August, 1998
Volume 1, Number 3
Research Update
by Bryan Haycock MSc., CSCS
bryan@thinkmuscle.com
Please send us your feedback
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.
1. Ever tried squeezing blood from a turnip? Try squeezing
"muscle extract" from a muscle!
Title: Skeletal Muscle Injury Repair and Regeneration Enhanced by
Muscle Mitogen.
Researchers: M. Li, JX Li, S. Lee, R. Xie, and KM Chan, from the
Department of Orthopedics & Traumatology, The Chinese University of
Hong Kong, Shatin, N.T., Hong Kong.
Source: Med Sci Sport Exer. 1998 May;30(5) Supplement;
S1-S1339
Summary: Previous studies suggested that muscle injuries lead to
the formation of wound fluid that can stimulate satellite cell
proliferation in cell culture. The present studies focused on the
identification of the functional role of the "muscle extract"
in muscle injury repair and regeneration in vivo. Two groups of rats
were subject to excessive exercise-induced muscle injury, and
strain-induced massive muscle injury respectively. Muscle extracts were
prepared from the red and white muscle tissue of young rats
respectively. Three rats of the first group (exercised group) were
injected beneath the epidermis of tibialis anterior muscle with 1 mg
muscle extract in one leg an hour after exercise. The remaining 3 rats
of the first group were injected with an equal amount of bovine serum
albumin (BSA) in PBS as control. The injection were repeated daily for 4
days. After two injections, bromodeoxyuridine (BrdU)(3mg/100g body wt.)
were injected along with the third and fourth injections of the extract
or control solution respectively. [BrdU is used as a marker of cell
proliferation.] The treatment for the "strain" group of rats
followed the exercised group’s treatment exactly. Rats of the two
groups were sacrificed 3 days after the last injection of the muscle
extract or control solution. After sacrifice, the tibialis anterior
muscle was removed and homogenized for measurement of DNA. For
histological examination, the sample of tibialis anterior was processed
for paraffin embedding, then proceeded with immunohistochemical
staining, and microscope examination. The results were significant, in
that the focal muscle injuries induced by excessive exercise were
undergoing better focal repair, with increased-number of myonuclei per
fiber after injection of muscle extract compared with that in control
injected with same amount of BSA. The result derived from strain-induced
model was even more significant, in that massive muscle regeneration was
observed with little focal fibrosis after injection of muscle extract,
in contrast, massive fibrosis was the main feature with little muscle
regeneration in control. Present evidences showed that muscle fibers
contain a preexisting muscle mitogen. Injury to the fiber, that cause
the release of the mitogen normally enclosed in the muscle fibers that
can enhance muscle injury repair. However, in normal course of
un-interfered healing of muscle injury, fibrous tissue grows faster to
replace the inflammatory reaction, although some little regenerating
muscle fibers are present, it is far to insufficient. Administration of
exogenous muscle mitogen can greatly improve muscle injury repair and
regeneration. Therefore, identification and further production of the
muscle mitogen are of great significance both clinically and
commercially.
Discussion: The role of muscle fiber injury has been an area of
interest for some time. It has been speculated that adaptive muscle
growth is analogous to other forms of tissue repair in response to
injury. The theory is that cell growth, connective tissue matrix
deposition, and angiogenesis (development of new blood vessels) are
stimulated by NAD+ depletion caused by a burst in lactate generation in
the would site. In the study above, it was demonstrated that if there is
insufficient "muscle mitogen", exercise induced muscle injury
leads to significant inflamation and as a result, an over production of
fibrous connective tissue that effectively replaces functional muscle
tissue. The exact composition of the muscle extract that was used was
not determined. Apparently it contains growth factors that accelerate
the rate of muscle fiber regeneration when injected locally at the site
of damage. It is probable that this muscle extract used by these
investigators contains chemicals (probably proteins) that act as signals
for myogenic stem cells, sometimes called satellite cells, to
proliferate and even relocate. Although satellite cells have long been
established as the providers of myoblastic cells, very little is really
known (apart from their anatomical location in relation to muscle fibers
and their ability to migrate) about the precise role of satellite cells
in myogenesis.
The results of this study indicate that for significant functional
muscle growth you must induce some amount of fiber damage during your
training. This damage must be sufficient to cause a release of this
"muscle mitogen" from within the muscle cells into the
surrounding space. The results of this study may also shed light on the
fact that as we age, we respond less favorably to muscle damage than
when we are young. Tissue response to injury in the aged is
characterized by a disproportional increase in fibrous tissue within the
muscle similar to that seen in the untreated groups in this study.
2. The "Zone" put on trial!
Title: Effects of Two Energy Restricted Diets on Fuel
Utilization, Blood Chemistry, and Body Composition.
Researchers: M. Kern, V. Schuab, and D. Harris, from the
Department of Kinesiology, San Francisco State University, SF, CA.
Source: Med Sci Sport Exer. 1998 May;30(5) Supplement;
S1-S1339
Summary: Researchers from the Department of Kinesiology from San
Francisco State University recently put the "Zone" diet to the
test. The purpose of the study was to determine the effect of two energy
restricted diets on fuel utilization during exercise, body composition
and fasting blood parameters. The two diets that were compared were a
typical high carb diet consisting of 65% carbohydrate, 20% protein, and
15% fat, and a second diet which was similar to the "Sears Zone
Diet" that was made up of 40% carbohydrate, 30% protein, and 30%
fat.
|
Parameter |
ZONE Pre |
Post |
HICHO Pre |
Post |
| Weight (kg) |
80.1 ± 3.8 |
76.5 ± 2.9* |
74.3 ± 2.6 |
70.4 ± 2.6* |
| % BF |
42.04 ± 7.5 |
32.2 ± 2.8* |
32.3 ± 1.7 |
30.2 ± 1.7* |
| FatMass(kg) |
32.07 ± 4.3 |
24.2 ± 1.8* |
23.8 ± 1.4 |
20.8 ± 1.5* |
| FFM(kg) |
47.4 ± 6.7 |
52.3 ± 3.8 |
50.5 ± 2.5 |
49.6 ± 2.43* |
| Trig(mg/dl) |
168.9 ± 57 |
96.4 ± 16* |
102.4 ± 25 |
103 ± 19 |
| TC(mg/dl) |
209.3 ± 10 |
189.1 ± 12* |
201.5 ± 18 |
183.6 ± 12* |
| LDL(mg/dl) |
139.9 ± 13 |
121.0 ± 10* |
125.6 ± 15 |
108.7 ± 9* |
| TC/HDL |
4.9 ± 0.7 |
4.1 ± 0.4* |
3.7 ± 0.3 |
3.4 ± 0.2 |
*indicates significance (p£0.05) between pre and post with the same
group.
Similar trends in blood lipid changes resulted from following either
diet, though Triglycerides and TC/HDL ratio only significantly decreased
on the "Zone" diet. Respiratory Exchange Ratio (RER) was not
different between or within groups. Most importantly, there was no loss
of Fat Free Mass on the "Zone" diet, unlike the "high
carb/low fat" diet.
Discussion: Before any conclusions are drawn, attention should be
paid to the relatively small sample size used in this study. Any time
you use so few people in a study, the statistical "power" of
the results are diminished. Inter-individual differences and
"unaccounted for" variables can greatly effect the outcome
when so few subjects are used. This aside, once again it appears that
the phobia about fat is probably unfounded. Weight loss is a matter of
burning more calories than one consumes. The difference between these
two diets was not in the amount of calories but in the composition of
those calories. The "Zone" diet contains 30% of calories from
fat, whereas the high carbohydrate diet used in this study contained
only 15% of calories from fat.
It is possible that the additional fat content of the
"ZONE" diet provided more fuel for muscle and organs, thereby
lowering the demand for amino acids (and thus muscle catabolism) as
gluconeogenic precursors. It would appear that when the body is given
the opportunity to adjust its metabolism towards utilizing fat for fuel
instead of sugar, a muscle sparing effect is observed due to a decrease
in gluconeogenesis. This theory might seem unlikely if you only look at
the RER as these authors did. The RER only measures the Vco2/Vo2 at the
lungs and is not an accurate indication of substrate utilization at the
cellular levels. Perhaps a more telling measurement would have been the
Respiratory Quotient (RQ) which measures the amount of O2 consumed and
the amount of CO2 produced at the cellular level. This would provide a
more accurate picture of substrate utilization by the tissues. Finally,
a favorable change in serum triglycerides and TC/HDL was only evident in
the "Zone" group.
Before you go announcing these results to your local dietician,
understand that they are firmly indoctrinated in the "food
pyramid" view of the universe. As a result, they find it very
difficult to stray from the ways of their upbringing. You must also
consider the fact that in order for them to acknowledge the value of
moderate fat diets, they must in essence, admit to being wrong for the
last two decades. This kind of paradigm shift will only happen with
time.
3. Keeping cortisol in check with carb drinks could lead to
greater muscle growth in only 12 weeks!
Title: Influence of Weight Training Exercise and Modification of
Hormonal Response on Skeletal Muscle Growth
Researchers: Tarpenning KM, Wiswell RA, Marcell TJ, Hawkins SA
from the University of Southern California, Los Angeles, and the Charles
Sturt University, Bathurst NSW, Australia
Source: Med Sci Sport Exer. 1998 May;30(5) Supplement;
S1-S1339
Summary: Skeletal muscle growth is influenced by a number of
physiological factors such as hormonal action, nutrient supply, and
level of contractile activity. Previous research has demonstrated that
the consumption of a carbohydrate (CHO) solution during weight lifting
exercise can modify the response of several hormones known to regulate
protein metabolism. The purpose of this study was to determine if the
chronic supplementation of a CHO solution and the resultant alteration
of hormone levels, would positively effect the hypertrophic response to
resistance exercise. Two groups of young men (21.3±1.5-y) engaged in 12
weeks of progressive resistance weight training exercise. Training for
one group included the ingestion of a non-caloric placebo beverage
(Ex+P1f), and the other, a 6% CHO solution (Ex+CHO) - each at a quantity
of 8.5-ml-kg body wt. The hormonal response to exercise was monitored
during weeks 1, 6, and 12, as determined by RIA, while muscle growth was
determined from differences in pre and post training muscle fiber area
as calculated from biopsy samples obtained from the vastus lateralis.
Throughout the twelve weeks of training, the Ex+CHO treatment group
continued to display a non-significant change in cortisol concentration
(pre to post to exercise). This is in contrast to significantly elevated
levels (post exercise) observed for the Ex+Pl control group.
Corresponding with these response patterns were differences in muscle
growth. Weight training exercise with CHO ingestion resulted in
significantly greater gains in both type I and type II muscle fiber area
than weight training exercise alone. The differences in cortisol release
accounted for 73.5% of the variance in change of type I muscle fiber
area, and 52.3% of the variance in change of type II muscle fiber area.
The results of this study suggest that the modification of the hormonal
response associated with CHO ingestion can positively impact exercise
induced muscle hypertrophy in young men.
Discussion: During exercise, cortisol accelerates lipolysis,
ketogenesis, and proteolysis (protein breakdown). This happens in order
to provide additional fuel substrates for continued exercise. The
effects of cortisol may also be necessary to provide an amino acid pool
from which the muscle can rebuild new contractile proteins. This ensures
that some degree of adaptation can occur regardless of the availability
of food. Over time however, if this process is not balanced with
additional dietary protein the net effect will be only a maintenance or
even a decrease in functional muscle tissue, as is evident during
periods of starvation or prolonged dieting. From the study above we see
that there was only a non-significant rise in cortisol levels when
carbohydrates were consumed during exercise. The net effect was a more
rapid increase in the cross sectional area of the muscle fibers with the
greatest effect seen in type-II fibers.
This may be a less expensive option for those who can not afford the
use of phosphatidylserine. In this case, carbohydrate administration
appears to down regulate the hypothalamic-pituitary-adrenal axis. This
would, in effect, greatly reduce the bodies catabolic response to
exercise stress. All good news for bodybuilders.
4. Does supplementing with Glutamine cause insulin resistance?
Title: The effect of Oral Glutamine Supplementation in the
Development of Insulin Resistance in Rat’s Muscles
Researchers: L.A. Swada, A.S. Costa, M.L. Marquezi, L.O. Pereira,
L.F.B.P. Costa Rosa, & A.H. Lancha Jr., from the School of Physical
Education and Sport, Laboratory of Nutrition, Metabolism and Applied
Exercise, University of Sao Paulo, Brazil.
Source: Med Sci Sport Exer. 1998 May;30(5) Supplement;
S1-S1339
Summary: Insulin resistance to glucose uptake is a metabolic
state that seems to be related to some pathological disorders such as
obesity and diabetes. One of the mechanisms of the development of
insulin resistance could be associated with the impairment of glucose
transporter (GLUT 4) translocation to the cellular membrane, which might
be related to some defect in one of the steps after insulin receptor
activation. Recently, some proteins that mediate the insulin signalizing
process have been described, GLUT4 translocation and the activity of
these proteins were also subjected to the influence of amino acids.
Females Wistar rats, weighting 200-250 g. received 0.4 g/kg of glutamine
(200 mM) daily for 10 days, by gavage. The soleus muscle was incubated
with labeled glucose C14 with or without glutamine to study glucose
uptake. The results showed a decrease in glucose uptake of 40% in the
supplemented group compared to the control group (1,099 mM/h). When
adding glutamine during incubation, the supplemented group showed a
reduction in glucose uptake of 42% and 54% in the control group.
Although the oral administration did not increase the plasma glutamine
concentration, there was a raise of 15% in plasmatic glutamate. We
conclude that the chronic glutamine supplementation decreases glucose
uptake in skeletal muscle probably due to the increase in palmitic
glutamate which is converted into glutamine in some tissues, such as
muscle of liver.
Discussion: Glutamine is an essential amino acid to rapidly
proliferating cells such as immune system cells and enterocytes.
Although a few studies have demonstrated an increase in glutamine plasma
concentration due to high oral supplementation, most of them emphasize
that this oral administration of glutamine does not raise plasma
concentrations because the enterocytes metabolize most all the
glutamine. The role of glutamine in the development of insulin
resistance has been described as a consequence of the hexosamine pathway
whose product, glucosamine, then prevents GLUT4 translocation in part by
induction of protein kinase C (PKC). In muscle cells, glutamine
stimulates the hexosamine pathway producing glucosamine, which then
leads to insulin resistance. This hypothesis is reinforced considering
the glucose uptake reduction when glutamine was added during incubation,
even in the control group.
Considering the popularity of glutamine supplementation, this should
be food for thought for many of you. The authors point out that although
most studies show that oral glutamine supplementation seldom results in
significant serum "glutamine" concentrations, it is plasmatic
glutamate that showed an 15% increase and eventually leads to an
increase in intracellular glutamine. It may be that using a glutamine
supplement may not be desirable during high calorie "bulking"
phases. It should be mentioned that an acute dose of glutamine only
produces acute (temporary) effects on glucose transport, however,
chronic supplementation has been shown to reduce the number of GLUT-4
transporters under basal conditions. In other words, overuse of
glutamine supplements may lead to chronic insulin resistance and
hyperglycaemic effects.
by Bryan Haycock MSc., CSCS
bryan@thinkmuscle.com
Please send us your feedback
on this article.
