ean

11 The questionable research practices of Dr.

Jerrold Petrofsky.
By Cameron Mochrie & Ian Capulet

14 Vertical Jump FAQ.

By Jamie Hale

Copyright © October 1st, 2009 by Alan Aragon

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

2 Adaptive thermogenesis, A.K.A. starvation mode:

the downfall of dieting?
By Alan Aragon

5 Short-term modified alternate-day fasting: a novel

dietary strategy for weight loss and
cardioprotection in obese adults.
Varady KA, et al. Am J Clin Nutr. 2009 Nov;90(5):1138-
43. [Medline]
6 Intermittent fasting does not affect whole-body
glucose, lipid, or protein metabolism.
Soeters MR, Am J Clin Nutr. 2009 Nov;90(5):1244-51.
[Medline]

7 Increased food energy supply is more than

sufficient to explain the US epidemic of obesity.
Swinburn B, et al. Am J Clin Nutr. 2009 Oct 14. [Epub
ahead of print] [Medline]

8 Protease supplementation improves muscle

function after eccentric exercise.
Buford TW, et al. Med Sci Sports Exerc. 2009 Sep 2. [Epub
ahead of print] [Medline]

9 Supplementation with a whey protein hydrolysate

enhances recovery of muscle force-generating
capacity following eccentric exercise.
Buckley JD, et al. J Sci Med Sport. 2008 Sep 1. [Epub
ahead of print] [Medline]

Alan Aragon’s Research Review – October, 2009 [Back to Contents] Page 1

 Looking at the two arguments, they bear an uncanny
resemblance to the modern debate between the pragmatic
Adaptive thermogenesis, A.K.A. starvation mode: the “calorie balance” camp, versus the “metabolic advantage” camp
downfall of dieting? (refer to the June 2009 AARR for a review of the metabolic
By Alan Aragon advantage research). Almost a century of study has elapsed since
this feud began, so who’s correct? Let’s take a look at the key
Introduction findings thus far.
Adaptive thermogenesis has varying definitions depending on
Subsequent investigations on adaptive thermogenesis
the context used. In the area of body composition regulation, it’s
been defined as “the decrease in energy expenditure (EE) In a seminal study by Apfelbaum et al in 1971, three groups of
beyond what could be predicted from the changes in fat mass or subjects were used to examine the effects of over- and under-
fat-free mass under conditions of standardized physical activity eating using a combination of means, including a metabolic
in response to a decreased energy intake.”1 This technical ward.4 The oxygen consumption of three groups of subjects was
definition describes what dieters in the public domain would call assessed at two 15-day intervals: 1) Nine control subjects ate a
“starvation mode,” characterized by a frustrating plateau in normal maintenance diet, 2) Nine subjects were overfed an
weight loss despite a low food intake and supposed hypocaloric isonitrogenous diet plus a 1500 kcal supplement, and 3) 41 obese
state. Aside from a halt in weight loss before the goal is reached, subjects consumed a 220 kcal diet consisting of 55 g casein,
adaptive thermogenesis can also present difficulties in potassium chloride, vitamins, and water. The resting metabolic
maintaining a weight goal, since the maintenance intake is so rate of the overfed fed group showed a 12.5% increase, while the
restricted. This article will assess the research, and propose underfed group’s resting metabolic rate decreased by 14.05%.
solutions to this challenging phenomenon that’s all-too-familiar
A little over a decade ago, Dulloo and Jacquet did a
to both dieters and the practitioners working to solve their
retrospective assessment of the impact of lean and fat tissue
weight loss problems.
depletion as determinants of the adaptive reduction in basal
Century-old controversy metabolic rate (BMR) in response to food deprivation by
reanalyzing the data of the Minnesota Experiment.5 In this study
Scientific reports of the body’s tenacious homeostatic drive spanning from November of 1944 to December of 1945, 36 men
overriding various caloric intakes date back about a century. I underwent a 12-week control phase followed by a 24-week
found the following quote by Gullick’s 1922 paper strikingly “semi-starvation” phase where subjects consumed 50% of their
similar to modern issues - down to the mentioning of copious estimated maintenance needs. A final 12-week rehabilitative
starch consumption:2 controlled refeed phase concluded the trial.
“...there is a rather discouraging inconclusiveness in the work that  At week 12 of the caloric restriction, the median and mean
has been done on factors that regulate the nutritive balance of the  adjusted basal metabolic rates (BMR) were lower than the
fat  tissue  of  the  body,  and  the balance  between  total  intake  and  control BMR by approximately 20%, and this value dropped
total output of potential kinetic energy in the adult warm‐blooded  further to about 25% at week 24. According to a recent review
organism.  [...]  The  problem  was  first  drawn  to  my  attention  by  by Major et al, this represents a reduction of roughly 356 and
observation of myself, [...] I had long noted my inclination toward  406 kcal greater than predicted.1 After 12 weeks of controlled
a  very  copious  diet  of  predominantly  starchy  nature,  in  spite  of  refeeding, the median and mean values for adjusted BMR were
which  my  weight  remained  fairly  constant,  even  on  a  moderate  still below control values by roughly 10%. Perhaps the most
round  of  activity,  at  a  figure  well  below  the  average  for  my  important finding of Dulloo and Jacquet’s assessment of this
stature.”  trial was a positive correlation between the reduction in
thermogenesis and the degree of fat mass lost. Interestingly,
There’s been longstanding disagreement among researchers despite these significant decreases in BMR, they found a lack of
about the nature of adaptive thermogenesis. Gullick first coined correlation between decreased thermogenesis and loss of fat-free
luxuskonsumption, which is a supercompensatory increase in mass (FFM). To quote them directly,
metabolic rate that can offset any significant gains resulting
from an increased caloric intake. However, disagreement with “…in  response  to  food  deprivation,  the  leaner  the  person,  the 
this concept has since been voiced in the literature. An early greater  the  capacity  to  conserve  energy  through  suppression  of 
example is a 1932 paper by Wiley and Newburgh, who assert a thermogenesis. Conversely, the more obese the person, the lesser 
less mystical position: 3 the suppression in thermogenesis for the same degree of body fat 
depletion,  a  contention  that  seems  to  be  in  line  with  a  cross‐
“Clearly  the  body  weight  is  affected  on  the  one  hand  by  the  comparison  of  studies  indicating  that,  in  general,  the  size  of  the 
individual  metabolic  requirement  and  on  the  other  hand  by  the  adaptive  fall  in  BMR  tended  to  be  less  marked  in  obese  than  in 
total intake of energy. Evidently the mechanism, commonly called  lean individuals (22).” 
appetite, functions to maintain a balance between the supply and 
the  demand.  […]  Observations  and  special  studies  on  appetite  in 
The above quote ends with a reference to another important
this clinic have convinced us that the abnormalities of body weight 
are regularly due to a failure of the appetite to make a complete 
retrospective analysis by Luke et al, who found that obese
adjustment between the inflow and outflow of energy.” individuals demonstrated less of a BMR reduction during
underfeeding than semi-starved lean individuals. Also in line

Alan Aragon’s Research Review – October, 2009 [Back to Contents] Page 2

with Dulloo and Jacquet’s findings was that the reduction in
BMR in semi-starved lean individuals was disproportionately
greater than the reduction in fat-free mass. This points to a
downregulation of cellular metabolism that exceeds what can be
assumed by mere losses in FFM.
A particularly illuminating study by Leibel et al measured 24-
hour total energy expenditure, resting & non-resting energy
expenditure, and the thermic effect of feeding in both obese and
subjects who had never been obese.7 Subjects were studied both
at their usual bodyweight and also after losing 10-20% of their
bodyweight by underfeeding (on an 800 kcal/day diet) or gaining
10% by overfeeding  (5000-8000 kcal per day). I’ll bullet the
results of this rather intricate design:
ƒ The maintenance of a bodyweight at 10 percent or
more below the initial weight was associated with a mean
reduction in total energy expenditure of roughly 6 kcal/kg
FFM per day in the subjects who had never been obese,
and 8 kcal/kg FFM per day in the obese subjects.
ƒ Resting energy expenditure and non-resting energy
expenditure each decreased 3 to 4 kcal/kg FFM per day in
both groups of subjects.
ƒ Maintenance of body weight at a level 10% above the
usual weight was associated with an increase in total
energy expenditure of roughly 9 kcal/kg FFM per day in
subjects who were never obese, and 8 kcal/kg FFM per
day in the obese.
ƒ The thermic effect of feeding and non-resting energy
expenditure after weight gain increased by approximately 1
to 2 and 8 to 9 kcal/kg FFM per day, in the never-obese
and obese, respectively. These changes in energy
expenditure were not related to the degree of fatness or the
sex of the subjects.
The authors concluded that as a result of a 10 percent (or greater)
decrease in body weight, the reduction in energy expenditure in
obese individuals is approximately 15% below what’s predicted
for body composition. They assert the point that this is a
clinically significant reduction, considering that an average daily
intake of 2500 kcal would be associated with a positive energy
balance of approximately 375 kcal per day.
The Latest research
Within the last year, an intriguing example of adaptive
thermogenesis by Tremblay and Chaput has surfaced.8 Using an
innovative design based on the outcomes of previous
investigations, the trial examined obese males during 3 separate
phases while maintaining a constant moderate energy deficit
(approximately 700 kcal below predicted maintenance needs):
1) This was a baseline period involving a pre-targeted 5 kg
loss. This lasted 78 days, and during this time, RMR
dropped 99.8 kcal/day, which was more than predicted.
2) The objective of the this second phase was to accumulate
a 10 kg loss – this took 63 days for another 5 kg loss, so
far everything is pretty stable.
3) This final phase was defined by the point that a weight
loss plateau was reached – this took 105 days to lose
Alan Aragon’s Research Review – October, 2009
another 2 kg, and by this time, RMR had dropped 168
kcal/day from baseline.
An interesting outcome of this trial was a lack of FFM loss. The
prescribed energy deficit of approximately -700 kcal was the
same for each phase. However, the actual measured energy
deficit progressively diminished through each successive phase:
1) -747 kcal, 2) -606 kcal, 3) -155 kcal. The authors pointed out
that during the first 2 phases, weight loss was stable at 75g/day,
but this drastically slowed to a mean rate of 19g/day in the 3rd
phase before reaching a zero value. I’ll quote the authors’
eloquent account of the 3rd phase leading to the plateau:
“During  this  period,  compensation  in  energy  balance  (2281 kJ/d) 
[editor’s  note:  this  is  544.8  kcal]  corresponded  to  78 %  of  the 
theoretical  energy  deficit.  Furthermore,  it  is  important  to  note 
that  at  plateau,  the  high  level  of  observed  adaptive  reduction  in 
thermogenesis at rest explained about 30 % of this compensation 
in  energy  balance.  [...]  The  link  observed  between  the  adaptive 
reduction  in  thermogenesis  and  the  degree  of  fat  loss  suggests 
that the greater the percentage reduction in body fat, the greater 
the  reduction  in  adaptive  thermogenesis,  and  hence  the  greater 
the total thermogenic economy.” 
Possible mechanisms & causes
I’ll emphasize the word “possible” because adaptive
thermogenesis is very poorly understood, and may never be
completely or accurately quantified from a mechanistic
standpoint. However, one aspect has been observationally
consistent: there appears to be a negative feedback loop between
the body’s overriding thermostat and the degree of fat mass
depletion resulting from prolonged dieting. Dullo and Jacquet
have proposed two distinct control systems.9 Non-specific
thermogenesis is a direct and immediate responder to
fluctuations in energy balance, and is governed by the
sympathetic nervous system (SNS). Being under SNS control,
this is dictated by environmental factors such as diet
composition, surrounding temperature, & psychological stress.
In contrast, adipose-specific thermogenesis has markedly slower
dynamics due to these changes occurring in response to the
relative depletion and synthesis of bodyfat. The schematic
below created by the aforementioned authors depicts the dual
action of these thermogenic regulators: 9
[Back to Contents] Page 3
In addition to various hypotheses involving the function (and
dysfunction) of thyroid, insulin, leptin, and uncoupling
proteins,1,10,11 another proposed mechanism behind adaptive
thermogenesis is rooted – oddly enough – in environmental
pollutants called organochlorines.12,13 Perhaps the first paper to
propose a direct link between organochlorines and obesity was
by Tremblay et al, who measured body composition and
sleeping metabolic rate in obese subjects before and after a
weight reduction program.14 It was determined that increased
plasma organochlorine concentration was the factor explaining
the greatest proportion of the difference between predicted and
measured sleeping metabolic rate decreases as a result of weight
loss. Other studies have linked organochlorine concentrations
with reduced oxidative capacity in skeletal muscle15 and
disruption of thyroid function.16,17 Thus far, the literature
indicting organochorines as obesogenic is still merely
correlative, not causal. Still, it’s been raising a few eyebrows in
the research community.
A computational model for determining body composition?
In a fit of extreme analytical capability, Kevin Hall assembled a
computational model of human energy metabolism during semi-
starvation and re-feeding.18 In this project, his aim was to use
published in vivo human data to create a quantitative framework
to study the regulation of body composition. Of relevance to the
present topic, he based much of his calculations on the measured
body weight and fat mass changes during the Minnesota semi-
starvation experiment discussed earlier. His mathematical model
ultimately was validated by successfully simulating a published
short-term caloric restriction study without changing any of the
model’s parameters.
The above schematic by Hall is one of the more simple yet
elegant ones I’ve seen that attempts to illustrate the
harmoniously integrated nature of nutrient balance. In this
abbreviated model, arrows representing daily metabolic fluxes
indicate changes in body fat (F), glycogen (G), and protein (P)
were determined by the balance of fat intake (FI), carbohydrate
intake (CI), and protein intake (PI), gluconeogenesis from fat
(GNGF) and protein (GNGP), de novo lipogenesis (DNL),
glycerol 3-P synthesis (G3P), and the oxidation of fat (Fat Ox),
carbohydrate (Carb Ox), and protein (Prot Ox), respectively. To
gain an appreciation for the complexity of the actual
mathematical models, the free full text is here.18
Conclusion & practical application
The mechanisms underlying adaptive thermogenesis are not well
understood. However, there’s no question that it’s an actual,
measurable phenomenon. Given that, it’s tempting to lose faith
in the dieting process, figuring that it’s a futile endeavor at the
Alan Aragon’s Research Review – October, 2009
mercy of body’s metabolic downregulation that occurs with fat
loss. But, that’s just the point. Fat loss still occurs despite the
decrease in RMR, it just has to be nudged. Depending on
someone's initial size, we’re looking at roughly 250-500 less
calories burned per day compared to baseline. So, dieters in the
throes of adaptive thermogenesis are at worst running a single-
meal disadvantage. In other words, a dieter nearing a plateau
must eat the daily caloric equivalent of one less mid- to full-size
meal than prior to dieting the weight off. Another solution would
be to combine half of that caloric cutback with a subtle increase
in exercise to make up the difference. A time-saver is just an
increase in training intensity. Wise dieters are on a plan that
consists mostly of their favorite foods, but still hits the
macronutrient targets. Most of my clients succeed by having a
“junk meal” per week, and a full week off of dieting every 4-8
weeks. Ultimately, it’s important to realize that the difficulties
surrounding obesity are more closely related to the psychology
of behavior than a decrease in metabolic rate.
References
1. Major GC, et al. Clinical significance of adaptive thermogenesis. Int J Obes
(Lond). 2007 Feb;31(2):204-12. [Medline]
2. Gulick A. A study of weight regulation in the adult human body during over-
nutrition. Am J Physiol 1922; 60: 371–395. [AJP]
3. Wiley FH, Newburgh LH. The doubtful nature of ‘luxuskonsumption’. J
Clin Invest 1931; 10: 733–744. [Medline]
4. Apfelbaum M, et al. Effect of caloric restriction and excessive caloric intake
on energy expenditure. Am J Clin Nutr. 1971 Dec;24(12):1405-9. [Medline]
5. Dulloo AG, Jacquet J. Adaptive reduction in basal metabolic rate in response
to food deprivation in humans: a role for feedback signals from fat stores.
Am J Clin Nutr. 1998 Sep;68(3):599-606. [Medline]
6. Luke A, Schoeller DA. Basal metabolic rate, fat-free mass, and body cell
mass during energy restriction. Metabolism. 1992 Apr;41(4):450-6.
[Medline]
7. Leibel RL, Rosenbaum M, Hirsch J. Changes in energy expenditure resulting
from altered body weight. N Engl J Med. 1995 Mar 9;332(10):621-8.
[Medline]
8. Tremblay A, Chaput JP. Adaptive reduction in thermogenesis and resistance
to lose fat in obese men. Br J Nutr. 2009 Aug;102(4):488-92. [Medline]
9. Dulloo AG, Jacquet J. An adipose-specific control of thermogenesis in body
weight regulation. Int J Obes Relat Metab Disord. 2001 Dec;25 Suppl 5:S22-
9. [Medline]
10. Dulloo AG. A role for suppressed skeletal muscle thermogenesis in
pathways from weight fluctuations to the insulin resistance syndrome. Acta
Physiol Scand. 2005 Aug;184(4):295-307. [Medline]
11. Dullo AG, et al. Adaptive thermogenesis and uncoupling proteins: a
reappraisal of their roles in fat metabolism and energy balance. Physiol
Behav. 2004 Dec 30;83(4):587-602. [Medline]
12. Pelletier C, et al. Associations between weight loss-induced changes in
plasma organochlorine concentrations, serum T(3) concentration, and resting
metabolic rate. Toxicol Sci 2002; 67: 46–51. [Medline]
13. Pelletier C, Imbeault P, Tremblay A. Energy balance and pollution by
organochlorines and polychlorinated biphenyls. Obes Rev 2003; 4: 17–24.
[Medline]
14. Tremblay A, et al. Thermogenesis and weight loss in obese individuals: a
primary association with organochlorine pollution. Int J Obes Relat Metab
Disord. 2004 Jul;28(7):936-9. [Medline]
15. Imbeault P, et al. Weight loss-induced rise in plasma pollutant is associated
with reduced skeletal muscle oxidative capacity. Am J Physiol Endocrinol
Metab. 2002 Mar;282(3):E574-9. [Medline]
16. Dellaire R, et al. Thyroid function and plasma concentrations of
polyhalogenated compounds in Inuit adults. Environ Health Perspect. 2009
Sep;117(9):1380-6. [Medline]
17. Pichietti S, et al. Thyroid disruptor 1,1,1-trichloro-2,2-bis(p-
chlorophenyl)ethane (DDT) prevents internalization of TSH receptor. Cell
Tissue Res. 2009 Apr;336(1):31-40. [Medline]
18. Hall KD. Computational model of in vivo human energy metabolism
during semistarvation and refeeding. Am J Physiol Endocrinol Metab. 2006
Jul;291(1):E23-37. [Medline]
[Back to Contents] Page 4

Short-term modified alternate-day fasting: a novel
dietary strategy for weight loss and cardioprotection
in obese adults.
Varady KA, et al. Am J Clin Nutr. 2009 Nov;90(5):1138-43.
[Medline]
BACKROUND: The ability of modified alternate-day fasting
(ADF; ie, consuming 25% of energy needs on the fast day and
ad libitum food intake on the following day) to facilitate weight
loss and lower vascular disease risk in obese individuals remains
unknown. OBJECTIVE: This study examined the effects of
ADF that is administered under controlled compared with self-
implemented conditions on body weight and coronary artery
disease (CAD) risk indicators in obese adults. DESIGN: Sixteen
obese subjects (12 women, 4 men) completed a 10-wk trial,
which consisted of 3 phases: 1) a 2-wk control phase, 2) a 4-wk
weight loss/ADF controlled food intake phase, and 3) a 4-wk
weight loss/ADF self-selected food intake phase. RESULTS:
Dietary adherence remained high throughout the controlled food
intake phase (days adherent: 86%) and the self-selected food
intake phase (days adherent: 89%). The rate of weight loss
remained constant during controlled food intake (0.67 +/- 0.1
kg/wk) and self-selected food intake phases (0.68 +/- 0.1 kg/wk).
Body weight decreased (P < 0.001) by 5.6 +/- 1.0 kg (5.8 +/-
1.1%) after 8 wk of diet. Percentage body fat decreased (P <
0.01) from 45 +/- 2% to 42 +/- 2%. Total cholesterol, LDL
cholesterol, and triacylglycerol concentrations decreased (P <
0.01) by 21 +/- 4%, 25 +/- 10%, and 32 +/- 6%, respectively,
after 8 wk of ADF, whereas HDL cholesterol remained
unchanged. Systolic blood pressure decreased (P < 0.05) from
124 +/- 5 to 116 +/- 3 mm Hg. CONCLUSION: These findings
suggest that ADF is a viable diet option to help obese individuals
lose weight and decrease CAD risk. This trial was registered at
clinicaltrials.gov as UIC-004-2009. SPONSORSHIP:
Departmental funding from the University of Illinois, at
Chicago.
preferences and targeted calorie levels for the fast day. The
dietitian also provided instruction on how to make healthy food
choices on the ad libitum (as-desired) days by choosing low-fat
meat and dairy foods.
Study Limitations
This trial’s outcomes would have been strengthened with a
parallel arm design. That is, it would help to preserve the current
design, but add a control group whose weekly caloric intake was
equal, but distributed linearly (the same amount each day). This
would not only answer the question of whether or uncontrolled
ADF is more effective than controlled ADF; it would also
answer another important question of whether ADF more
effective than linear dieting. Another common limitation of diet
studies is the absence of a structured exercise program. While
this presents another variable and thus more confounding
potential, it’s more reflective of what dieters should be doing.
Comment/application
While the body of human trials on ADF is still scant,1-3 this is
the first one to show that ADF is an effective means for the
obese to lose weight and lower cardiovascular risk. Overall,
adherence was good in both the controlled (86%) and
uncontrolled phases (89%). Only 2 out of 20 subjects dropped
out of the study due to the inability to endure the fasting days. 2
others dropped out due to time constraints. Improvements in
body composition, heart rate, blood pressure, and plasma lipids
are consistent with what normally occurs as a result of
significant weight loss (in this case, a 5.8% decrease). Perhaps
the most important finding of this study is that the rate of weight
loss was similar between the controlled and uncontrolled phases,
as illustrated below. For dieters who would prefer to experience
“non-dieting days” for half the week, and can endure the fasting
on alternate days, ADF appears to be worth a try. A more
methodical way to go about this would be to fast on days off
from training, and train on non-fasting days.

Study strengths
I’m interested in the study of reduced meal frequency, mainly
because increased meal frequency is simply burdensome. The 6-
a-day dictum in fitness circles has become somewhat Gospel.
The common more-is-better mentality has been applied to meal
frequency, despite a lack of scientific support. While lab-
provided meals and metabolic ward conditions are the gold
standard of control, the next level up from that would be to
compare how a given treatment might fare in under free-living
conditions. This trial does just that – albeit for relatively brief (4-
week) periods. The 4-week control period was a fasting regimen
consisting of 25% of the subjects’ maintenance needs. All meals
were prepared and provided by the lab. All fast day meals were
consumed between 1200 and 1400 in order to standardize the
duration of fasting. During the Subjects met with a registered
dietitian at the beginning of each week to learn how to maintain
the ADF regimen on their own at home. The following 4-week
uncontrolled phase, a dietitian worked with each subject to
develop individualized fast day meal plans. These plans included
menus, portion sizes, and food lists based on the subjects’
Alan Aragon’s Research Review – October, 2009 [Back to Contents] Page 5
Intermittent fasting does not affect whole-body
glucose, lipid, or protein metabolism.
Soeters MR, Am J Clin Nutr. 2009 Nov;90(5):1244-51.
[Medline]
BACKROUND: Intermittent fasting (IF) was shown to increase
whole-body insulin sensitivity, but it is uncertain whether IF
selectively influences intermediary metabolism. Such selectivity
might be advantageous when adapting to periods of food
abundance and food shortage. OBJECTIVE: The objective was
to assess effects of IF on intermediary metabolism and energy
expenditure. DESIGN: Glucose, glycerol, and valine fluxes
were measured after 2 wk of IF and a standard diet (SD) in 8
lean healthy volunteers in a crossover design, in the basal state
and during a 2-step hyperinsulinemic euglycemic clamp, with
assessment of energy expenditure and phosphorylation of muscle
protein kinase B (AKT), glycogen synthase kinase (GSK), and
mammalian target of rapamycine (mTOR). We hypothesized
that IF selectively increases peripheral glucose uptake and
lowers proteolysis, thereby protecting protein
stores. RESULTS: No differences in body weight were
observed between the IF and SD groups. Peripheral glucose
uptake and hepatic insulin sensitivity during the clamp did not
significantly differ between the IF and SD groups. Likewise,
lipolysis and proteolysis were not different between the IF and
SD groups. IF decreased resting energy expenditure. IF had no
effect on the phosphorylation of AKT but significantly increased
the phosphorylation of glycogen synthase kinase.
Phosphorylation of mTOR was significantly lower after IF than
after the SD. CONCLUSION: IF does not affect whole-body
glucose, lipid, or protein metabolism in healthy lean men despite
changes in muscle phosphorylation of GSK and mTOR. The
decrease in resting energy expenditure after IF indicates the
possibility of an increase in weight during IF when caloric intake
is not adjusted. This study was registered at www.trialregister.nl
as NTR1841. SPONSORSHIP: None listed.
Study strengths
A crossover design helped alleviate the small sample size and
also hedged against variability of intersubject response; all
subjects served as their own controls. Unlike previous IF
research, this is the first trial to include a control treatment
(standard linear diet) matched for calories and macronutrition.
To increase the standardization, the volunteers ate mainly bread,
fruit, and dairy products (60% of daily calories) and
supplemented with liquid meals (40% of daily calories). Resting
energy expenditure (REE) was measured with indirect
calorimetry in attempt to accurately determine maintenance
energy needs (which happened to be estimated at 130–140% of
REE). Since the objective was to preserve weight maintenance,
the diets were adjusted in the event of a 1-kg weight change. To
insure close monitoring for this purpose, the volunteers visited
the lab for weight control on a validated scale on day 1 of each
diet and then twice per week thereafter.
Study limitations
Not that it would be incredibly useful to know given the short
durations of the treatments, but the method of body composition
assessment was not specified. It can also be argued that
Alan Aragon’s Research Review – October, 2009
differences may have been detected if the treatments were longer
than a measly 2 weeks each. This is perhaps the most critical
weakness of this study. Confining the subjects to a metabolic
ward would have made the best use of the brevity of the trial
periods, but this was not the case. Very little was reported in the
text regarding specific measures of dietary control and
supervision. An often-overlooked limitation in trials like these is
the lack of a structured training protocol. My hope is that future
research on IF incorporates exercise variations, which might
significantly alter the outcomes.
Comment/application
The main findings of the present trial were that compared to
standard/linear intake at weight maintenance levels, 1) IF
(fasting for 20 hours every second day) did not alter insulin-
mediated peripheral glucose uptake, hepatic insulin sensitivity,
insulin sensitivity of adipose tissue, or proteolysis; 2) IF
significantly increased the phosphorylation of glycogen
synthase; 3) IF caused a lower phosphorylation of mTOR; 4) IF
caused a greater reduction of resting energy expenditure from
baseline; 5) No significant differences in body composition were
detected between treatments. Given this, the primary expectation
of IF increasing insulin sensitivity better than standard eating
were not fulfilled, making these results somewhat anticlimactic.
The drop in resting energy expenditure in the IF group gave the
authors some concern about whether or not IF might have
negative consequences. To quote them, “The decrease in REE
after IF may precede weight gain during IF when caloric intake
is not adjusted. Whether IF is beneficial at improving peripheral
insulin resistance in obese, insulin-resistant subjects remains to
be established.” Looking at the exact numbers, the mean
decrease in REE was 59 kcals/day, which – given a static set of
surrounding variables – can amount to a monthly difference of
half a pound. Although the decrease was found to be a
statistically significant difference, the real-world significance of
this difference is highly questionable.
Despite the above, there were a couple of outcomes in favor of
IF. LBM and fat mass were unaffected by either treatment,
which challenges the widely held belief that routinely going
without food for more than a few hours causes muscle
catabolism. Further supporting this observation was a lack of
difference proteolysis between treatments (measured via isotope-
enriched valine). The other positive outcome was an increase in
glycogen synthase activity, which might benefit endurance sport
applications. Interestingly, although mTOR activation was lower
in the IF group, there were no significant differences in fatty
acid oxidation. Heilbronn et al observed an increase in fat
oxidation as a result of a 36-hour fast,1 but the present study’s
20-hour fasting cycle didn’t yield such an increase. Additionally,
no group differences were seen in basal levels of insulin, thyroid
hormones, cortisol, glucagon, or adiponectin.
IF’s potential for improving adherence through convenience,
simplicity, and flexibility is tough to dispute. But thus far,
inherent physiological benefits of intermittent fasting over a
conventional eating pattern have not been seen. Would this still
be the case in longer trials? Would this still be the case in trials
imposing an energy deficit instead of maintenance as in the
present study? These questions are yet unanswered, but
hopefully will be resolved by further research.
[Back to Contents] Page 6
Increased food energy supply is more than sufficient
to explain the US epidemic of obesity.
Swinburn B, et al. Am J Clin Nutr. 2009 Oct 14. [Epub ahead of
print] [Medline]
BACKGROUND: The major drivers of the obesity epidemic
are much debated and have considerable policy importance for
the population-wide prevention of obesity. OBJECTIVE: The
objective was to determine the relative contributions of
increased energy intake and reduced physical activity to the US
obesity epidemic. DESIGN: We predicted the changes in weight
from the changes in estimated energy intakes in US children and
adults between the 1970s and 2000s. The increased US food
energy supply (adjusted for wastage and assumed to be
proportional to energy intake) was apportioned to children and
adults and inserted into equations that relate energy intake to
body weight derived from doubly labeled water studies. The
weight increases predicted from the equations were compared
with weight increases measured in representative US surveys
over the same period. RESULTS: For children, the measured
weight gain was 4.0 kg, and the predicted weight gain for the
increased energy intake was identical at 4.0 kg. For adults, the
measured weight gain was 8.6 kg, whereas the predicted weight
gain was somewhat higher (10.8 kg). CONCLUSIONS:
Increased energy intake appears to be more than sufficient to
explain weight gain in the US population. A reversal of the
increase in energy intake of approximately 2000 kJ/d (500
kcal/d) for adults and of 1500 kJ/d (350 kcal/d) for children
would be needed for a reversal to the mean body weights of the
1970s. Alternatively, large compensatory increases in physical
activity (eg, 110-150 min/d walking), or a combination of both,
would achieve the same outcome. Population approaches to
reducing obesity should emphasize a reduction in the drivers of
increased energy intake. SPONSORSHIP: None listed.
Study strengths
This trial examines approximately 3 decades of population data
to investigate the impact of what I would expect be the most
obvious and critical factor in determining weight gain: chronic
positive thermodynamic balance. The data was stratified
between children and adults by using census data to derive
chilled:adult population proportions. Doubly labeled water
studies were used to generate data for energy intake proportions
between children and adults (by using the appropriate average
age and weight from the census and NHANES data). The
apportioned energy supply data were then included in the
equations for children and adults to derive predicted weight
gains, which were then compared with their respective measured
gains.
Study limitations
Like all epidemiological/observational data, only correlational or
associative relationships can be established between variables.
Unlike the case of randomized controlled trials (RCTs – also
called controlled interventions), uncontrolled research cannot
establish cause-and-effect relationships between the variables in
question. Another potential limitation is that the food supply
data represent the food available for consumption rather than the
Alan Aragon’s Research Review – October, 2009
amount of food actually ingested, so these are likely to be
overestimates of actual consumption, even after adjustment for
food loss. Also, food loss is inherently difficult to measure
accurately. Thus, even the US Department of Agriculture
(USDA) acknowledges their estimates of retail, food service,
and consumer food losses are potentially under what the actual
amounts are. Despite this, the USDA food supply data are a
useful indicator of consumption trends, since many of these
errors are likely to be consistent and systematic. As such, their
relatively constant contribution is not likely to interfere
significantly with the tracking of intake changes over time.4
Comment/application
This article has special relevance because there seems to be a
persistent wave of press of both academic and lay press
concentrating on the “controversial” role of calories in the
obesity epidemic. That is, instead of total calories, there’s been a
lot of focus on diet composition – both in terms of macronutrient
proportion, as well as nit-picky food choices based on glycemic
index, insulin index, and glycemic load. The common theme
here is the concern over glycemia and/or insulinemia being
critical factors in gaining excess bodyweight and incurring
diseases related to the metabolic syndrome.5-9
As I’ve pointed out in previous articles, in spite of the fear of the
insulin response, or the hope of a strong metabolic advantage of
carbohydrate restriction (or any number of dietary
manipulations), total caloric balance – energy in versus energy
out – is the prime determinant of bodyweight and body fat. The
idea that diet composition is secondary to total caloric content is
supported by not just the majority long-term intervention trials,
but also the majority of controlled metabolic ward studies (I’ll
refer you to 2 excellent review papers by Schoeller and
Buchholz covering the metabolic ward research).10,11 In the
following quote, the authors sum up their findings (see the graph
below), and provide the take-home point as well:
“For the US population to return to the mean weights of the
1970s, the increased energy intake of ~1500 kJ/d (350 kcal/d)
for children (about one can of soda and a small order of French
fries) and 2000 kJ/d (500 kcal/d) for adults (about one large
hamburger) would need to be reversed. Alternatively,
compensatory increases in physical activity (~150 and 110 min/d
of extra walking respectively) would achieve similar results.”
[Back to Contents] Page 7

Protease supplementation improves muscle function
after eccentric exercise.
Buford TW, et al. Med Sci Sports Exerc. 2009 Sep 2. [Epub
ahead of print] [Medline]
BACKGROUND: Protease supplementation has been purported
to reduce the damaging effects of eccentric exercise and
accelerate recovery of muscle function, possibly by regulating
inflammation. PURPOSE: To determine the effectiveness of
protease supplementation in attenuating eccentric exercise-
induced skeletal muscle damage and inflammation.
METHODS: After standard physical and hemodynamic
assessment and fasting venous blood samples, subjects
performed isokinetic extension/flexion of the quadriceps group
on a Biodex isokinetic dynamometer at 60 degrees .s, followed
by V O2max testing. Subjects were randomly assigned to
consume 5.83 g daily of either a cellulose placebo (N = 15;
22.27 +/- 3.33 yr, 71.17 +/- 2.91 inches, 179.4 +/- 24.05 lb,
50.55 +/- 5.66 mL.kg.min) or a proteolytic supplement
containing fungal proteases, bromelain, and papain (N = 14;
22.85 +/- 5.9 yr, 70.0 +/- 2.67 inches, 173.11 +/- 29.94 lb, 49.69
+/- 6.15 mL.kg.min) for a period of 21 d. After the
supplementation period, subjects donated blood samples before
performing a 45-min downhill (-17.5%) treadmill protocol at
60% of V O2max. An additional four blood draws and three
muscle function tests were performed during the next 48 h.
Blood was analyzed using standard hematology and clinical
chemistry, enzyme-linked immunosorbent assay, and bead array.
Blood data were analyzed using multivariate analysis of variance
(MANOVA) with repeated measures, whereas Biodex data were
analyzed using a MANOVA on %Delta values. RESULTS:
Significant group differences (T1-T3, P = 0.033; T1-T4, P =
0.043) and another strong trend (T1-3 h, P = 0.055) were
observed for flexion (peak torque %Delta at 60 degrees .s)
indicating higher force production in the protease group.
Significant group x time interactions (P < 0.05) were observed,
including elevations in circulating eosinophils and basophils in
the protease group coinciding with lower levels of serum
cyclooxygenase 2, interleukin 6, and interleukin 12 in this group.
CONCLUSIONS: Protease supplementation seems to attenuate
muscle strength losses after eccentric exercise by regulating
leukocyte activity and inflammation. SPONSORSHIP: Funding
for this study was provided through research grants awarded to
Baylor University by the Transformation Enzyme Corporation
(Houston, TX) and the Texas Regional Chapter of ACSM.
Study strengths
This trial involved 29 recreationally active subjects,
characterized by “consistent, structured exercise at least three
times per week.” This population – as opposed to a
sedentary/deconditioned one is less susceptible to newbie
effects. Subjects were required to keep a daily record of their
dietary intake, which was analyzed with software to determine
the macronutrient makeup, as well as intake of vitamins C & E
(which might have affected the outcomes postulated to be
mediated in part by altering the inflammatory response.
Alan Aragon’s Research Review – October, 2009
Study limitations
As is typical with supplementation studies (particularly studies
funded by the company providing the experimental agent), there
was no dietary control. Despite daily recording, there was no
standardization of the diet, so the validity of the results hinges
upon the consistency of the subjects’ dietary habits at both pre
and during the trial period. Another limitation is the inherent
room for inapplicability to the real-word field challenges when
lab-based strength tests (i.e., isokinetic devices) are used.
Comment/application
Protease supplementation has for the most part far flown under
my radar of interest. However, it turns out there’s been two
human studies preceding this one showing the benefit of
protease on muscle function and reduction of delayed-onset
muscle soreness (DOMS) after eccentrically damaging
exercise.12,13 The present trial adds to this small body of research
in support of protease supplementation. An interesting find was
that although the protease group showed no force decrements
during flexion, a similar decrease in force production to placebo
occurred during the extension portion of the exercise.
The authors cite the most intriguing finding as the increase in
circulating eosinophils and basophils in the protease group. One
of the functions of eosinophils and basophils is to increase
inflammation. Their surprise is likely based on the traditional
approach to recovery which is geared toward reducing training-
induced inflammation. The release of cytokines can increase
tissue permeability and cause further damage. In the present
case, no such harmful cascade occurred in spite of the rise in
these particular leukocytes in the protease group.
Although the authors concede that the exact mechanism remains
a mystery, they speculate that regulation of the inflammatory
response is likely to be responsible for the benefit of protease
supplementation. Lending fairly strong support to this idea was
the suppression of COX2, the primary signal for the production
of prostaglandins. As a related aside, non-steroidal anti-
inflammatory drugs (NSAIDs) such as ibuprofen and naproxen
are COX2 inhibitors.
So, how can the increase in eosinophils be reconciled? The
authors propose two possibilities. First, it’s possible that the
ingested protease increased the recruitment of macrophages
and/or neutrophils (white blood cells) to the site of injury in
order to promote recovery by clearing cellular debris. The
infiltration of phagocytes into damaged tissue is accomplished
by passing into the interstitial space after vascular dilation and
swelling. A second possibility is that protease-mediated
improvements in muscle function are due to extracellular matrix
(ECM) remodeling. The ECM helps facilitate the transmission of
force by providing structural support for skeletal muscle.
Eccentric exercise contributes significantly to the remodeling of
the ECM. The authors thus propose that protease ingestion might
activate the production of matrix metalloproteases (MMP),
which also contribute to ECM remodeling.
As in the case of many trials, the outcomes of this trial warrant
further investigation under better-controlled, longer-term
conditions, preferably incorporating field performance tests.
[Back to Contents] Page 8

Supplementation with a whey protein hydrolysate
enhances recovery of muscle force-generating
capacity following eccentric exercise.
Buckley JD, et al. J Sci Med Sport. 2008 Sep 1. [Epub ahead of
print] [Medline]
BACKGROUND/PURPOSE: There is evidence that protein
hydrolysates can speed tissue repair following damage and may
therefore be useful for accelerating recovery from exercise
induced muscle damage. The potential for a hydrolysate
(WPI(HD)) of whey protein isolate (WPI) to speed recovery
following eccentric exercise was evaluated by assessing effects
on recovery of peak isometric torque (PIT).: METHODS In a
double-blind randomised parallel trial, 28 sedentary males had
muscle soreness (MS), serum creatine kinase (CK) activity,
plasma TNFalpha, and PIT assessed at baseline and after 100
maximal eccentric contractions (ECC) of their knee extensors.
Participants then consumed 250ml of flavoured water (FW;
n=11), or FW containing 25g WPI (n=11) or 25g WPI(HD)
(n=6) and the assessments were repeated 1, 2, 6 and 24h later.
RESULTS: PIT decreased approximately 23% following ECC,
remained suppressed in FW and WPI, but recovered fully in
WPI(HD) by 6h (P=0.006, treatmentxtime interaction). MS
increased following ECC (P<0.001 for time), and remained
elevated with no difference between groups (P=0.61). TNFalpha
and CK did not change (P>0.45). CONCLUSION: WPI(HD)
may be a useful supplement for assisting athletes to recover from
fatiguing eccentric exercise. SPONSORSHIP: MG Nutritionals
(Brunswick, Australia) and a Food Innovation Grant from the
National Food Industry Strategy, Australia. MG Nutritionals
provided the supplements used in this study.
Study strengths
This study addresses a hot topic in sports nutrition: are protein
hydrolysates superior to isolates for postexercise recovery? This
question is far from adequately investigated. But with the
barrage of marketing hype surrounding hydrolysates, another
question remains of whether it’s justified paying double the price
of the regular stuff (usually a combination of concentrate and
isolate). This trial is one of the forerunners to examine this issue.
Study limitations
Perhaps the most glaring limitation of this study was the
troublesome sample. What began as a group of 43 sedentary
males dropped down to 28. Incapability (or unwillingness) of
putting maximal effort into the baseline strength testing was seen
in 15 of the original subjects. This was evidenced by a lack of
decrease in peak isometric torque (PIT) after 100 maximal
eccentric contractions (ECC). After this 34.8% dropout, the
treatment groups were severely imbalanced. The flavored water
control and the whey protein isolate group had 11 subjects each,
while the hydrolysate group was left with only 6. Although the
dropouts were excluded from the data analysis, this doesn’t
change that fact that the hydrolysate group’s significantly
smaller size greatly increases the potential for inter-subject
variability error. In other words, the smaller the group, the
greater the ability for outlying (unusually high or low)
Alan Aragon’s Research Review – October, 2009
responders to skew the results. Another important confounder
was the use of sedentary subjects. To quote the criteria:
“Volunteers were excluded if they participated in regular
physical activity more than once per week for the purpose of
improving or maintaining their physical fitness; had undertaken
resistance training of the quadricep muscles during the previous
3 months” Based on this, it makes sense that if you subject
completely deconditioned individuals to intense eccentric loads,
a good portion of those individuals will be incapable (both
neurologically and/or psychologically) to generate maximal
effort. This led to a 34.8% dropout rate due to what the authors
called ‘noncompliance.’ In reality, it was likely less a matter of
compliance as it was a matter of experience and training
capability. This crucial shortcoming could have easily been
alleviated by choosing moderately trained subjects rather than
rank couch potatoes.
Comment/application
This trial adds food for thought to the scant, equivocal body of
research on hydrolysates versus isolates. Preceding this one,
only one other human study comparing the whey hydrolysate
and intact whey isolate had contrary outcomes. Farnfield et al
found that whey isolate caused a more rapid absorption of amino
acids and greater overall anabolic response than whey
hydrolysate.14 Contradictions continue to plague this area of
investigation. Koopman et al (reviewed in AARR, May 2009)
found that casein hydrolysate, as opposed to its intact protein,
tends to increase the incorporation rate of dietary amino acids
into skeletal muscle protein.15 To my knowledge, the only trial
(other than the present one) comparing a protein hydrolysate
with its parent isolate on performance measures used casein, not
whey. Deglaire et al (reviewed in AARR, Aug 2009) found that
casein hydrolysate resulted in greater splanchnic dietary nitrogen
delivery than its peripheral anabolic use.16 In other words,
nitrogen from casein hydrolysate was preferentially taken up by
the visceral organs, whereas that of isolate was preferentially
taken up by skeletal muscle. However, to the credit of the
present trial, Farnfield et al and Deglaire et al did not directly
measure exercise performance or recovery endpoints were not
assessed.
Currently, there’s a lack of literature comparing hydrolysates
head-to-head with their native intact protein isolates for the
sports/fitness-related purposes. To my knowledge, there’s no
other trial besides the present one comparing performance
effects of whey hydrolysate versus whey isolate. Furthermore,
the available literature has only measured acute effects, so the
more important question of chronic effects remains open. A
recent review by Manninen17 cites the present trial and another
trial by Cribb et al18 as evidence of whey hydrolysate’s potential
utility for improving body composition and performance.
However, Cribb et al compared VP2 (a whey hydrolysate sold
by the trial’s sponsor, AST) with casein, not with whey isolate.
What it all comes down to is that the whey hydrolysate
campaign is basing all of its claims of superiority (and premium
pricing) over whey isolate on a single study. Early adopters and
optimistic types will undoubtedly fuel this campaign, but I think
it’s premature to shell out the bucks for hydrolysates when the
difference in the long term is likely to be miniscule, if anything.
[Back to Contents] Page 9
1. Heilbronn, et al. Alternate-day fasting in nonobese subjects:
effects on body weight, body composition, and energy
metabolism. Am J Clin Nutr. 2005 Jan;81(1):69-73. [Medline]
2. Heilbronn, et al. Glucose tolerance and skeletal muscle gene
expression in response to alternate day fasting. Obes Res. 2005
Mar;13(3):574-81. [Medline]
3. Halberg, et al. Effect of intermittent fasting and refeeding on
insulin action in healthy men. J Appl Phsiol. 2005
Dec;99(6):2128-36. [Medline]
4. US Department of Agriculture, Economic Research Service.
Loss-adjusted food availability data: documentation. June
2008. [ERS/USDA]
5. Bao J, et al. Food insulin index: physiologic basis for
predicting insulin demand evoked by composite meals. Am J
Clin Nutr. 2009 Oct;90(4):986-92. [Medline]
6. Livesey G, et al. Glycemic response and health--a systematic
review and meta-analysis: relations between dietary glycemic
properties and health outcomes. Am J Clin Nutr. 2008
Jan;87(1):258S-268S. [Medline]
7. Livesey G, et al. Glycemic response and health--a systematic
review and meta-analysis: the database, study characteristics,
and macronutrient intakes. Am J Clin Nutr. 2008
Jan;87(1):223S-236S. [Medline]
8. Venn BJ, Green TJ. Glycemic index and glycemic load:
measurement issues and their effect on diet-disease
relationships. Eur J Clin Nutr. 2007 Dec;61 Suppl 1:S122-31.
[Medline]
9. Galani J, et al. Nutr J. 2006 Sep 5;5:22. Acute effect of meal
glycemic index and glycemic load on blood glucose and insulin
responses in humans. [Medline]
10. Schoeller DA, Buchholz AC. Energetics of obesity and weight
control: does diet composition matter? J Am Diet Assoc. 2005
May;105(5 Suppl 1):S24-8. [Medline]
11. Buchholz AC, Schoeller DA. Is a calorie a calorie? Am J Clin
Nutr. 2004 May;79(5):899S-906S. [Medline]
12. Beck TW, et al. Effects of a protease supplement on eccentric
exercise-induced markers of delayed-onset muscle soreness and
muscle damage. J Strength Cond Res. 2007 Aug;21(3):661-7.
[Medline]
13. Miller PC, et al. The effects of protease supplementation on
skeletal muscle function and DOMS following downhill
running. J Sports Sci. 2004 Apr;22(4):365-72. [Medline]
14. Farnfield MM, et al. Plasma amino acid response after
ingestion of different whey protein fractions. Int J Food Sci
Nutr. 2008 May 8:1-11. [Medline]
15. Koopman R, et al. Ingestion of a protein hydrolysate is
accompanied by an accelerated in vivo digestion and
absorption rate when compared with its intact protein. Am J
Clin Nutr. 2009 May 27. [Epub ahead of print] [Medline]
16. Deglaire A, et al. Hydrolyzed dietary casein as compared with
the intact protein reduces postprandial peripheral, but not
whole-body, uptake of nitrogen in humans.Am J Clin Nutr.
2009 Aug 19. [Epub ahead of print] [Medline]
17. Manninen AH. Protein hydrolysates in sports nutrition. Nutr
Metab (Lond). 2009 Sep 28;6:38. [Medline]
18. Cribb PJ, et al. The effect of whey isolate and resistance
training on strength, body composition, and plasma glutamine.
Int J Sport Nutr Exerc Metab. 2006 Oct;16(5):494-509.
[Medline]

Alan Aragon’s Research Review – October, 2009 [Back to Contents] Page 10


The questionable research practices of Dr. Jerrold
Petrofsky
By Cameron Mochrie & Ian Capulet
Introduction
Between 2003 and 2008, Dr. Jerrold Petrofsky, a professor of
physical therapy of Loma Linda University and Azusa Pacific
University, published 19 papers measuring the efficacy of fitness
products marketed by Savvier LP.1,2 The products featured in
each of these papers received a favorable evaluation. Quotes and
results from these papers were later used by Savvier LP for
marketing purposes, with portions from the papers often
appearing within product websites and infomercials to sell them
as “university tested” equipment.3
The methodology used in these studies, along with the general
research design, is highly questionable upon closer
inspection. Furthermore, each paper was published in the Journal
of Applied Research in Clinical and Experimental Theraputics
(JAR, also called JARCET), which is a journal “committed to
rapid publication (we guarantee publication, if the article is
accepted by our board, within 120 days of receipt of the
manuscript) with the sole criterion for acceptance by our board
as scientific accuracy.”4 Dr. Petrofsky is also a member of JAR's
review board.5 As for what the journal’s criteria for “scientific
accuracy” amounts to, though never explicitly provided, the
quality of Dr. Petrofsky's publications suggests the bar isn’t set
to widely-held standards. At best, the research done by Petrofsky
was of dubious value, and at worst…we will let the readers draw
their own conclusions.
Easy Curves™
One of the many papers authored by Dr. Jerrold Petrofsky is, “A
Bidirectional Resistance Device for Increasing the Strength and
Tone in Upper Body Core Muscles and Chest Girth.”6 While
difficult to tell from the loquacious title, the device concerned in
this paper is the Easy Curves™ (although referred to in the paper
as the “Bustmaster”), a product of Savvier LP that supposedly
“Lifts, Firms, and Enlarges Your Bustline.”7 The purpose of the
study was to test the ability of the exercise device's ability to
improve core muscle strength, firmness, girth, and toning of the
upper body. The subjects were 29 women, ages 22 to 48, who
used the product at home 5 minutes a day, 5 days a week for 30
days. Muscle strength, tone, and girth were measured on the
strength and back with a tensionometer and measuring tape.
Ultrasound was used to measure muscle thickness on the chest
and back. The abstract for the paper itself reads like something
out of an infomercial: “The results showed that only 5 minutes
of exercise per day on a resistance trainer can cause dramatic
effects on core muscle strength, firmness, girth, and toning of the
upper body.”
Along the same lines, Petrofsky et al. present, “One significant
problem in women that is often overlooked is that as aging
progresses, muscle weakness in the chest causes the breasts to
sag. This in turn can create a lever arm that causes back and neck
Alan Aragon’s Research Review – October, 2009
muscle strain and soreness. This has been a major problem in
women.” Contrary to this, ptosis is not likely a “major” problem
in women, at least not in terms of general health concerns.8 Like
Petrofsky says, sagging of the breasts is a natural occurrence in
aging, much like increased incidence of skin folds and creases,
i.e. wrinkles. But as for ptosis contributing to back and neck
soreness, Petrofsky provides no citation of relevant reports, nor
could any be found independently. Even if ptosis-caused pain
occurs, it is hardly a major problem of aging like, for instance,
degenerative heart disease.
As for the structuring of the groups in the study, the only
compliance monitoring mentioned is the amount of days each
subject performed the workout. No indication is given as to
whether the subject groups, both the control and experimental,
were monitored for other, potentially confounding factors. For
instance, the groups were not monitored for nutrition, calorie
intake, or additional exercise. This allows for the possibility, for
example, that the experimental group could have changed their
nutritional habits or exercise regime on a whole in some way.
Neither is unreasonable to imagine: “Well, I'm already working
my chest for 5 minutes a day; I'm going to cut out that morning
donut and maybe go on daily jogs.” Because the team instituted
no other controls or monitoring, we simply can’t trust that the
evaluation was thorough enough.
Additionally, some of the data collected are not relevant to the
topics of study. For instance, Petrofsky reports in the results
section that “...firming in the upper body caused the breast line
to rise (measured from digital measurements is the distance from
the acromion to the nipple), an average of 0.45 ± 0.22 cm.” (sic)
It is not clear what measuring the breast line of the subjects tells
us about chest girth, muscle tone, or strength. Therefore, one
wonders why it was reported, let alone measured, to begin with.
Bender Ball™
In another article, “Muscle use During Exercise With a Mini
Medicine Ball Compared to Other Abdominal Exercise
Modalities,”9 Petrofsky's team compares muscle activity from
various movements with and without 2 and 6lb mini-medicine
balls, which are marketed by Savvier LP as "Bender Balls".
Trivial as the study seems at first, the true purpose is revealed in
the discussion section.
Abdominal crunches were compared with “tuck-up abdominal
crunches” with the addition of the 6lb ball: “...during the tuck-up
abdominal crunches exercises, the average core muscle
recruitment for the 4 core muscle groups examined here
was 37.1% of muscle activity compared with 13.68% for an
abdominal crunch. This core muscle use was almost 300%
higher for this exercise.” The article goes on to say, “when the
weight was progressively increased to the 6-lb ball, muscle
activity was substantially higher, averaging 49.9% of total
muscle activity for the abdominal muscles, showing an increase
of about 400% over an abdominal crunch.” The scientific value
of these comparisons isn't entirely clear: it just reports muscle
activity in completely different exercises with the addition of a
weight. Nevertheless, it is a great selling point for the maker of
[Back to Contents] Page 11
the Bender Ball. Sure enough, the Bender Ball website
(www.benderball.com) claims it to be 408% more effective.
Petrofsky studies the Bender Ball three more times in 2008:
ƒ “The Effect of a Diet and Exercise Program with a Mini
Medicine Ball on Cardiovascular Fitness, Weight Loss, and
Strength.”10 where overweight to obese individuals went on
a 10 day crash diet and exercise program, and not
surprisingly, achieved weight loss and strength gains.
ƒ “Aerobic Energy Expenditure on a 60-Minute Exercise
Video with Mini Medicine Balls”11 wherein 13 subjects
screened for illness or orthopedic problems followed a 1
hour exercise video from Savvier LP and used the Bender
Ball.
ƒ “Improving the Outcomes after Back Injury by a Core
Muscle Strengthening Program”12 wherein subjects
suffering from lower back pain underwent a 1 month
exercise protocol (The Bender Method for Core Training,
marketed by Savvier LP). While the subjects that took part
in the strengthening program improved their strength and
reduced pain, the study neglected to compare the Bender
Ball training to any other modality. This makes the actual
results of the study largely meaningless, as untrained
individuals doing ANY sort of training are almost certain to
achieve at least a measure of progress.
There are instances where complex devices are tested in multiple
studies, but the Bender Ball is hardly novel or complex. It is
strikingly odd that it was the focus of one scientific study, let
alone four. In case anyone is counting, these and “A
Bidirectional...” constitute about one-fourth of the papers
Petrofsky coauthored in the last six years.
The Journal of Applied Research
The very publication Petrofsky uses, JAR, is suspect. It is
published by a Pennsylvania company, Therapeutic Solutions
LLC,4 and the registered Office of Address lists Bob Issler of
Newton PA.13 Bob Issler is the managing editor of JAR, who
also oversees "operations" for its sister publication, The
International Journal of Applied Research in Veterinary
Medicine (also published by Therapeutic Solutions LLC).14,15
Both journals’ fax numbers resolve to a private residence in
Apopka, FL and are listed to an R Issler.16 This same fax number
is listed (also as Bob Issler’s) for a direct mail and telemarketing
company, Plan B Marketing, a New Jersey registered company
of which Bob Issler is also an officer.17,18 This strikes us as
loose, unprofessional, and shady - as always, we encourage
readers to draw their own conclusions about an academic journal
whose fax number belongs to another journal, and a direct
mail/telemarketing company, edited by a man who is also an
officer of said marketing company.
Savvier LP
Savvier LP, maker of Easy Curves™ and Bender Ball™, is
located less than 100 miles from Loma Linda University and
Azusa Pacific University.19 It was sued by the FTC in 2003, and
awarded a judgment in 2004 for making false claims in regards
to the BodyFlex exercise routine and forced to refund customers
Alan Aragon’s Research Review – October, 2009
$2.6 million.20 The judgment also, “prohibits the defendants
from making claims, for any product, service, or program that
purports to provide weight-loss, inch- loss, fat-loss, exercise or
fitness benefits, and for any dietary supplement, food or drug,
without scientific substantiation.” Petrofsky first began studying
Savvier products in the fall of 2003 publishing two papers on the
6 Second Abs™.21 We don’t know what, if any, effect the FTC’s
lawsuit had on Savvier LP’s marketing policies.
The president and co-founder of Savvier LP is Jeff Tuller.22 He
was recently elected as Chair-Elect of the Electronic Retailing
Association, a trade association and lobbying group for direct
response marketers.23 Savvier LP is a “Platinum Member” in the
organization, and Tuller also serves on two committees and an
advisory board within the organization.24,25
Conclusion (& an Oddity)
Before concluding we thought we would share one of the first
(and funniest) tidbits that turned us on to this investigation. 5
seconds in to the Easy Curves™ commercial, a doctor, Jan S.
Kodat, appears on screen endorsing the product. It turns out that
Kodat earned her MPT and DPTSc at Loma Linda University.
She went on to teach at Azusa Pacific University, and while
there published a paper with Petrofsky and Laymon (a co-author
on several Savvier LP product papers).26 Kodat now teaches at
California Baptist University.27 Unfortunately for her, a Google
search of her name returns this page in 2nd position.
Despite what Dr. Petrofsky says about the pertinence and
authenticity of his research into these commercial exercise
products, the question remains: what is really going on here? Dr.
Petrofsky, along with dozens of his grad students and several
colleagues, published twenty research papers in the same suspect
journal. In every paper overwhelming positive results are
achieved. Has Petrofsky got a line on the best designed,
effective, and affordable exercise gadgets known to man? We
think it's more plausible instead that there some undisclosed
relationship between Petrofsky, his colleagues, Savvier LP, and
the Journal of Applied Research. Surely, Savvier LP looks to
benefit the most from independent confirmation of the efficacy
of nearly their entire catalogue of direct marketed exercise
equipment and videos, not consumers.
References
1. Jerry Petrofsky’s faculty page. [Azusa Pacific University]
2. [Petrofsky PDF search results]
3. [Bender Ball Official site]; [Easy Curves Official site]
4. JARCET company profile [JARCET]
5. JARCET review board [JARCET]
6. Petrofsky  JS,  et  al.  A bidirectional resistance device for
increasing the strength and tone in upper body core muscles
and chest girth. JARCET. 2005;5(4):553‐68 [Fulltext PDF]
7. [Easy Curves Official site]
8. Geffen A, Benny B. Mechanics of the normal woman’s
breast. Technol Health Care. 2007;15(4):259-71.
[Medline][Fulltext PDF]
9. Petrofsky JS, et al. Muscle use during exercise with a mini
medicine ball compared to other abdominal exercise
Modalities. JARCET. 2005;5(4):553‐68. [Fulltext PDF]
[Back to Contents] Page 12
10. Petrofsky JS, et al. The effect of a diet and exercise program
with a mini medicine ball on cardiovascular fitness, weight
loss, and strength. JARCET. 2008;8(2):116-29. [Fulltext
PDF]
11. Laymon M, et al. aerobic energy expenditure on a 60-
minute exercise video with mini medicine Balls. JARCET.
2008;8(2):130-4. [Fulltext PDF]
12. Petrofsky  JS,  et  al. Improving  the  outcomes  after  back 
injury  by  a  core  muscle  strengthening  program. 
JARCET. 2008;8(1):62-75. [Fulltext PDF]
13. Therepeutinc Solutions, LLC [Corporate Filing]
14. Staff Directory [JARCET]
15. Staff Directory [JARVM]
16. R. Issler [Contact]
17. [Plan B Marketing - Home Page]
18. Filing #0400143471 - search "Robert Issler" for officer
information [New Jersey State Business Gateway Service]
19. LLU, APU, Savvier LP [Located on Google Maps]
20. Bodyflex Marketers Settle FTC Charges of False and
Unsubstantiated Inch and Fat Loss Claims. Sept 2004.
[FTC]
21. JARCET table of contents [Vol. 3, No. 4, Fall 2003]
22. Jeffrey Tuller [Home Page]
23. Electronic Retailing Association [About ERA]
24. ERA Names Newly Elected Board of Directors for 2009-
2010. Reuters. Sep 2009. [Reuters]
25. [ERA Membership Committee]; [ERA Retail Council];
[ERA Advisory Board]
26. Jan Kodat’s faculty page. [Azusa Pacific University]
27. Jan Kodat’s faculty page. [California Baptist University]
___________________________________________________
Cameron Mochrie graduated from Amherst College, majoring in physics. He put
himself through college playing online poker and after graduation worked for a
time in the financial sector. After the meltdown, he left to start his own personal
training business in Toronto, ON. You can check him out at http://sfbfitness.com.

Also a graduate of Amherst College, Ian Capulet double majored (with honors)
in political science and philosophy. He is an aspiring screenwriter, fashion
consultant/blogger, movie reviewer, and essayist. He blogs about fashion for
men at http://cefashion.net.

Alan Aragon’s Research Review – October, 2009 [Back to Contents] Page 13


Vertical Jump FAQ
By Jamie Hale
Question: How much
do you need to train
calves to help enhance
my vertical leap?
Answer: Approximately
80% of the force pro-
duced in the vertical
leap comes from the
posterior chain and
quads, while the calves
and upper body contri-
bute the other 20%. It
probably won’t hurt to
do some direct lower
leg training, but spend
the majority of your
time training the muscles
that contribute the most.
Question: Do you recommend strength shoes for increasing
lower leg strength and vertical?
Answer: I do not recommend strength shoes. I have never seen
anyone increase their vertical because they were using strength
shoes. Cook and colleagues evaluated in a prospective,
randomized trial the efficacy and safety of the strength shoe
training regimen for increasing lower leg flexibility and strength
in intercollegiate track and field participants.1 No enhancement
of flexibility, strength, or performance was observed for
participants wearing the strength shoe at the end of an eight-
week training program following the suggested regimen of the
manufacturer. The authors concluded that the strength shoe
couldn’t be recommended as a safe, effective training method
for developing lower leg strength and flexibility. The results of
this study did not surprise me. The mechanical factors involved
with wearing a strength shoe are not conducive to increases in
strength or power. In most cases, fancy gadgets equal
deconditioned athletes.
Question: If I get stronger, will my vertical increase?
Answer: If maximal strength increases but relative strength
decreases (usually signifying rapid weight gain) your vertical
will probably decrease. However, if relative strength increases,
your vertical will usually increase.
Question: Does weighted vest training contribute to vertical
jump?
Answer: If used appropriately, you can probably expect some
gains in vertical leap. Don’t were a weighted vest while
performing sport-specific skill work.
Question: What is the best exercise for increasing vertical
jump?
Alan Aragon’s Research Review – October, 2009
Answer: There is no single best exercise. Concentrate primarily
on developing power in the quads and hamstrings, using mostly
squats, variants of squats, Olympic lifting variants, good
mornings, and plyometrics.
Question: For my nutrition-entrenched readers who might not
be privy to the details of it, please elaborate a bit about
plyometrics – what it is, what people mistake it for, and what are
the key technical aspects.
Answer: Plyometric training was developed by Yuri
Verkhoshansky as a means to enhance speed strength. What is
now referred to as plyometrics was originally called the shock
method. The original meaning of the word plyometric (originally
spelled pliometric) was intended to mean eccentric contraction.
Plyometrics became popular in America in the 70s according to
most authorities. Soviet sprinters were displaying very
impressive sprint times so U.S. coaches decided to travel to the
Soviet Union to figure out what was going on.
The Americans saw an athlete step off a box, jump up in the air
and the rest, as they say, is history. On their return to the United
States, they spread the word of the magic training method.
Needless to say they never took into consideration the planning
and conditioning that existed in addition to this type of magic
training. In the Soviet Union the shock method was used in a
cyclic nature which involved varying intensity levels and
conditioning methods.
Today every coach and fitness instructor in the world is probably
using some type of supposed plyometrics. As an example, a
coach might have an athlete jump ten minutes with no regard to
times spent on the ground or quality. According to the founder
of shock method training, if you spend an excess of 0.2 of a
second on the ground after landing this does not constitute true
plyometric activity. This is where the misconception lies –
plenty of activities administered by trainers are referred to as
plyometrics, when they really are not.
The ultimate goal in shock method training is to maximize the
benefits of the stretch-shortening cycle (SSC) The athlete needs
sufficient strength in the musculoskeletal system before adhering
to this type of training. A great deal of force is produced in the
joints when performing any type of jumping or falling.
Concentrate on quality training when using plyometrics. This
should not be a fatiguing endeavor; remember, the goal is speed-
strength. When used properly, plyometrics is an excellent
training method for increasing speed-strength, or the ability to
quickly execute an unloaded movement or a movement against a
relatively small external resistance. Plyometrics take advantage
of the myotatic stretch reflex and its contribution to force
production.
Question: What is the stretch reflex, and how does it relate to
improving the vertical leap?
The stretch shortening cycle (SSC) occurs in a specific order. As
the body performs an eccentric action, the body will store
potential kinetic energy. When the concentric action quickly
[Back to Contents] Page 14
follows the eccentric action, the kinetic energy is utilized. The
stretch shortening cycle is evident in numerous sporting events.
Examples of the stretch shortening cycle include the wind up by
the pitcher in baseball. In power lifting squatting is a SSC
maneuver. The success of sprinters and throwers is to a large
extent dependent on the efficiency of the SSC.

The key to utilizing stored elastic energy involved in the SSC is

the ability to minimize the conversion time between the ending
of the eccentric and beginning of the concentric phase of the
movement. The attachment time between myosin and actin
strands is very brief, usually 15 to 120 milliseconds. A long
delay between the stretching and contracting phase of the
movement results in increasing detachment of the myofilaments
which negates the potential to utilize the elastic energy stored in
the muscle.

The neural mechanisms most prominent in the SSC are the

myotatic stretch reflex and the golgi tendon organ. The myotatic
reflex receptors (muscle spindles) are specialized muscle fibers
which detect length change within the muscle. The primary role
of the muscle spindles is to set the muscle to a preset length.
When the muscles are stretched the muscle spindles are also
stretched. This causes muscle spindle discharge which results in
alpha motoneuron release which, in turn, results in reflex
contraction of the stretched muscle. This reflex enables the
muscle to return to its preset length. The golgi tendon organ is
located in the muscle-tendinous junction and senses change in
the tension of muscle. The primary role of the golgi tendon
organ is to prevent potentially injurious muscle tension. When
this organ senses forces are excessive, muscular contraction is
inhibited.

One of the primary training goals for enhancing the SSC is to

maximize the positive effects of the myotatic stretch reflex while
minimizing the negative effects of the golgi tendon organ. This
type of training could involve accelerative movements with or
without weights. Accelerative training, in this case, would refer
to very rapid stretching followed by accelerative contraction.
The goal is to maximize the benefits of the stretch reflex and
In the spirit of Mochrie & Capulet’s excellent investigative
minimize the actions of the golgi tendon organ.
report on Dr. Petrofsky et al, here is the home page of an
amusing product called the “Shake Weight.” I originally saw the
Reference Cited
video ad on youtube, but had to make sure that the product was
1. Cook SD, et al. Development of lower leg strength and actual and not merely a parody (yup, it’s real). Imagine my
flexibility with the strength shoe. Am J Sports Med. delight at finding out there’s a version for men, which can be
1993;21(3):445–8. [AJSM] marveled at here.
___________________________________________________
Jamie Hale is a sports conditioning coach, author, lecturer, outdoor enthusiast
and exercise and nutrition consultant. He is the owner and founder of
MaxCondition Training, MaxCondition Nutrition and HNE Research Group. He
is also a member of Kentucky Association of Science Educators and Skeptics. He Researcher James Krieger grabs the bull by the horns and takes
has contributed to numerous exercise and sports publications (nationally and
internationally) and has authored six books. Jamie is a member of the World
an evidence-based dump on all that is dumpy in the fitness
Marital Arts Hall of Fame in recognition of his conditioning work with martial information realm. Visit his blog here.
artists. To learn more about Jamie, visit his websites at www.maxcondition.com
and www.knowledgesummit.net

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

contention, cheers, jeers, guest articles you’d like to submit, or
any feedback at all, send it over to aarrsupport@gmail.com.

Alan Aragon’s Research Review – October, 2009 [Back to Contents] Page 15