ean

13 An open label study to determine the effects of an

oral proteolytic enzyme system on whey protein
concentrate metabolism in healthy males.
Oben J, et al. J Int Soc Sports Nutr. 2008 Jul 24;5:10.
[Medline]

15 Hidden blessings Part 2: What do Alwyn Cosgrove,

Lyle McDonald, and gay porn have in common?
By Alan Aragon
Copyright © October 1st, 2008 by Alan Aragon
Home: www.alanaragon.com/researchreview
Correspondence: aarrsupport@gmail.com

2 So much ado about insulin hindering fat loss, so

little evidence.
By Alan Aragon

5 Olympic speedskater Maria Garcia drops some

insight for the hopefuls.
Interviewed by Alan Aragon

8 International society of sports nutrition position

stand: nutrient timing.
Kerksick C, et al. J Int Soc Sports Nutr. 2008 Oct 3;5(1):17.
[Medline]

10 Long-term persistence of adaptive thermogenesis in

subjects who have maintained a reduced body
weight.
Rosenbaum M, et al. Am J Clin Nutr. 2008 Oct;88(4):906-
12. [AJCN]

11 Caffeine supplementation and multiple sprint

running performance.
Glaister M, et al. Med Sci Sports Exerc. 2008
Oct;40(10):1835-40. [Medline]

12 Postexercise Muscle Glycogen Synthesis with

Combined Glucose and Fructose Ingestion.
Wallis GA, et al. Med Sci Sports Exerc. 2008
Oct;40(10):1789-94. [Medline]

Alan Aragon’s Research Review – October, 2008                                  [Back to Contents]                  Page 1 

So much ado about insulin hindering fat loss, so little
evidence. By Alan Aragon
INTRODUCTION
Fear is a bestseller
An ongoing debate amongst the fitness pundits is insulin’s effect
on bodyfat reduction compared to merely a hypocaloric state. A
barrage of bestselling pop-diet books including Protein Power,
Enter The Zone, Sugarbusters, Atkins New Diet Revolution, the
South Beach Diet have been instrumental in kickstarting a global
concern over insulin levels. The authors collectively blame
impaired insulin metabolism as the root of all cardiovascular
disease. Although there’s some disagreement on the exact
definition, a combination of truncal obesity, glucose intolerance,
high blood pressure, inflammation, and dyslipidemia is generally
known as the metabolic syndrome,1 also called syndrome X.
With the lay public’s fear primed toward anything insulinogenic
“causing” syndrome X, it makes sense that carbohydrate got the
brunt of the blame, since a major function of insulin is to lower
blood glucose levels. Protein and amino acids are insulinogenic
as well, but that complicates the neat little anti-carb stance.
Things get funny when we cross over into the fitness realm,
where a sizable faction of enthusiasts place insulin concerns
above thermodynamics when discussing fat loss. Rather than
comparing the fat loss effects of low- and high-carb diets per se,
I’ll examine the evidence behind the claim that calories matter
little compared to controlling insulin levels.
INSULIN & BEYOND
The multifaceted multitasker
Insulin is a hormone secreted by the beta-cells of the pancreas.
Its primary function is to direct energy metabolism in the fed
state. Research has focused predominantly on insulin’s
regulatory action on blood glucose. Insulin serves a vital set of
functions within the body; a complete absence of insulin would
result in coma and eventually death. The actions of insulin can
be stratified into 4 levels of immediacy.2 Very fast effects
(occurring within seconds) involve changes in the membranes of
cells involved with glucose transport. Fast effects (within
minutes) involve the suppression of catabolic processes while
upregulating anabolic enzyme systems that promote
glycogenesis, protein synthesis, and lipogenesis. Naturally, the
latter function is where all of the assumptions and
misinformation lies. Slower effects (minutes to several hours)
involve further activity of anabolic enzymes and concurrent
suppression of catabolic enzymes. The slowest effect is the
promotion of anabolism through cell replication and
mitogenesis.
The fat storage hormone?
Insulin can suppress fatty acid oxidation on a micro-level under
certain conditions. However, under hypocaloric conditions, these
micro-effects cannot and do not develop into macro-effects.
Alan Aragon’s Research Review – October, 2008                                  [Back to Contents]                  Page 2
given the aforementioned multitude of anabolic and anticatabolic
functions, insulin’s lay moniker as the “fat storage hormone” is
clearly an oversimplification. While it’s true that insulin can
antagonize the fat-mobilizing effects of counterregulatory agents
such as hormone-sensitive lipase (HSL), it’s not the only
endogenous compound that does this.
In contrast to the multifunctional role of insulin, Acylation
stimulating protein (ASP) is a hormone whose primary function
appears to be to increase fat storage.3 It accomplishes this by at
least three separate mechanisms.4 ASP first increases the activity
of diacylglycerol transferase which in turn increases fatty acid
esterification in the adipocytes. It also stimulates glucose
transport in preadipocytes. Finally, it inhibits the activity of
HSL, and thus decreases lipolysis. The clincher is that ASP can
increase lipogenesis in the adipocytes independently of any
insulin elevation. Similarly, a compound known as fat-specific
protein 27 (FSP27) promotes triacylglycerol deposition in
adipocytes via inhibition of lipolysis.5 FSP27 binds to lipid
droplets and regulates their enlargement. Expression of FSP27 in
subcutaneous adipose tissue was seen to decrease with total fat
mass, but this was unrelated to measures of insulin resistance.6
INSULIN’S ELUSIVE ROLE IN WEIGHT & FAT GAIN
Lack of effect on appetite
Contrary to popular assumption, lower insulin response to a
meal does not consistently correlate with greater satiety. Bowen
and colleagues compared the appetite effects (measured by
subsequent buffet lunch intake) of either glucose, fructose,
whey, or whey plus fructose.7 No differences were observed
despite a significantly greater insulin response elicited by the
glucose treatment compared to the whey and/or fructose.
In another example, Akhavan and Anderson compared the
satiating effects of solutions with varying glucose-to-fructose
ratios.8 Expectedly, the 80% glucose/20% fructose solution caused
the highest insulin response, and the 20% glucose/80% fructose
solution caused the lowest insulin response. The high-glucose
solution caused the lowest subsequent food intake despite having
the highest insulinemic effect.
The latter results are in agreement with a previous trial by
Anderson and colleagues who found an inverse relationship
between mealtime energy intake and the glycemic effect of the
preload.9 In other words, It’s safe to assume that insulinemic
response correlated directly with glycemic response given the
carbohydrate sources compared in this study (polycose, sucrose,
amylopectin, a fructose-glucose mixture, and amylase). In a
recent trial, Flint and colleagues found that a higher insulin
response (but not glycemic response) correlated with an
increased feeling of fullness and decreased desire to eat.10
Insulin response bows to caloric restriction
Energy restriction improves glycemic control (and thus insulin
metabolism) regardless of a wide array of carbohydrate
proportions ranging from 15-73% of dietary calories.11 Plasma
insulin levels decrease concurrently with decreases in
bodyweight regardless of diet composition. Conversely, as
 
bodyfat increases, overeating in addition to the development of
insulin resistance results in higher circulating insulin levels – not
the other way around.
No clear weight/fat-loss advantage to lower-insulinemic diets
Almost a decade ago, a 2-month trial by McLaughlin and
colleagues demonstrated that under hypocaloric conditions, the
most insulin-resistant and hyperinsulinemic subjects lost weight
as effectively as the most insulin-sensitive subjects with the
lowest insulin responses.12 Similarly, a recent 3-month trial by
de Luis and colleagues, basal glycemic status (impaired vs
normal glucose metabolism) and insulin response had no
influence on weight or fat loss.13 In another recent study, Noakes
and colleagues found no difference in weight or fat loss among 3
diets varying from 4%-70% carbohydrate over a 2-month
period.14 This lack of difference was seen despite a 33% greater
reduction in fasting insulin levels caused by the lowest-carb
treatment compared to no insulin reduction in the highest-carb
treatment.
Glycemic index (GI) of foods is very closely correlated with
insulin response.15 So, if the insulinemic effect of a diet was a
major determinant of its ability to regulate fat gain or loss, then
we’d see low-GI diets decisively beating high-GI diets for
weight or fat loss. However, the majority of long-term trials
lasting 6 months or longer show that this is simply not the case;
GI indeed makes no significant difference in weight and/or fat
loss.16-20 Along these lines, low-carbohydrate diets almost
always have greater insulin-lowering effects than high-
carbohydrate diets. Most trials spanning up to 6 months show the
superiority of low-carb diets for weight loss. However, with
scant exception,21 controlled trials whose duration or follow-up
points reach the 12-month mark, low-carb diets offer no weight
loss benefits over their high-carb counterparts. 22-24
It’s important to note that the lackluster long-term results of the
low-carb diets occurred despite the use of obese/de-conditioned
subjects. If these comparisons were applied to the athletic
population, the differences would be even more miniscule
considering that fit folks have better glucose tolerance than the
deconditioned obese. As I’ve mentioned in past articles,
sufficient protein beats insufficient protein on a number of
metabolic and body composition parameters. However, for the
purpose of altering bodyweight or composition, a diet’s ability to
raise or lower insulin levels pales in comparison to a diet’s
influence on thermodynamics. A diet’s insulin-eliciting capacity
might have minor bearing in the short term, but this disappears
in the long-term in most cases.
No clear effect on body composition even when drug-suppressed
In a poignant example of the non-relation of insulin secretion to
bodyfat reduction, Due and colleagues examined the effect of
inhibiting insulin secretion by pharmacological means
(diazoxide).25 After 8 weeks of calorie restriction, insulin-
resistant obese subjects experienced no difference in weight or
fat loss whether on placebo or diazoxide. Furthermore, no
differences were seen in appetite, resting energy expenditure, or
respiratory quotient. The authors concluded that despite
contrasting results seen in a previous study,26 suppression of
Alan Aragon’s Research Review – October, 2008                                  [Back to Contents]                  Page 3
insulin output is not likely to be an effective strategy for obese
patients.
SUMMARY POINTS
Insulin & beyond
• Insulin is a hormone secreted by the beta-cells of the
pancreas. Its primary function is to orchestrate energy
metabolism in the fed state.
• Insulin plays a vital set of anabolic and anticatabolic roles
within the body; a complete absence of insulin would result
in coma and eventually death.
• Insulin can suppress fatty acid oxidation under certain
transient conditions. However, given its diverse functions,
it’s grossly oversimplified to refer to it as the “fat storage
hormone”.
• In contrast to the multifunctional role of insulin, Acylation
stimulating protein (ASP) is a hormone whose primary
function appears to be to increase fat storage.
• Similarly, a compound known as fat-specific protein 27
(FSP27) promotes triacylglycerol deposition in adipocytes
via inhibition of lipolysis.
Insulin’s elusive role in weight and fat loss
• Contrary to popular assumption, lower insulin response to a
meal does not consistently correlate with greater satiety.
• Energy restriction improves glycemic control (and thus
insulin metabolism) regardless of a wide array of
carbohydrate proportions.
• The current body of research evidence shows that there is
little to no weight or fat loss advantage in diets that that are
less insulinemic.
• Despite the close correlation of glycemic index (GI) and
insulin index, the majority of trials lasting 6 months or longer
show GI makes no difference in bodyweight & bodyfat loss.
• Suppression of insulin secretion via pharmacological means
is not a reliable method for enhancing weight or fat loss in
obese hyperinsulinemic subjects.
• Calorie flux (thus changes in mass) can influence hormonal
flux – not the other way around.
• Obesity can lead to hyperinsulinemia – not the other way
around.
CONCLUSION
It always makes me chuckle when I tool around the forums and
see that a large segment of the dieting population has a mortal
fear of insulin. Many of these same folks will copiously
consume protein hydrolysates along with amino acid
supplements during exercise and between meals. This only
serves to keep insulin jacked skyward all day long – but no need
to tell them this and ruin their bliss. The majority of dieters are
far more vigilant about carb restriction rather than total caloric
restriction. Their fear is that along with carbs comes a hike in
insulin levels and inability to lose fat. But behold, oh insulin-
phobes, reams of research demonstrate that this fear is rooted in
paranoia. Still, an excess of carb-free calories are sucked down
the hatch, and bewilderment over a lack of weight loss
continues… Keyword: calories.
 
REFERENCES 18. Sichieri R, et al. An 18-mo randomized trial of a low-
glycemic-index diet and weight change in Brazilian women.
1. Reaven GM. The metabolic syndrome: is this diagnosis Am J Clin Nutr. 2007 Sep;86(3):707-13. [Medline]
necessary? Am J Clin Nutr. 2006 Jun;83(6):1237-47. 19. Raatz SK et al. Reduced glycemic index and glycemic load
[Medline] diets do not increase the effects of energy restriction on
2. Groff JL, et al. Advanced Nutrition and Human Metabolism, weight loss and insulin sensitivity in obese men and women.
2nd Edition. St. Paul, MN. West Publishing Company, 1995. J Nutr. 2005 Oct;135(10):2387-91. [Medline]
3. Miner JL. The adipocyte as an endocrine cell. J Anim Sci. 20. Raben A. Should obese patients be counselled to follow a
2004 Mar;82(3):935-41. [Medline] low-glycaemic index diet? No. Obes Rev. 2002
4. Jazet IM, et al. Adipose tissue as an endocrine organ: impact Nov;3(4):245-56. [Medline]
on insulin resistance. Neth J Med. 2003 Jun;61(6):194-212. 21. Gardner CD, et al. Comparison of the Atkins, Zone, Ornish,
[Medline] and LEARN diets for change in weight and related risk
5. Puti V, et al. Fat-specific protein 27, a novel lipid droplet factors among overweight premenopausal women: the A TO
protein that enhances triglyceride storage. J Biol Chem. Z Weight Loss Study: a randomized trial. JAMA. 2007 Mar
2007 Nov 23;282(47):34213-8. [Medline] 7;297(9):969-77. [Medline]
6. Keller P, et al. Fat-specific protein 27 regulates storage of 22. Dansiger ML, et al. Comparison of the Atkins, Ornish,
triacylglycerol. J Biol Chem. 2008 May 23;283(21):14355- Weight Watchers, and Zone diets for weight loss and heart
65. [Medline] disease risk reduction: a randomized trial. JAMA. 2005 Jan
7. Bowen J, et al. Appetite hormones and energy intake in 5;293(1):43-53. [Medline]
obese men after consumption of fructose, glucose and whey 23. Foster GD, et al. A randomized trial of a low-
protein beverages. Int J Obes (Lond). 2007 Nov;31(11):1696- carbohydrate diet for obesity. N Engl J Med. 2003 May
703. [Medline] 22;348(21):2082-90. [Medline]
8. Akhavan T, Anderson GH. Effects of glucose-to-fructose 24. Stern L, et al. The effects of low-carbohydrate versus
ratios in solutions on subjective satiety, food intake, and conventional weight loss diets in severely obese adults: one-
satiety hormones in young men. Am J Clin Nutr. 2007 year follow-up of a randomized trial. Ann Intern Med. 2004
Nov;86(5):1354-63. [Medline] May 18;140(10):778-85. [Medline]
9. Anderson GH, et al. Inverse association between the effect 25. Due A, et al. No effect of inhibition of insulin secretion by
of carbohydrates on blood glucose and subsequent short- diazoxide on weight loss in hyperinsulinaemic obese
term food intake in young men. Am J Clin Nutr. 2002 subjects during an 8-week weight-loss diet. Diabetes Obes
Nov;76(5):1023-30. [Medline] Metab. 2007 Jul;9(4):566-74. [Medline]
10. Flint A, et al. Glycemic and insulinemic responses as 26. Alemzadeh R, et al. Beneficial effect of diazoxide in obese
determinants of appetite in humans. Am J Clin Nutr. 2006 hyperinsulinemic adults. J Clin Endocrinol Metab. 1998
Dec;84(6):1365-73. [Medline] Jun;83(6):1911-5. [Medline]
11. Freedman MR, et al. Popular diets: a scientific review. Obes
Res. 2001 Mar;9 Suppl 1:1S-40S. [Medline]
12. McLaughlin T, et al. Differences in insulin resistance do not
predict weight loss in response to hypocaloric diets in
healthy obese women. J Clin Endocrinol Metab. 1999
Feb;84(2):578-81. [Medline]
13. de Luis DA, et al. Differences in glycaemic status do not
predict weight loss in response to hypocaloric diets in obese
patients. Clin Nutr. 2006 Feb;25(1):117-22. Epub 2005 Nov
8. [Medline]
14. Noakes M, et al. Comparison of isocaloric very low
carbohydrate/high saturated fat and high carbohydrate/low
saturated fat diets on body composition and cardiovascular
risk. Nutr Metab (Lond). 2006 Jan 11;3:7. [Medline]
15. Holt SH, et al. An insulin index of foods: the insulin
demand generated by 1000-kJ portions of common foods.
Am J Clin Nutr. 1997 Nov;66(5):1264-76. [Medline]
16. Das SK, et al. Long-term effects of 2 energy-restricted diets
differing in glycemic load on dietary adherence, body
composition, and metabolism in CALERIE: a 1-y
randomized controlled trial. Am J Clin Nutr. 2007
Apr;85(4):1023-30. [Medline]
17. Aston LM, et al. No effect of a diet with a reduced
glycaemic index on satiety, energy intake and body weight
in overweight and obese women. Int J Obes (Lond). 2008
Jan;32(1):160-5. [Medline]

Alan Aragon’s Research Review – October, 2008                                  [Back to Contents]                  Page 4 

Olympic speedskater Maria Garcia drops some insight
for the hopefuls.
Interviewed by Alan Aragon
Maria Garcia is a rare breed of individual I like to refer to as the
pure athlete. She’s blessed with talent, and possesses a work
ethic that I simply stand in awe of. She just qualified for the
World Cups, so she’s at an exciting position to ascend the ranks
and continue on towards making the Olympic team once again.
I find her story educational and inspirational, and here it is.
__________________________________________________
Let's go way back and start with where you grew up, and
how you initially got involved in skating, and eventually
competitive speedskating.
I grew up inner city in Carson, CA. My parents got me involved
with many sports to keep me out of trouble. I ran track and Field,
played tennis, and figure skated. One day when I was at a public
session figure skating my mom saw a poster advertising to come
try speedskating for $3.00. Figure skating was financially the
wrong move for my family, so in order to remain on the ice I
switched to speedskating. Within three months I went to my first
Nationals in West Point, NY and placed third overall and
continued competitively within the sport ever since. I was lucky
that I had a natural talent for ice and enjoyed it just as much.
What are your most significant or proudest career
accomplishments on and off the ice?
My proudest accomplishment has been being a member of the
2006 Winter Olympic Team in Torino, Italy and being the only
member to do so training outside of an Olympic Training Center.
Off the ice I am currently in school I try to maintain 1-2 classes
per semester until I can be a full time student. I also dedicate my
time to volunteering with the Southern California Olympians
Association and the Ready Set, Gold! program where Olympians
go to schools throughout the Los Angeles Unified School
District to help spread Olympic spirit, help students set goals for
Alan Aragon’s Research Review – October, 2008                                  [Back to Contents]                  Page 5
fitness gram testing and to help promote a healthy lifestyle. I
also am a proud member of the American Heart Association (I
have a pulmonary valve insufficiency).
What were some of the decisions you've made in your
athletic career that you wish you could rewind the clock and
do differently?
I truly believe in growing and learning about myself mentally
and physically from mistakes. There may have been incidents in
my athletic career when I look back thinking I should have done
something differently. But, the most important thing is to learn
valuable lessons from the different steps and paths taken in life.
Are there any major pitfalls you'd warn aspiring competitive
athletes to watch out for?
I choose to live outside the Olympic training center and train
with my local club in southern California. I do my best to prove
that you can accomplish your dreams without having to leave
your home at an early age to move to a training center. I do
believe that the Olympic training center is a great facility, with
some of the best coaches, trainers, dietitians, and it may offer
some financial relief to athletes. However, the training center
was not the right fit for me. I think it’s important for athletes to
decide what they want out of their own athletic career. Compete
for the right reasons and never feel as though sport is a job. I
love training at my local club because I think it reminds me why
I even began speedskating watching the younger skaters try to
reach their athletic dreams, and have so much passion for the
sport. I hope that skaters can look to me for encouragement as I
look to them for encouragement.
What have been the most effective training techniques that
have helped you reach your current level of skill and
conditioning?
I am still learning about myself mentally and physically. I have
developed a program that has helped me remain injury free and
physically and mentally strong. Financially it may be a struggle
but, I have a wonderful group of intelligent professionals all
working toward the same goal.
How much effort have you personally needed to dedicate to
the mental/psychological aspect of competitive skating?
I love sports psychology in fact that is what I hope to call my
career one day. Short-rack speedskating happens to be an
extremely unique and exciting sport because you are racing 5-6
other skaters in one race so it requires far more than just being
physically in great shape. Mental endurance, strategy, and
composure play a big part in racing.
Is there any particular way(s) you train that you feel are
different from the norm that other athletes might benefit
from trying?
I would love to answer this question in more detail upon retiring.
I do feel as though I have a different outlook on training at an
 
Olympic level especially in comparison to my teammates that
train within the Olympic training center.
Can you give us a typical day (off-season, in-season, or pre-
season, your choice) in the life of Maria Garcia?
I always try to get 8-10 hours of sleep. I eat a very balanced diet
(which I can thank you for, I now understand the important
details of fueling my workouts) and include sports drinks
throughout training. I train 2-4 hours every day except for
Sundays which is my recovery day.
We’ve discussed your back injury in Beijing, and I would
love for you to share the details with my readers. I certainly
gained a new perspective of the term “crisis management”
after hearing it.
I was in Beijing for a world cup. I was skating as a member of
the woman's 3000m relay. I came out for an exchange and
within one lap of the exchange I crashed. It was an interesting
fall (which I have on video and watched countless times trying
to come to some conclusion as to why I fell). When I hit the
wall, I immediately lost feeling in the left side of my body. I
remember falling just under the coach's box where the national
training coach was yelling for me to get up and out of the corner
which is dangerous in case of another fall. What seemed liked a
lifetime was only just under a minute on the video replay. I
managed to get up and get to the middle where I waited for the
race to finish up and upon completion got off the ice lied on my
back. I remained on my back for the following 5 days.
Upon exiting the ice, I was met by the team medical staff and the
medical staff of other countries. I was duct taped to a board and
told that I must have a serious back injury due to the paralysis
in my left side. I was Lifted onto a gurney, rolled on a
cobblestone walkway, and loaded into an ambulance. When I
say Ambulance it’s not of those I speak of in America. It literally
was a minivan with the seats taken out. I remember thinking to
myself, “I hope this car has amazing shocks because I don't think
I could handle any more cobblestone streets.” But, to my
discomfort, I was driven painfully along a cobblestone street to a
Military Hospital where I was not going to be treated because of
being an American.
I remember the hospital to be the classic nurses in white skirted
outfits and the doctor leaning over me with a headlamp. Upon
deciding to treat me, the doctor was ecstatic because they just
received their very first MRI machine the previous day. The
doctor then asked me if I could walk to the MRI room. Sarah,
our sports med staff nurse, insisted that with a back injury I
shouldn't be moved – let alone walk. About five nurses and two
doctors began to grab my limbs and insist that I be carried into
the room since the gurney was made of metal. There was lots of
arguing about what to do and not to do.
Sarah came to the conclusion that I could not be treated here. I
lied on a metal gurney for a few hours as Sarah was on the
phone making arrangements for transportation to a hospital that
could treat me. Every so often a female nurse would lean over
Alan Aragon’s Research Review – October, 2008                                  [Back to Contents]                  Page 6
with excitement and adjust my sheets. I refused to have an IV or
any medication – even pain killers – because being an athlete I
need to trust the source and have an understanding of what I was
taking.
I remember waking to Sarah telling me that I was going to be
driven to the opposite side of Beijing where a doctor from
Canada was doing an internship at a westernized hospital. This is
where it ended... Long story short... I was driven to the opposite
side of Beijing to be treated at a westernized hospital. I was
diagnosed with a fracture in C-1, C-5 and congenital fusion in C-
3 and C-4. The doctor said he did not have the medical supplies
or staff to treat my injury. I was told by my program director that
he needed a credit card to pay the hospital. I was wearing only a
skinsuit and did not have a credit card in my name nor access in
handing over one. US Speedskating said they would not be
responsible for paying my medical bills. The nurse rolled me out
into the hallway until I could come up with payment. I lied there
for hours calling my family who luckily got in touch with a
family friend that could supply a credit card to cover my medical
bills.
I spent the night in Beijing a waiting an Air Ambulance to fly
me to Hong Kong for further treatment. That following morning
I was air ambulanced to Hong Hong for treatment. The doctor
there said it was a clean break, and that until the ligament and
sternum damage I had sustained could stabilize my spin, I was to
remain in the hospital. About five days later I was released from
the hospital to fly back home. Again I had difficulty with US
Speedskating agreeing to purchase my plane ticket. But they did.
I was then sent to the Olympic Training Center to see the Team
doctor that said upon reading my results I did not have any
spinal injuries. I flew home back to California after deciding to
compete a month later at my US Junior Nationals which I placed
first under the impression I had not fractured my back. I then
competed in Junior Worlds in Belgrade, Serbia, placing ninth to
return home with back pain. I then saw my Orthopedic doctor
and he again confirmed that I indeed had a fractured back and
had sustained sternum and ligament damage.
It’s amazing how you were able to get through that and get
back into competition full-force. Who do you consider to be
your main influences in your athletic career?
I never had a particular athlete that I idolized. I love all great
athletes and I have a respect for all great athletic
accomplishments. My parents have always taught me to immerse
myself physically and mentally in anything I decide to do.
Are there any special ways you deal with the rigors of travel
and its effects on training and performance?
This is something I still struggle with. I am a terrible traveler. I
always find myself extremely hungry, jet-lagged, dehydrated,
and almost always end up coming down with a sickness. I try to
reduce stress by packing and arriving to the airport early, I have
a travel blanket, headphones that are supposed to reduce the
effects of jet-lag, an eye mask etc. On international flights I walk
 
around, change my clothes, wash my face, brush my teeth. I try
to make myself as comfortable as possible.
Being a full-time athlete obviously requires a delicate
balance of training and rest. Are there any specific things
you do to relax?
weight. My training work level has increased due to supplying
enough calories all while decreasing body fat. I have also
noticed how fueling before and after workouts plays a huge part
in my recovery.
Thanks very much, Maria!

Catch up with family and friends. They take a backseat to my

EDITOR’S  NOTE:  I  know  that  was  cheesy  of  me  to  put  Maria 
training and competition schedule. I also really enjoy yoga, and
through  that  final  question.  But  since  she’s  my  client,  I  just 
trying anything new and adventurous, skydiving, curling,
couldn’t resist. Big thanks to Maria for doing this interview. 
Trapeze.

What are your current projects, your plans for the

immediate future, and plans for life after competitive
skating?

I am currently in school maintaining 1-2 classes per semester.

After skating I plan to become a full-time student. I plan to join
a nursing program. While I am working as a nurse I plan to
finish my bachelors and masters in psychology. My dream
career is to become a clinical psychologist. I plan to always
volunteer my time to my local speedskating club and hopefully
start a non-profit to get youth, especially inner city youth,
involved in the winter Olympics – particularly in my realm of
expertise, speedskating. I also plan to volunteer time with the
American Heart Association to promote a healthy heart since I
struggle with a pulmonary insufficiency. I also would love to be
part of Doctors without Borders as a nurse and do some
volunteer work abroad.

What are some key gems of advice that you'd give a young
athlete aspiring to reach Olympic-level competition?

Set goals! Focus on your dreams and always be aware that

achieving is believing.

Favorite book?

The inner game of Tennis, Wooden

Favorite movie?

City of God, Maria full of grace.

Favorite food?

Mexican food. Carne Asada tacos.

Favorite way to get motivated or psyched up for training?

I train to compete! If I don't train hard I wont see the results

competitively I want. It all works together. You have to put in
the work to see results.

Favorite nutritionist?

Alan Aragon!! I have always had difficulty losing and

maintaining a steady weight. Especially being an athlete I am
aware of supplying enough calories to perform but could never
find a balance of understanding what to cut out in order to lose

Alan Aragon’s Research Review – October, 2008                                  [Back to Contents]                  Page 7 
 I have no major criticisms here other than that consuming 8-16
oz of fluid every 10-15 minutes is definitely on the high end. Try
International society of sports nutrition position stand: consuming this amount at this rate and you’ll see what I mean. I
nutrient timing. can see this level of consumption being realistic if the training is
at a relatively high intensity in a high-temperature environment.
Kerksick C, et al. J Int Soc Sports Nutr. 2008 Oct 3;5(1):17. Aside from those conditions, the fluid demand would be
[Medline] substantially less. I recommend starting with a lower dose of
150-350mL (6-12oz) every 15-20 minutes in order to minimize
Competitive sports cover the gamut from the strength/power- gastric discomfort, and you can always ratchet up from there.
focused all the way to ultraendurance events. One glaring                 
deficiency in this position stand’s text was the absence of the 3) Ingesting CHO alone or in combination with PRO during resistance 
acknowledgement of a broad continuum that the various sports exercise  increases  muscle  glycogen,  offsets  muscle  damage,  and 
fall upon. Without mentioning this, it makes for a simpler facilitates  greater  training  adaptations  after  either  acute  or 
position stand, but it also ignores the distinctly different energy prolonged periods of supplementation with resistance training.      
and substrate demands of each type of sport. Ultimately, it
overshoots the needs of one sport while undershooting the needs The addition of protein to the carbohydrate solution as suggested
of another. It would have been a better idea for the Journal of is not likely to increase performance, but it indeed can prevent
International Society of Sports Nutrition to stratify their muscle protein breakdown. Again, this is application benefits
recommendations according to demands of fuel timing, type, prolonged endurance training, and may or may not be necessary
amount, and form (refer to the January, February, and March or optimal given that pretraining nutrition was not neglected. It’s
Issues of AARR to see what I mean). crucial to note that the overwhelming majority of nutrient timing
                 research has been done on fasted subjects. Consumption of
The position of the Society regarding nutrient timing and the intake  additional substrates in the fed state is very likely an exercise in
of  carbohydrates,  proteins,  and  fats  in  reference  to  healthy,  redundancy. Let’s not forget that depending on its size, a meal
exercising individuals is summarized by the following eight points: 1)  takes at least 3-6 hours to digest and absorb. A properly placed
Maximal  endogenous  glycogen  stores  are  best  promoted  by  pretraining meal will keep substrate levels sufficiently elevated
following a high‐glycemic, high‐carbohydrate (CHO) diet (600 ‐ 1000  during training bouts that don’t approach or exceed 2 hours. This
grams  CHO  or  ~  8  ‐  10  g  CHO/kg/d),  and  ingestion  of  free  amino  includes most non-endurance training bouts.
acids  and  protein  (PRO)  alone  or  in  combination  with  CHO  before 
resistance exercise can maximally stimulate protein synthesis.     
                
4)  Post‐exercise  (within  30  minutes)  consumption  of  CHO  at  high 
dosages (8 ‐ 10 g CHO/kg/day) have been shown to stimulate muscle 
While it’s true that high-glycemic carbohydrates are the fastest glycogen  re‐synthesis,  while  adding  PRO  (0.2  g  ‐  0.5  g  PRO/kg/day) 
at resynthesizing glycogen, they are neither necessary nor to  CHO  at  a  ratio  of  3  ‐  4:1  (CHO:  PRO)  may  further  enhance 
optimal for sports that do not involve multiple glycogen- glycogen re‐synthesis.              
depleting events in a single day. This high-GI obsession that
pervades the recommendations is one of the most persistent Again, these recommendations are fine for endurance
examples of mythology in the literature. The fact of the matter applications. However, it’s rather odd to suggest that additional
is, fully depleted glycogen stores get completely replenished protein at 0.2-0.5g/kg/day will be of any benefit if an adequate
within 24 hours regardless of the glycemic nature of the daily protein intake (roughly 2g/kg/d) is already in place.
carbohydrate ingested. This occurs regardless of the presence of                 
other macronutrients. Even high amounts of fat (165g), which 5) Post‐exercise ingestion (immediately to 3 h post) of amino acids, 
undoubtedly would lower the glycemic effect, still do not primarily essential amino acids (EAA), has been shown to stimulate 
prevent full glycogen repletion from occurring within 24 hours.2 robust  increases  in  muscle  protein  synthesis,  while  the  addition  of 
CHO  may  stimulate  even  greater  levels  of  protein  synthesis. 
The total amount suggested (8-10g/kg/d, or 600-1000g/d) is Additionally, pre‐exercise consumption of a CHO + PRO supplement 
suitable for competitive endurance athletes, but is excessive for may result in peak levels of protein synthesis.          
all other populations. It’s grossly excessive for noncompetitive
recreational athletes. Burke and colleagues have suggested a The basic premise that protein and carbohydrate intake should
more reasonable dosing stratification of 5-7g/d for competitive sandwich both sides of the training bout is correct. However, a
strength/power and general training needs, and 7-10g/d for glaring deficiency of this review is the lack of emphasis that
endurance athletes.1 non-supplemental means to fulfill nutrient requirements pre- and
                 postexercise can be done with ease. Most high-quality protein
2)  During  exercise,  CHO  should  be  consumed  at  a  rate  of  30  ‐  60  sources contain 40-50% EAA. Animal proteins range from 18-
grams  of  CHO/hour  in  a  6  ‐  8  %  CHO  solution  (8  ‐  16  fluid  ounces)  26% BCAA. Even soy protein is 18% BCAA. Supplemental
every 10 ‐ 15 minutes. Adding PRO to create a CHO:PRO ratio of 3 ‐  EAA and BCAA beyond what's already present in a typical
4:1  may  increase  endurance  performance  and  maximally  promotes  athlete's protein-rich diet will very likely do nothing other than
glycogen  re‐synthesis  during  acute  and  subsequent  bouts  of  add unnecessary metabolic stress. Exceptions to the “whole food
endurance exercise.              
suffices” application are endurance and endurance-type athletes

Alan Aragon’s Research Review – October, 2008                                  [Back to Contents]                  Page 8 
whose training approaches or exceeds 2 hours of continuous
work; they may benefit from mid-training intake.
                
6)  During  consistent,  prolonged  resistance  training,  post‐exercise 
consumption of varying doses of CHO + PRO supplements in varying 
dosages  have  been  shown  to  stimulate  improvements  in  strength 
and  body  composition  when  compared  to  control  or  placebo 
conditions.                  

I agree.
                
7) The addition of creatine (Cr) (0.1 g Cr/kg/day) to a CHO +
PRO supplement may facilitate even greater adaptations to
resistance training.              

This is correct if muscle creatine stores are not yet saturated, in

which case, concurrent ingestion with protein and/or
carbohydrate can speed up this process. However, after roughly
a month of regular creatine dosing at 2-5 g/day (or about a week
of high-dose loading at roughly 20g/day), a saturation point is
reached, and the timing of creatine ingestion with other
substrates will have little additional benefit, if at all.
                
8) Nutrient timing incorporates the use of methodical planning
and eating of whole foods, nutrients extracted from food, and
other sources. The timing of the energy intake and the ratio of
certain ingested macronutrients are likely the attributes which
allow for enhanced recovery and tissue repair following high-
volume exercise, augmented muscle protein synthesis, and
improved mood states when compared with unplanned or
traditional strategies of nutrient intake.

The above summary point contains the only two mentions of the
word “food’ in the entire document. After reading through the
entire manuscript, it’s easy to come away with the message that
you must consume quick sugars and isolated amino acids during
and around training for maximal results. Except for endurance
athletes and those with multiple depletion bouts of the same
muscles in a day, this just isn’t the case. To conclude, I’ll leave
you with the hierarchy of importance that I reiterated throughout
the nutrient timing series I wrote at the beginning of the year:

T  HE HIERARCHY OF IMPORTANCE  
When  speaking  of  nutrition  for  improving  body  composition  or 
athletic  performance,  it’s  crucial  to  realize  there’s  an  underlying 
hierarchy  of  importance.  At  the  top  of  the  hierarchy  of  effects  is 
total amount of the macronutrients by the end of the day. Below 
that  –  and  I  mean  distantly  below  that  –  is  the  precise  timing  of 
those  nutrients.  With  very  few  exceptions  (i.e.,  the  intermittent 
fasting  populace),  athletes  and  active  individuals  eat  multiple 
times per day, to the tune of at least four meals, and up to 6 or 7. 
Thus,  the  majority  of  their  day  is  spent  in  the  postprandial  (fed) 
rather  than  a  post‐absorptive  (fasted)  state.  The  vast  majority  of 
nutrient  timing  studies  have  been  done  on  overnight‐fasted 
subjects,  which  obviously  limits  the  applicability  of  the  studies’ 
conclusions.  Pre‐exercise  (and/or  during‐exercise)  nutrient  intake 
often  has  a  lingering  carry‐over  effect  into  the  during‐  and  post‐
exercise period. Throughout the day, there’s a constant overlap of 
meal  absorption.  Therefore,  nutrient  timing  is  NOT  a  strategy 
that’s only effective if done with chronometric precision. 

Alan Aragon’s Research Review – October, 2008                                  [Back to Contents]                  Page 9 
Long-term persistence of adaptive thermogenesis in
subjects who have maintained a reduced body weight.
Rosenbaum M, et al. Am J Clin Nutr. 2008 Oct;88(4):906-12.
[AJCN]
PURPOSE: After weight loss, total energy expenditure—in
particular, energy expenditure at low levels of physical
activity—is lower than predicted by actual changes in body
weight and composition. An important clinical issue is whether
this reduction, which predisposes to weight regain, persists over
time. We aimed to determine whether this disproportionate
reduction in energy expenditure persists in persons who have
maintained a body-weight reduction of 10% for >1 y.
METHODS: Seven trios of sex- and weight-matched subjects
were studied in an in-patient setting while receiving a weight-
maintaining liquid formula diet of identical composition. Each
trio consisted of a subject at usual weight (Wtinitial), a subject
maintaining a weight reduction of 10% after recent (5–8 wk)
completion of weight loss (Wtloss-recent), and a subject who had
maintained a documented reduction in body weight of >10% for
>1 y (Wtloss-sustained). Twenty-four-hour total energy expenditure
(TEE) was assessed by precise titration of fed calories of a liquid
formula diet necessary to maintain body weight. Resting energy
expenditure (REE) and the thermic effect of feeding (TEF) were
measured by indirect calorimetry. Nonresting energy
expenditure (NREE) was calculated as NREE = TEE – (REE
+TEF). RESULTS: TEE, NREE, and (to a lesser extent) REE
were significantly lower in the Wtloss-sustained and Wtloss-recent
groups than in the Wtinitial group. Differences from the Wtinitial
group in energy expenditure were qualitatively and quantitatively
similar after recent and sustained weight loss. CONCLUSION:
Declines in energy expenditure favoring the regain of lost weight
persist well beyond the period of dynamic weight loss..
SPONSORSHIP: National Institutes of Health
Study strengths
Great concept; it begins to answer the important question of just
how metabolically disadvantaged dieters are in the long term
once they’ve lost 10% or more of their bodyweight. As the old
saying goes, anyone can lose weight; keeping it off is the true
challenge. The investigators drew subjects from a pool of their
own studies of energy metabolism before and after weight
reduction in obese and nonobese subjects in an in-patient setting.
Physical activity was closely monitored, weight stability was
clearly documented, and only a liquid formula diet was
undergone while living in a clinical research center (CRC). This
design made it possible to control for differences in diet
composition, subject compliance, and physical activity to a
degree that is not possible in out-patient studies.
Hydrodensitometry was used to assess body composition; this
method is more reliable than skinfolds or BIA, although not
quite as highly regarded as DEXA or ADP.
Study limitations
The study population maintained a low level of physical activity,
which limits the application of these results to the relatively
sedentary. Although the lab setting enforces a greater degree of
control and closer monitoring, it presents a confined space for
physical activity that may not represent free-living conditions.
Alan Aragon’s Research Review – October, 2008                                  [Back to Contents]                  Page 10
Comment/application
The major finding of the present study is that there were
significant declines in total energy expenditure (TEE), non-
resting energy expenditure (NREE), and to a lesser degree,
resting energy expenditure (REE) in subjects maintaining a
reduced body weight. Importantly, this decline persists
regardless of whether that reduced weight has been maintained
for weeks or even years. To quote the authors directly,
“bioenergetic responses to maintenance of a reduced body
weight do not wane with time.”
Based on their previous investigations, the authors further
confirm the dismal reality that the systems regulating energy
intake and output that occur during post-reduction weight
maintenance act coordinately to favor weight re-gain. Since
many of these changes are reversed by restoring circulating
leptin concentrations to pre-weight-loss levels, the authors assert
that they are the consequences of persistent relative
hypoleptinemia long after weight loss has ended. This line of
thought clicks well with the importance of periodic refeeds
consisting of foods that reignite leptin production, particularly
carb-rich foods.
Although not emphasized by the authors, a rich history of their
own research indicates that a decline in energy expended in low-
level physical activity is responsible for most of the TEE
decrease in weight-stable subjects after weight loss.3-6 Given
this, it seems that aside from ramping up physical activity, a
solution to the decreased EE would either be to somehow
increase the metabolic activity of the lean mass, or increase the
amount of lean mass. Achieving both is not out of the question.
As I’ve mentioned previously, it’s possible for the deconditioned
obese to actually increase muscle mass in the face of a severe
caloric deficit if a strength training program is employed. Given
this, it’s certainly not impossible for the more fit population to at
the very least maintain muscle mass in the midst of moderately
hypocaloric conditions. Apparently, the key is in not only
adhering to the diet, but also maintaining somewhat of a
progressive exercise program that includes resistance training.
A recent trial by Hackney and colleagues found that full-body
resistance training (with a concentration on eccentric resistance)
elevated REE for up to 72 hours in both trained and untrained
subjects.7 In another recent example, Hunter and colleagues
compared the effects of 12 kg weight loss in combination with
either aerobic training or resistance training on body
composition and REE.8 Both the aerobic training and no-training
control groups experienced a drop in REE along with the weight
loss, but the resistance training group did not. Predictably, the
resistance group conserved fat-free mass and strength as well.
The take-home message is that we’re finally beginning to
understand the mechanisms underlying the setup for common
weight re-gain in the sedentary population. However, we need to
examine the metabolic effects of sustained weight loss under
optimal diet and training circumstances. I’m sure they’d be a lot
more favorable than what’s been seen in the literature thus far.
 

Caffeine supplementation and multiple sprint running
performance.
Glaister M, et al. Med Sci Sports Exerc. 2008 Oct;40(10):1835-
40. [Medline]
PURPOSE: The aim of this study was to examine the effects of
caffeine supplementation on multiple sprint running
performance. METHODS: Using a randomized double-blind
research design, 21 physically active men ingested a gelatin
capsule containing either caffeine (5 mg x kg(-1) body mass) or
placebo (maltodextrin) 1 h before completing an indoor multiple
sprint running trial (12 x 30 m; repeated at 35-s intervals).
Venous blood samples were drawn to evaluate plasma caffeine
and primary metabolite concentrations. Sprint times were
recorded via twin-beam photocells, and earlobe blood samples
were drawn to evaluate pretest and posttest lactate
concentrations. Heart rate was monitored continuously
throughout the tests, with RPE recorded after every third sprint.
RESULTS: Relative to placebo, caffeine supplementation
resulted in a 0.06-s (1.4%) reduction in fastest sprint time (95%
likely range = 0.04-0.09 s), which corresponded with a 1.2%
increase in fatigue (95% likely range = 0.3-2.2%). Caffeine
supplementation also resulted in a 3.4-bpm increase in mean
heart rate (95% likely range = 0.1-6.6 bpm) and elevations in
pretest (+0.7 mmol x L(-1); 95% likely range = 0.1-1.3 mmol x
L(-1)) and posttest (+1.8 mmol x L(-1); 95% likely range = 0.3-
3.2 mmol x L(-1)) blood lactate concentrations. In contrast, there
was no significant effect of caffeine supplementation on RPE.
CONCLUSION: Although the effect of recovery duration on
caffeine-induced responses to multiple sprint work requires
further investigation, the results of the present study show that
caffeine has ergogenic properties with the potential to benefit
performance in both single and multiple sprint sports.
SPONSORSHIP: St. Mary's University College Research
Support Committee.
Study strengths
A major shortcoming of the majority of previous caffeine
research has been small sample size (10 subjects or less). The
present trial used 21 subjects, strengthening its statistical power.
Four trials of the multiple sprint test were conducted in order to
iron out confounders. Trial 1 was a familiarization test to limit
the effects of learning on the outcome of the experiment. Trial 2
was a baseline test to enable the effects of both caffeine and
placebo to be compared. Trials 3 and 4 were the experimental
trials that were randomized and conducted in a double-blind
manner. All trials were completed at the same time of day in an
indoor, thermostatically controlled environment with a minimum
of 4 days between trials. Perhaps the most critical strength of
this trial was its measurement of resting and preexercise caffeine
levels; a procedure missing in much of the previous research.
Study limitations
Although subjects were instructed to maintain their normal diet
throughout the testing period, no records were kept, and we’re
Alan Aragon’s Research Review – October, 2008                                  [Back to Contents]                  Page 11
talking about college students here. They’re notorious for having
erratic, haphazard eating habits. The subjects were instructed to
abstain from eating 1 hour prior to testing. Since no control or
standardization was assigned to the pre-test meal consumption,
substrate utilization could have varied considerably during the
experimental trials.
Comment/application
Unlike the bulk of previous research, caffeine did not reduce rate
of perceived exertion (RPE) in spite of its performance
enhancement. Another interesting find was that although
caffeine improved sprint performance in the initial stages of the
test, the benefits were offset by an overall increase in fatigue.
Interpreting these results is difficult; a longer series of sprint
tests is necessary to determine whether this would ultimately
neutralize the ergogenesis seen in the present design. Given that
no ergolytic effects of caffeine in previous research have been
seen, it’s not likely that ergolytic effects would occur if the
present design’s work volume was increased.
The mechanisms responsible for caffeine-induced performance
enhancement in the present study are unclear. Current research
points to the antagonism of adenosine receptors, which in turn
stimulates the CNS. A possible limitation of the present study
was that the subjects’ habitual consumption of caffeine was
significantly less than the average amount consumed by the
general population. This opens up the possibility that folks with
a higher habitual intake may be less responsive to the dosing in
the present protocol.
Nevertheless, the possibility of desensitization in chronic
caffeine users is questionable since moderately habituated
subjects have been responsive to caffeine’s ergogenic effects.
For example, Hogervorst and colleagues recently investigated
the effect of a caffeine-containing sports bar on well-trained
endurance athletes.9 An ergogenic effect occurred in spite of two
subjects reporting an intake of over 6 cups of coffee per day,
while the others consumed less than 4 cups (but were still
regular coffee drinkers). Those who were caffeine-naïve upon
initial selection were assigned to increase their caffeine
consumption before the study to reach a moderate level of
habituation as confirmed by salivary caffeine levels.
The authors of the present study emphasize the tentative nature
of the results, since caffeine’s effect on repeated short-term high-
intensity exercise has been inconsistent. Caffeine is no longer on
the banned list of the World Anti-Doping Agency, and is legal to
use in professional sports. Thus, the results of the present study
(and other trials with similar outcomes) have important potential
application to sports involving repeated anaerobic thresholds.
As is the typical problem with the majority of caffeine research,
coffee drinkers are left in the lurch with questions regarding the
effectiveness of an equivalent coffee dose versus isolated
caffeine. Although it’s controversial, a possible advantage of
using coffee instead of caffeine pills (other than a distinguished
yellow smile) is that it contains various compounds associated
with chronic disease prevention.10
 
Postexercise Muscle Glycogen Synthesis
Combined Glucose and Fructose Ingestion.
Wallis GA, et al. Med Sci Sports Exerc. 2008 Oct;40(10):1789-94.
[Medline]
PURPOSE: To evaluate the efficacy of using combined glucose
and fructose (GF) ingestion as a means to stimulate short-term (4
h) postexercise muscle glycogen synthesis compared to glucose
only (G). METHODS: On two separate occasions, six
endurance-trained men performed an exhaustive glycogen-
depleting exercise bout followed by a 4-h recovery period.
Muscle biopsy samples were obtained from the vastus lateralis
muscle at 0, 1, and 4 h after exercise. Subjects ingested
carbohydrate solutions containing G (90 g x h(-1)) or GF (G =
60 g x h(-1); F = 30 g x h(-1)) commencing immediately after
exercise and every 30 min thereafter. RESULTS: Immediate
postexercise muscle glycogen concentrations were similar in
both trials (G = 128 +/- 25 mmol x kg(-1) dry muscle (dm) vs
GF = 112 +/- 16 mmol x kg(-1) dm. Total glycogen storage
during the 4-h recovery period was 176 +/- 33 and 155 +/- 31
mmol x kg(-1) dm for G and GF, respectively (G vs GF). Hence,
mean muscle glycogen synthesis rates during the 4-h recovery
period did not differ between the two conditions (G = 44 +/- 8
mmol x kg(-1) dm x h(-1) vs GF = 39 +/- 8 mmol x kg(-1) dm x
h(-1). Plasma glucose and serum insulin responses during the
recovery period were similar in both conditions, although plasma
lactate concentrations were significantly elevated during GF
compared to G (by approximately 0.8 mmol x L(-1).
CONCLUSION: Glucose and glucose/fructose (2:1 ratio)
solutions, ingested at a rate of 90 g x h(-1), are equally effective
at restoring muscle glycogen in exercised muscles during the
recovery from exhaustive exercise. SPONSORSHIP: Glaxo-
SmithKline Consumer Healthcare, United Kingdom.
Study strengths
Subjects were trained endurance athletes, which is a good thing
in terms of eliminating the newbie effect. In order to minimize
the differences in resting muscle glycogen concentration,
subjects completed a diet recall log in which they recorded diet
patterns 24 h before the first trial. I personally feel that the
investigation of this topic is long overdue.
Study Limitations
The experimental protocol for this and similar studies is
relatively simple and straightforward. It’s tough to really screw
up the design. However, with only 6 participants, we can safely
conclude that a larger sample size could have strengthened the
results considerably.
Comment/application
Plenty of hype in the past half-decade or so has centered on the
use of dextrose postworkout, with the implication that any
fructose at all during this time would be a bad idea. However,
research has been mounting in favor of a combined ingestion of
glucose and fructose (or sucrose) during exercise for the dual
benefit maximal oxidation rate and absence of gastric upset
(unlike single-source solutions).11-13 Since glucose and fructose
Alan Aragon’s Research Review – October, 2008                                  [Back to Contents]                  Page 12
with have different transporters, this opens up the possibility that their
combination may enhance their systemic availability. As the
authors point out, systemic carbohydrate availability has been
speculated as the rate-limiting step in mucle glycogen synthesis,
at least in the early phase. I would also add to this that this
combination might be optimal from the standpoint of supporting
not just muscle glycogen (via glucose), but liver glycogen as
well (via fructose).
The ratio of glucose to fructose in the combination treatment
was 2:1. Which interestingly enough is a figure I’ve speculated
to be optimal for postworkut glycogen resynthesis, given the
relative glycogen capacities of muscle and liver glycogen. To be
specific, I’ve advocated that fructose (or galactose) should be
anywhere from a 25-33% of the postworkout mix. Granted, rapid
glygoenesis has limited application, but in the case of nitpicking
over what’s optimal for this purpose, my original
recommendations are enjoying a semblance of validation.
The authors of the present study originally hypothesized that the
combination treatment would be more effective than the straight
glucose treatment. After seeing that both treatments produced
similar results, their speculation was that a significant portion of
the ingested fructose could have been directed toward lactate
production. This could occur in the liver or kidneys, as well as
the more obvious site – skeletal muscle. Elevated lactate levels
as a result of the combination treatment could potentially explain
the lack of extra muscle glycogen synthesis sine the primary fate
of lactate is oxidation, with glycogen synthesis being a
secondary fate. Nevertheless, the authors (and myself) now have
the license to gloat over these novel findings. To quote the
investigators directly,
“As mentioned in the introduction, previous studies would
indicate that fructose is a relatively poor nutritional precursor
for glycogen synthesis compared with glucose. However, our
results demonstrate that fructose is not detrimental to
postexercise muscle glycogen synthesis when coingested with
glucose using the strategy adopted herein.”
An important detail to consider is that a high-end dosing scheme
was used in this trial. An initial postexercise bolus of
approximately 83 g carbohydrate was followed by about 40 g
every half hour for a total of 4 hours. Therefore, extrapolating
these results to less aggressive dosing schemes should be done
with caution. I previously reviewed a trial by Pedersen and
colleagues, who set the record for the highest rate of glycogen
resynthesis via oral means in humans.15 In the latter trial, a
single dose of caffeine (8mg/kg) and a carbohydrate intake
totaling 4g/kg by the end of a 4 hour recovery period was used to
achieve an overall glycogenesis rate of 57.7 mmol/kg/hr, as
opposed to 44 & 39 mmol/kg/hr seen in the glucose and
combination treatments, respectively. What’s interesting is that
the Pedersen trial used less carbohydrate; an average of 1.0g/kg
per hour as opposed to the 1.2g/kg/hr of the present trial. Looks
like it’s time to test a 2:1 ratio of glucose:fructose with
additional caffeine. Better yet, the glucose-fructose combination
should be pitted against waxy maize starch, without a financially
vested sponsor. For now, you can include some fructose
postworkout without fear of critical impedance of glycogenesis.
 

An open label study to determine the effects of an oral
proteolytic enzyme system on whey protein concentrate
metabolism in healthy males.
Oben J, et al. J Int Soc Sports Nutr. 2008 Jul 24;5:10. [Medline]
PURPOSE: The purpose of this study was to determine if
Aminogen(R), a patented blend of digestive proteases from
Aspergillus niger and Aspergillus oryzae, would significantly
increase the in-vivo absorption rate of processed WPC over
control values. It also investigated if any increase would be
sufficient to significantly alter nitrogen (N2) balance and C-
reactive protein (CRP) levels over control values as further
evidence of increased WPC absorption rate. METHODS: Two
groups of healthy male subjects were assigned a specified
balanced diet before and after each of two legs of the study.
Subjects served as their own controls. In the first leg each
control group (CG) was dosed with 50 g of WPC following an
overnight fast. Nine days later each test group (TG) was dosed
following an overnight fast with 50 g of WPC containing either
2.5 g (A2.5) or 5 g (A5) of Aminogen(R). Blood samples were
collected during each leg at 0 hr, 0.5 hr, 1 hr, 2 hr, 3 hr, 3.5 hr
and 4 hr for amino acid (AA) and CRP analyses. The following
18 AAs were quantified: alanine, arginine, aspartic acid,
cysteine, glutamic acid, glycine, histidine, isoleucine, leucine,
lysine, methionine, phenylalanine, proline, serine, threonine,
tryptophan, tyrosine and valine. Urine was collected for 24 hours
from 0 hr for total N2 analysis.. RESULTS: After baseline
subtraction the mean AUC was significantly greater in each TG
compared the corresponding CG. Comparison of the mean AUC
between each TG and each CG was not significantly different.
Total serum amino acid (TSAA) levels were significantly greater
in each TG compared the corresponding CG. They were also
significantly different between each TG but not between each
CG. All individual serum amino acid (ISAA) levels in TG-A2.5
except glycine, histidine, methionine and serine were
significantly higher than in CG-A2.5 at 4 hr. All ISAA levels in
TG-A5 except methionine and serine were significantly higher
than in CG-A5 at 4 hr. The N2 balance was significantly higher
in each TG compared to the corresponding CG, but not
significantly different between each CG and between each TG.
Significant differences in CRP levels are reported between each
TG compared to the corresponding CG, but not significantly
different between each TG and between each CG.
CONCLUSION: A patented blend of digestive proteases
(Aminogen(R)) increased the absorption rate of processed WPC
over controls, as measured by statistically significant increases
in AUC, TSAA levels, ISAA levels and N2 balance. Significant
decreases in CRP levels and fluxes in AA levels are also
reported. SPONSORSHIP: Triarco Industries, Inc. (Wayne, NJ)
through the contract research organization (CRO) Gateway
Health Alliances, Inc.
Study strengths
At a total of 42 subjects, a sample size this large is unusual in
studies examining the effects of sports supplements; it almost
seems like a fabricated figure. Subjects carried out a specified,
Alan Aragon’s Research Review – October, 2008                                  [Back to Contents]                  Page 13
balanced diet of 2200 kcal/day during a one week
standardization period prior to the start of the study and for nine
days between each leg of the study. Nutrient composition was
reasonably balanced (as opposed to the typical ultra-low protein
regimen). The precise weight and composition was established
for each individual by a registered dietician. Subjects were
provided a main meal at the and given precise take-out portions
for the rest of their meals.
Study limitations
This trial is mainly limited by its acute nature. The effects seen
in the short-term may or may not play out as initially indicated
in the long-term. A perfect follow-up for this study would be to
administer the supplement over a period of months to subjects
on a structured resistance training program. As it stands, we can
only speculate. It’s also open to speculation what sort of
differences may have occurred if they used whey isolate instead
of concentrate.
Comment/application
The results of the present study are rather dramatic, assuming
that these results actually occurred. The Aminogen treatment
arm’s dose-dependent 220% and 350% greater postprandial
amino acid AUC’s coupled with markedly reduced nitrogen
losses seem downright magical. This study wins the award for
having the longest abstract I’ve ever come across (I actually
truncated about 200 words from what you see on the left). It’s
well and good to provide a lot of detail in the abstract, but it’s
also a little fishy; it’s almost as if the abstract is glorified enough
for the reader to skip the full text.
One particularly fishy aspect of this study is the high likelihood
of funding bias. One of the three investigators of this trial (Mark
Anderson) is the director of research and development of Triarco
Industries, Inc., whose featured product is – you guessed it –
Aminogen. As listed in the section outlining the author’s
contributions, Anderson assisted in protocol development,
clinical supply management and manuscript preparation. As
director of R & D of the company that produces the product
under investigation, bias is inevitable. For amusement purposes,
let me quote the manuscript’s section on competing interests:
“None of the researchers have any financial interests
concerning the outcome of this investigation and the results do
not constitute an endorsement by the authors and/or their
institutions concerning the ingredient tested.”
Based on this claim, they should have covered their tracks by not
disclosing Anderson’s employment with Triarco. Another
indication of funding bias is the use of Gateway Health
Alliances, Inc., a contract research organization (CRO).
Although hiring a CRO can produce high-quality research on
paper, a CRO’s underlying function is to efficiently shuttle
manuscripts through every step of the publication process, from
study design, all the way to acceptance in the target journals. An
increasingly popular tactic of CROs is the outsourcing of
research to third parties in foreign countries. For example, the
present trial was carried out in Cameroon, a unitary republic of
central and western Africa. Sure, this cuts costs, but in my view,
it also reduces accountability and credibility (no offense to the
good citizens of Cameroon).
 
1. Burke LM, et al. Guidelines for daily carbohydrate intake:
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9. Hogervorst E, et al. Caffeine improves physical and
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Sports Exerc. 2008 Oct;40(10):1841-51. [Medline]
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Nutr. 2005 Apr;93(4):485-92. [Medline]
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Alan Aragon’s Research Review – October, 2008                                  [Back to Contents]                  Page 14 

Hidden blessings Part 2: What do Alwyn Cosgrove,
Lyle McDonald, and gay porn have in common?
By Alan Aragon
Last month I discussed the unexpected returns of what initially
seemed like doors slamming shut in my face. This month I’ll
continue with the final part of the saga involving a couple of
pivotal office moves, and yes, gay porn.
The importance of putting things in writing
When people go into private practice, the smart ones don’t trust
anyone and have everything laid out in writing. Over the course
of a decade, I built a strong relationship with the personnel of the
health club where I held my nutritional counseling practice.
Regarding competition, I assumed I was protected by an
unwritten code of honor. In other words I was positive that the
health club management felt that it would benefit them to
preserve our relationship, and would do whatever it took to
sustain it since we worked symbiotically. They used my services
to promote memberships, while I relied on them for referrals. It
worked great for quite a while; the club had about 30 trainers
who all trusted and appreciated effectiveness in helping them
help their clients reach their goals.
Short-sightedness 101
I was an independent contractor, not an employee of the club. As
such, I didn’t funnel a cut of my revenue to the club’s bottom
line, I merely gave the trainers referral fees – generous ones. It
was a win-win situation. That is, until a new fitness manager was
hired. Shortly thereafter, he hired a friend. She was a trainer who
wanted to be the nutritionist of the club. She tried her damndest,
but the trainers kept referring clients to this outside contractor
renting space in the building (me) instead of her. So, this conflict
created the new manager’s plot to get rid of me. By this time, it
was a smidge too late to whip up a non-compete agreement. My
eventual departure was a darkly entertaining turn of events. Stick
with me here.
The call of fate
I was tipped off by one of the club personnel to a very large
corporation who was looking for a corporate wellness presenter
to whip their upper management into shape. I interviewed for the
gig (a series of lectures), and got it pretty darn swiftly, thank you
very much. And now the plot thickens. Within a couple of days I
got a call from several of the training staff telling me that Mr.
Manager left a broadcast voicemail threatening to fire anyone
who referred business to me. I wondered what the hell was going
on. Why the sudden, aggressive, un-chesslike move? I did some
digging and found out that one of his subordinates interviewed
for the gig that I ended up getting hired for. Guess who failed
her interview?
As someone who likes to keep things simple, I had my eggs all
in one basket; the trainers of the club were my primary referral
source. So when that critical resource was pulled from under me,
I was in some genuine trouble.
Alan Aragon’s Research Review – October, 2008                                  [Back to Contents]                  Page 15
And now for the kicker
I shortly after found out that Mr. Manager had a rather lengthy
gay porn career. He was a self-proclaimed “bottom” (for those
unfamiliar with the term, go ahead and wikipedia it). I found that
quite amusing. It turns out that he's fairly well-known in those
circles. There was even an instance when a gay guy was hired to
work the front desk, and he was instantly fired for recognizing
Mr. Manager as an ‘actor’ in one of the flicks he saw. Oh, and
by the way, I’m keeping Mr. Manager nameless to protect the
guilty; I’ve gotten over this fiasco, and I just hope that I can pass
along some wisdom by sharing my mistakes.
Back to the saga. Eventually, Mr. Manager got word that I was
blabbering to the training staff about his former film career. Fact
of the matter is, everyone seemed to know about it before I did.
Nevertheless, I never felt the need to hide what was commercial
entertainment available for public consumption. The likely
scenario was that in order to avoid termination, someone
implicated me as the lead loudmouth exposing Mr. Manager’s
shenanigans. So the shit finally hit the fan (so to speak), and I
was banned from the club. Given that my office was located in
the same building as the health club I was banned from, this was
a pretty clear sign that I needed to set up shop elsewhere.
The turning point
So, with my referrals diminished to a handful of clandestine calls
and messages by trainers who knew full-well they were risking
their necks, I relocated to a different facility. At this point I had
less in-person client time, and more downtime on the internet as
I rebuilt my in-person clientele. It was during this downtime that
I was able to further solidify the structure and function of this
research review. This time period forced me to polish up my
distance counseling methods. It also afforded me more time to
generate more online interest in my writing. Had my focus not
shifted from reality to virtual reality, I wouldn’t be as excited as
I am today about how I can educate and communicate to the
public on a broader scale with this review.
The twist
An unexpected twist occurred in last week. I got an offer to set
up my practice in a new training “studio” just a short jog from
my former office. I put the word studio in quotes, because this
place is enormous and extremely busy. My new office is worlds
better than the previous, and several universes better than the
office before that. In short, I’m finally an overworked bastard
who has to put prospective clients on a waiting list. As far as my
in-person practice goes, this will be the apex. All other moves
will be lateral, and in the direction of my keyboard, my monitor,
and the warm solace of Pub Med.
The final bit of news I’m excited about is that I’m working on a
book idea. I might find myself castrated if I start dishing out
details, but it looks like it will be a good year in the making, and
if this project materializes, I will take bro-bashing to the shelves
of your favorite book store. Even if it doesn’t materialize, the
career sector of life will still be better than it ever was.
My main point is that the really good stuff has tended to happen
for me soon after the really bad stuff. So, my advice is to hang
in there and leave the quitting for those in the wrong film genre.
 
The photograph below entitled “Senses” is by Wojtek
Kwiatkowski. I met him at Starbuck’s a couple of weeks back.
Long story, he didn’t have the English skills to communicate
effectively enough with tech support, so I got on the phone and
helped him out. At any rate, the guy periodically travels here
from Poland just to photograph horses. This is how he makes his
living. It seems insane to me to travel alone to a continent on the
far side of the planet to barely profit at all. He says it’s mostly
for the love of the art. Strangely, I didn’t find myself too
skeptical of that claim.
“Senses” is the first photograph Wojtek directed me towards.
I’m going to assume that it’s one of his personal favourites,
because his gravitation towards it was immediate. I find the
image particularly intense and downright haunting. I’ve never
had any remote interest in horses, but his photography has a
classic, otherworldly quality that I think any artist can
here
appreciate. More of his work can be seen here.

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

contention, cheers, jeers, guest articles you’d like to submit, or
any feedback at all, send it over to aarrsupport@gmail.com. All
suggestions are taken very seriously. I want to make sure this
publication continues to stand alone in its excellence.

Alan Aragon’s Research Review – October, 2008                                  [Back to Contents]                  Page 16