it an ‘impairment effect’. This is in part
due to the down regulation of PDH, showing a
decrease in metabolic flexibility. [12]
•It is unknown how long it takes in the face of
increased CHO availability to wash out the
‘retooling’ effects of a LCHF diet – though we
know they persist in the face of at least 36
hours of aggressive CHO loading and
consumption.
There is little in the research to indicate the
LCHF diets are beneficial to endurance
performance, though studies have shown very
mixed results. In general, only submaximal/low
intensity exercise was benefited- and even
those findings were mixed [6].
8
9
Training Status LCHF adaption
protocol
Performance
protocol
Nutritional
protocol
Performance
advantage
Moderately
trained cyclists
n=7 F
[7]
7 days
LCHF = 1.2g/kg
bw CHO
HC = 6.4 g/kg bw
CHO
Cycling TTE at
80% VO2max
3-4 h after meal,
no CHO intake
during exercise
No, TTE reduced
47%
Well-trained
cyclists
N=5 M
[8]
14 days
LCHF= 17% E CHO
HC= 74% E CHO
Cycling 30s
wingate test +
TTE @ 90%
VO2max + TTE @
60% VO2max
Overnight-fasted
+ no CHO intake
during exercise
No: high intensity
tests
Yes: Submaximal
by 87%
Well-trained
cyclists
n=16 M
[9]
14 days
LCHF = 17% E
CHO
HC= 74% E CHO
Cycling 150 min
at 70% VO2max +
40 km TT
Performance
measured day
0,5,10 and 15
MCT intake 1.5 h
before event
(14g)
MCT and CHO (.8
g/kg/h) during
exercise
No
TT Performance
increased in both
groups, but no
differences.
Adaptions of high
fat diet were
found by day 5.
Well-trained
cyclists
N=7 M
[10]
14 days
LCHF = 2.4g/kg
bm CHO
HC= 8.6g/kg bm
CHO
Cycling 5h
including 15 min
TT + 100 km TT
LCHF = high fat
pre-event meal
HC = high CHO
pre-event meal
Both = 0.8 g/kg/h
CHO during
Yes: Submaximal
No: Higher
intensity
Small NS
differences
between groups.
Well-trained
duathletes
N=11 M
[11]
5 weeks
LCHF = 3.6g/kg
bm CHO
HC = 6.9g/kg bm
CHO
Cycling 40 min
Incremental
protocol + 20 min
TT @ 89% VO2
max
Running 21km TT
(another day)
LCHF = high fat
pre-event meal
HC = high CHO
pre-event meal
No data on 21km
TT run
No
Self-selected
work output was
similar among
treatments. No
difference in run
TT.
BM body mass, CHO carbohydrate, E energy F female, HC high-carbohydrate diet, LCHF low-
carbohydrate high-fat diet, M male, MCT medium chain triglyceride, NS not significant, TT time trial,
TTE time to exhaustion, VO2 max maximal oxygen uptake
Regardless of the lack of immediate
benefits – the muscle ‘retooling’ effects of a
LCHF diet are very intriguing and have lead
many, including myself to consider what the
results would be once CHO are
reintroduced in the diet of the LCHF athlete.
This might mean that we introduce CHO for
days leading up to competition day, shorter
duration < 3 days, or only during exercise.
To the rightare the findings of the majority
of current research behind the hypothesis
of ‘training low, competing high’:
It would appear that there are no clear
benefits of adapting an athlete to a LCHF
diet and then flooding the system with
available CHO to improve performance. It is
very important to mention that with all the
studies cited up to this point there are
limitations. Varying dietary protocols,
exercise prescription, statistical crunching,
and training levels of the subjects. Though
as the number of interventions and
adaptions increase, the likelihood that
individual variation in underlying factors
such as insulin sensitivity, cellular level
adaptions, hormonal and cognitive
influencers, and even daily life stresses and
activities will undermine the validity of the
study’s results.
So what’s the point of discussing this? A
recent study by Marquet LA, et al. called
Enhanced Endurance Performance by
Periodization of CHO Intake: "Sleep Low"
Strategy peaked my interest in this topic once
again and lends valid consideration that
CHO/glycogen manipulation in accordance with
training may work under certain training and
timing conditions. This study is summarized
below:
• 21 triathletes were split into two groups for 3
weeks- a ‘sleep low’ group and a control group.
• Both groups consumed 6g/kg/day CHO, but
with different timing to manipulate availability
during training sessions.
• The ‘sleep low’ group performed interval
training sessions (HIT) in the evening with high-
CHO availability, and then were restricted of
CHO overnight (‘sleeping low’), and then
performed ‘train-low’ sessions with low
endogenous and exogenous CHO availability.
• The control group undertook the same
training protocol, but without CHO restriction
and with high CHO availability for all training
sessions.
• The sleep low treatment significantly
improved TTE at 150% of aerobic peak power
and 10km running performance. Fat mass was
also decreased to a larger extent in the sleep
low treatment while muscle mass was not. [20]
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Training Status LCHF protocol CHO restoration Performance
protocol
Nutritional
strategy
Performance
advantage
Well-trained
cyclists/triathletes
N=8 M
[13]
5 days LCHF
adapt
LCHF = 2.5g/kg
bm CHO
HC = 9.6 g/kg bm
CHO
1 day rest + high
CHO 10g/kg bm
Cycling 120min @
70% VO2 max +
30min TT
Fasted + no CHO
intake during
Varied between
individuals. NS
difference
between trials in
TT, though an 8%
enhancement with
LCHF trial
Well-trained cyclists
and triathletes
N=8 M
[14]
5 days LCHF
adapt
LCHF = 2.5g/kg
bm CHO
HC= 9.3g/kg bm
CHO
1 day rest + high
CHO 10g/kg bm
Cycling 120min @
70% VO2 max +
30 min TT
CHO intake 2 h
before exercise
(2g/kg bm) and
during (0.8g/kg/h)
No
NS differences
between trials.
Highly-trained cyclists
and triathletes
N=7 M
[15]
6 days LCHF
adapt
LCHF = 2.5g/kg
bm CHO
HC = 11g/kg bm
CHO
1 day rest + high
CHO 11g/kg bm
Cycling 240 min @
65% VO2 max + 60
min TT
CHO intake
before exercise
(3g/kg bm)
and during (1.3
g/kg/h)
No difference
between trials, but
possible TT
enhancement with
LCHF adapt (4%)
Highly-trained cyclists
and triathletes
N=7 M
[16]
5 days LCHF
adapt
LCHF = 2.5g/kg
bm CHO
HC= 11g/kg bm
CHO
1 day rest + high
CHO 11g/kg bm
Cycling 240min @
65% VO2 max + 60
min TT
CHO intake
before exercise
(3g/kg bm)
and during (1.3
g/kg/h)
No difference
Trained cyclists and
triathletes
N=5 M
[17]
10 days LCHF
adapt
LCHF = 1.6 g/kg
bm CHO
HC = 5.8 g/kg bm
CHO
3 days high CHO
7g/kg bm + 1 day
rest
Cycling 150min at
70% VO2max +
20km TT
MCT intake 1 hr
before event
(14g) & CHO
during (0.8
g/kg/h)
Yes
4% enhancement
with LCHF adapt
Well-trained cyclists
N=7 M
[18]
11.5 days LCHF
adapt
LCHF = 2.4g/kg
bm CHO
HC = 8.6g/kg bm
CHO
2.5 days high CHO
6.8 g/kg bm
Cycling 5-hr
protocol with 15-
min TT + 100km
TT
HC = High CHO
pre-exercise meal
Both = 0.8 g/kg/h
CHO during
exercise
Maybe for
submaximal
exercise, small NS
benefit in 100-km
TT
Well-trained cyclists
N=8 M
[19]
6 days LCHF
adapt
LCHF = 1.8g/kg
bm CHO
HC = 7.5g/kg bm
CHO
1 day rest + high
CHO
8-10 g/kg bm
Cycling 100km TT
including 4x4-km
sprints + 5x1-km
sprints
CHO consumption
during ride.
No, NS differences
between TT and
4km sprints.
Significant
reduction in
power for 1-km
sprints in LCHF
adapt.
This study is important because it used a
novel approach to CHO manipulation and
showed significant performance benefits. It
sheds some light on the possible protocols
to ‘retool’ muscles for fat adaption without
compromising high intensity performance,
while working them into a program that
utilizes both exercise intensities. It shines
light on the gray area of CHO manipulation.
In this study, over-all CHO intake is not
limited, only the timing is changed. Athletes
were also completing all high-intensity work
with high CHO availability. However, this
study utilizes both exercise intensities on
the same day – not necessarily a common
practice amongst most athletes or cyclists –
though more common among triathletes,
track cyclists, and professional athletes. It
would be interesting to see this study
undertaken on a more macro-scale –
restricting CHO during training periods of
prolonged submaximal exercise, and
ensuring high CHO availability during the
‘peak’ or times when mostly high intensity
exercise is performed.
Consider periodization in the role of program
creation for athlete’s in terms of strength or
endurance training. All coaches will tell you
that it is important in order to elicit training
adaptions. Why shouldn’t nutrition
periodization beyond caloric totals and timing
of macronutrients be implemented in
accordance with training under the supervision
of a sports nutritionist? The research doesn’t
indicate a clear path towards how this will
happen, and more research certainly needs to
be done in the area – but the idea is an
interesting one.
Why should a cyclist who’s clocking in 25+
hours of training in a week at very low
intensities be consuming roughly the same diet
(besides caloric content) of when they are
training at other intensities, durations, and
frequencies later in the season? No study has
been done where cyclists consume a LCHF diet
over their ‘base’ period where all exercise is
done at sub-maximal intensities, and then
switched to a high-CHO diet once they
commence higher-intensity training. Based off
studies done and an understanding of the
underlying mechanisms, this could be of
benefit to athletes
12
In a more acute sense, in regards to the
previously mentioned study, some cyclists
(or any other athlete who partakes in both
aerobic and high intensity exercise) could
benefit from manipulating CHO intake
between sessions.
Too often in the realm of nutrition are
things stated in black and white. We as
humans like to compartmentalize overly-
complex processes and make them easier
to understand and adhere to- and we often
like to think about diets in black and white
terms. It is important that research, as well
as the field, attempts to bridge this
understanding in the body’s adaptions to
low CHO availability, and how to implement
it without raising the fatigue levels of
athletes to a compromising degree. Training
‘low’ has many implications for fatigue and
therefore requires careful treading. It is
also abundantly clear that a lack of CHO is
detrimental to high intensity performance.
As a sports nutritionist, I think it’s important
that we continue to advance our field and
not settle for blanket dietary
recommendations regardless of
interpersonal, lifestyle and environmental
differences for athletes.
With the advancement of personalized
testing for nutritional, enzymatic, and
hormonal inadequacies – this change is
already taking place. I believe it is possible,
with further research and field work that
we can use these tests in the future to
make evidence-based nutrition programs
utilizing micro and macro periodization of
CHO intake for athletes in order to improve
their performance, and ultimately hit their
peak when they need to – rather than
searching for a yearlong dietary strategy
that will improve performance all year long.
Author Bio
Luke Harris is the founder and owner of
Enclave Performance Nutrition in Portland,
Oregon. He is a recent transplant from
Colorado, where he studied nutrition at
Colorado State University at the
undergraduate and graduate level. Luke is a
certified sports nutritionist with the ISSN, a
certified strength and conditioning
specialist, and CF-L1 coach who works with
CrossFit athletes, weight lifters, and cyclists
to improve their performance, body
composition, and health.
http://lucaaharris.wix.com/enclave
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1. Cox GR, Clark SA, Cox AJ, Halson SL, Hargreaves M, Hawley JA, et al. Daily training with high carbohydrate availability increases exogenous carbohydrate oxidation during endurance cycling. J Appl Physiol (1985) 2010;109:126–134. doi: 10.1152/japplphysiol.00950.2009.
2. Blomstrand E, Saltin B. Effect of muscle glycogen on glucose, lactate and amino acid metabolism during exercise and recovery in human subjects. J Physiol. 1999;514(Pt 1):293–302. doi: 10.1111/j.1469-7793.1999.293af.x. [
3. Bartlett JD, Hawley JA, Morton JP. Carbohydrate availability and exercise training adaptation: Too much of a good thing? Eur J Sport Sci. 2015;15:3–12. doi: 10.1080/17461391.2014.920926.
4. Goedecke JH, Christie C, Wilson G, et al. Metabolic adaptations to a high-fat diet in endurance cyclists. Metabolism. 1999;48:1509–1517. doi: 10.1016/S0026-0495(99)90238-X.
5. Yeo WK, Carey AL, Burke L, et al. Fat adaptation in well-trained athletes: effects on cell metabolism. Appl Physiol Nutr Metab. 2011;36:12–22. doi: 10.1139/H10-089.
6. Burke LM. Re-Examining High-Fat Diets for Sports Performance: Did We Call the ‘Nail in the Coffin’ Too Soon? Sports Med. 2015; 45(Suppl 1): 33–49. Published online 2015 Nov 9. doi: 10.1007/s40279-015-0393-9 PMCID: PMC4672014
7. O’Keeffe KA, Keith RE, Wilson GD, et al. Dietary carbohydrate intake and endurance exercise performance of trained female cyclists. Nutr Res. 1989;9:819–830. doi: 10.1016/S0271-5317(89)80027-2.
8. Lambert EV, Speechly DP, Dennis SC, et al. Enhanced endurance in trained cyclists during moderate intensity exercise following 2 weeks adaptation to a high fat diet. Eur J Appl Physiol. 1994;69:287–293. doi: 10.1007/BF00392032.
9. Goedecke JH, Christie C, Wilson G, et al. Metabolic adaptations to a high-fat diet in endurance cyclists. Metabolism. 1999;48:1509–1517. doi: 10.1016/S0026-0495(99)90238-X.
10. Rowlands DS, Hopkins WG. Effects of high-fat and high-carbohydrate diets on metabolism and performance in cycling. Metabolism. 2002;51:678–690. doi: 10.1053/meta.2002.32723.
11. Vogt M, Puntschart A, Howald H, et al. Effects of dietary fat on muscle substrates, metabolism, and performance in athletes. Med Sci Sports Exerc. 2003;35:952–960. doi: 10.1249/01.MSS.0000069336.30649.BD.
12. Stellingwerff T, Spriet LL, Watt MJ, et al. Decreased PDH activation and glycogenolysisduring exercise following fat adaptation with carbohydrate restoration. Am J Physiol. 2006;290:E380–E388.
13. Burke LM, Angus DJ, Cox GR, et al. Effect of fat adaptation and carbohydrate restoration on metabolism and performance during prolonged cycling. J Appl Physiol. 2000;89:2413–2421.
14. Burke LM, Hawley JA, Angus DJ, et al. Adaptations to short-term high-fat diet persist during exercise despite high carbohydrate availability. Med Sci Sports Exerc. 2002;34:83–91. doi: 10.1097/00005768-200201000-00014.
15. Carey AL, Staudacher HM, Cummings NK, et al. Effects of fat adaptation and carbohydrate restoration on prolonged endurance exercise. J Appl Physiol. 2001;91:115–122.
16. Noakes T. Fat adaptation and prolonged exercise performance. J Appl Physiol. 2004;96:1243
17. Lambert EV, Goedecke JH, Van Zyl CG, et al. High-fat versus habitual diet prior to carbohydrate loading: effects on exercise metabolism and cycling performance. Int J Sport Nutr Exerc Metab. 2001;11:209–225.
18. Rowlands DS, Hopkins WG. Effects of high-fat and high-carbohydrate diets on metabolism and performance in cycling. Metabolism. 2002;51:678–690. doi: 10.1053/meta.2002.32723.
19. Havemann L, West S, Goedecke JH, et al. Fat adaptation followed by carbohydrate-loading compromises high-intensity sprint performance. J Appl Physiol. 2006;100:194–202. doi: 10.1152/japplphysiol.00813.2005.
20. Marquet LA, et al. Enhanced Endurance Performance by Periodization of CHO Intake: "Sleep Low" Strategy. Med Sci Sports Exerc. 2016 Jan 7. [Epub ahead of print]
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Editorial note: the following email has been edited. It
was edited only to correct grammatical mistakes and no
content has been changed. Additionally, the reader has
agreed to have our discussion made available as this is
an excellent example of discourse in which differences in
data interpretation and clarification can make a
thought process better and more coherent.
Readers Comment (Joakim)
Got the free November issue of Science
Driven Nutrition. Have just read one article
yet, but found a couple of, what I believe,
faulty interpretations of the science. I’m
completely open to that I myself can have
interpreted it incorrectly (I am not a
researcher), but maybe you could shed some
light here.
It is regarding the article, “Is nitrogen spiking a
joke” by Filipe Teixeira.
The first is regarding the statement
”Although adding leucine to a suboptimal dose
of whey enhances muscle protein synthesis
(MPS) to the same extent as 25g of whey at
rest, only whey can enhance MPS post-
exercise [31].”
I read the referenced article and my
interpretation is that leucine increased MPS
similar to whey in the first hour whereas
whey where the only protocol that were
able to sustain MPS for longer periods of
time (3-5h) (the faster uptake and peak for
EAA compared to whey is no news, and
does not mean that EAA is ineffective post-
exercise).
Below is some excerpts for the article
backing up my claims:
”MPS were increased above FAST over 1–3
h post-exercise recovery (P = 0.001; EAA-
LEU = 0.069 ± 0.012; LEU = 0.068 ± 0.014;
WHEY = 0.064 ± 0.007). However, the rates
of MPS remained increased above FAST at
3–5h exercise recovery only after ingestion
of WHEY versus LEU and EAA-LEU (EAA-LEU
= 0.050 ± 0.005; LEU = 0.048 ± 0.012; WHEY
= 0.088 ± 0.010; Fig. 3B).”
”In this study we report that a dose of whey
protein, previously shown to be less than
maximally effective for stimulating muscle
protein synthesis after resistance exercise
(Moore et al. 2009a), supplemented with
leucine (LEU) resulted in an early (1–3 h
post-exercise recovery) increase in both FED
and EX-FED rates of MPS equal to that seen
following ingestion of 25 g of whey protein
(WHEY).”16
”However, despite similar early responses of
MPS, EX-FED rates over 3–5 h were only sustained
following WHEY, whereas EX-FED rates of MPS in
both LEU and EAA-LEU had decreased to values
not significantly different from FAST.”
Frankly, it seems like he just read the part
above the abstract named “key points” and not
the entire article.
The second thing in the SDN article I reacted to
was: ”Adulteration with amino acids probably
does not pose a risk to consumer’s health,
however it defrauds costumers both financially
and physiologically, since consuming free amino
acids does not have the same effect than whey
protein on MPS [39].”
I think this statement misrepresent the body of
research regarding protein and amino acids when
it relates to MPS. The study referenced compared
15g of whey and its constituent EAA content
amounting to only 6.72g of amino acids. And since
the dose was ingested in a fasted state, after an
overnight fast, adding the fact that whey is not
free form amino acids and thus requires more
time for uptake, I think it is no wonder that the
group consuming twice the amount of more
slowly digested protein showed a more positive
protein balance.
The authors of the referenced study even
note that in a previous study they found that
ingestion of 15 of EAA promotes muscle protein
accrual more so than 15 of whey, clearly
showing, I believe, that its more so the amount
and essentiality of the amino acids that makes
the difference, and not that EAA is simply less
effective than whey, regardless, that Teixeira
seems to claim.
Article quote to back this: ”These findings
may appear to differ from our previous findings
in the elderly that ingestion of 15g of EAA
promotes muscle protein accrual [8], and that
the response following ingestion of 15 g of EAA
is greater than that following ingestion of 15g of
whey protein [14]. These apparent discrepancies
are likely explained by the total EAA content of
the mixtures (15 g vs 6.72 in the present study).”
Once again it seems like barely the abstract
was read and that the body of research was not
taken into consideration. Teixeira does however
partly disclaim this statement with, “However,
more recent research in older women shows
equivocal results in this subject matter [41].”
But I think the first part of that paragraph is
misleading should not have been there in the
first place, just adding confusion.
17
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I’m not claiming that I am even close to fully
proficient in interpreting science, so I’m open to
the fact that I myself have done some
misinterpretations.
Response from the Editor (Brad Dieter)
I thank you for the insightful comments and
thorough read of the supporting literature in
the article presented in the November issue. As
the editor I try to review every article
thoroughly but will admit that I do not have
time to read every single reference in every
single article to confirm every statement. I
appreciate your thoroughness and bringing this
point to my attention I think this serves as an
excellent place to begin a discussion regarding
this topic
After a thorough read of the referenced
paper I find that Filipe’s statement that, “only
whey can enhance MPS post-exercise” holds
true. When you look at the Figure 3 please
compare the data in panel A showing the effect
of Leucine and Whey on FSR in a purely fed
state (no exercise) and in panel B showing the
effect of leucine and whey (shown below for
ease of reading). Upon examination you will
notice that 1-3 hours post feeding shows an
increase in FSR for both whey and leucine in a
non-exercise and an exercise state.
This suggests that there is no effect of
exercise on whey or leucine induced FSR
between 1-3 hours in this cohort. When we
examine the data at 3-5 hours there is
increased FSR in only the whey group, not
the leucine group. Also compare the
amounts between the leucine in the
exercised and non-exercised state, they
both appear to be around 0.068 in the non-
exercised group at 1-3h and 0.068 in the
exercised group. So my interpretation is
that leucine induced FSR similarly between
exercised and non-exercised states,
whereas the whey group showed increased
FSR at 3-5 hours in only the exercise group.
This suggests that at the dose of leucine
given (~3.0g), there is no real difference in
FSR in an exercised and non-exercised state.
In the whey group there was enhanced FSR
in the exercised group, thus I feel his
interpretation, “Although adding leucine to
a suboptimal dose of whey enhances
muscle protein synthesis (MPS) to the same
extent as 25g of whey at rest, only whey
can enhance MPS post-exercise.” is indeed
correct
19
Data referenced from Churchward-Venne et al. 2012 J Physiol
20
I believe you make some excellent points
in regards to the specificity of which Filipe
mentions free amino acids and better care
could have been taken in that sentence.
Indeed, it appears that free-form essential
amino acids can induce greater accrual of
muscle protein than whey in an elderly
population of individuals as noted in the
study by Paddon-Jones and colleagues
(Paddon-Jones et al., 2006). However, to
date, no studies (that I am aware of) show
that non-essential amino acids are a large
contributor to muscle protein synthesis. For
example, Volpi and showed that 18 grams
of amino acids lead to similar increases in
FSR as 18 grams of essential amino acids +
22g of amino acids, indicating that while
essential amino acids account for virtually
the entirety of amino acid induced muscle
protein synthesis (Volpi et al., 2003).*
This brings us to the point at hand. Your
comment of “I think this statement
misrepresents the body of research
regarding protein and aminoacids when it
relates to MPS”.
A slight change of a word or two in that
sentence (will rectify at the end of this
paragraph) should clear up the confusion,
also remember the context of the
statement as I do believe the context of
that statement is important and can
illuminate the message that sentence
(while not written as clear as possible)
meant to send. The article, “Is Nitrogen
Spiking a Joke” discusses primarily using
non-essential amino acids such as glycine
and taurine, along with arginine to increase
nitrogen content.
Would altering the sentence to read,
“Adulteration with non-essential amino
acids probably does not pose a risk to
consumer’s health, however it defrauds
costumers both financially and
physiologically, since consuming non-
essential free amino acids does not have
the same effect as whey protein on MPS”
alleviate your concerns regarding the
representation of the literature?
21
Also, as a note of decorum, when bringing
issues to light in a discussion aimed at
forwarding knowledge and fostering
understanding, ad hominem ought to be
avoided, especially when they are
assumptions. Claiming an author only read
the abstract distracts from the conversation
in a mud-throwing manner.
*The use of sedentary, non-exercising
participants helps elucidate the direct role
of exercise-independent effects of specific
amino acids on muscle protein synthesis.
References
Paddon-Jones D, Sheffield-Moore M,
Katsanos CS, Zhang XJ, Wolfe RR: 2006.
Differential stimulation of muscle protein
synthesis in elderly humans following
isocaloric ingestion of amino acids or whey
protein. Experimental gerontology 41:215-
219.
Volpi E, Kobayashi H, Sheffield-Moore M,
Mittendorfer B, Wolfe RR: 2003. Essential
amino acids are primarily responsible for
the amino acid stimulation of muscle
protein anabolism in healthy elderly adults.
The American journal of clinical nutrition
78:250-258.
Response from the Author (Filipe Teixeira)
I feel the editor fully addressed the first
issue raise so I shall focus my attention on
the second issue.
Editorial Note: I have taken the liberty of
putting the reader’s comments in bold and
the author’s response in normal type.
First we need to address the claim that,
“adding the fact that whey is not free form
amino acids and thus requires more time
for uptake”.
In fact whey is mainly absorbed in di and
tripeptide form through PEPT1 transporters
in the gut. These are high capacity
transporters that can further allow the
hydrolysis e di and tripeptide inside the
enterocyte (a small part passes intact since
di and tripeptides are found in circulation)
(Grimble et al. 1986, Lis et al. 1971,
Gromova and Gruzdkov 2003). Peptides are
responsible for over 60 % of the absorption
of amino acids while free amino acids are
only responsible for ≈40 % (Grimble et al.
1987, Zaloga et al.).
22
Assuming that whey is digested at a slower
rate than free amino acids is wishful thinking
and is debatable at least. This is not an
argument to dismiss the work made by
Katsanos et al.
The authors of the referenced study even
notes that in a previous study they found that
ingestion of 15 of EAA promotes muscle
protein accrual more so than 15 of whey,
clearly showing, i believe, that its more so the
amount and essentiality of the aminoacids that
makes the difference, and not that EAA is
simply less effective than whey, regardless,
that Teixeira seems to claim. What I seem to
claim is the interpretation of the reader. The
mentioned study showing that 15 g of EAA
promotes muscle protein accrual more than 15
g of whey has limitations that the reader
seems to have missed… So I have to state that
the interpretation of the research quoted is
faulty indeed but from the reader’s side. I
would suggest the reader to read the review
below from Hulmi et al :
It pretty much wraps all the whole discussion,
since it quotes both studies cited by the
reader (excerpt below for ease of reading).
“As alluded to previously, the effects of
whey on muscle adaptations may not be solely
dependent upon its EAA concentration. A
study that may confuse that argument was
one in which the consumption of 15 g of EAA
almost doubled the muscle protein balance in
elderly subjects, compared to consuming
whey [118]. Of note, however, the subjects
consumed isocaloric amounts of either EAA or
whey, and thus the whey trial consisted of
~50% less EAA. From this study, it would
appear that whey may be energetically less
efficient than consumption of its constituent
EAA for increasing muscle protein balance, at
least for elderly individuals, as its constituent
non-essential amino acids do not seem to be
as important in enhancing protein
balance/synthesis [3,108,109].
Contrastingly, acute whey PRO ingestion
(15 g), under resting conditions and in
elderly men and women, resulted in greater
muscle protein balance than consumption
of its constituent EAAs (6.72 g) or non-
essential amino acids (7.57 g) [10]. This
result may suggest that something other
than EAAs within whey are important for
muscle hypertrophy. For example, it is
possible that via the PEPT-1 cotransporters'
high capacity, low specificity rate of
transport, and an apparent increased
transport affinity for L-valine bound
peptides, that the bound form of an EAA
may be more efficiently utilized than when
delivered in its free-form [119]. Similarly,
new discoveries continue to surface
regarding bioactive peptides present within
dairy, and specifically in whey that may
facilitate improved recovery and
antioxidative capacity to support
physiological adaptations to exercise
[104].However, possible long term
superiority of whey compared to its
constituent amino acids (all, or just its
EAAs) is not known.”
23
References
Grimble GK, Silk DB. The optimum form of
dietary nitrogen in gastrointestinal disease:
proteins, peptides or amino acids?
Verhandlungen der Deutschen Gesellschaft
fur Innere Medizin 1986; 92: 674-685.
Grimble GK, Rees RG, Keohane PP, Cartwright T, Desreumaux M, Silk DB. Effect of peptide chain length on absorption of egg protein hydrolysates in the normal human jejunum. Gastroenterology. 1987 Jan;92(1):136–42.
Gromova LV, Gruzdkov AA. [Kinetic analysis of glycine and glycylglycine absorption in rat small intestine in chronic experiment]. Rossiiskii fiziologicheskii zhurnal imeni IM Sechenova / Rossiiskaia akademiia nauk2003; 89: 173-183.
Hulmi JJ, Lockwood CM, Stout JR. Effect of protein/essential amino acids and resistance training on skeletal muscle hypertrophy: A case for whey protein. Nutrition & Metabolism. 2010;7:51. doi:10.1186/1743-7075-7-51.
M.T. Lis, R.F. Crampton, D.M. Matthews, Rates of absorption of a dipeptide and the equivalent free amino acid in various mammalian species, Biochimica et Biophysica Acta (BBA) - Biomembranes, Volume 233, Issue 2, 1971, Pages 453-455, ISSN 0005-2736, http://dx.doi.org/10.1016/0005-2736(71)90342-7.
(http://www.sciencedirect.com/science/article/pii/0005273671903427)
Zaloga GP, Siddiqui RA. Biologically active dietary peptides. Mini Rev Med Chem. 2004 Oct;4(8):815–21.
Reader’s Response to Editor and Author’s
Comments
Again, below is edited solely for
grammar, content remains intact. Reader’s
comments in bold
Once again thank you for answering my
comment so thoroughly. Here is my reply.
Filipe
”Reading the full article not knowing the
all body of research or not having a critical
view of what is being claimed can be more
misleading to some people than just
reading the abstract.”
Completely agree. Want to expand a bit on
that also
One should never use only the info in
an abstract as evidence. When one does
not understand the article then one can at
most use the abstract as a very rough hint
as to whats going on, but never to prove
ones point and as evidence.
And when one does have the ability to
understand the article, then i do not think
that an abstract should ever be used as
anything else than an aid in helping one
decide whether the article is relevant and
worth reading.
Also, I am not claiming that you
didn't read the full-length article here,
it just seemed like that to me based
on my interpretation of the article,
which, I now realize, after
correspondence with B. Dieter, was
faulty.
Dieter
”After a thorough read of the
referenced paper I find that Filipe’s
statement that, “only whey can enhance
MPS post-exercise” holds true. When
you look at the Figure 3 please compare
the data in panel A showing the effect of
Leucine and Whey on FSR in a purely
fed state (no exercise) and in panel B
showing the effect of leucine and whey
(shown below for ease of reading).
Upon examination you will notice that 1-
3 hours post feeding shows an increase
in FSR for both whey and leucine in a
non-exercise and an exercise state. This
suggests that there is no effect of
exercise on whey or leucine induced
FSR between 1-3 hours in this cohort.
When we examine the data at 3-5 hours
there is increased FSR in only the whey
group, not the leucine group.
24
Also compare the amounts between the
leucine in the exercised and non-exercised
state, they both appear to be around 0.068
in the non-exercised group at 1-3h and
0.068 in the exercised group. So my
interpretation is that leucine induced FSR
similarly between exercised and non-
exercised states, whereas the whey group
showed increased FSR at 3-5 hours in only
the exercise group. This suggests that at the
dose of leucine given (~3.0g), there is no
real difference in FSR in an exercised and
non-exercised state. In the whey group
there was enhanced FSR in the exercised
group, thus I feel his interpretation,
“Although adding leucine to a suboptimal
dose of whey enhances muscle protein
synthesis (MPS) to the same extent as 25g
of whey at rest, only whey
can enhance MPS post-exercise.” is indeed
correct”
Yes, I see. Thanks for clarifying that. I
withdraw my previous remark.
”I believe you make some excellent
points in regards to the specificity of
which Filipe mentions free amino acids
and better care could have been taken
in that sentence. Indeed, it appears that
free-form essential amino acids can
induce greater accrual of muscle protein
than whey in an elderly population of
individuals as noted in the study by
Paddon-Jones and colleagues (Paddon-
Jones et al., 2006). However, to date,
no studies (that I am aware of) show
that non-essential amino acids are a
large contributor to muscle protein
synthesis. For example, Volpi and
showed that 18 grams of amino acids
lead to similar increases in FSR as 18
grams of essential amino acids + 22g of
amino acids, indicating that essential
amino acids account for virtually the
entirety of amino acid induced muscle
protein synthesis (Volpi et al., 2003).*”
25
I didnt mean that NEAA is responsible
for MPS (aware that EAA is the major, if
not sole, contributor to MPS), i meant that
in a situation where sub-optimal amounts
of protein is consumed the total amount of
AA (i speculate) might be important in the
sense that NEAA might contribute to other
bodily processes and thus work somewhat
sparingly. (i dont have any research to back
this up).
”This brings us to the point at hand. Your
comment of “I think this statement
misrepresents the body of research
regarding protein and aminoacids when it
relates to MPS”. A slight change of a word
or two in that sentence (will rectify at the
end of this paragraph) should clear up the
confusion, also remember the context of
the statement as I do believe the context of
that statement is important and can
illuminate the message that sentence
(while not written as clear as possible)
meant to send. The article, “Is Nitrogen
Spiking a Joke” discusses primarily using
non-essential amino acids such as glycine
and taurine, along with arginine to increase
nitrogen content.
Would altering the sentence to read,
“Adulteration with non-essential amino
acids probably does not pose a risk to
consumer’s health, however it defrauds
costumers both financially and
physiologically, since consuming non-
essential free amino acids does not
have the same effect as whey protein on
MPS” alleviate your concerns regarding
the representation of the literature?”
Yes, that would be excellently put!
26
27
B
u
r
n
F
a
t
G
a
i
n
M
u
s
c
l
e
The single biggest marketing slogan for
nutrition or fitness programs is “Lose Fat
and Gain Muscle”.
Whether it is actually possible to do so
has remained a topic of great debate over
the last several decades. Recent studies in
the past years have given us the data
needed to draw a conclusion on whether it
is indeed possible.
Before we dive into the studies and the
data lets discuss the hypothesis and
arguments surrounding the issue.
REGULATING BODY MASS
The main argument against the idea of
losing fat and gaining muscle
simultaneously is essentially the notion of
calories in versus calories out.
The argument goes something like this:
depending on your caloric balance your
body is either in a net state of anabolism
(building new tissue) or catabolism
(breaking down tissue)
The calories in calories out (CICO) model
holds a lot of truth and can explain a lot of
the variation in body weight, yet it is
incomplete.
I like to compare the CICO model with
Newtonian Physics… it is accurate and
describes gravity for a majority of cases but
it is not complete. We need Einstein’s
theories of relativity to describe the
enormously large* and fast and we need
quantum theory for the incredibly small.
28
I believe the CICO model breaks down in
certain situations.
One such area where it breaks down is
for anabolism and catabolism to be
occurring simultaneously in different
“compartments” of the body.
The CICO model essentially treats the
body as a bomb calorimeter and an isolated
system immune to perturbations. This is
inaccurate. The body is not simply a bomb
calorimeter, nor is it an isolated system.
The body is dynamic and responds to both
internal and external stimuli (Figure 1).
29
I want to take the internal stimuli first and
relate it to the topic at hand (building
muscle).
Without even touching nutrition we have
data to show that the body has internal
signals that simultaneously induce muscle
protein synthesis and increase fat oxidation,
namely the hormone testosterone. It is well
documented that testosterone increases
muscle protein synthesis and that it can do so
without increased amino acid uptake into
cells (1,2,3). Additionally testosterone can
simultaneously increase lean mass and
decrease fat mass in an older population (4).
Now onto external signals. It is clear that
ingestion of protein elicits muscle protein
synthesis in humans (5,6,7). Now there are
good arguments for what type of
protein/amino acids are the biggest
inducers of muscle protein synthesis but
that is superfluous to the point at hand. It is
enough for this argument that as a nutrient,
protein elicits an anabolic signal of muscle
protein accretion in humans. This effect is
robust and reproducible in various
populations.
The next external signal that elicits a robust,
repeatable signal for muscle protein synthesis is
exercise, with resistance training showing the
greatest amount of muscle protein
synthesis(8,9,10). In addition to signaling muscle
accretion, exercise can also induce a signal for
lipolysis and fat oxidation.
So let’s stop and review. The CICO model only
really accounts for total body mass and predicts
overall changes in the mass of a system. The
body is more than a bomb calorimeter, it is
dynamic and responds to signals and can change
the masses of different “compartments” in
accordance with the signals.
We have two easily modifiable signals we can
use to elicit our goal of increasing muscle mass:
1) consuming protein, 2) engaging in resistance
exercise. We also have covered 1 signal for
eliciting our goal of fat loss: exercise.**
This figure wraps up these ideas quite nicely.
30
Dietary protein and exercise essentially
can act as leverage points. So to take
Archimedes favorite quote, “Give me a
place to stand and with a lever I will move
the whole world” and spin it … “Give me
some protein and with a good resistance
training program I will build muscle and lose
fat simultaneously”.
So without getting too far into the weeds
we have a mechanism by which the goal of
“gaining muscle while losing fat” is, at least
in theory, possible.
Now let’s look at two separate studies
using two very different approaches to see
how this translates into practice.
I am going to summarize the findings
over the next few paragraphs but a full
discussion of each can be found at
www.sciencedrivennutrition.com
STUDY 1
The first study was a protein overfeeding
study in which they had resistance-trained
volunteers consume either a “normal”
protein diet or an overfeed protein diet in
which they were instructed to consumer
more than 3g/kg of protein per day (see
table below for macronutrient and calorie
breakdown) (11). Briefly, the high protein
group consumed about 500 calories more
per day, with about 80 of those calories
coming from carbohydrates (not statistically
significant from the normal protein) and
about 350 calories extra from protein (this
was statistically different), and about 60
calories from fat (also not statistically
different).
31
During the dietary intervention the
participants continued to resistance train
for 5days/week for 8 weeks.
At the conclusion of this study the high
protein group lost an average of 1.6 kg of
fat mass with the normal protein group only
lost 0.3 kg. Additionally, the high protein
group saw a 2.4% decrease in body fat with
the normal protein group saw a 0.6%
decrease in body fat.
Although the high protein group
consumed 350 more kcals per day than the
normal protein group, the high protein diet
group saw no change in body weight (-0.1
kg) while the normal protein diet group saw
an increase in body weight (1.3 kg). This is
quite interesting in that the increase in total
body weight suggests that the normal
protein group was likely already in a
hypercaloric state as they increased their
body weight, yet the high protein group
which consumed even more calories (about
20,000 kcals more over the whole study)
did not see an increase in BW.
STUDY 2
Where the first study was considered
“protein overfeeding” and hypercaloric, the
second study is presented in the context of
eating higher protein in the context of
caloric restriction***.
32
In this study the researchers recruited 40
overweight (BMI >25) young men (mean
age 23 years old) for this single-blind,
prospective trial. All the participants were
recreationally active, but were not regularly
performing resistance training (so this is a
relatively untrained population compared
to the study from the Antonio lab)
(12)****.
The participants were randomly assigned
to either a high protein (2.4 gkg/day) or
control protein (1.2g/kg.day) diet that was
energy restricted by approximately 40%.
Please see Table 2 for a complete
breakdown of the diets and the differences
between them. Briefly, one was a high
protein, low fat diet, while the other was a
“normal protein”, “normal fat” diet.
33
These tables and figures are directly from the Longland et al. 2016 AJCN paper
The participants also began a 6 days/week
exercise program for the duration of the study (4
weeks).
When we look at the results of the study, we see, as
expected in a 40% calorie restricted diet, that both
groups lost body weight with similar weight losses
between groups.
Now here is, in my opinion the big result from
this study. The LBM stayed the same in the CON
group but increased in the PRO group. Meaning the
PRO group lost fat and simultaneously increased
LBM.
34
THE WRAP UP
The CICO model only really accounts for total
body mass and predicts overall changes in the mass
of a system. The body is more than a bomb
calorimeter, it is dynamic and responds to signals
and can change the masses of different
“compartments” in accordance with the signals.
By manipulating the signals going into the system
through proper diet and exercise it is indeed
possible to simultaneously increase lean mass while
reducing fat mass. It appears that this
phenomenon may be more robust in untrained
individuals than trained individuals, yet based on
the studies from the Antonio lab it appears possible
in trained populations as well.
For the interested reader please continue to the
work below for more in-depth analysis of the two
studies.
References
1. Griggs RC, Kingston W, Jozefowicz RF, et al.Effect of testosterone on muscle mass and muscle protein synthesis. Journal of applied physiology 1989; 66: 498-503.
2. Brodsky IG, Balagopal P, Nair KS. Effects of testosterone replacement on muscle mass and muscle protein synthesis in hypogonadal men--a clinical research center study. The Journal of clinical endocrinology and metabolism 1996; 81: 3469-3475.
3. Ferrando AA, Tipton KD, Doyle D, et al.Testosterone injection stimulates net protein synthesis but not tissue amino acid transport. The American journal of physiology 1998; 275: E864-871.
4. Wittert GA, Chapman IM, Haren MT, et al. Oral testosterone supplementation increases muscle and decreases fat mass in healthy elderly males with low-normal gonadal status. The journals of gerontology Series A, Biological sciences and medical sciences 2003; 58: 618-625
5. Tang JE, Moore DR, Kujbida GW, et al. Ingestion of whey hydrolysate, casein, or soy protein isolate: effects on mixed muscle protein synthesis at rest and following resistance exercise in young men. Journal of applied physiology 2009; 107: 987-992.
6. Moore DR, Robinson MJ, Fry JL, et al. Ingested protein dose response of muscle and albumin protein synthesis after resistance exercise in young men. The American journal of clinical nutrition 2009; 89: 161-168.
7. Burd NA, Gorissen SH, van Vliet S, et al.Differences in postprandial protein handling after beef compared with milk ingestion during postexercise recovery: a randomized controlled trial. The American journal of clinical nutrition2015; 102: 828-836
8. MacDougall JD, Gibala MJ, Tarnopolsky MA, et al. The time course for elevated muscle protein synthesis following heavy resistance exercise. Canadian journal of applied physiology = Revue canadienne de physiologie appliquee 1995; 20: 480-486.
9. Phillips SM, Tipton KD, Aarsland A, et al. Mixed muscle protein synthesis and breakdown after resistance exercise in humans. The American journal of physiology 1997; 273: E99-107.
10. Hasten DL, Pak-Loduca J, Obert KA, et al.Resistance exercise acutely increases MHC and mixed muscle protein synthesis rates in 78-84 and 23-32 yr olds. American journal of physiology Endocrinology and metabolism 2000; 278: E620-626.
11. Antonio J, Ellerbroek A, Silver T, et al. A high protein diet (3.4 g/kg/d) combined with a heavy resistance training program improves body composition in healthy trained men and women--a follow-up investigation. Journal of the International Society of Sports Nutrition 2015; 12: 39.
12. Longland TM, Oikawa SY, Mitchell CJ, et al.Higher compared with lower dietary protein during an energy deficit combined with intense exercise promotes greater lean mass gain and fat mass loss: a randomized trial. The American journal of clinical nutrition 2016.
35
Glutamine
Glutamine is one of the twenty amino
acids used by humans in metabolism. It is
conditionally essential, meaning your body
can manufacture it, but not in sufficient
quantities during times of extreme stress
(i.e. disease or extreme exercise).
Glutamine has been highly touted as being
able to increase muscle mass. Interestingly,
glutamine is a critical component of gut
health and for the immune system due to
the fact that glutamine is often a
preferential fuel source in gut and immune
cells.
What the Research Says
The research behind glutamine is vast in
both breadth and depth. After a thorough
reading of over 50+ papers on glutamine
supplementation, I have made the following
conclusions.
1. Glutamine does not increase muscle
protein synthesis above normal in
healthy individuals. In people who are
sick, have significant muscle trauma, or
a wasting disease, glutamine can be
effective in building muscle.
2. Glutamine supplementation is
beneficial for individuals with GI
dysfunction and can aid in reducing
symptoms of GI distress, especially in
those who engage in heavy training.
3. During heavy training cycles, or times
of stress, glutamine supplementation
can improve the function of the
immune system
36
Dosing
Typical dosing is approximately 5g per
day, with an upper limit of about 14g.
Typically, individuals who consume a high-
protein diet, especially those who
supplement with whey protein are unlikely
to need additional glutamine
supplementation.
Individuals with gut or immune issues
could benefit from additional glutamine
supplementation in pill form as more
glutamine is available to the intestines
when consumed in that form.
Bottom Line
Glutamine supplementation is effective
in muscle building for those in an infirmed
state. It can help improve gut health and
augment immune function in those
engaged in heavy training. Most people
who consume a higher protein diet (i.e.
1g/lb/day) get adequate glutamine and
further supplementation is not needed.
37
Pros
• Can be beneficial for gut health
• In periods of heavy training in may have an
immune boosting effect
Cons
• You can get enough glutamine in your diet.
• There is no real benefit of glutamine for
building muscle
