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

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

The study below shows that even moderate resistance training executed while a
muscle is compressed can produce a greater increase in strength, hypertrophy
and local muscle endurance than if one trains without the muscle being
compressed. Note that the exercise was performed with only 50% of 1RM and
that the compression only amounted to less than one-third of atmospheric
pressure, so it would be interesting to see how the results would change with
greater resistance and somewhat greater levels of compression.

Let us now recall the typical loading used in explosive lifting training
(i.e. with loads of 50-67% of 1RM), which is of the same order of magnitude
as was used in this experiment. Suppose, instead of not wearing supportive
garb, we chose to train regularly with firm wraps, powerlifting suits/vests
or neoprene sleeves. Would this not possibly result in increases in strength
and all those other performance factors?

Maybe all that theoretical advice that supportive apparel is detrimental to
training might be proved to be very wrong indeed — after all, the evidence
quoted is based entirely on theoretical grounds and anecdotes, while the
below study proved experimentally that compression-aided training improves
several fitness and strength qualities of high-level athletes. Maybe wearing
a belt not only enhances proprioceptive sensitivity, confidence and some
“core” stability, but it actually may increase the strength and growth of the
trunk musculature. Similarly, wraps around the thighs, chest and arms may
produce the same effects in those regions. What then about doing
crunches and other abdominal exercises while wearing wraps or a very flexible
corset around the trunk?

Only one way to find out about this theory without waiting for scientists to
take many months and a few years to have their research published – we can
personally try this (moderate) compression training method for a few months
and see what happens. There is nothing to lose and something to gain. We
could try squatting or cleaning with wraps (or neoprene sleeves) around the
thighs and bench pressing with lifting shirt and wraps around the upper arms
- and keep careful records of lifts and limb girths (and skinfolds) to
monitor any changes (and compare them with our usual patterns of change).

Now read the study for yourselves:

—————-

Effects of resistance exercise combined with vascular occlusion on muscle
function in athletes

Yudai Takarada, Yoshiaki Sato & Naokata Ishii

Eur J Appl Physiol (2002) 86: 308-314

The effects of resistance exercise combined with vascular occlusion on muscle
function were investigated in highly trained athletes. Elite rugby players
(n=17) took part in an 8 week study of exercise training of the knee extensor
muscles, in which low-intensity [about 50% of one repetition maximum]
exercise combined with an occlusion pressure of about 200 mmHg (LIO, n=6),
low-intensity exercise without the occlusion (LI, n=6), and no exercise
training (untrained control, n=5) were included. The exercise in the LI
[non-compression] group was of the same intensity and amount as in the LIO
[compression - MCS] group.

1. The LIO [compression] group showed a significantly larger increase in
isokinetic knee extension torque than that in the other two groups at all the
velocities studied.

2. On the other hand, no significant difference was seen between LI
[non-compression] and the control group.

3. In the LIO [compression] group, the cross-sectional area of knee
extensors increased significantly, suggesting that the increase in knee
extension strength was mainly caused by muscle hypertrophy.

4. The dynamic endurance of knee extensors estimated from the decreases in
mechanical work production and peak force after 50 repeated concentric
contractions was also improved after LIO [compression], whereas no
significant change was observed in the LI [non-compression] and control
groups.

The results indicated that low-intensity resistance exercise causes, in
almost fully trained athletes, increases in muscle size, strength and
endurance, when combined with vascular occlusion [compression].

————-

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

—————

PART 2

Silent Period and Reciprocal Inhibition

The “silent period” of muscle is the period of cessation of activity which
occurs when a twitch contraction is superimposed on a voluntary effort (e.g.,
electrically or by a tendon tap). Its normal range (in adductor pollicis) is
87 to 151 msec (Higgins & Lieberman, 1968). It also occurs following the
sudden release of a voluntarily innervated muscle provided a certain minimum
rate of shortening is achieved; if shortening is not permitted or is slow, no
silent period results (Struppler, 1975).

Struppler has shown clearly that the silent period is NOT the result of
reciprocal inhibition (autogenic inhibition); rather it is primarily due to
the cessation of facilitatory impulses in the primary afferent fibres from
the muscle spindles. At the end of the silent period, there is a rebound
burst of EMG activity. A sudden stretch of a relaxed muscle does not recruit
a monosynaptic (muscle-spindle) reflex in man (Marsden, Merton & Morton,
1976).

Garland & Angel (1971) showed that during a rapid voluntary movement, the
agonist produces two distinct volleys of EMG activity separated by a relative
silence. When the active limb was unloaded during the movement, the second
burst was significantly reduced. Apparently, the second burst is due to
spinal reflexes. The mechanical properties of the muscle were shown by
Agarwal & Gottlieb (1972) to have a significant influence on the duration of
the silent period that follows the electrically induced H-wave in soleus
muscle. The primary contraction in soleus (M-wave) coincides with reciprocal
inhibition of the tibialis anterior.

Yabe & Tamaki (1976) have shown the voluntary elbow extension is immediately
preceded by a silent period in the unexercised contralateral agonist
(“contralateral agonist silent period”), without any contralateral antagonist
contraction occurring. Obviously this occurrence cannot be a unilateral type
of reciprocal inhibition at the spinal level.

A different kind of silent period has been demonstrated in the muscles of
mastication. Single stimulation of the teeth induces inhibition in actively
contracting temporalis and masseter muscles with a 30 to 40 msec latency. The
same type of inhibition occurs from sudden unload of the muscles (Ahlgren,
1969; Beaudreau et al., 1969; Griffin & Munro, 1969). Munro and I (1971) more
recently demonstrated that the inhibition in all the elevators of the
mandible was almost synchronous; in most subjects there was a synchronous
burst of activity in the chief depressor muscle (anterior belly of digastric)
some 15 to 27 msec after initial tooth contact.

Hannam (1972) has demonstrated that an enhancement of the masseteric reflex
by voluntary contraction of the jaw-closing muscles may be due to autogenic
factors, synergistic factors or both. Stimulation of the muscle spindles and
facilitation caused by the voluntary activity before tooth contact must be
involved.

Effects of Cross Exercise

The hypothesis that there is a transfer of activity to the contralateral limb
during prescr ibed exercise on one side has been frequently postulated, but
now it is being seriously questioned. Probably it is invalid except in very
special circumstances. Gregg, Mastellone & Gersten (1957) of Denver,
Colorado, found that overflow to the unexercised, contralateral muscles did
not occur during simple non-resistive exercises or during isometric
contractions of one biceps brachii. As the exercise stress increased,
however, there was some “overflow” to the opposite triceps and, after even
greater stress, to the biceps. Increasing fatigue played an important role in
the “overflow” but was reversible, for after a rest of two minutes “overflow”
would at first be absent. Moore (1975) found overflow activity to be between
10% and 20% of the maximal intensity of activity in the exercised limb. She
believed that even this small amount of overflow gives sufficient
justification for it to be used in maintaining muscular tone in immobilized
limbs.

Samilson & Morris (1964) confirm the finding that in normal man activity of
one upper limb is not accompanied by activity in the contralateral resting
limb. However, in spastic children, there is such a spread. On the other hand
Podivinsky (1964) of Bratislava, Czechoslovakia finds a slight motor
irradiation occurs from the strong contraction of finger flexors to the
related muscles of the opposite limb (“crossed motor irradiation”).

This perhaps is related to the findings of Hellebrandt and her colleagues
regarding indirect learning, i.e., the improvement of strength in one limb by
exercising the opposite limb (Hellebrandt & Waterland, 1962a, b). Its
practical significance in ordinary life is unknown and appears to have been
exaggerated since the days of Scripture et aL (1894). We have shown that at
the finest levels of control in motor unit training the role of
cross-training is not significant (Basmajian & Simard, 1966).

Further, the crossed reflex phenomenon described by Ikai (1956) of Tokyo is
not really the same phenomenon as cross exercise. Ikai showed that the
crossed reflex of limbs in spinal animals can be reproduced under certain
conditions as a brief overflow of monosynaptic reflexes to the opposite limb.

Panin, Lindenauer, Weiss & Ebel (1961) seem to have delivered a serious blow
to the concept of “cross exercise.” In their extensive study they found that
the spread of activity was minimal to insignificant. Insignificant potentials
of low amplitude and frequency appeared in all non-exercised muscles in a
widespread distribution in all four limbs. They appeared most in areas
required for postural stabilization of the subject’s body. Even then the
amount of activity was so slight as not to constitute exercise effect.

Our own studies on quadriceps (p 250) and those of Sills and Olsen (see
above) largely confirm the conclusions of Gregg and his colleagues. We found
in our studies of spastic patients (p 83), however, that an exuberant
overflow occurs to the opposite limb. Walshe (1923) and, more recently, Hopf
et al. (1974) and Soto et al (1974) have written about a similar phenomenon
in hemiplegia. We must conclude that “cross education” is, at best, of
dubious value in normal subjects……

Motor Learning and Control

There is mounting evidence that motor learning and control are not a process
of accretion but depend on patterning of inhibition in motor neurons. Elect
rom yo graphic studies in health and disease indicate that the acquisition of
skills occurs through selective inhibition of unnecessary muscular activity
rather than the activation of additional motor units.

As noted in other sections, almost all resting muscles throughout the bodies
of adults, both human and general mammalian, fall to a level of neuromuscular
silence. This total relaxation occurs unless the muscles are needed to be
tensed for a posture or movement or unless the person suffers from
uncontrolled apprehension or neurotic and neurological disturbances. With
this in mind, MacConaill and I (1969) enunciated the principle that there
should be a minimal expenditure of energy consistent with the ends to-be
achieved. This self-evident principle embraces two laws:

1. The Law of minimal spurt action – no more muscle fibres are brought into
action than are both necessary and sufficient to stabilize or move a bone
against gravity or other resistant forces, and none are used insofar as
gravity can supply the motive force for movement;

2. The law of minimal shunt action – only such muscle fibres are used as are
necessary and sufficient to ensure that the transarticular force directed
toward a joint is equal to the weight of the stabilized or moving part
together with such additional centripetal force as may be required because of
the velocity of that part when it is in motion.

Control of Movement

The neurophysiological literature is encrusted with the barnacle that “the
brain does not order a muscle to contract but orders movement of a joint.”
Recently, Phillips (1975) made a concerted effort to dispel this myth which
has stultified research on the learning of motor behavior. In fact, the best
movements are performed with an economy of muscular movements dependent upon
impulses being sent to only one or two muscles or even a localized area of
one muscle. What the brain has “learned” is patterning of these actions by
means of a progressive inhibition of the inefficient mass responses that were
natural to the child.

Some movements are extremely economical in the well-trained person. For
example, most of us are fairly well-trained in turning our hand over through
pronation and supination of the forearm; in this learned act our nervous
system calls upon only one or two muscles to produce the movements.
Fortunately, the normally plastic human brain quickly adapts to shifts of
function; otherwise tendon-transfer operations would be useless.

Physiologists and even some kinesiologists do not appreciate that each and
every muscle has several (sometime many) component parts which are recruited
in different functions at different times. Many investigations with
intramuscular electrodes in many thousands of muscles lead me to believe that
this local activity is patterned by progressive inhibition of motoneurons
until an acceptable performance is achieved. Our studies of elbow flexion and
thenar muscles, which show the interplay of motor unit functions dedicated to
specific postures and movements, clearly indicate that the positioning of
limbs is predetermined by sets of motor units which are permitted to act for
that position. The same appears to be true for welllearned movements.

I believe that a mosaic of spinal motoneurons is dedicated to the learned
response of a specific posture or movement of a joint through space. The
ultimately superior performance of a skilled movement depends on the
reproducibility of the ideal, an economically spare mosaic of motoneuronal
activity (Basmajian, 1977).

With different objects in mind, Payton et al. (1976) put it slightly
differently: they found no statistically significant difference between
pre-learning and post-learning of a simple task in regard in the EMG
activity, movement time and range of movement. They concluded that all the
prime movers that are going to contribute to the final learned act take part
even before the skill is learned; thus as motor learning takes place, there
is a marked reduction of activity only in the auxiliary muscles while the
prime movers neither gain nor lose (Payton et al., 1976).

When I first described the precision possible in controlling single
motorneutons, I believed (as did many others) that this type of control was
the building block of motor performance. Given visual and auditory cues
through electronic amplification and feedback, subjects could be quickly
trained to consciously activate single motoneurons with great precision. But
conscious activation of single motoneurons in the single-motor-unit training
paradigm depends on the same principles as the learning of any other novel
task, that is, progressive (and sometimes rapid) inhibition of the
motoneuronal activity that adds no useful function in producing a desired
motor response (Smith, Basmajian & Vanderstoep, 1974).

Training, whether it is the unconscious process of the child learning simple
social motor responses or the preparation for a specific skilled act (such as
those of a musician or athlete), is a progressive inhibition of many muscles
that flood into play when one first attempts to produce the required
response. The athlete’s continued drill to perfect a skilled movement
exhibits a large element of progressively more successful repression of
undesired contractions. Among others, O’Connell (1958) has demonstrated this
convincingly. A group of physical education majors required to perform “head
stands” while being studied electromyographically could be graded as to their
actual experience by the amount of overflow of undesired activity in muscles
that were only casually related to the exercise.

The young animal has enormous amounts of overactivity and reactive
contractions in muscles that are serving no directed purpose in producing the
desired movement or posture. Among others, Janda & Stara (1965) demonstrated
in children a high incidence of mass responses in a predictable pattern even
in muscles that are far removed from those which produce a required movement.
As children mature, this overactivity disappears and is absent in normal
adults. It reappears in adults under psychological stress, but people can be
trained to inhibit it to varying degrees. In patients with diseases and
injuries of the central nervous system, the normal inhibition pattern is
lacking; then mass responses from local interoceptive and exteroceptive
bombardments of the motoneurons result in an exaggerated mass response
described as spasticity.

The Moscow investigators led by Yusevich (see, for example, Okhnyanskaya et
al., 1974) attribute normal motor hyperactivity in infants and children to
synkinesis or synergies of suprasegmental origin, pointing out the fact that
they normally disappear by the time a person is adult.

The patterning of the inhibition would seem to come in part from obscure
processes in diffuse centers of the cerebral cortex; since inhibition is a
central feature, one must consider the possibility that brainstem centres and
perhaps the cerebellum are critically important in the imprinting of the
learning. It is too simplistic to consider a schema where an impulse is
started at a tiny area of the cerebral cortex and is thence passed directly
along a facilitatory path to a desired set of motoneurons. The motor learning
process probably employs a neuronal network with the “main” pathway for motor
activation being almost a small part of the whole.

Proprioceptive Effects

Gellhorn (1960) has described electromyographic studies which disclose the
effects of central proprioceptive influences on movements elicited by the
electrical stimulation of the motor cortex. Movements so produced are
strongly reinforced by proprioceptive impulses which also determine, by and
large, the type of movement that results. He showed, for example, that the
contraction of triceps and flexor carpi muscles when stimulated through the
cerebral cortex is greater if the elbow is at 45 degs than if it is at 110
degs or 160 degs. Furthermore, a cortical stimulus that is below threshold
when a muscle is slack may become effective when the muscle is put on the
stretch…………

END OF SERIES

Mel Siff

————————–

PART 1

Coordination, Antagonists and Synergy

One often sees the owlish statement that the brain does not order a muscle to
contract but orders movements of a joint. As clever as it sounds, this
statement is only true in part. Under certain circumstances the movement is,
in fact, the result of contraction in only one or two muscles. This we have
shown repeatedly by our various studies.

For example, pronation of the forearm is usually produced by one muscle alone
- pronator quadratus – unless added resistance is offered to the movement;
then, more muscles are called upon (Basmajian and Travill, 1961). My
colleagues and I have found this to be true in elbow flexion too, where
brachialis alone often suffices, and in other movements. Therefore, it is
wrong and misleading to believe that nature always calls upon groups of
muscles to produce simple movements. On the other hand, there are complex
movements (such as rotation of the scapula on the chest wall during elevation
of the limb) which obviously call upon groups of cooperating muscles (see p.
191).

Antagonists, too, have been misrepresented in the normal functioning of
muscles. The unfortunate and incorrect impression has been fostered by many
physiologists and even more anatomists that during the movement of a joint in
one direction muscles that move it in the opposite direction show some sort
of antagonism.

The truth of the matter, first proposed by Sherrington as “reciprocal
inhibition” is that the so-called antagonist relaxes completely (Travill &
Basmajian, 1961) except perhaps with one exception-at the end of a whip-like
motion of a hinge Joint. Here, apparently, the short sharp burst of activity
in some antagonists occurs to prevent damage to the joint; this was first
implied by Barnett and Harding (1955) and later supported by our own work
(Basmajian, 1957, 1959) (see Fig 4.9) and that of Bierman & Ralston (1965).
These investigators at the Biomechanics Laboratory of the University of
California in San Francisco recorded the EMG potentials in rectus femoris and
biceps femoris while subjects had their knee moved passively and when they
actively performed flexion and extension of the knee (Fig 4.10).

When they turned their attention to what the antagonists are doing during
active movements, they found that toward the end of such a movement,
potentials occurred in the antagonist (Fig 4.10). They did not ascribe this
to a stretch reflex as such, but they did consider the action as a regulatory
one acting in proper timing through central feedback loops. They would agree
that this brief terminal activity in antagonists serves a protective function
to “avoid damage which such a force [in the prime mover] could produce.”

Equally concerned with antagonist function are a group of French workers
(Goubel & Bouisset, 1967; Bouisset & Goubel, 1967; Lestienne & Bouisset,
1967; Goubel, Lestienne & Bouisset, 1968; Pertuzon & Lestienne, 1968;
Lestienne & Goubel, 1969; Bertoz & Metral, 1970).

In summary, they find a pattern of responses in which low unsustained
activity occurs in antagonists at low speeds of voluntary flexion and
extension of the elbow; at middle speeds there are successive activities in
the agonist and antagonist, including common electrical silence; at high
speed of flexion and extension there was partial overlapping of phasic
activities in agonist and antagonist. They focus their attention not on the
speed per se, but on the tension in the agonist and draw attention to the
reflex activity during muscular recruitment especially in extension movements.

Patton & Mortensen (1970) also have studied the mechanical factors which
affect agonist-antagonist interaction at the elbow joint. Extension of the
elbow always causes more cocontraction of antagonists than does flexion.
Increasing load increases cocontraction during both flexion and extension.
Skilled subjects have reduced cocontraction. When voluntary cocontraction
preceded a movement, there was marked reciprocal inhibition in the antagonist
during an active movement. These findings assume an intermediate position in
the continuing dialogue concerning the existence of cocontraction and
probably come close to the truth in this complicated area of muscle
physiology.

Holt et al. (1969) found a reflex effect of antagonist contraction and head
position on the responses of the agonist muscle which, for example, was
augmented by prior strong contractions of the antagonist. Cohen (1970) goes
even further in demonstrating that what is being done by the opposite limb
affects the EMG of rhythmic movements in the studied limb in a varying
manner. Generally it is agreed that voluntary slow movements in normal man
do not cause stretch-reflex cocontraction of the antagonists, but rather,
when it occurs, it occurs with rapid movements (Patton and Mortensen, 197 1;
Angel, 1975; Hallett et al., 1975; de Sousa et al., 1975; Morin et al., 1976;
Jacobs, 1976).

In effect, cocontraction of antagonists occurs to greater or lesser degree in
some movements, in some people, at some ages and under some circumstances.
With increasing age and training and at slower speeds, it tends to reduce to
nil. When it occurs, it sometimes is due to reflexes and sometimes appears to
be extravagant overflow.

The oft-used term “antagonist” should be replaced, in my opinion, by the
companion word “synergist”. When “antagonists” act they really act just to
prevent undesired movement, and their only important application as
antagonists is in their acting against gravity. Because nervous coordination
is so fine, there is no need for muscles to act in antagonism to others
simultaneously. The rule, then, is for the “antagonist” to relax.

Wiesendanger et al. (1967) in a study on reaction-time at the elbow found
that the muscular activity of a volitional reaction movement was short and
usually showed reciprocal activity of the antagonist; in some cases there was
reciprocal inhibition. Triceps activity in the position of the antagonist
always was less marked than that of biceps as the antagonist.

One finds that the activity of muscles in the position of antagonists during
a movement is a sign of nervous abnormality (e.g., the spasticity of
paraplegia) or, in the case of fine movements requiring training, a sign of
ineptitude. Indeed, the athlete’s continued drill to perfect a skilled
movement exhibits a large element of progressively more successful repression
of undesired contractions. O’Connell has demonstrated this convincingly in
her unpublished EMG studies at Boston University. A group of physical
education majors required to perform “head stands” while being studied
electromyographically could be graded as to their actual experience by the
amount of overflow of undesired activity in muscles that were only casually
related to the exercise. (See also section under “Training,” p. 105.)

Hirschberg & Dacso (1953), on the other hand, would seem to disagree with my
opinion. In an early EMG study, they appeared to conclude that simultaneous
activity of agonists and antagonists is a common phenomenon, but
unconsciously they come closer to my own position with their almost
parenthetical statement that such activity is seen in ” . . . strenuous
motion or in tense experimental subjects.”

Furthermore, Lundervold’s extensive experiments (1951) referred to on page
84, appear also to contradict Hirschberg and Dacso. Miles, Mortensen &
Sullivan (1947) in an early study stated that potentials could be recorded
from topographical antagonists, but the circumstances of their experiments
were somewhat too specialized to make so sweeping a generalization today.

Dempster & Finerty (1947) in an early EMG study set out to determine the
influence of varying gravitational effects on the large number of muscles
that may cross one joint-specifically, for 15 muscles that cross the wrist
held in a horizontal position. Furthermore, they were concerned with the
influence of torques or moments of force at the pivot. Finally, they employed
rather esoteric calculations (of no interest to the general reader) to
explain their findings.

For static support, the torque at the wrist produced by gravity must be
balanced neatly by the torque of those muscles which are in an advantageous
position, i.e., crossing above the horizontal level of the wrist pivot.
However, Dempster & Finerty found that synergists were active as well and
these were obviously not in a position to exert an antigravity torque. This
activity in the synergists or stabilizers was about half that in the
antigravity or main group (which they referred to as “agonists”). Muscles
that were below the wrist pivot and therefore in no position to act against
gravity showed activity too; this was one quarter as much as that in the
agonists, according to Dempster and Finerty. They then unfortunately dubbed
these muscles “antagonists.” If indeed any true activity of this nature
occurs – and refined EMG techniques seem to deny it – the activity is not a
matter of antagonism to the agonists, for gravity does not require help.
Rather it must be due to secondary synergic and postural functions of the
muscles of the wrist and fingers.

By rotating the horizontally held wrist (supination and pronation) different
groups of muscles were brought to a superior position. Here they assumed the
burden of the gravity torque; others were placed in less advantageous
positions in which, however, they continued activity as synergists, but with
reduced intensity.

Using as a model the act of prehension of the hand, Livingston, Paillard,
Tournay & Fessard (1951) of Paris demonstrated the plasticity of synergists
during voluntary movements. Thus, the interplay of activity of the flexors of
the fingers and of the thumb with those of the forearm was shown during
normal activity to vary significantly depending on the information of
peripheral origin, e.g., position of joints, angle at which the synergists
act, the nature of objects grasped, etc. More recently, Weathersby (1966)
reported that there is considerable synergistic activity in certain forearm
flexors during ordinary movements of the thumb.

Missiuro & Kozlowski (1961) illustrated the ultimate plasticity of
synergists. In a study of rabbit muscle transplanted to the place of its
“antagonist,” they found the transplant took on the function of the
anatomical and functional “antagonist.” Obviously the nervous system is able
to adapt readily to such changes.

We know that many contractions of any one particular muscle may be
accompanied by synergistic activity in other muscles to steady the adjacent
joints. Gellhorn (1947) thus demonstrated the role of far-removed synergists
in movements of the wrist. While flexor carpi radialis was activated in very
slight flexion of the wrist, triceps brachii became active with the
increasing effort in the prime movers (the extensors of the wrist remaining
relaxed meanwhile). Only with very strong static flexion of the wrist would
activity-and that only occasionally-appear in the antagonists.

Gellhorn found three stages of recruitment of synergists, depending on the
stress:

1. In the first, the activity is confined to the agonist at the wrist.

2. In the second, action potentials appear in the agonist and a muscle of the
upper arm according to the following rule: biceps muscle becomes active with
flexion of the supine wrist and with extension of the prone wrist, whereas
the triceps becomes active with the reverse conditions (i.e., extension of
the supine and flexion of the prone wrist).

3. In the third stage, with excessive straining, some activity appears in
antagonists as well but it is never equal to the activity of the prime mover
and of the synergists.

The exact significance of Gellhorn’s patterns of recruitment are obscure but
may be of fundamental importance. In any case, they stress the concept that
“antagonists” are really only synergists.

Along the same line, experiments were done by Sills & Olsen (1958) in the
hope of demonstrating activity in the unexercised arm while the opposite arm
was exercised by normal subjects. There was, in these normal persons, little
if any such “spread” to the opposite limb musculature unless extremely
powerful movements were made. (See also our similar findings, p 257 and the
section under “Effects of Cross Exercise.”) Their conclusions effectively
demolish the basis for certain contralateral exercises that have been
advocated for developing muscles, especially for an injured limb too painful
or too immobilized to be moved itself. [Note the importance of this finding
for anyone who believes that modest training of an uninjured limb offers
significant "cross training" of the injured limb. Mel Siff]

Novel electromyographic studies of abnormalities in the plantar reflex
response have fallen neatly into this general concept, too. The “up-going
toe” of upper motor neuron lesions has been found by Landau & Clare (1959) to
be the result of an exuberant overflow of activity to the great toe
extensors; even though the flexors continue to contract, the extensors
overpower them (Fig 4. 11).

In the very young normal child and especially premature babies, the same sort
of phenomenon was demonstrated by Fenyes, Gergely & Toth (1960) with “flexion
reflexes” observed electromyographically. Both agonists and antagonists
contract in what they term a “co-reflex phenomenon.” The same is true in
spastic children with cerebral palsy during locomotion (Kenney and Heaberlin,
1962; Feldkamp et al., 1976). There is an abrupt onset of the agonists and a
rapid response of the antagonists with sufficient power to be obstructive.
Under considerable resistance, normal children give the same response of
exuberant (but wasteful or useless) overactivity of antagonists.

Rao (1965) has shown by EMG that, contrary to general opinion, *reciprocal
inhibition* does not occur with the ankle jerk reflex. But he confirms its
validity when voluntary actions are performed. Motor units in tibialis
anterior act as briskly as those in gastrocnemius when the tendon of Achilles
is tapped. He explains this reversal of normal inhibition in the
“antagonist” as part of the positive supporting reaction (PSR) in which the
principle of reciprocal innervation is not applicable. [Note that I have
discussed the PSR in previous posts -- it is also discussed in
"Supertraining" and in Guyton's "Textbook of Medical Physiology". Mel Siff]

Agonist-antagonist interactions have been widely studied in the Soviet Union
(Baranov-Krylov, 1969; Person, 1965, 1969; Kozmyan, 1965) from the viewpoint
of central motor controls. Person’s work has been the most thorough and
extensive. She showed that relaxation and tensing of an antagonist is learned
and can be trained to increase or decrease. Kozmyan revealed that the latency
of antagonist inhibition and agonist excitation varied most frequently during
movements responding to non-rhythmic stimulation. With rhythmic repetitive
movements, the latencies as well as dissociation of reciprocal inhibition
diminished. Thus, inhibition of the antagonist muscles were to be expected in
rhythmic activity with any element of supraspinal control or learning.

Bratanova (1966) of Sofia found essentially the same thing with rhythmic
activity of biceps and triceps brachii. In the “training” stages,
coactivation was common apparently as the result of excitation radiation but
later it was extinguished, Gatev (1967) also of Bulgaria, but working
independently, found that as infants mature the excessive cocontraction
typical of childhood diminishes progressively. This appears again to be the
result of learned or patterned supraspinal control eliminating “undesirable”
or “useless” cocontraction.

In a study of reflex reactivity of biceps and triceps in children at
different developmental stages, the Polish investigator, Missiuro (1963),
found a spread of electrical activity to other muscles of the same extremity.
With increasing age this decreases so that in adult life it is minimal.

Vladimir Janda (1966, personal communication) of Prague has shown a
significant linkage of EMG activity in certain separate muscle groups,
especially in children. During a strong effort in a particular muscle, he
finds a high incidence of activity (in a predictable pattern) in far removed
muscles of the same limb and trunk musculature.

Hellebrandt and her colleagues have convincingly drawn our attention to a
patterned spread of gross muscular activity to wider and wider areas during
forceful effort or exercise stress (Hellebrandt & Waterland, 1962a, b;
Waterland & Hellebrandt, 1964; Waterland & Munson, 1964a, b). Employing the
Fukuda Stepping Test, Waterland & Shambes (t970) showed that the
head-shoulder linkage of muscular activity was the key to body displacement
and rotational directions when allowed to respond spontaneously.

In insects, simultaneous EMG activity in antagonist muscles has been reported
(Hoyle, 1964, in grasshoppers; Wilson, 1965, in cockroaches and locusts).
These have no simple relationship and probably do not bear on the problem of
synergy in mammals. The only possible connection is in the findings of
Stuart, Eldred, Hemingway & Kawamura (1963) who showed that in shivering
there are synchronous contractions in antagonistic muscles of mammals….

END OF PART 1

————————–

Mel Siff

“Tonic muscles… perform extensor actions including abduction or lateral
rotation. Phasic muscles… perform flexor functions, including adduction
and medial rotation.”

What are the references for these comments, and do you have any speculations
as to why these diffentiations exist?>

*** I have been hunting through my library for that specific definition, but
have not managed to locate it yet. Note that I stated that this is one of
the categorisations that are used to classify muscles, not that this is MY
preferred approach. In fact, I even wrote a Puzzle & Paradox on this very
issue several years ago, which you might like to address:

PUZZLE & PARADOX 98

Classification of muscles into tonic and phasic groups may be inaccurate and
misleading

————————

Muscles are commonly divided into those which stabilise (tonic) and those
which mobilise or move (phasic). Sometimes we also read that the tonic
muscles comprise predominantly slow twitch muscle fibres, whereas phasic
muscles are largely fast twitch.

If we consult research publications, however, we note that some postural or
tonic muscles, such as some of the trunk muscles, are predominantly fast
twitch.

At the same time, we appreciate that stabilisation is sometimes dynamic,
sometimes static and that some limbs undergo concurrent stabilisation and
movement by the same muscle groups. For instance, consider the actions of
the lower extremity during running and jumping – is it entirely appropriate
to separate the actions of certain muscles into stabilisation and
mobilisation processes. What about the actions which take place in cyclical
movements such as cycling and swimming?

Possibly we can talk about tonic and phasic functions, but to rigidly define
muscles as either one or the other may well be more confusing and misleading
than enlightening and accurate. Is there any real need to persist with this
type of classification, particularly if attempts are made to justify it on a
simplistic basis of muscle fibre types (which usually neglects to implicate
the actions of the nervous system in orchestrating the complex interactive
processes of stabilisation and mobilisation)?

Draw on appropriate references or your own powers of logical analysis to
resolve this issue.

——————

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

———————————–

Types of Muscle Contraction

[Siff M C "Supertraining" 2000 Ch 1: 51-52]

Traditionally, the following types of muscle “contraction” beginning with the
prefix ‘-iso’ (meaning ‘the same’) are defined: isotonic (constant muscle
tension), isometric (constant muscle length), isokinetic (constant velocity
of motion) and isoinertial (constant load). In addition, movement may occur
under concentric (so-called “muscle shortening”) and eccentric (so-called
“muscle lengthening”) conditions. Before these terms are unquestioningly
applied to exercise, it is important to examine their validity.

In all of the above cases, it is more accurate to speak about muscle
“contraction” (action) taking place under various movement conditions. It
is well known that a muscle can only contract or relax relative to its
resting or inactivated state, so that it is a misnomer to refer to eccentric
muscle contraction as a “contraction” in which a muscle contracts and
lengthens simultaneously. Actually, this means that a muscle which has
contracted under concentric or isometric conditions is simply returning under
eccentric conditions to its original resting length. To avoid confusion like
this, it is preferable to define muscle action as follows:

* Concentric – Action in which the proximal and distal muscle attachments
move towards one another
* Eccentric – Action in which the proximal and distal muscle attachments
move away from one another
* Isometric – Action in which the proximal and distal muscle attachments do
not move relative to one another

“Isometric” literally means ’same length’, a state which occurs only in a
relaxed muscle. Actually, it is not muscle length, but joint angle which
remains constant. Contraction means ’shortening’, so that isometric
contraction, like all other forms of muscle contraction, involves internal
movement processes which shorten the muscle fibres. Isometric contraction
may be defined more accurately to mean muscle contraction which occurs when
there is no external movement or change in joint angle (or distance between
origin and insertion). It occurs when the force produced by a muscle exactly
balances the resistance imposed upon it and no movement results.

Although not incorrect, the term “isometric” may be replaced by the simple
word static, without sacrificing any scientific rigour. It is interesting to
note that, during isometric contraction, mechanical work, some of which is
absorbed by the tendinous tissue, is generated by the shortening of muscle
fibres (Masamitsu et al, 1998).

The term “isotonic”, however, should be avoided under most circumstances,
since it is virtually impossible for muscle tension to remain the same while
joint movement occurs over any extended range. Constancy is possible only
over a very small range under very slow or quasi-isometric (almost isometric)
conditions of movement for a limited time (since fatigue rapidly decreases
tension). Naturally, constant tone also exists when a muscle is relaxed, a
state known as resting tonus. Whenever movement occurs, muscle tension
increases or decreases, since acceleration or deceleration is always involved
and one of the stretch reflexes may be activated.
European and Russian scientists often prefer to use the term “auxotonic”,
which refers to muscle contraction involving changes in muscle tension and
length. Other authors use the term “allodynamic”, from the Greek ‘allos’
meaning ‘other’ or ‘not the same’. Both terms are more accurate than
“isotonic” in this context.

Isotonic action is most likely to occur under static conditions, in which
case we have isotonic isometric action. Even then, as is the case with all
muscle activation, there is rise time of tension build up, an intermediate
phase of maximal tension and a final decay time of tension decrease. For any
prolonged action, the tension changes irregularly over a range of values.
If the load is near maximal, the muscles are unable to sustain the same
level of static muscle tension for more than a few seconds and the situation
rapidly becomes “anisotonic isometric”. In general, the term “isotonic”
should be reserved for the highly limited, short-movement range situations in
which muscle tension definitely remains approximately constant.

The word “isokinetic” is encountered in two contexts: firstly, some textbooks
regard it as a specific type of muscle contraction, and secondly, so-called
isokinetic rehabilitation and testing machines are often used by physical
therapists.

The term “isokinetic contraction” is inappropriately applied in most cases,
since it is impossible to produce a full-range muscle contraction at constant
velocity. To produce any movement from rest, Newton’s first two Laws of
Motion reveal that acceleration must be involved, so that constant velocity
cannot exist in a muscle which contracts from rest and returns to that state.
Constant velocity can occur only over a part of the range of action.

Similarly, it is biomechanically impossible to design a purely isokinetic
machine, since the user has to start a given limb from rest and push against
the machine until it can constrain the motion to approximately constant
angular velocity over part of its range. The resistance offered by these
devices increases in response to increases in the force produced by the
muscles, thereby limiting the velocity of movement to roughly isokinetic
conditions over part of their range. They are designed in this way since
some authorities maintain that strength is best developed if muscle tension
is kept at a maximum at every point throughout the range, a proposition which
has neither been proved nor universally accepted with reference to all types
of strength.

Moreover, research has shown that torque (and force) produced under
isokinetic conditions is usually much lower than that produced isometrically
at the same joint angle (see Figs 2.8, 2.9). In other words, it is
impossible to use isokinetic machines to develop maximal strength throughout
the range of joint movement.
The presence of any acceleration or deceleration always reveals the absence
of full-range constant velocity. Isokinetic machines should more accurately
be referred to as “quasi-isokinetic” (or pseudo-isokinetic) machines.

One of the few occasions when isokinetic action takes place is during
isometric contraction. In this case, the velocity of limb movement is
constant and equal to zero. Approximately isokinetic action also occurs
during very brief mid-range movement phases in swimming and aquarobics, with
water resistance serving to limit increases in velocity to a certain extent.
However, even if a machine manages to constrain an external movement to take
place at constant velocity, the underlying muscle contraction is not
occurring at constant velocity.

Two remaining terms applied to dynamic muscle action need elaboration.
“Concentric contraction” refers to muscle action which produces a force to
overcome the load being acted upon. For this reason, Russian scientists
call it “overcoming” contraction. The work done during concentric
contraction is referred to as positive. “Eccentric contraction” refers to
muscle action in which the muscle force yields to the imposed load. Thus, in
Russia, it is referred to as “yielding” or succumbing contraction. The work
done during eccentric contraction is called “negative”.

Concentric contraction occurs, for example, during the upward thrust in the
bench press or squat, while eccentric contraction occurs during the downward
phase. Apparently, more post-exercise soreness (DOMS – Delayed Onset Muscle
Soreness) is produced by eccentric contraction than the other types of muscle
contraction. However, it should be noted that adaptation processes minimise
the occurrence of DOMS in the musculoskeletal systems of well-conditioned
athletes. Apparently, microtrauma of connective tissue plays a significant
role in the DOMS phenomenon, but the relationship between the intensity and
volume of eccentric muscle activity, biochemical changes, the influence of
adaptation processes and the extent of DOMS is still poorly understood.

A little appreciated fact concerning eccentric muscle contraction is that the
muscle tension over any full range movement (from starting position through a
full cycle back to the starting position) is lower during the eccentric phase
than the isometric or concentric phases, yet eccentric activity is generally
identified as being the major cause of muscle soreness. Certainly, muscle
tension of 30-40% greater than concentric or isometric contraction can be
produced by maximal eccentric muscle contraction, as when an athlete lowers a
supramaximal load in a squat or bench press (but can never raise the same
load), but this degree of tension is not produced during the eccentric phase
of normal sporting movements. Clearly, it would be foolhardy to assume that
our current understanding of all aspects of muscle contraction is adequate
for offering optimal physical conditioning or rehabilitation…..

——————-

Mel Siff