Advanced Bodybuilding - part II

[global]

Here is part 2 as some people have said they are interested. I will post part 3 when I receive it.

In part I we discussed some very basic principles at work during adaptation to
resistance training. Specificity was outlined as a governing principle with
which we can predict the outcomes of our training. Low volume/high load training
produce increases in neuromuscular efficiency and motor unit recruitment, while
high volume/moderate load training produces only moderate increases in strength
and neuromuscular adaptations along with marked hypertrophy of both slow and
fast twitch fibres. Also discussed were issues such as rational and irrational
adaptation. Dramatic increases in sarcomere volume without increases in
myo-nuclear number, seen during irrational adaptation, effectively inhibits
further increases in the production of contractile proteins and diminishes
recovery and performance. Slower increases in sarcomere volume, as seen in
rational adaptation, actually facilitates recovery and leads to a more steady
increase in both size and strength. In part two we will discuss the mechanisms
responsible for the specific nature of adaptation and look at ways of applying
this knowledge to build size and strength.

The Stimulus for Muscle Growth

To most people, the way to get a muscle to grow larger is simply a matter of
"exercising" the muscle you want to grow. This is a very simplistic way of
looking at it. Those individuals who fail to realise that there is a right way
and a wrong way to train a muscle never go on to develop out of the ordinary
physiques. Don’t get me wrong, the knowledge of how muscle tissue grows in
response to training is not a requirement to be a successful bodybuilder.
Anabolics have become the ultimate "cheat sheet". They effectively reduce the
overload threshold necessary for compensatory hypertrophy and elevate the
genetic limit or plateau. If you chose not to use potent synthetic hormones you
are in for a much more difficult road, and a good understanding of muscle
hypertrophy will be invaluable to you as you train over the years.

At the very foundation of muscle hypertrophy is load induced tissue strain.
Muscle tissue must undergo mechanical strain in order to begin the biochemical
steps necessary for adaptive growth (Clarke,1996). This "strain" induced by the
loading of the tissue leads to sarcolemma micro trauma. The wounding of the
muscle cell after training is characterised by myofibrillar disruption, Z line
smearing, discontinuity of sarcomeres and an increase in the porosity, or
permeability, of the sarcolemma. The effect or result of this nonfatal cellular
damage is the production, and release of growth factors that then interact with
the damaged cell itself and also very importantly, with satellite cells.

Satellite cells are myogenic stem cells that serve to assist postnatal growth
and regeneration in adult skeletal muscle. Following proliferation
(reproduction) and subsequent differentiation (to become a specific type of
cell), these satellite cells will fuse with one another or with the adjacent
damaged muscle fibre, thereby increasing myonuclei numbers for fibre growth and
repair. Proliferation is necessary in order to meet the needs of thousands of
muscle cells all potentially requiring additional nuclei. Differentiation is
necessary in order for the new nucleus to behave as a nucleus of muscle origin.
In order to better understand what is physically happening between satellite
cells and muscle cells, try to picture 2 oil droplets floating on water. The two
droplets represent a muscle cell and a satellite cell. Because the lipid bilayer
of cells are hydrophobic just like common oil droplets, when brought into
proximity to one another in an aqueous environment, they will come into contact
for a moment and then fuse together to form one larger oil droplet. Now whatever
(i.e. nuclei) was dissolved within one droplet will then mix with the contents
of the other droplet. This is a simplified model of how satellite cells donate
nuclei to existing muscle cells.

There appears to be a finite limit placed on the cytoplasmic / nuclear ratio
(Rosenblatt,1994). Whenever a muscle grows in response to functional overload
there is a positive correlation between the increase in the number of myonuclei
and the increase in fibre cross sectional area (CSA). When satellite cells are
prohibited from donating viable nuclei, overloaded muscle will not grow
(Rosenblatt,1992; Phelan,1997). It is not a stretch to say that satellite cell
activity is a required step, or prerequisite, in compensatory muscle
hypertrophy, for without it, a muscle simply cannot significantly increase total
protein content nor CSA.

Some factors which regulate this process are exercise, trauma, passive stretch,
massage, innovation, and the activity of soluble growth factors. Three classes
of growth factors in particular have been studied extensively with respect to
their effects on satellite cell proliferation and differentiation in vitro. They
are; fibroblast growth factors (FGF), insulin-like growth factors (IGF), and the
transforming growth factor-beta superfamily (TGF-beta). When administered in
combination, these factors can induce satellite cell activities in vitro which
mimic those typical of satellite cells found in vivo in growing, regenerating,
or healthy mature muscle. In essence they can mimic the effects of loading
without any micro trauma actually being done.

FGF is one growth factor being actively studied. Recent studies have shown that
an increase in the permeability of the sarcolemma is necessary for the release
of fibroblast growth factor (FGF). This is because FGF does not contain a signal
transduction peptide sequence (Abraham,1986) and thus does not exit the source
cell through vesicle mediated exocytosis. This "signal transduction peptide
sequence" is necessary for the protein to be incorporated into intracellular
vesicles and actively transported to the cell surface, and then ultimately
released. Instead, it must be able to pass directly through the phospholipid
bilayer of the wounded sarcomere in order to have an autocrine and paracrine
effect on target tissues. This is accomplished in adult muscle fibres by
inflicting microtrauma.

FGF, specifically FGF-beta, has been shown to stimulate proliferation but
suppress differentiation of myogenic stem cells. This has the result of
increasing the availability of satellite cells but reduces the number of them
that are actively fusing with nearby muscle cells. In a study where FGF was
injected directly into healthy muscle tissue, it had the effect of increasing
muscle DNA content and IGF-1 peptides, but had no significant effect on total
protein content or gross muscle weight (Adams,1998). These researchers speculate
that the increase in DNA content was the result of increased satellite cell
number. The fact that FGF was unable to induce hypertrophy reflects the fact
that FGF inhibits satellite cell differentiation (i.e. the satellite cells never
actually became of the muscle cell type) preventing the nuclei from producing
muscle specific proteins and thereby short circuiting a critical step the growth
process. An additional study involving both local injection and local
implantation of FGF pellets into "regenerating", or damaged muscle, failed to
show any effect of FGF on the ability of muscle tissue to regenerate after
microtrauma (Mitchell,1996). In this study FGF did have the effect of enhancing
satellite cell proliferation as well as angiogenesis (capillary formation)
nevertheless, it appears that FGF is not the limiting factor in compensatory
muscle hypertrophy.
Insulin-like growth factor (specifically IGF-1) stimulates both proliferation
and differentiation in an autocrine-paracrine manner, although it induces
differentiation to a much greater degree. IGF-1, when injected locally,
increases satellite cell activity, muscle DNA, muscle protein content, muscle
weight and muscle cross sectional area (Adams,1998). As discussed earlier, the
proliferation and differentiation of satellite cells is critical part of
compensatory hypertrophy. The importance of IGF-1 lies in the fact that all of
its apparent functions act to induce muscle growth with or without overload
although it really shines as a growth promoter when combined with physical
loading of the muscle.

IGF-1 also acts as an endocrine growth factor having an anabolic effect on
distant tissues once released into the blood stream by the liver. In human
volunteers, detailed information on the effect of IGF-1 on protein synthesis,
degradation and balance has been obtained by using the arteriovenous difference
of labelled and unlabeled phenylalanine across the forearm (Barrett & Gelfand
1989). In the aforementioned studies, "systemic" IGF-1 infusion for 6 h caused
positive amino acid balance, both by inhibiting protein degradation and
stimulating protein synthesis (Fryburg, 1994). This differs from the effect of
peptide "hormones" such as insulin, which does not stimulate synthesis in adults
(Bennet et al. 1990, Fryburg 1990, Gelfand & Barrett 1987, McNurlan, 1994).
Therefore IGF-1 possesses the insulin-like property of inhibiting degradation,
but in addition can stimulate protein synthesis (Fryburg 1991). The insulin-like
effects are probably due to the similarity of the signalling pathways between
insulin and IGF-1 following ligand binding at the receptors (Schumacher 1991,
Gual 1998).

The ability of IGF-I to stimulate protein synthesis resembles the action of GH,
which was shown in separate studies on volunteers to stimulate protein synthesis
without affecting protein degradation (Fryburg et al. 1991, Fryburg and Barrett
1993). Although it is often believed that the effects of GH are mediated through
IGF-1, this cannot be the case entirely. First, the effects of the two hormones
were different, in that GH did not change protein degradation. Second, the
effect of GH was observed with little or no change in systemic IGF-1 and GH
concentrations because the GH was infused directly into the brachial artery
(Fryburg et al. 1991).
Transforming growth factor-beta (TGF-beta) slightly depresses proliferation but
inhibits differentiation. So although it is called a growth factor, it is an
"inhibitory" factor involved in muscle growth. For example, one TGF-beta member
known as growth/differentiation factor-8 (GDF-8), was found to have profound
effects on muscle growth (McPherron & Lawler,1997). GDF-8 was found to exist in
many muscles throughout the body. In order to identify the function of this
protein, researchers "targeted", or "knocked out" the gene responsible for
producing it. The result was nothing less than miraculous. The mice who lacked
the gene went on to grow muscles up to 3 times larger than normal mice. This is
a 300% increase in muscle weight with no specific exercise or mechanical
loading! You may remember pictures of these mice published in issue number 188
in MuscleMag International (MuscleMag,1998). The increase in the mass of the
"mutant" mice muscles was a result of both increased hypertrophy and hyperplasia
(an increase in fibre number). There are also naturally occurring mutations to
this gene that result in "double muscling" of animals such as livestock. Two
breeds of cattle known as Belgian Blue and Piedmontese exhibit naturally
occurring mutations on the myostatin gene (McPherron & Lee,1997). This changes
the amino acid sequence of the GDF-8 peptide and greatly attenuates its
physiological activity.

All of these growth factors are brought into play in human models of
compensatory hypertrophy. In summary, resistance exercise of sufficient load and
volume causes microtrauma to the sarcolemma which increases the release and
production of growth factors. This is done through increased permeability of the
wounded cell membrane allowing soluble growth factors to "leak" out into the
intercellular space. The growth factors then go on to increase the number, or
"proliferation" of satellite cells, also called myogenic stem cells. This is
done through interaction with growth factor receptors on the surface of these
cells. These growth factors then go further to induce the conversion, or
"differentiation" of these undifferentiated cells into cells expressing DNA of
muscle origin. Once these satellite cells have undergone differentiation they
can then fuse to existing muscle cells. This fusion allows the satellite cell to
donate needed myonuclei to the wounded or developing muscle cell. The effect of
increasing the number of nuclei within a cell allows for increased protein
synthesis and ultimately hypertrophy. As mentioned earlier, there is a nuclear
to cytoplasmic ratio, or "nuclear domain", that is closely regulated by the
cell. If the muscle cell is prevented from increasing the number of nuclei, it
does not grow in response to overload (Phelan,1997).
All of the aforementioned processes occur with or without systemic hormonal
influence or nutritional abundance (Borer,1995). In this way the hypertrophic
response can be limited to the overloaded tissue. I do not mean to imply that
exercise induced growth is not effected by systemic hormones and/or nutritional
abundance, only that mechanisms are in place that allow for growth in localised
muscle tissue in the absence of endocrine support and adequate nutritional
status.

The Stimulus for Strength

The foundation for the development of strength is neuromuscular in nature.
Increases in strength from resistance exercise has been attributed to several
neural adaptations including altered recruitment patterns, rate coding, motor
unit synchronisation, reflex potentiation, prime mover antagonist activity, and
prime mover agonist activity. Aside from incremental changes in the number of
contractile filaments, voluntary force production is largely a matter of
"activating" motor units. In order to ascertain the relative contribution of
each of these mechanisms, various measurement techniques have been utilised.
Hereafter we will briefly discuss each of these mechanisms as they relate to
resistance training.

Recruitment of motor units can be measured with Electromyography (EMG). As a
muscle contracts, the electrical signal initiated by the motor nerve can be
detected with EMG. The intensity or magnitude of this signal is sometimes
described as "neural drive". In order to explain increases in strength from
resistance exercise, researchers have measured the changes in EMG activity in
weight training subjects.

Hakkinen and co-workers have shown that there is an increase in EMG activity
with strength training as well as a decrease in EMG activity upon cessation of
training (Hakkinen,1983). Fourteen male subjects (20-30 yr) accustomed to weight
training went through progressive strength training of combined concentric and
eccentric contractions three times per week for 16 wk. The active training
period was followed by an eight week detraining period. The training program
consisted mainly of dynamic exercises for leg extensors with the loads of
80-120% of one maximum concentric repetition (1RM). Significant improvements in
muscle function were observed in early conditioning; however, the increase in
maximal force during the very late training period was greatly limited. Marked
improvements in muscle strength were accompanied by significant increases in the
neural activation (EMG) of the leg extensor muscles. The relationship between
EMG and high absolute forces changed during the training period. The occurrence
of these changes varied during the course of training. During detraining, there
was a decline in EMG activity.
Now those who would argue that increases in strength are solely due to increased
recruitment of motor units would have a difficult time defending themselves in
light of other research. The is a method of measuring motor unit activity called
"Interpolated Twitch Technique", or ITT. ITT is used to determine the extent of
activation of the entire muscle. Merton (Merton, 1954) was the first to use this
technique to describe whole muscle activation. He showed full activation of the
adductor pollicis with fatigue in untrained subjects. Several other studies have
since shown a similar ability of untrained subjects to voluntarily fully
activate various muscle groups (Bellemare 1983, Chapman 1985, Gandevia 1988,
Belanger 1981). This directly contradicts the theory of strength increases due
to the ability to activate more motor units.

The activation of motor units is done in an asynchronous fashion, meaning that
not all fibres contract at the same time within a given muscle. There is a
hierarchy to the order of fibre recruitment in muscle tissue. Because fibre
activation is not "analogue" or variable in nature, in other words, a fibre is
either fully activated or fully quiescent, the brain must control contraction
intensity by altering the number of fibres it activates. In general, slow twitch
fibres are activated first followed by larger fast twitch fibres. Now when
muscles begin to fatigue the asynchronous firing of fibres become more and more
synchronised (Butchal, 1950). This allows for greater force production. This
synchronisation of muscle fibres has been linked to increases in voluntary
strength (Milner-Brown, 1975). Now although increases in motor unit
synchronisation have been reported with training, studies involving artificial
stimulation show that force development with asynchronous stimulation is greater
and smoother (Clamann, 1988). In addition, researchers have shown that the rate
of force development in brief maximal contractions is faster in voluntary than
in evoked contractions (Miller, 1981). So from these studies we see that
although synchronization of motor units can increase with training, asynchronous
motor unit activation is more advantageous to rate and magnitude of force
development than is synchronous activation.
Increases in "reflex potentiation" have also been linked to resistance training
(Sale & Upton 1983, Sale & MacDougall 1983) as well as decreases with
immobilisation (Sale, 1982). The actual benefit, if any, of this adaptation is
unclear. An increase in reflex potentiation would contribute to the voluntary
EMG signal augmenting the motor or neuronal drive. Nevertheless, because
untrained individuals have been shown to be able to fully recruit their motor
units, the purpose of increased reflex potential remains undecided.

Finally, that activity of prime mover agonists and antagonists plays a role in
directed voluntary strength. The obvious role of agonists is to assist the prime
mover by guidance and stabilisation. This could be termed "co-ordination". It is
well known that any unaccustomed exercise requires practice in order to develop
sufficient co-ordination to allow maximum efficiency of muscular effort. The
role of antagonistic muscle groups is more complicated. They serve to prevent
damage through co-contraction as well as ensure less resistance through
relaxation to prime mover contractility.
The protective mechanisms function by way of golgi tendon organs (GTO). The GTO
is sensitive to force output or tension within the muscle. They are located at
the musculo-tendonous junction and is contained within a compressible
collagenous capsule. Fibres of the GTO are connected directly to muscle fibres
as well as to Type "Ib" inhibitory neuron within the muscle. The physical
structure of the GTO allows it to be sensitive to stretch or load present in the
muscle. Think of the notorious "Chinese finger trap". You first stick you
fingers in each end. Then as you pull your fingers apart, the structure of the
woven tube causes it shrink (or in the case of GTO it compresses) in diameter in
order to stretch. The GTO works very much like this. When the collagen around
the GTO is compressed because of contraction or stretch by the muscle, the Ib
neurons generate an impulse that is proportional to the amount of GTO
deformation. In this way the GTO can decrease contraction of a muscle being
stretched in order to protect it from being torn. Likewise, GTO are thought to
prevent unusually high contractions of a muscle in order to protect it from
tearing itself apart. So in an antagonist muscle, the GTO can serve to inhibit
co-contraction, facilitating contraction of the prime mover. In a prime mover,
the GTO acts to prevent torn pecs, biceps and whatever else you are using to
lift insanely heavy weights.
Another neuronal structure regulating involuntary muscle activity is the muscle
spindle. The muscle spindle is found in greater abundance in the muscle belly as
apposed to the musculotendonous junction. The muscle spindle also responds to
stretch. However, the spindle is less like a Chinese finger trap and more like
spring. When the muscle undergoes stretch, the centre of the spindle is
stretched. These spindles contain neurons that are sensitive to this stretching.
Unlike with the GTO, when a muscle spindle is stretched its excitatory neurons
fire in order to counteract the stretch. When a stretch is imposed on a muscle,
the Type-I sensory neuron sends impulses into the spinal cord and connects with
interneurons, generating an excitatory local-graded potential that is sent back
to the muscle being stretched. If the stretch is of sufficient magnitude and/or
rate, a local graded impulse will be sent back to the same muscle with
sufficient strength to initiate a contraction via alpha motoneurons. This reflex
arc in known as the "stretch-reflex" and is characterised by a quick muscular
contraction following a rapid stretch of the same muscle. Now this stretch
reflex primarily functions in slow twitch muscle fibres.

Alterations in the sensitivity of these two regulatory mechanisms have been seen
with training. Carolan (Carolan, 1992) showed a decrease in antagonist
co-activation of the lex extensors with training. On the other hand, increases
in co-activation have been seen in longitudinal studies comparing explosive
trained athletes to non-explosive trained athletes (Osternig 1986, Barrata
1988). These somewhat contradictory results may reflect the possibility that
co-activation alterations are very specific in nature and depend on things such
as contraction velocity, range of motion, and training specific effects.
Training for Size
Of primary interest to bodybuilders is training for size. After all, what is
bodybuilding but doing whatever you can to make your muscles larger. The goal
now is to use the current knowledge of the way muscle tissue reacts to imposed
mechanical overload and microtrauma to plan a training strategy or routine that
best elicits a growth effect.

Understand that from here on out you are going to see areas where different
approaches would be equally valid. One reason for this is the lack of quality
research looking specifically at muscle hypertrophy in humans using typical (or
atypical for that matter) exercise protocols that last for more than 8-12 weeks.
In part 1 of this article we mentioned the fact that the length of a standard
school semester or quarter usually dictate the length of a given study.
Volunteers are hard to keep track of when their schedules change or when summer
starts.

Conclusion

Thus far in Part II we have discussed the various mechanisms by which muscle
adapts to resistance exercise. This is very important to understand if we are
going to make advances in training techniques and planning. We know that in
order for a muscle to undergo compensatory hypertrophy it must be subjected to
sufficient trauma to activate satellite cells. This is done through the activity
of various growth factors which all act in concert to regulate muscle
hypertrophy. We also know that in order to increase our strength we must
increase the "efficiency" of nerve conduction and motor unit co-ordination.
Training to accomplish this relies heavily upon the principle of specificity
which was spoken of in Part 1 of "Advanced Training Planning for Bodybuilders".
If you simply want brute force you must train the nervous system and the
resultant increase in strength will reflect the manner in which you trained. Now
one should not assume that training for size will automatically lead to
significant increases in size. This simply isn’t true. In Part III we will
examine specifically what methods can be adopted to cause increases in muscle
size or increases in muscular strength. You might be surprised with what we come
up with so stay tuned.

primobolan
global@elitefitness.com

[SteelPreacher]

I'm sorry global but that is some boring shit. The bottom line is in part three and I hate watching a show that is "To be continued..." [img]/infopop/emoticons/icon_mad.gif[/img] [img]/infopop/emoticons/icon_wink.gif[/img]

[global]

yes , and I hope they do send me part 3 or you will have been bored for nothing!!

primobolan
global@elitefitness.com

I have rear and copied the first two,
hope they send you #3..

Boring yes but interesting so far.

Thanks for the info.

Doggy