Originally posted by nicodipietro:
PS:
Gaw, sono curioso di leggere una tua risposta al mio post di sopra!
PS:
Gaw, sono curioso di leggere una tua risposta al mio post di sopra!
---------------------------------------------
In part 1, Akerfeldt cites the major research he uses to back the
ABCDE diet. First he cites Jebb et. al. (1). Akerfeldt implies that
the same subjects were first overfed and then underfed (which would be
identical to what he suggests in the ABCDE diet). However, close
reading of the Jebb study shows that this is not the case. There were
three subjects who were ONLY overfed. There were three subjects who
were ONLY underfed. One subject was included in both groups and was
first overfed AND then subsequently underfed. This is an important
distinction to be made (one that Akerfeldt did not explicitly make in
the article). Akerfeldt's theoretical basis for the ABCDE diet is
based on two week periods of over and under feeding. Jebb's study did
not examine the effects of 12 days of overfeeding followed by 12 days
of underfeeding in the same subjects. Rather it simply looked at the
effects of over- or under-feeding in general terms. Over 12 days of
overfeeding (1/3 above maintenance levels), the subjects gained an
average of 6.4 pounds of Lean Body Mass (LBM) and 2 pounds of fat.
During underfeeding (2/3 below maintenance), the subjects lost an
average of 4.6 pounds of fat and 2.4 pounds of lean body mass. The
subjects were confined to a metabolic ward and performed cycling as
their only exercise.
The problem with this study is that there is no distinction made
between changes in muscle mass (i.e. actual contractile tissue) vs.
changes in water and glycogen. The researchers do note that protein
oxidation (burning) did not increase during overfeeding and that
nitrogen retention may have been higher due to the inclusion of
exercise. This study wasn't actually looking at LBM/fat mass gains
in the first place, making it understandable (but frustrating) that
techniques were not used to differentiate between changes in
glycogen/water and muscle. Because glycogen and water can easily make
up 5-10 pounds of body weight (depending on the size of the
individual), it's entirely possible that the subjects gained primarily
glycogen and water during overfeeding. It would be expected that
individuals involved in resistance training would gain proportionally
more lean body mass and less fat (and perhaps more of the lean body
mass as actual muscle tissue) but it is not possible to make that
distinction from this study. Additionally, a sample size of 3
subjects is fairly low. However, this is a problem endemic with any
nutritional research. The cost of running the study makes large
numbers of subjects infeasible.
The second major study cited is Forbes et. al. (2) which examined
the hormonal response to overfeeding for 21 days. Thirteen females
were given 1200-1600 calories/day above maintenance for 19 of the 21
days. At the end of the study, the subjects had gained from 6.8 to
12.3 pounds of total body weight with an average of 9.5 pounds. Of
this weight, 4 pounds was lean body mass and 5.5 pounds was fat. The
women did not exercise. Additionally, there were increases in plasma
insulin, testosterone and IGF-1 during overfeeding, all of which would
contribute to increases in LBM. Lean body mass was measured by
Potassium 40 measurement (a very high tech body composition method)
and the researchers imply in the discussion that most of the LBM
gained was actual lean tissue, not simply glycogen and water. As with
all studies, it is unknown if males would receive the same hormonal
boost as women (for example, women get much greater boosts in
testosterone with DHEA or androstene than men do) but it is
interesting nonetheless.
A similar study using resistance training (which would likely
increase gains in LBM and decreased gains in fat) would be nice to
see. Another observation from the study was a trend towards a decrease
in hormone levels into the third week despite a continued increase in
LBM. The researchers were unable to explain this phenomenon but this
hormonal reduction, after two weeks of overfeeding, was the basis for
Akerfeldt's choice of a 2 week overfeeding cycle. Again, a longer
study would be enlightening to see if chronic overfeeding can maintain
the hormonal increase.
The third major study Akerfeldt cites is Ravussin et. al. (3)
commenting that overfeeding can cause LBM gain without any exercise.
The study in question was actually examining the concept of
luxoconsumption, a process quite similar to thermogenesis whereby the
body dissipates excess calories in a fashion that cannot be accounted
for. Five males were overfed for 9 days at 1.6 times their maintenance
needs. The subjects gained an average of 7 pounds with 4 pounds as
fat (the remaining 3 pounds as LBM) as measured by underwater
weighing. It should be noted that most of the weight gain (almost
half) occurred in the first 2 days of overfeeding, highly suggesting
that the gains in LBM were due to changes in muscle glycogen and water
and not actual muscle tissue. Nitrogen balance increased during the
study indicating that more protein was being stored in the body.
Unfortunately, without more accurate measurement methods, it is
impossible to know where the protein was stored.
The final major study cited is Chiang et. al. (4) which
examined nitrogen retention at different calorie levels. Not
surprisingly, as caloric intake went up, nitrogen retention also
increased. This agrees very closely with the first studies described
above and has been well known for years (i.e. nitrogen balance is
correlated to both protein levels and caloric intake).
Overall comments on these 4 studies
The biggest problem with the studies cited is their general lack
of applicability to bodybuilders as well as some basic methodological
problems. First and foremost, only one study (1) used a structured
exercise program (which was cycling). While we can assume rigorous
weight training would shift the ratios of gains towards more muscle
and less fat, it can not be confirmed from these studies.
Additionally, it is impossible to tell whether the gains in Lean Body
Mass (all non-fat tissues) is water and glycogen or actual muscle
tissue. Each gram of carbohydrate stored in the muscle stores an
additional 3 grams of water.
Athletes, such as precontest bodybuilders or endurance athletes,
who perform the standard 3 day period of severe or moderately severe
carbohydrate restriction and then subsequently follow these 3 days
with a very high carbohydrate diet will see major shifts in body
weight and lean body mass over this 6 day period. As much as a 5-7
pound weight loss can be attributed to total glycogen and water
depletion. With glycogen compensation to normal levels, those same
5-7 pounds can be regained. Glycogen supercompensation (at 50-100%
above normal levels) can increase body weight by 10 pounds or more.
The 5-10 pounds gained with glycogen supercompensation may fully
explain the weight gains observed with the overfeeding models (1,2,3)
above. In the Jebb study (1) (which used a cycling model), it is
attractive to assume that the exercise increased nitrogen retention.
However it is equally plausible to argue that the exercise helped
reduce muscle glycogen levels initially but then, during overfeeding,
triggered the same supercompensation of glycogen described above.
Without more accurate methods of measurement (or even a muscle biopsy
to measure glycogen levels to see if they are changing), it is
impossible to know.
Other aspects of the diet
In part II of the article series, Akerfeldt goes into detail about
several other aspects of the ABCDE system including an important
distinction that the overfeeding studies of Jebb, Forbes, Tseng and
Chiang (1,2,3,4) do not discriminate between gains in glycogen, water,
etc. and gains of actual contractile tissue.
In defense of this argument, he cites Deiraz et. al. (5) which
found an increase of only skeletal muscle mass during overfeeding.
This was a major error, one he perhaps thought would go unnoticed. The
study in question used an overfeeding model of 100 days, quite unlike
the 14 day overfeeding Akerfeldt suggests. This is a perfect example
of how cited research can be misused to support one's point of view.
Comparing data of a 100 day overfeeding study to 14 days of
overfeeding cannot be done and detracts from the credibility of the
concept being supported. During less severe long term overfeeding,
such as in Deiraz et.al., and considering in general, the slow rate of
muscle tissue synthesis, it seems much more likely that the gains in
lean body mass observed by Deirz et.al. were actual contractile muscle
tissue rather than short term changes in glycogen and water. Quite
simply, it seems highly unlikely, especially in trained bodybuilders
with significant muscle mass, that a gain of 1-2 pounds of actual
contractile tissue could be realized in a 14 day span. A gain of 1-2
pounds of contractile tissue over a 14 day period may only occur in
beginning weight trainers. More studies are needed to confirm this,
however.
In addition to citing an inapplicable study to defend the argument
that the gains in LBM aren't just glycogen and water, Akerfeldt also
claims that true muscle growth will occur AFTER the muscle cell is
filled with glycogen, amino acids, water, etc. That is, that actual
growth of actin and myosin (the cellular components of contractile
tissue) will occur after such time that the muscle is full of
glycogen, protein, water, etc.. He argues that the cell wants to keep
the relationship between cell volume and the number of nuclei citing
Moss et. al. (6), a study on chickens. Additionally, he claims that
muscle nucleus number is correlated with mitochondrial density, citing
Tseng et. al. (7), a rat study. The problem with both of these
studies is that animal models may or may not be an accurate model of
human muscle growth. For example, animals have frequently been shown
to undergo muscle cell hyperplasia (an increase in muscle fiber
number), a phenomenon which has never been supported in humans (8). In
weight training studies, mitochondrial density has been repeatedly
shown to go down with increases in muscle size (10,11) directly
contradicting the claims of Tseng et. al. (7).
One slight curiosity in the article series occurs in part 2
when Akerfeldt claims that intramuscular triglycerides (which increase
during overfeeding) are a controller of muscle growth, stating
matter-of-factly that "intracellular triglycerides play a very
important role in weight-training-induced muscle growth." Strangely,
especially considering the large number of references for other
claims, he provides no references for this statement.
---------------------------------------------
Inoltre M. Colgan In "Optimum Sports Nutrition" fa notare che la crescita di tessuto muscolare non supera mai i 25-28 gr al giorno.
Per quanto riguarda la dieta a Zona, non credo che sia possibile aumentare la massa magra e contemporaneamente diminuire il grasso corporeo. Casomai si può limitarne l'accumulo. L'aumento di GH non è così sostanziale come si vuole fare credere.
Prendiamo la "zona" per quello che è, ovvero una buona dieta per la perdita di peso, piuttosto "salutista, e dimentichiamoci le implicazioni "miracolistiche".
Commenta