August 30, 1999
Volume 2, Number 15
Research Update
by Bryan Haycock MSc., CSCS
bryan@thinkmuscle.com
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on this article.
As we approach the new millennium we find the science of building
muscle progressing faster than ever before. Long gone are the days of
simple trial and error when it comes to building muscle. The modern
bodybuilder demands more than just "hear say" if they are to
adopt a new training routine or nutritional supplement. This column was
created to keep today’s bodybuilder on the cutting edge of scientific
research that might benefit them in their quest for body perfection.
Weight Training Miraculously Shown to Preserve Muscle
While Dieting.....Again.
Title:
Effects of resistance vs. aerobic training combined
with an 800 calorie liquid diet on lean body mass and resting metabolic
rate.
Researchers:
Bryner RW, Ullrich IH, Sauers J, Donley D,
Hornsby G, Kolar M, Yeater R; Department of Human Performance and
Applied Exercise Science, West Virginia; University, Morgantown 26506,
USA.
Source:
Journal of the American College of Nutrition 1999
Apr;18(2):115-21
Summary:
The purpose of this study was to examine the
effect of intensive, high volume resistance training combined with a
very low calorie diet (VLCD) on weight loss, lean body weight loss
(LBW), and resting metabolic rate (RMR). METHODS: Twenty subjects (17
women, three men), mean age 38 years, were randomly assigned to either
standard treatment control plus diet (C+D), n = 10, or resistance
exercise plus diet (R+D), n = 10. Both groups consumed 800 kcal/day
liquid formula diets for 12 weeks. The C+D group exercised 1 hour four
times/week by walking, biking or stair climbing. The R+D group performed
resistance training 3 days/week at 10 stations increasing from two sets
of 8 to 15 repetitions to four sets of 8 to 15 repetitions by 12 weeks.
Groups were similar at baseline with respect to weight, body
composition, aerobic capacity, and resting metabolic rate. RESULTS:
Maximum oxygen consumption (Max VO2) increased significantly but equally
in both groups. Body weight decreased significantly more in C+D than
R+D. The C+D group lost a significant amount of LBW (~ 4 kg or 8.8
pounds). No decrease in LBW was observed in R+D. In addition, R+D had an
increase in RMR O2 ml/kg/min (2.6 to 3.1). The 24 hour RMR decreased in
the C+D group. CONCLUSION: The addition of an intensive, high volume
resistance training program resulted in preservation of LBW and RMR
during weight loss with a VLCD.
Discussion:
When caloric expenditure is greater than
caloric intake (e.g. while dieting), the body converts it’s tissues
into burnable forms of energy such as glucose, amino acids and free
fatty acids. This is carried out in response to heightened activity of
catabolic hormones. These hormones are able to mobilize energy buy
causing cells to disassemble proteins, sugars and fats that make up the
cells enzymes and internal structures.
With an increase in catabolic hormones it is only natural that the
body will begin to lose mass and get smaller. When calories are
restricted the body not only draws upon fat stores but also upon tissues
such as muscle, blood and even your internal organs in order to get
amino acids used in gluconeogenesis.
Due to the central nervous systems’ constant need for glucose,
gluconeogenesis increases sharply when calories are restricted. This
means that protein is broken down to make key amino acids available to
be converted into glucose as well as for other essential functions. All
this is done at the expense of protein rich tissues such as muscle and
internal organs.
During starvation diets as much as 50% of the total amount of weight
lost has been observed to come from lean tissue. This is disastrous for
anyone trying to lose fat! Imagine that you have a car and your goal is
to use up all of the gas in the gas tank. The catch, is that the more
gas you use, the smaller the engine gets, and the less gas it requires.
(It must be one of those foreign jobs.) This illustrates the impact of
losing lean tissue as you try to lose fat. Muscle tissue, through its
own metabolic activity as well as it’s relation to thyroid output, is
almost 90% responsible for the number of calories that you burn in a
day. As you lose muscle it becomes harder and harder to continue to lose
weight because fewer calories are needed by the body. The usual response
is to cut calories even further which only exacerbates the situation.
This predicament is the result of normal metabolic adaptations to
caloric restriction.
Although the effects of weight training on the preservation of lean
mass during caloric restriction is very old knowledge to bodybuilders,
the medical community must once again try to feel responsible for making
the discovery. In the study above we see subjects put on what has
previously been considered a dangerous very low caloric intake of 800
liquid Kcals per day. Some of the people on the diet were put on a
resistance training program. This group performed resistance training 3
days/week at 10 stations increasing from two sets of 8 to 15 repetitions
to four sets of 8 to 15 repetitions by the end of 12 weeks. The control
group used the same diet but performed aerobics or endurance exercise.
The result? As expected the weight training group held on to their
muscle while the aerobics group lost almost 9 pounds of theirs.
A couple of issues need to be brought up while interpreting these
results. First, these were regular non-weight training, non-athletic
people. The anabolic stimulus created by their meager attempts at
pumping iron was sufficient to completely counter the catabolic effects
of an 800 Kcal per day liquid diet. They were not holding on to any
hypertrophied lean tissue before dieting. This being the case, their
muscle was already somewhat resistant to catabolism when compared to
some one who must bust their butt most days of the week just to keep
from getting "small".
The second issue that must be recognized is that they adhered to a
very important principle of resistance exercise, namely the principle
of progressive resistance. This means that over the period of their
diet, the amount of resistance as well as the volume lifted increased
steadily. This seems to be problematic for most bodybuilders. In fact it
is common practice to actually decrease the poundages for most lifts
over the course of a pre-contest diet. This happens because they make no
effort to cycle their training to accommodate the diet. Starting a diet
at the peak of a strength plateau is not the best method to keep
your size for an upcoming show. A period of "strategic
deconditioning" during which size is maintained while intensity and
volume slowly decrease is necessary to prepare for dieting. Then, the
diet begins at the same time a progressive resistance cycle is begun.
This simulates the conditions under which a novice experiences
significant muscle gains at the onset of a weight training program and
is more conducive to keeping, if not increasing, lean mass while
dieting. Of course this is a simplification yet the principle is sound
and the results reproducible.
Claims About the Dangers of Creatine May Be
Overstated.
Title:
Long term oral creatine supplementation does not
impair renal function in healthy athletes.
Researchers:
Poortmans JR., & Francaux M.
Source: Medicine and
Science in Sports and Exercise 31(8): 1108-1110, 1999
Summary:
Side effects have been postulated from the use of
creatine supplements yet no thorough investigations have been conducted
to support these assertions. The purpose of this study was to determine
if indeed long term creatine use was detrimental to the kidneys of
healthy individuals. METHODS: Creatinine, urea, and plasma albumin
clearances were measured in oral creatine consumers (taken regularly for
10 months to 5 years) and in control subjects (never used creatine).
RESULTS: There were no statistical differences between the control group
and the creatine consumers group for plasma contents and urine excretion
rates for creatinine, urea, and albumin. Clearance of these compounds
did not differ between the two groups. Thus glomerular filtration rate,
tubular reabsorption, and glomerular membrane permeability were normal
in both groups. The authors conclude that neither short-term,
medium-term, nor long-term oral creatine consumption induce detrimental
effects on the kidney of healthy individuals.
Discussion:
Any time something good comes from the
supplement industry (a rare yet highly anticipated occurrence) there
will be nay sayers quick to declare the evils of the new super
supplement. Creatine was not immune to such opponents of progress. Add
to this rumors of kids peeing blood after loading the stuff for football
practice and you have a full blown controversy. There has even been a
published case study detailing the dangers of creatine on kidney
function (Pritchard, 1998). Upon closer examination you will find that
their one subject had a pre-existing kidney disease for the last 8
years. Not only that but the subject had been taking drugs that are
toxic to the kidney for the last 5 years prior to their case study. Not
surprisingly, their subject experienced kidney dysfunction after 7 weeks
of creatine supplementation. This subject would probably have
experienced kidney dysfunction after 7 weeks of mother’s milk!
The subjects in this study did not have any pre-existing
kidney problems. Nine athletes were chosen to represent "long
term" creatine supplementation. Eighty five subjects served as
controls. Those who consumed creatine regularly did so in the following
manner. Individual doses from 1 - 20 grams of creatine were taken from 1
to 4 times per day. Total daily doses ranged from 1 to 80 grams per day
taken 7 days per week for a period ranging from 10 months to 5 years.
As you are aware from the above summary of the study, long term
creatine supplementation does not appear to cause any kind of kidney
dysfunction. All of the parameters looked at by these researchers showed
no difference between the experimental group and the control group.
There is one thing that I can promise you, you will not here about this
study on the morning news. They only focus on sensationalizing
supplements in the context that they are dangerous and their use is akin
to drug abuse. Rest assured they will have someone with no actual
knowledge of supplements or science extolling the dangers of
supplements. All of this misinforms the general public making the work
of actual experts in the field of nutritional supplementation all the
more difficult as they have to go back and try to undo all of the
hysteria. I’m afraid this is turning into some sort of rant. That’s
a sure sign that I have said enough on this subject.
References:
Pritchard NR., Kalra PA. Renal dysfunction accompanying oral creatine
supplements. Lancet 351:1252-1253, 1998.
When It Comes to Building Tendons, Not All
Steroids are Created Equal.
Title:
Stimulation of collagen synthesis by the anabolic
steroid stanozolol.
Researchers:
Falanga V, Greenberg AS, Zhou L, Ochoa SM,
Roberts AB, Falabella A, Yamaguchi Y; University of Miami School of
Medicine, Department of Dermatology, Miami, Veterans Affairs Medical
Center, Florida, USA.
Source:
J Invest Dermatol 1998 Dec;111(6):1193-7
Summary:
In this report, we measured the effect of the
anabolic steroid stanozolol on cell replication and collagen synthesis
in cultures of adult human dermal fibroblasts. Stanozolol (0.625-5
micrograms per ml) had no effect on fibroblast replication and cell
viability but enhanced collagen synthesis in a dose-dependent manner.
Stanozolol also increased (by 2-fold) the mRNA levels of alpha1 (I) and
alpha1 (III) procollagen and, to a similar extent, upregulated
transforming growth factor-beta1 (TGF-beta1) mRNA and peptide levels.
There was no stimulation of collagen synthesis by testosterone. The
stimulatory effects of stanozolol on collagen synthesis were blocked by
a TGF-beta1 anti-sense oligonucleotide, by antibodies to TGF-beta, and
in dermal fibroblast cultures derived from TGF-beta-1 knockout mice. We
conclude that collagen synthesis is increased by the anabolic steroid
stanozolol and that, for the most part, this effect is due to
TGF-beta-1. These findings point to a novel mechanism of action of
anabolic steroids.
Discussion:
I must first acknowledge that the commonly
held belief is that anabolic steroids predispose an athlete to tendon
rupture. This conclusion is drawn from animal studies showing that some
steroids produce a larger, stiffer tendon in rats and that these
steroid-induced tendons "fail" before the tendons from the
control animals. The term fail refers to the breaking point.
The interesting thing about the present study is that the steroid
stanozolol (Winstrol) had a different effect than testosterone. If you
are a regular reader of Mesomorphosis you should be well aware that not
all steroids act in the same manner. And that because of subtle
differences in there molecular structure they are able to elicit
different responses. For example, Deca seems to act primarily through
the androgen receptor (AR) where as Dianabol has effects beyond those
associated with the AR.
Because synthetic steroids have differ in their chemical properties
it should not be surprising that testosterone did not have the same
effect as Winstrol. Winstrol increased collagen synthesis as opposed to
testosterone which did not in this study. Interpreting the results of
this study are more difficult than simply describing them. Other
researchers have suggested that steroids cause a rapid increase in
protein synthesis within tendon fibroblasts which results in fibroids or
fibrous nodules within the tendon (Michna,1988). These fibroids alter
the mechanical properties of the tendon perhaps predisposing it to
rupture. It is also noted that during short term use of steroids there
is an alteration in the alignment of collagen fibers which may also lead
to rupture. Interestingly these alterations in collagen metabolism are
transient with markers of collagen turnover returning more or less to
baseline after 3-4 weeks of steroid administration (Karpakka,1992).
These same researchers noted that low dose anabolics effect primarily
muscle collagenous tissue with tendon being effected only at higher
doses (i.e. 5 times the therapeutic dose) which would more closely
represent what is needed by bodybuilders to put on mass.
The question remains, dose this mean that Winstrol will actually help
prevent tendon injury or will it lead to bigger yet stiffer tendons
prone to injury? It is difficult to take animal research and extrapolate
the results to humans. Stanozolol is used therapeutically in humans to
treat a variety of connective tissue and vascular disorders and its
clinical effects suggest that it can modulate connective tissue
breakdown in people. Despite being labeled as "ineffective" by
many bodybuilders it is very popular among athletes. As with most
hormones, dosage plays a role in what effects are seen, be they positive
or negative. Hopefully future studies will shed light on the therapeutic
effects of different steroids on tendons in humans.
References:
Michna H Appearance and ultrastructure of intranuclear crystalloids
in tendon fibroblasts induced by an anabolic steroid hormone in the
mouse. Acta Anat (Basel) 1988;133(3):247-50
Karpakka JA, Pesola MK, Takala TE. The effects of anabolic steroids
on collagen synthesis in rat skeletal muscle and tendon. A preliminary
report. Am J Sports Med 1992 May-Jun;20(3):262-6
Please send us your feedback
on this article.
by Bryan Haycock MSc., CSCS
bryan@thinkmuscle.com
