Here is the original letter:

<< I’ve just been awarded a research bursary and am planning to investigate
the possible link between hamstring strength and core trunk stability. I’m
planning to measure concentric/eccentric hams strength intially, send
subjects off to do hams strength work, transversus abdominus strength work
and placebo exercises. I’ve been able to get lots of literature re hams
strength, transversus abdominus (mainly Hodges, Jull and Richardson) and hams
injury prevention. What I haven’t been able to get is much information on
hamstring/muscular trunk control interaction. Anybody out there able to point
me in the right direction? >>

Here is my response:

***Just a small point about which I have written before – how does one assess
“core stability” statically or dynamically under conditions in which
peripheral stabilisation does not play a significant role in the overall
stabilisation process or confound the results? For instance, if one wishes
to assess “core stability” in a standing position, then how do we rule out
the major role played by the lower extremity musculature in the process?

Moreover, stability is not necessarily a result of adequate strength, but the
amount of “strength”, force or torque exerted at crucial stages of joint
action throughout any given movement. If someone produces inappropriate
patterns or timings of motion, then, no matter how strong a given muscle may
be, then stability will be severely compromised. This point often seems to
be forgotten in many studies of relationship between injuries and muscle
strength. Though the intrinsic strength of a muscle may be adequate in the
execution of a given task, it may not be utilised efficiently in that or
other tasks.

Moreover, if strength is adjudged to be adequate as estimated by static or
isokinetic tests in a given action, this does not imply that strength under
other conditions will be adequate. We simply cannot ignore the vital fact
that strength is not only the result of muscle action, but of neuromuscular
facilitation in response to specific stimulation in a given motor task. It
is not valid to extrapolate findings from isolated joint testing to a process
as multifactorial as dynamic stabilisation.

In this regard, articles such as the following can be very revealing:

Zajac FE & Gordon MF(1989) Determining muscle’s force and action in
multi-articular movement Exerc Sport Sci Revs 17: 187-230

Andrews JG (1985) A general method for determining the functional role of a
muscle J Biomech Eng 107: 348-353

Andrews JG (1982) On the relationship between resultant joint torques and
muscular activity Med Sci Sports Exerc 14: 361-7

What does all of this imply for the researcher? Well, it means that the
research protocol, and possibly the title of the project, needs to be devised
very carefully to take these problems into account. One has to be especially
careful as to how one defines and measures “stability”, especially the
“stability” of a portion of a dynamically linked system. So far, I am not
very convinced that many researchers are adequately addressing this problem -
maybe you could take a significant step forward to rise above the
perpetuation of some dubious traditional and relatively unchallenged
hypotheses. Best wishes in your task!

Mel Siff
Denver, USA
Mel Siff Dot Com
Supertraining Twitter Feed

Member<< I might take issue with some of this and ask for greater clarification.
While it is true that for general purposes a muscle is “measured relative to
its resting, unactivated length”, the relationship between lengthening and
shortening is relative to the extremes of the specific action being examined
and would seem to have nothing to do with “resting, unactivated length”….

While it is true, that the “attempt” to contract against opposing force
provides tension to the muscle in all three muscle action/contractions, true
contraction “only” occurs when the filaments actually “slide”, providing
a “shortening”. So even though we might be able to loosely term the act of
tensioning, “contracting”, we would be acknowledging that the “attempt to
contract” is “understood”. >>

Mel Siff:

***I was clarifying the definitions and analysis of muscle action according
to what is accepted in standard high level texts and was not trying to create
a new body of knowledge, because literature that I came across did not
reflect an adequate degree of accuracy on the topic. You have offered
comments which apply to muscles in different states of excitation, including
altered cognitive states, which intentionally have been excluded from the
accepted definitions because they are acknowledged not to be true resting
states. It would also help if you provided some references to support any
opinions, so that we don’t simply end up having a jolly good rumble in the
playground of speculation.

Member:

<<It is also true that due to the elastic nature of the “muscle complex” that
it is possible to have a small amount of “shortening” during an isometric or
eccentric action, this action is limited to the elastic properties and “is
not” representitive of the total action in these cases.>>

Mel Siff:

***This is not exactly correct, since the sliding filament model of muscle
and photomicrographs of muscle action show clearly that the actin-myosin
units shorten and thereby tension the other non-contractile elements in the
muscle complex. Also, there are elastic and viscoelastic components in the
muscle complex, so that the issue is not one of simple elastic extension.

Member:

<<I think we more accurately would say during a “forced lengthening” eccentric
action, the muscle “attempts” to contract. >>

Mel Siff:

***No, whether the action is “forced” by a heavy load or allowed to happen
voluntarily when a person lowers a light load, the muscle will contract. It
does not “attempt” to contract – it contracts. Muscle contraction is not a
matter of ‘half-hearted’, semi-committed action, but the result of all or
nothing excitation of muscle fibres. If there are any “attempts” to initiate
a motor action, then this process happens at a neural level, not at a
muscular level.

Member:

<<I am pressed to see that a true contraction (shortening) can happen under
these conditions. Even though, as I have stated, a muscle has a degree of
elasticity that may allow a small amount of actual contracting (within the
limits of structural integrity), I think somehow we are confusing the
“attempt to contract” with the actual “act of contracting”. The resistive
action in the muscle to a “forced lengthening” is not called an eccentric
contraction. It is called an eccentric action (or attempt to contract
against an active/superior force)>>

Member:

*** How can elasticity allow for contraction? Elasticity is always
associated with lengthening in extensible tissues such as the muscles and
elastic bands. This elasticity and possibly some ’sliding’ within the muscle
complex contribute to the electromechanical delay associated with the
activation of a muscle from its relaxed to its contracting state.

You will notice that I referred to eccentric “action” throughout my post, so
that this comment has no bearing on what I wrote. I take great care not to
confuse action with contraction, as do any biomechanists working in the same
field. As noted above, the concept of “attempting” to contract is not a
local muscular process or even one of spinal motor reflex action.

In one of my recent posts I even mentioned that the resting length in some
cases (as in individuals suffering measurement of muscle length is a relative
one. I simply emphasized that there happens to be a well-accepted definition
of resting (unexcited) muscle length in every individual.

Member:

<<Biomechanically, the two actions (concentric-eccentric) are distinct and
different. You might simply say that one acts as a brake and the other acts
as a motor.>>

Mel Siff:

***Interestingly, though research has shown that isometric action is
controlled by different brain mechanisms from dynamic action, no such
difference has been found between concentric and eccentric muscle action (we
discuss this point in Ch 1 of “Supertraining”). During all forms of JOINT
action, the underlying process of muscle CONTRACTION is the same, though
there are differences in the utilisation of deformable passive tissues and
the various reflexes.

I can anticipate your possibly detouring into some lengthy semantic arguments
about what we are discussing, and that will simply induce me to summarise
even more information on this topic from some very competent authorities.
So, to fill the gaps in your interpretation of muscle structure and function,
first please read the summaries of current muscle research such as that in
“Supertraining” (1999, pages 38-39) and go to the references cited. Other
relevant texts are:

Fung Y Biomechanics: Mechanical Properties of Living Tissue 1981
Frankel V & Nordin M Basic Biomechanics of the Skeletal System 1980

Scientific American has also featured more recent work on this topic, plus a
Medline search will also yield a huge amount of useful information.

Mel Siff
Denver, USA
Mel Siff Dot Com
Supertraining Twitter Feed

Dr Mel Siff and a Supertraining Yahoogroup member going back and forth

<If you hit bounce off the box correctly you will not experience any problems
with the lower back. The bounce needs to be make on the hamstrings and not
directly with your butt. If you perform it correctly you will the hamstrings
and to some extent the gluts will absorb the impact.

If you perform it incorrectly, you will experience some pressure in the
spine. Sitting back on the box places a lot of pressure on the lower back.
If you perform the bounce correctly, this is no more loading on the
spine…maybe even less that sitting back on the box. >

*** It certainly is useful advice to make most of the contact with the back
of the thighs rather than ever sitting with any significant pressure on the
glutes. However, cases have occurred where poorly understood and
technically hazardous bouncing off a box has caused fractures of area such as
the lumbosacral region of the lower spine, while back pain is also not
uncommon among those who use a definite bounce — and that is the problem
with novice users of the box squat. One cannot emphasize Kenny’s advice
strongly enough that the exercise be done with a correct, very light touching
bounce which does not longitudinally impose impact along the spinal column or
cause the spine to lose its lumbar concavity

Remember that the act of sitting down tends to elicit a relaxation of the
lumbar spine and posterior tilting of the pelvis, which leads to flattening
of the lumbar concavity. If you sit down on a box, you have to make very
definite actions to prevent these spinal relaxing processes from happening,
as is constantly stressed by the Westsiders.

<Bouncing off the box provides a greater stretch reflex. Minimize the risk
by performing it correctly and you’ll illicit a greater training effect in
the stretch reflex.

*** Bouncing off the prestretched muscle complex stimulates the myotatic
stretch reflex more strongly if you do not sit on a box at all. Any
superficial contact with the skin that you sit on will tend to diminish the
intensity of this reflex, plus any delay incurred while you are sitting (even
for less than a second) will diminish it further. Advocates of the box
squat do not even advocate “bouncing” off the box, especially under heavy
loading with a weight or a weight and bands combination.

If you wish to retain enough of the stretch reflex in the muscles of the
“posterior chain”, you should not use the box to offer anything more than a
slight brief touch to the backs of the thighs to enhance proprioceptive
awareness of the position at which you wish to commence your upward drive.
You can gain a good awareness of the prestretch in that position by using a
“Romanian” deadlift — i.e., by lowering and raising the bar from upper thigh
to below the knees by pushing your rear end backwards. Bent-knee good
mornings with glutes thrust back (rather than relying solely on hip flexion
or simple “leaning forwards”) will also enhance one’s awareness of that same
prestretch process.

<You should ease into ballistic box squatting. Once you learn to do it
you’ll illicit a greater training effect in the stretch reflex.>

*** See above – ballistic box squatting will not elicit a greater “training
effect in the stretch reflex”. If you are using box squats to enhance
performance in the squat, the reason is not mainly because you are trying to
“train” the stretch reflex, especially since the competition squat has to be
done without a box and methods of acquiring specific neural programmes tend
to be rather specific to the way in which they were learned. Anyway, I am
sure that this is what Kenny is advising – namely not using the box to sit
upon, but to serve as just a gentle warning system to offer tactile contact
so that you know exactly when to begin your upward drive in the squat. In
this way, you will retain the necessary prestretch and manage to execute the
movement explosively.

There are several reasons why one may use some forms of box squatting, but
“training the stretch reflex” is not one of them. However, the main problem
here is more a matter of scientific correctness and differences in phrasing
the advice more accurately. Some of the box squatting and Westside fans out
there might like to list some of their reasons for using box squats with and
without the added effect of bands for those who have never used box squats.

Mel Siff
Denver, USA
Mel Siff Dot Com
Supertraining Twitter Feed

PUZZLE & PARADOX 72

The effects of joint manipulation or mobilisation may not be as clearly
related to traditional explanations of their underlying mechanisms as
suggested by various therapists.

Most sports scientists, physiotherapists and athletes are very aware of the
various classes of mechanical ‘realignment’ of joints (including
manipulation and mobilisation) that are applied by physical therapists or
chiropractors. These twists, thrust, pulls or pushes of the spinal column,
in particular, are often accompanied by an audible ‘click’ or ‘pop’.

The professional therapists who apply this form of treatment attribute any
subsequent relief from pain or mobility symptoms to processes such as the
reduction of subluxations, stretching of connective tissue, the release of
nitrogen bubbles within the joint fluids, the realignment of joint surfaces,
nerve release and so forth.

This type of procedure is the central foundation of chiropractic and to
manipulative therapy in physiotherapy, with its users totally committed to
its effectiveness. Some long-term studies, however, indicate that joint
manipulation or mobilisation makes no statistically significant difference to
the rate or degree of recovery of the client from pain or malfunction. In
some cases, these procedures have resulted in far greater damage to the
patient, with periodic reports of hemiplegia, quadriplegia or exacerbation
of existing spinal damage appearing (frequently a result of inadequate
collaboration with medical, radiographic or surgical experts).

While the controversy between the merits and demerits of manipulative
procedures will no doubt continue to rage, this is not the main thrust of
this P&P. What appears to remain uncertain is the reason why these
procedures are successful in certain instances. All of the reasons
mentioned above need to be examined carefully before we can state
scientifically that there is a cause-effect relationship between any of them
and rehabilitation from back pain and/or dysfunction.

For instance, let us examine the contention that a quick, sharp thrust of
certain vertebrae will stretch the ligaments in that region and produce
greater mobility at that level. This presumes that a rapid movement will
cause permanent plastic deformation of the connective tissue, which happens
to be viscoelastic in nature. This means that rapid thrusts should evoke a
more elastic response from the appropriate vertebral ligaments, rather than
plastic deformation, which usually is a result of prolonged stretching above
a certain threshold level of strain in the tissues. So, if plastic
deformation is unlikely, this leaves only one other alternative, namely
tissue rupture, which is the last thing that any therapist wants.

However, all of this presumes that the therapist can produce sufficient
manual force to deform ligamentous tissue, which is highly unlikely, because
of its enormous mechanical tensile strength.

This immediately leads us to the hypothesis that many ‘back problems’ are
due to subluxations (small dislocations) of the vertebrae relative to one
another. We immediately have to ask if normal daily activities can
temporarily stretch enormously strong ligaments sufficiently to permit these
subluxations to persist for prolonged periods until the therapist
intervenes.

We have to examine the proof for the existence of these temporary
subluxations such as MRIs or CAT scans – is there unequivocal evidence to
show that ligaments (which are extremely inextensible) can be temporarily
stretched to allow adjacent vertebrae to stay dislocated relative to one
another? If so, then it will be interesting to carry out a biomechanical
analysis of the stresses and strains involved. It will be even more
interesting to understand how the slightly, but powerfully stretched,
ligaments manage to return to their original length along an hysteresis path
that shows no residual strain after prolonged stretching.

Even if one suggests that the subluxation or displacement that is reduced by
manipulation is the sum of tiny contributions from many vertebrae, it does
not eliminate the fact that ligament is very difficult to deform, especially
if subjected to a single sharp thrust.

What then of traction, that is probably used as widely as manipulation? Can
one state that traction stretches ligaments as well and relieves pressure on
nerves? Or is the idea of traction simply to overcome a persistent myotatic
stretch reflex which has temporarily forgotten to become inoperative or a
Golgi tendon reflex that has omitted becoming involved?

Possibly this would then offer a more rational approach to explain why
manipulation might relieve back pain or dysfunction. Such an hypothesis
would suggest that the muscles cause the ligaments to be pulled in a certain
direction, thereby producing and sustaining a subluxation. Of course, we
then have to examine how long a stretch reflex can remain operative and how
long a muscle can remain submaximally contracted. In the case of some back
pain sufferers, we might have to wonder at the impressive local muscle
endurance involved.

There are several other questions remaining regarding manipulation, such as
the cause of the ‘pop’ or click’. If it is indeed produced by the release
of air or nitrogen bubbles into the joints, then this would imply the
occurrence of cavitation, which is known to produce very detrimental shock
waves in engineering systems. If gas bubbles are released in the
cerebrospinal fluid, does this not imply the possibility of micro-shock wave
damage to structures in the spine, especially if manipulation is applied
regularly? Is there any evidence for the release of gas bubbles with
manipulation and, if so, are there any studies to show that they are
harmless artifacts?

Maybe the acute relief afforded in certain cases is more a consequence of
neural stimulation rather than mechanical realignment, caused by stimulation
of the nerves passing from the foramina of the spine. Would this also be a
reasonable hypothesis? Naturally, this would give us the opportunity of
invoking the ubiquitous placebo effect!

This P&P could be extended into the broader territory of deep transverse
friction, structural integration (‘Rolfing’) and so on to create a broader
base for examining the mechanical manipulation of the entire musculoskeletal
system. Indeed, this would probably be of enormous value in removing some
of the controversy associated with all of these procedures.

Comment on any of the issues raised by the above focus on manipulation and
mobilisation as currently practised by various therapists, quoting any
scientific studies which appear to support or disprove the value of these
procedures and the explanations presently given to validate them. Regarding
the mechanisms involved – Is it in the back or is it all in the head?

——————

Mel Siff
Denver, USA
Mel Siff Dot Com
Supertraining Twitter Feed

Note the conclusion that the sticking region does not appear to be caused by
worse leverage (“an increase in the moment arm of the weight about the
shoulder or elbow joints”) or by a significant decrease in muscle activity
during this region. The authors suggest that the problem may lie in the
possibility that the sticking region represents a force-reduced transition
zone between the earlier stretch-assisted acceleration-strength phase and the
later mechanically efficient maximum strength region. The use of limited
range elastic band and chain training (e.g. by Louie Simmons and the Westside
team) may play a useful role in attending to this specific deficit in the
transition zone referred to in this paper.

The relevance of analysing the force-time curve in terms of strength
qualities such as starting strength, acceleration-strength, maximal strength,
explosive strength then becomes more obvious, as discussed in Ch 2 of
“Supertraining”. A better understanding of these fundamental biomechanical
factors then enables one to plan one’s training more effectively.

————————

Elliott BC, Wilson GJ, Kerr GK.

A biomechanical analysis of the sticking region in the Bench Press

Medicine & Science in Sports & Exercise. 21(4):450-62, Aug 1989.

The performance of ten elite powerlifters were analyzed in a simulated
competition environment using three-dimensional cinematography and surface
electromyography while bench pressing approximately 80% of maximum, a maximal
load, and an unsuccessful supramaximal attempt.

The resultant moment arm (from the sagittal and transverse planes) of the
weight about the shoulder axis decreased throughout the upward movement of
the bar. The resultant moment arm of the weight about the elbow axis
decreased throughout the initial portion of the ascent of the bar, recording
a minimum value during the sticking region, and subsequently increased
throughout the remainder of the ascent of the bar.

The electromyograms produced by the prime mover muscles (sternal portion of
pectoralis major, anterior deltoid, long head of triceps brachii) achieved
maximal activation at the beginning of the ascent phase of the lift and
maintained this level essentially unchanged throughout the upward movement of
the bar.

The sticking region, therefore, did not appear to be caused by an increase in
the moment arm of the weight about the shoulder or elbow joints or by a
minimization of muscular activity during this region.

A possible mechanism which envisages the sticking region as a force-reduced
transition phase between a strain energy-assisted *acceleration phase* and a
mechanically advantageous *maximum strength* region is postulated.

—————-

Mel Siff
Denver, USA
Mel Siff Dot Com
Supertraining Twitter Feed

<http://netra.exploratorium.edu/sport/faq11.html#anchor445332>

Q: How does Michael Jordan manage to hang in the air for so long when he goes
up for a slam dunk?

A: Actually, he doesn’t hang in the air any longer than any other basketball
player. It just looks that way. Once he leaves the ground, Jordan is governed
by the same laws of physics as the rest of us. How high he jumps depends
entirely on how much force he generates with his legs as he leaves the
ground. And how long he stays aloft is directly related to the height of the
jump: the higher the jump, the longer he stays in the air.

A vertical jump of four feet leads to a hang time of one second. That’s an
unusually high jump and, it turns out, most basketball players, including
Michael Jordan, don’t jump that high. A three-foot-high jump has a hang time
of 0.87 seconds. All the artistry of a slam dunk takes place in just eight-
or nine-tenths of a second!

Jordan makes it seem longer because he holds onto the ball longer than other
players before shooting or dunking, waiting until he’s on the way down to let
go of the ball. His tendency to pull his legs up as the jump progresses also
makes it seem like he’s staying higher than he really is.

Next time you watch the Bulls play, try to time how long Jordan stays aloft
and compare it to other players’ hang times. You’ll see there’s not much
difference.

—————

Q: Why do long jumpers “run” several steps in the air after they take off?

<http://netra.exploratorium.edu/sport/faq7.html#anchor452653>

A: The hitch-kick, as the running motion is called, stops the forward
rotation of the jumper’s body that he gets when he springs into the air. As
the jumper plants his foot for takeoff, the motion of his lower body stops
for the fraction of a second his foot is in contact with the board. But his
upper body continues to move forward, which makes him start to rotate forward
around his center of gravity. If unchecked, this rotation would send him
face-down into the sand.

Long jumpers have learned to counteract this rotation by moving their hands
and arms in the hitch-kick. During the hitch-kick, jumpers hold each leg
straight as it moves backward and bent at the knees as it comes forward. This
difference in leg position causes the jumper’s lower body to move forward.

Similarly, the jumper’s arm movements during the hitch-kick pushes the
jumper’s upper body backward. These body motions neutralize the takeoff
rotation and allow the jumper to get into a better position for landing

When the jumper stops hitch-kicking, the take-off rotation continues
unchecked. The jumper rotates forward around a line that goes from side to
side through his center of gravity. This rotation forces his legs (now
stretched out in front of him) downward.

—————–

Mel Siff
Denver, USA
Mel Siff Dot Com
Supertraining Twitter Feed

INTRODUCTORY NOTE

For newcomers, these P&Ps are Propositions, not facts or dogmatic
proclamations. They are intended to stimulate interaction among users working
in different fields, to re-examine traditional concepts, foster distance
education, question our beliefs and suggest new lines of research or
approaches to training. We look forward to responses from anyone who has
views or relevant information on the topics.

PUZZLE & PARADOX 70

The treatment of knee conditions such as chondromalacia patellae by leg
extension exercises to alter ‘muscle balance’ may be based on faulty or
doubtful premises.

Treatment of the condition involving deterioration of the articulating
surface beneath the patella (often referred to as chondromalacia patellae -
CPAT) is usually based on the premise that some muscular imbalance between
vastus medialis and vastus lateralis causes the patella to track imprecisely
over the femur.

Apparently, a weaker v medialis relative to the v lateralis permits the
patella to be pulled laterally out of its most efficient trajectory over the
femur, thereby leading to uneven wear of the cartilagenous bearing surface
beneath the patella.

Consequently, therapists have tried to strengthen the v medialis with knee
extension exercises on isokinetic dynamometers or with various forms of
electrostimulation (faradism, interferentialism or so-called ‘Russian
stimulation’) in an attempt to improve the medialis/lateralis strength ratio.
Many clinical and theoretical studies have attested to its success and
validity, but the underlying mechanical process might not be as clearcut as
has been suggested.

The traditional explanation of strengthening v medialis implies that
strengthening of this muscle causes the patella to be ‘pulled in’ closer to
its ‘ideal’ trajectory during any movement which involves significant knee
flexion. A simple geometric analysis of the situation implies further that :

1. v medialis must then shorten more than it did before treatment; or
2. v medialis has been shortened chronically by the treatment.

If either of these implications is correct, then there must be some evidence
either that training causes any given muscle to contract to a greater extent
than the same unexercised muscle or that extended range training causes a
muscle to shorten progressively. If this suggested analysis is incorrect,
then another possible explanation has to be sought, possibly in altered
neuromuscular control or kinaesthetic processes.

This does not deny the fact that this type of therapy often may diminish
peripatellar pain and improve knee extension strength, but it serves to point
out that some of the traditional rationales for this type of injury
management may not be correct or as simple as are implied by the current
theories.

This analysis may also have profound implications for the entire concept of
testing and training muscles to enhance performance, facilitate
rehabilitation or prevent injury. In trying to understand the relevance of
muscle ratios, we have to search for rational hypotheses in structural,
functional or combined (structural-functional) processes.

For instance, has it been proved beyond a shadow of doubt that ‘muscle
imbalances’ are a major cause of injury or impaired performance? Or is the
cause of any problem rather to be sought in inappropriate patterns of muscle
recruitment, irrespective of the balance between the strength of any muscles
involved? In other words, is the dominant cause of injury or impaired
performance due more to neuromuscular control or motor skill factors than
‘muscle imbalances’?

Moreover, in attempts to analyse muscle balance and imbalance, how solid are
the current norms against which these balances are measured? We also have to
examine differences in muscle balance under static or static stabilising
conditions, as well as under dynamic conditions at different velocities and
in different patterns of cocontrative and ballistic action.

We cannot simply assume that balance under dynamic conditions implies equal
balance under explosive, slower or static conditions. Is this type of
biomechanical analysis carried out yet with this degree of thoroughness or
are therapists quite blindly extrapolating fixed path analysis on an
isokinetic dynamometer to all other multi-dimensional stabilising and moving
conditions to be encountered by the athlete? If the latter, why do
therapists continue to use such a flawed and dubious method of treatment and
assessment?

So, our critical analysis of the idea of an idealised perfect patella
trajectory under ‘balanced’ muscle action has led us to re-examine the entire
concept of testing and rehabilitation based on machine measurement under very
rigid mechanical conditions.

Comment on the current explanations for the validity of CPAT rehabilitation
and on the general concept of specific, fixed muscle balances concerning all
other joints in the body. The validity of extrapolating machine testing to
sports functional performance may also bear some critical analysis.

—————-

Mel Siff
Denver, USA
Mel Siff Dot Com
Supertraining Twitter Feed

For example: shoulder flexion with elbow extension, where one part of the
bicep is shortening (as in shoulder
flexion) and the other part is lengthening (as in elbow extension).

Have you heard of this before? Does it go by another name? And is it good to
train certain muscles using
that principle (maybe hamstrings?). The lecturer provided no references for
his remarks. >
Mel Siff responded with the following;
*** First of all, many scientists today prefer not to refer to muscle
“contraction” and instead use the word, “action”, to minimise any of the
existing confusion about “lengthening” of muscle during eccentric action and
to eliminate the need for creation of any new such words or ideas such as
what you have just mentioned. Anyhow, what you described happens very
commonly with any muscles that cross more than one joint. Many jumps,
throws, “plyometric” drills, the so-called “double knee-bend” in the Olympic
pull, and other ballistic movements automatically invoke this sort of action,
so there is no need to do anything special to make use of it.

The speaker more accurately should have referred to one joint angle
increasing and another decreasing during the movements that he was
addressing, as is conventional for any kinesiological analysis of
bi-articular (two jointed) muscle action. It is misleading to imply that
one end of a muscle is lengthening while its other end is shortening. That
sort of curious event does not happen in a uniform, continuous elastic band
and it does not happen in a continuous muscle.

The ability of some muscles to activate locally (some work has been done in
this regard with respect to the deltoids) does not depend on local
lengthening or shortening, but as a consequence of neural excitation.
However, the act of flexing the shoulder, e.g., in a “biceps curl”, can
prestretch the elbow flexors and produce greater force at some stages of the
exercise. There is absolutely no need to use that term “ecconcentric muscle
contraction” because the entire biceps group of muscles (and some other elbow
flexors) is in concentric (or “overcoming”, as the Russians would call it)
action during that exercise. There is no such “new” type of muscle action
called ecconcentric.

Many years ago, some scientists vainly attempted to resolve all this
confusion and dissatisfaction with existing terminology by creating these
definitions:

- isometric (no external joint action evident)
- pliometric ( “eccentric” action)
- miometric (“concentric” action)

What happened? Well, someone decided that the Russians (as usual, those
crafty bearers of all the training secrets in the world!) were using a
special type of training which looked like it relied mainly on “pliometric”
action – the person/s concerned misspelled the word in the form of
“plyometrics” and that label has stuck so well that the original Russian
concept upon which it was based, namely shock method (udarniye metod), has
largely fallen into disuse in the West.

It would be preferable if that speaker and all others in future simplified
the whole muscle mechanics issue by talking about “muscle action” and dropped
all reference to contraction, ecconcentrics and any other such confounding
terminology — or at least placed inverted commas about those terms to remind
us of their limitations.

Mel Siff

So, let me draw on some biomechanics to offer you some standard definitions
that are essential for understanding strength science (see Chs 1 and 2 of
“Supertraining” for further details):

1. Strength is the ability of a living system (or a muscle or a person) to
exert force (in a given action)

2. Maximum strength is the ability of a person to produce maximal force in a
specific action or exercise.

3. Power is the rate of doing work (P = work/time)

4. Peak power is the maximum power produced at any instant in a specific
movement under specific conditions

5. Mean power is the average power exerted over a given range of movement in
a specific exercise

6. Rate of Force Development (RFD) is the rate at which force is produced in
a given action. It is described by the slope of the force vs time curve.
The maximum value of RFD describes explosive strength (see below).

7. Explosive strength is the ability to exert strength or force as rapidly
as possible in a given action. A measure that is used to describe it is the
“Index of Explosive Strength” (IES), which is the maximum value reached by
the Rate of Force development in that action.

Mel Siff

<I am having considerable disagreement with my teacher on the topic of
reciprocal inhibition. As someone who is still a student, I don’t feel that I
have the background knowledge to rebut any of his proclamations, in spite of
delving into the Supertraining archives. This is due to the fact that he my
knowledge as conjectured or claimed and his as “proven documented fact”.
Could anyone please critique the following statement which he declared as
“fact”, not hypothesis?

“A muscle that is overdeveloped compared with its antagonist, will
continually create a situation of reciprocal inhibition to the antagonist,
which results in comparative disuse atrophy of the antagonist over time. This
in effect will weaken the antagonist. Many references (both physio, chiro and
related refer to this).” >

*** Before we take this any further, could you please obtain from that
teacher a representative list of some of those references to ensure that we
are discussing exactly the same issues, otherwise his arguments also have to
be considered as conjecture and belief? Note that, if those references rely
largely on clinical observations and anecdotes based upon a few case studies,
instead of on quantitative measurements, then they, too, may be worthless in
resolving this issue. I look forward to studying those “many” references.

Once upon a time it used to be claimed, on the basis of lower extremity
isokinetic tests, that balance between “agonists” and “antagonists” should
be 60:40. Then others came along and stated that it should be 50:50 if
evaluation relied on treadmill activities. Vorobyev cited figures nearer
70:30 for the knee muscles of Olympic lifters, apparently based upon
isometric dynamometry over a range of joint angles. And so on…..

Finally, do you know what transpired? Maybe you guessed it – further
examination of all of those tests led to any reliance upon them as being
regarded as being highly suspect, especially because all “agonist-antagonist”
ratios change with joint angle, speed of movement, pattern of joint action
and with multi-articular action.

Take one basic example, namely the action of the lower extremity structures
in movements such as walking, running, jumping, squatting and power cleaning.
It is almost entirely meaningless to refer to agonist-antagonist
deficiencies of the knee muscles because, in all of these activities, some of
those muscles cross both the hip and knee joints, with the exact instant to
instant contribution to each activity by each separate muscle depending on
individual characteristics and capabilities. Some of those muscles also
cross both the ankle and the knee joint, so the issue becomes even more
complex.

Then there is the fact that muscles which do not cross any of the lower
extremity joints can also have a profound effect on all of those activities
– for instance, the muscles involved with arm swing and trunk rotation and
extension can all play a major role in the overall movement patterns. The
following article offers invaluable comments in this regard: Zajac F E &
Gordon M F Determining muscle’s force and action in multi-articular movement
Exerc Sport Sci Revs 1989, 17: 187-230. In the light of these
biomechanical and anatomical facts, any reliance on highly limited analysis
of uni-articular agonism-antagonism may be seen to be highly simplistic and
inaccurate.

To all of this, we must now add the fact that all joint action does not
involve continuous action of “agonists” and “antagonists”, because this is
not the case with explosive and ballistic actions, where constant
antagonistic action would impede the concentric movement and lead to the real
possibility of injury. In this respect, I would suggest that your teacher
reads the work of Basmajian (“Muscles Alive”), which stresses that joint
actions may be either concontractive (which involves ongoing interaction of
“agonists” and “antagonists”) or ballistic (in which antagonistic action will
take place only to terminate the movement so as to prevent joint
dislocation).

As yet, nobody has ever determined what the hypothetical ratios should be
between “agonist” and “antagonist” under very rapid or ballistic conditions.
In other words, your teacher seems to have no evidence to prove that the
alleged “agonist-antagonist” ratios or imbalances apply to any situations
other than possibly a few archaic uni-articular tests in a laboratory or
clinic (a la Francis Kendall and co). What’s more, these types of action are
commonplace in many sports, because without them we could not run, throw,
strike, jump or weightlift, so they cannot be dismissed as being unusual or
infrequent.

Having now learned how complex and multifaceted real world muscle action is,
we can now see the even greater weaknesses in the argument that any “muscle
that is overdeveloped compared with its antagonist, will continually create a
situation of reciprocal inhibition to the antagonist, which results in
comparative disuse atrophy of the antagonist over time.”

Of course, one has to ask how it can be determined that a given muscle is
“overdeveloped”? Is this in terms of hypertrophy, isokinetic testing, manual
testing, or functional performance in a given simple or complex motor act?

Several weeks ago I discussed similar comments about agonism, antagonism and
inhibitory processes, where I stressed that it is not really accurate to
refer to muscles in this way. All muscles can play agonistic or antagonistic
roles, depending on the situation. There is no such entity as a muscle that
is only an agonist or only an antagonist, so that any comments on
“overdeveloped” agonists are unscientific and misleading. No biomechanist or
anatomist today will universally classify muscles according to that archaic
and limited schema.

If your teacher is willing to enter our discussions to rebut the evidence
which I have presented here, I would be most happy to welcome him/her here.
The ensuing discussion certainly could be of great interest and value to many
list members.

Any further coments from others?

Mel Siff