I brought up EMG to my trainer, and he said it was useless because it has no
way of giving any indication of how a muscle is being worked. He said he can’t
figure out for the life of him how they can relate that to a muscle. He said EMG
had nothing to do with muscular activity. He also said that either an entire
muscle group contracts or it doesn’t contract at all. He said it’s the all or
none law, and you can’t break a law as its set in stone and science has
confirmed this. That’s why he said you only need like one exercise to stimulate
an entire muscle. What are your thoughts?
Very flawed, very flawed indeed.
Your trainer is showing a classic example of how a scientific
concept, namely the all or none principal can be grossly misinterpreted and then
used to come to an extremely illogical conclusion.
In fact, I would go so far as to say, that the concept of all
or none is the most frequently misunderstood principle in all of bodybuilding.
Whole books have based their techniques on what I call the all or none from
another dimension. In other words, your trainer’s interpretation has nothing to
do with reality. And I would caution people to use the word science with
a more skilled grip. The term science means " to know. " What we do not
know at the cellular level far exceeds what we do know. Therefore, one must use
knowledge to properly move forward, and not backwards. For example, many of the
training methods used by Old School bodybuilders were interpreted by so called
science to be flawed. As new discoveries have been made, we are finding that
these so called outdated methods, are validated keys to building optimal mass.
In fact, what must be understood, is that bodybuilders have been far ahead of
the scientific world of published journals, in the realm of hypertrophy for a
tremendously long amount of time. What also must be understood, is that
scientists study the hypertrophy athlete, and his methods, and then use that
data to enrich their own studies. William J. Gonyea, a scientist who many
consider to be the leading authority in the world in both hypertrophy and
hyperplasia has this to say about the subject:
" Despite progressively increasing resistance’s long history, relatively
little scientific information has been published regarding various training
techniques and their effects on muscle mass.
A large part of the information concerning weight training has been
gained through practical experiences and empirical observations of
bodybuilders. The current body of scientific information regarding weight
training’s effects on muscle mass is small...( 1 )"
Translation – Even The badest scientists in the world base
their studies on what bodybuilders have proven over and over again through
hardcore, balls to the wall hypertrophy training! This is not to say, that there
is not a tremendous amount of published data. Only, that everyday discoveries
are being made, which have already been confirmed in the hardcore, die hard
bodybuilding world. And, just as countless great scientists feed off
of bodybuilding methods to fuel their studies, the athlete would do well to
realize why they do so. Because it is apparent that the techniques work. This is
why Dr. Benhamin F. Timson, in the journal of the American Physiological Society
pointed out after doing a study on the subject that " bodybuilders have a 76
percent greater cross sectional area in the biceps brachii then the normal
Indeed, one would be a fool not to tap into a resource as rich as that to build
scientifically on what has already been shown to be true. Afterall, if hardcore
training has continually been shown to work, then one must study why this is the
case, and that is exactly what Scientists such as Dr. Timson, and Dr. Gonyea do.
What we will now do, is delve further into, what exactly the all or none
principle is, and what it definitely is not.
All Or None Principle
This principle is based on an electrical event. Think of
the electrical event as a signal stimulating a cell to perform a certain action.
Notice my wording here, I said " cell. " That is – the all or none principle is
based on single cellular units. It is not, and I repeat not applicable to
multiple cells. To demonstrate this concept I want you to perform an experiment
using your special sensory neurons from the auditory nerve. This is known as
cranial nerve 8 and contains several sensory neurons in it. These neurons are
stimulated by sound. As sound waves are generated, they cause small graded
electrical impulses( receptor potentials ) to occur in the neurons contained in
this nerve. If, the wave is large enough for a particular neuron, then it
completely depolarizes and an electrical impulse is carried across the entire
neuron, and carries that signal to your brain where it is translated. I will
explain depolarization further in a minute. Let me just say this: either a
neuron( which is a single cell ) is stimulated to conduct an electrical current
across its entire self, or it is not( called an action potential ).
The question now, is what are these impulses to which I am
referring? Simply put, an electrical current is defined as a positive charge
flowing towards a negative charge. If you recall from my article on the nervous
system, I discussed the fact that certain cells are specialized at conducting
electrical currents. This is where electrolytes such as sodium, potassium and
Seksi’s article this month
) show their extreme importance to functions throughout the entire body! An
electrolyte is an ion or a group of charged atoms which can carry such a
current. Similar to magnets, opposites attract each other. Sodium ( Na + ) and
Calcium are therefore attracted to any negatively charged area( this is called
an electrical force ). However, there are also chemical forces at work here.
Everyone here knows the process of diffusion. Atoms or molecules always move
randomly from areas of higher concentration, to areas of lower concentration.
Now to the experiment. Tap on your desk lightly, now progressively tap with
increasing force. What did you notice? The sound got louder and louder correct?
This is due to the fact, that more and more neurons were stimulated to
threshold. The more neurons stimulated, the more intense the sound became. If
the all or none principle were applicable to all the cells in that nerve, then
every time someone whispered, it would sound as if Roseanne Bar came into your
house and yelled at the top of her lungs straight into your ear drums! That is
frightening is it not!? The point is, that this principle is not,
and I repeat not applicable outside of a single neuron, and the
experiment you just conducted proved that.
To make a long story short, in the membrane of both muscle
cells and neurons are several complex structures. There are voltage gated
channels which allow sodium into the cell, and there voltage gated channels
which let potassium out of the cell. Additionally there are sodium / potassium
pumps, which literally pump three sodiums( against their electrical and chemical
gradients ) out of the cell, while only pumping two potassiums into the cell.
Three positives out, and two positives in, translates to the inside of the cell,
being more negative then the outside of the cell. In addition to this, there are
also channels in the membrane which allow more potassium to escape then sodium
to enter, which means that more positive charge leaves the cell, then enters.
Finally, negatively charged proteins are manufactured inside of the cell. The
point is simple, by complex machinery, both neurons and muscle cells set up what
is called a negative membrane potential. Which means that the inside of the cell
is more negative then the outside. Secondly, the cell has driven Sodium outside
of the cell, against its chemical and electrical gradient – that is - if you
could make the membrane more permeable to sodium it would rush into the cell
like a bullet out of a gun!
This is precisely what occurs in an action potential. Without
going into horrid detail, there is a certain threshold for each cell or action
potential. This means that enough positive charge flowing toward negative charge
has to occur in order for the entire cell to conduct an electrical impulse. Once
this is reached however, the entire cell will go through an action potential(
actually its more similar to tiny action potentials propagating themselves
across the cell ). Finally, once threshold has been reached there is no stopping
the action potential from spreading across the entire cell! This is why it is
the all or none principle.
Remember what Gonyea stated. We must use our eyes to
understand why this process is applicable to a cell, and not an entire nerve, or
an entire muscle. Think about it for a second, if every muscle cell in your
shoulder was activated, how would you comb your hair? You’d reach to comb and
your arm would jerk at unforeseen speeds! The reason why we are designed to
recruit muscle fibers in an orderly fashion, is due to the different demands of
our bodies( which can be mimicked through a variety of exercises for maximum
stimulation across the gaster or belly). I will obviously use less force with my
fingers to type, then during a deadlift with hundreds of pounds!
All Or None As it Applies to Muscular
The end plate of a muscle cell is one of the most
features in the human body. In the future we will analyze just how
design truly is. In it, you will find an intriquate array of gated and non
and a countless array of complex machinery.
As stated, an all or none propagation always leads to a
physiological action. In the case of a neuron, that action may be to release a
neurotransmitter. This is a specialized messenger, and it is vital to muscular
contraction. The muscle cell has what is called an end plate. On this end plate
are gated channels for sodium which are closed at rest. As you recall, if
opened, sodium will flow into the cell at an accelerated rate( + to - =
electrical current ). After an action potential travels along a neuron, its axon
terminal( essentially the end of the neuron ), which communicates with the end
plate of the muscle cell, will release its neurotransmitter. This transmitter
which stimulates depolarization( to make a cell more positive, again by letting
in sodium ) is always Ach or acetylcholine. That is more detail, then we need.
But the point is, that this neurotransmitter acts like a key to a locked gate.
When released, the key opens the gate, and sodium rushes in, causing the cell
membrane of the muscle cell( the cell membrane of a myofiber is called the
anatomy of a muscle
) to reach threshold. This means that an electrical current will travel
throughout the entire cell!
Remember what I stated! An electrical current( the action potential which
operates on the all or none principle ) always precedes the physiological action
which the cell carries out. What is the action of a muscle cell? To
contract correct!? I can tell you right now, the contraction mechanism of the
cell, initiated by the action potential is sheer genius! One could easily talk
for all day on how stupendous the mechanism is! However, I will get to the
As You can see, the action potential is in reference to the electrical events
taken place within this particular cell being studied. The long wave
actual contraction of the muscle cell. Consequently, the AC is noticeably
is contraction. Yu Yevon was discussing some extremely fascinating
subjects with me
this month on how this can apply to the sport of bodybuilding, and what effect
potentials, fired one after the other can have on muscular tension. This
is definitely a subject
of consequence for future articles.
In the cytosplasm( called sarcoplasm in a muscle ), which is the intracellular
environment, are literal storage bins of calcium( again I would refer you to
Seksi’s article on Ca ++).
Calcium, is the key to muscular contraction. As you know, from my muscle fiber
article, a muscle cell is made up of myofibrils, which are long cylindrical
contractile units, made up of smaller units called sarcomeres(
click here for more info ).
The sarcomeres are lined up one after the other to form a
myofibril, and the myofibrils are lined up parallel to eachother to form the
An action potential causes the calcium, stored in bins(
these bins are called the sarcoplasmic reticulum ) to be released, thus allowing
contraction to begin. A contraction, followed by a relaxation is known as
a " twitch. "
( its more in depth but that is the overall concept ). Now, inside the sarcomere
are contractile proteins called actin and myosin. Myosin has protrusions called
heads, and actin has binding sites for these heads to bind to. The heads are
continually breaking down atp to bind to the actin, but, the binding sites are
masked by another protein called the troponin-tropomyosin complex( actually two
seperate globular proteins ). Calcium, like a key unmasks the binding sites, and
allows the myosin to bind to the actin. The binding of myosin to actin is called
a cross bridge, and this is defined as " tension. " The more myosin bound to
actin, the more tension is built up in the muscle!
Consequently, this is where we derive the term, slow twitch and fast twitch
muscle cells. You see, myosin must hydrolyze( break down ) ATP before it can
bind to actin. Its quite simple, a slow twitch fiber contains the so
called " slow myosin ATPase. " The fast twitch fiber contains fast myosin
ATPase( whenever you see an ase it is an enzyme, ATP is what it breaks down ).
The latter breaks down ATP quicker and can subsequently bind to actin at a
faster rate then can the former. Note: For More Information On ATP -
Click Here and
Click Here For Old
School's article on how to optimize ATP levels
Does EMG have to do with Muscular Contraction?
Now to directly address your first question. The answer is
yes! EMG stands for Electromyography. Myo stands for muscle. It measures
electrical activity within an entire muscle. Before a muscle cell contracts, it
must conduct an electrical current. Putting two and two together, it doesn’t
take an Einstein to figure out, why this is a vital tool of research! The fact,
that someone would state that it has nothing to do with the action of an entire
muscle, simply means that the person does not understand what an action
potential is, or how any type of muscle, be it skeletal, cardiac or smooth work.
Does it have limitations? Sure it does. We will discuss these
in a moment. This is why true science, collectively uses knowledge. In other
words, one cannot rely on one method to study something as complex as an entire
Let me delve deeper into this. Electromyography has shown that
specific exercises elicit more electrical activity in the long head of the
biceps brachii, then the short head, and of course vice versa.
I have heard people state, " Yes, but electromyography is best
at measuring the superficial muscle cells of an entire muscle, so it doesn’t
count to show that an entire muscle functions in a non uniform manner. "
On the contrary! It shows that it actually reacts in an even
more complex manner! You see, if the superficial cells are activated in a non
uniform manner, then we can realize that this is also occurring in the deep
aspects of the muscle! A quote from an earlier article of mine discusses this:
" There are also many signs of compartmentalization, where we cannot
physically see septum. Septum is what the connective tissue is called when it
spans out and forms the barrier( i.e. your nasal cavity is separated into two
cavities by a septum ). For example, if we look at motor nuclei and
examine them closely in the biceps brachii, we actually find that "
" speaking there is compartmentalization. Meaning, that different aspects
of this muscle, function differently. English, A.W., S.L. Wolf, and R.L. Segal.
In their study, Compartmentalization of muscles and their motor nuclei found
this to be so, not only for this muscle, but several others( 10 ). "
To compound the situation, muscle biopsies reveal that this
complexity is reflected by different fiber ratios superficially, as opposed to
deep. I can reference example after example of this! The adductor magnus is 53
percent type I muscle cells superficially and yet when you go deeper it has a
slow twitch make up of 64 percent( 12 )! That’s a large increase! And one only
has to study fiber makeup to realize that there is always a purpose behind it(
i.e. functional compartmentalization ). The same discrepancy can be found in the
biceps muscle as well and every single other muscle examined. Therefore, what
EMG is demonstrating is that muscle groups are far more complex than we ever
believed them to be, in both functionality and force recruitment patterns!
Clarifying The All Or None To An Entire Muscle
Note The display here and discrepancy presented. Each motor unit
is separate from its counter parts, and are separate structures. Also
note, that each contains a different number of muscle cells. This is
of extreme significance as you will see below.
To recap past articles, a motor unit is the neuron and all the
muscle fibers it innervates. This can range from as low as 2 cells to thousands
of cells. Now, each motor unit fires as a unit. Which means when the neuron is
fired, that the muscle fibers innervated will undergo action potentials. Even a
small muscle such as the brachialis has over 150, 000 muscle fibers. This means,
a tremendously large amount of motor units, and therefore a tremendous amount of
complexity. This is why studies show non-uniform hypertrophy in experiment,
after experiment( 7, 13, 14, )!
Therefore to answer this question. No, all the muscle fibers
in an entire muscle group are not all activated at the same time, and the all or
none is not applicable to an entire muscle group.
Is it Always Applicable Even Across a Single
Indeed, the extreme complexities of skeletal muscles are
tremendous. What I am now going to do, is go deeper, and I mean extremely deep.
I say this, because an all or none action potential leads to the contraction of
a cell, but, when that cell is fatigued, though it depolarizes, it does not,
under conditions of fatigue( which is where a bodybuilder lives ) always do so
uniformly. Buckle up and I will expound on this concept!
We need to take a look at what has been found when muscle
fibers have been analyzed. Through a deepened look, via electrophoresis it has
been found that many of these cells express varying forms of myosin throughout
the fiber. As you now know from earlier in the article, myosin atpase
hydrolysizes atp at differing rates. Thus, it would stand to reason, that
differing contractions would effect a cell nonuniformly. For more information on
click here. "
To compound this situation, it has been demonstrated on countless occasions,
when studying individual fibers that indeed non-uniform hypertrophy had clearly
taken place( 1, 2, 3, 4, 5, 7, 18 ). For example, in a quote from my article on
this subject states the following:
" Sakuma, K., A. Yamaguchi, and S. Katsuta.
entered experimentation with the same question we have. In fact the title
of their journal was Are region-specific changes in fibre types attributable
to nonuniform muscle hypertrophy by overloading? They discovered that
type IIB fiber areas increased more in the middle and distal regions of the
muscle cells they tested rather than the proximal regions( 18 )! "
What is the explanation for this clear nonuniform growth?
While there are several reasons, I intend to expound on this from a cytoskeleton
standpoint in the present article, as this is what is responsible for the
organization found within a single muscle fiber. The cytoskeleton protects, and
organizes a cell, much like your bones do for your entire body. Several areas on
this structure can be examined and shown to have a non uniform effect under
fatigue. I am going to address two aspects of this today to highlight just how
non-uniform a muscle acts when trained( though I can and will go deeper into
this subject in the near future ).
Desmin proteins connect in series sarcomere units, allowing
them to work together over long distances( 9 ). Desmin is also responsible for
unifying parallel force across a muscle fiber. That is, combining the force of
two sarcomere units which are side by side. Consequently this means that one
damaged sarcomere can effect tension levels on its parallel counterpart. A
second and fascinating protein is Titin. It is an extremely elastic molecule,
and has the ability to store energy much like a rubber band ( 18, 19),
additionally it aids in the alignment of the thick myosin filaments relative to
actin binding sites( 18, 19, ). When a muscle is stretched, the elasticity of
Titin assists greatly in bringing it back to its optimal length.
I intend to delve further into this subject in the near future. I
believe that Titin is a key to
several physiological aspects, including enhanced athletic field performance.
This is important to understand, because at this stage I will address what
occurs during an eccentric contraction. In the Biophysical Journal, Dr. Dl
Morgan explained the following:
" Lengthening of active muscle on or beyond the plateau of the
length tension curve will take place very nonuniformly( 9 ). "
What he is saying needs to be further analyzed. An eccentric
contraction of a muscle fiber, involves the lengthening of that fiber as it is
being activated. That is-it is contracting-and lengthening at the same time.
to be understood is that a muscle fiber has an optimal length. This length
produces optimal tension in the cell, as tension is defined as, or rather
measured by the number of cross bridges formed between myosin heads and actin
binding sites. Think of it this way: when pushing a large and heavy object, what
will generate more force-one person or 10 people parallel to each other? The
same principle applies. When a myofiber is at optimal length, myosin and actin
filaments overlap so that each head on the myosin filament has access to a
binding site. However, when stretched, the actin filaments are pulled out of
range of the myosin filaments, and they have less to bind to.
Lets carry this one step further. What happens, when actin is
pulled completely out of reach of the myosin filaments? All the weight that the
load being placed on the muscle has now been transferred to the cytoskeleton.
This is similar to the deadlift. When my spine is flexed, by extensors or
erectors spinae are relaxed. If I lift the weight when flexed, my spine bares
the load, and consequently this leads to tendon and ligament strain. Dr. Morgan
explains that during eccentric contractions, this lengthening, or rather the
extent of lengthening per sarcomere unit does not take place uniformly. In fact,
depending on the exercise it can be quite selective.
When a sarcomere is lengthened to a point in which
myosin can no longer bind to actin, a vulnerable position will have been
reached. Desmin can lose its integrity in connecting adjacent Z-lines, and Titan
can be stretched to a point beyond its capacity to bring a sarcomere unit back
to resting length. This occurs when its association with thick filaments is
broken( 19 ). As a consequence, the effected area on the myofibril can lose its
ability to build maximum tension, or completely lose its ability all together to
build tension! This in turn places further stress on sarcomere units that are
parallel and increases their risk for high tension damage( 9 ).
What does this mean? Simply put, if an area loses its ability
to form cross bridges, that muscle fiber is no longer contracting as a complete
unit, even though the membrane in the sarcomere region is still depolarizing!
Secondly, the specific regions associated with this area that is now weakened
would become more susceptible to damage, and subsequent hypertrophy( 15, 16, 17,
21, ), then another area of the muscle fiber. It does not get more nonuniform
Considering the fact, that bodybuilders are continually
training to fatigue, it would be contradictory to ever make a generalized
statement in regards to such a complex subject, especially when that generalized
statement can be shown to be overtly false.
One cannot even phantom the complexities found at the
cytological level in a muscle cell. The integral proteins embedded in the
sarcolema alone are worth countless articles. This is why a high is reached when
discussing such insanely advanced levels of technology. I intend on capitalizing
on such physiological aspects in the future.
Yours In Sport
President Abcbodybuilding / Beyond Failure Magzine
1. Alen E. Mikeysky, William Matthews,
Catherine J. Giddings and William J. Gonyea
2. Alway, S.E. Stretch induces
non-uniform isomyosin expression in the quail anterior latissimus dorsi muscle.
Anat. Rec. 237:1–7. 1993
3. Alway, S.E., W.H. Grumbt, J. Stray-Gundersen,
and W.J. Gonyea. Effects of resistance training on elbow flexors of highly
competitive bodybuilders. J. Appl. Physiol. 72:1512–1521. 1992
4. Alway, S.E., P.K. Winchester, M.E.
Davis, and W.J. Gonyea. Regionalized adaptations and muscle fiber proliferation
in stretch-induced enlargement. J. Appl. Physiol. 66:771–781. 1989
5. Antonio, J., and W.J. Gonyea.
Skeletal muscle fiber hyperplasia. Med. Sci. Sports Exerc. 25:1333–1345.
6. Antonio, J., and W.J. Gonyea. Muscle fiber splitting in
stretch-enlarged avian muscle. Med. Sci. Sports Exerc. 26:973–977. 1994..
7 ANTONIO, JOSE, 2000: Nonuniform Response of
Skeletal Muscle to Heavy Resistance Training: Can Bodybuilders Induce Regional
The Journal of Strength and Conditioning Research: Vol. 14, No. 1, pp.
8. Benhamin F. Timson
Evaluation of animal models for the study of exercise induced muscle
enlargement. Copyright 1990 the American Physiological Society
9. D. L.
Morgan and D. G. Allen
Early events in stretch-induced muscle damage. J Appl Physiol 87:
Vol. 87, Issue 6, 2007-2015, December 1999
10. English, A.W., S.L. Wolf, and R.L. Segal.
Compartmentalization of muscles and their motor nuclei: The partitioning
hypothesis. Phys. Ther. 73:857–867. 1993
11. Gardiner, P.F., B.J. Jasmin, and P.
Corriveau. Rostrocaudal pattern of fiber-type changes in an overloaded rat ankle
extensor. J. Appl. Physiol. 71:558–564. 1991.
12. Johnson, M.A., Polgar, J., Weightman, D.,
Appleton, D. Data on the distribution of fibre types in thirty-six human
muscles. An autopsy study. J. Neurol. Sci: 18:111-129, 1973.
13. Kawakami, Y., T. Abe, S.-Y. Kuno, and T.
Fukunaga. Training-induced changes in muscle architecture and specific tension.
Eur. J. Appl. Physiol. 72:37-43 1995.
14.. 4.Kawakami, Y., T. Abe, S.-Y. Kuno,
and T. Fukunaga. Training-induced changes in muscle architecture and specific
tension. Eur. J. Appl. Physiol. 72:37-43 1995.
15. Millward DJ, Garlick PJ, Stewart RJ,
Nnanyelugo DO, Waterlow JC
Skeletal-muscle growth and protein turnover. Biochem J 1975 Aug;150(2):235-43
16. N. Stupka1, M. A. Tarnopolsky1,2,
N. J. Yardley1, and S. M. Phillips1,2Cellular adaptation to
repeated eccentric exercise-induced muscle damage. J Appl Physiol 91:
1669-1678, 2001; Vol. 91, Issue 4, 1669-1678, October 2001
17 P. M.
Clarkson and I. Tremblay
Exercise-induced muscle damage, repair, and adaptation in humans.
Journal of Applied Physiology, Vol 65, Issue 1 1-6, Copyright © 1988 by American
18. Sakuma, K., A. Yamaguchi, and S. Katsuta.
Are region-specific changes in fibre types attributable to nonuniform muscle
hypertrophy by overloading?.
Eur. J. Appl. Physiol. 71:499–504. 1995.
19. S. Staron, D. L. Karapondo, W. J. Kraemer,
A. C. Fry, S. E. Gordon, J. E. Falkel, F. C. Hagerman and R. S. HikidaSkeletal muscle adaptations during early
phase of heavy-resistance training in men and women. Journal of Applied
Physiology, Vol 76, Issue 3 1247-1255, Copyright © 1994 by American
20. Stan L. Lindstedt, Trude E. Reich, Paul
Keim and Paul C. LaStayo
The Journal of Experimental Biology
205, 2211-2216 (2002)
Do muscles function as adaptable locomotor springs?
21. Tibor Hortobágyi, Joseph Houmard, David
Fraser, Ronald Dudek, Jean Lambert and James TracyNormal forces and myofibrillar disruption
after repeated eccentric exercise. J Appl Physiol 84: 492-498, 1998; Vol. 84,
Issue 2, 492-498, February 1998
22. Morgan, D. L. New insights into the
behavior of muscle during active lengthening. Biophys. J. 57: 209-221
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