Muscle Interaction and Reciprocal Inhibition Part 2 by Mel Siff

Posted by: Mel Siff Blog  :  Category: Mel Siff Mind/Brain Stuff, Mel Siff on Anatomy/Physiology, Training Theory

Here continues the information on reciprocal inhibition and muscle
interaction from Basmajian (“Muscles Alive”).

—————

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

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Muscle Interaction and Reciprocal Inhibition Part 1 by Mel Siff

Posted by: Mel Siff Blog  :  Category: Mel Siff Mind/Brain Stuff, Mel Siff on Anatomy/Physiology, Training Theory

Because of a recent request for more information on the nature of reciprocal
inhibition and what it means for training, I am posting some thorough details
on this topic from Basmajian (Muscles Alive) in a series of two articles:

————————–

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

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Specificity and Neural Confusion by Mel Siff

Posted by: Mel Siff Blog  :  Category: Mel Siff Mind/Brain Stuff, Training Theory

The issue of neuromuscular confusion being caused by training with exercises
that supposedly are not specific enough to assist in enhancing one’s
abilities in another movement or sport often comes up, as we have noted in
some of our recent discussions on the strengths and weaknesses of lifting
exercises and “functional” training.

Science indeed has shown that each part of the cerebral cortex has a
different job to do, and when one region is attending to a given task, it can
interferes with the ability of its nearest neighbors to perform their
relevant tasks at a given time. I have already pointed out that this type
of “neurological confusion” is not caused just by using tasks that are not
specifically the same or very similar to the actions of one’s specific sport,
but that even greater confusion may be cause by tasks that are very similar
in nature.

I promised to offer some practical tutorials to let you experience firsthand
some tasks which can cause great neuromuscular confusion, so here we go with
some excellent examples from Discover journal at:

http://www.discover.com/

Take, for example, the motor cortex, where voluntary movements of your limbs
originate. Neurons that control your right arm and leg are located near each
other within the left “precentral gyrus” of the brain, while nerve cells that
command arm and leg muscles on the left side reside in the right precentral
gyrus.

Now, try a few experiments to see how cooperative these different regions of
the brain are.

EXPERIMENT 1: Ipsilateral Arm-Leg Interaction

Sit in a comfortable chair and hold out your RIGHT ARM, palm down, then
polish an imaginary piece of furniture, using a continuous counterclockwise
motion. As soon as you have a good rhythm going, start your RIGHT FOOT
circling counterclockwise in synchrony with the motion of your arm. After
mastering this coordinated effort, REVERSE the rotation direction of your
foot while keeping your arm on its original counterclockwise path.

Pretty difficult to do, isn’t it? When the neurons controlling your arm and
the nearby leg neurons work together, they don’t disturb each other much,
just as someone playing a radio right next to you doesn’t disturb your
equilibrium if it’s tuned to a station you like. But if the person next to
you is playing punk rock and you like country, one of you has to move.

EXPERIMENT 2: Contralateral Arm-Leg Interaction

If your right arm has not become too fatigued by the above exercise, keep it
polishing that nonexistent surface and repeat Experiment 1. This time,
however, use your LEFT foot.

Circling your RIGHT ARM and LEFT FOOT in opposite directions should be very
simple. That is because the control centres for the two limbs inhabit
opposite sides of the brain and don’t interfere much with each other, even
when executing conflicting motor tasks (i.e. ones that are not similar or
specifically the same).

EXPERIMENT 3: Head-Limb Interaction

Don’t stop polishing with that right arm just yet. To polish the imaginary
table to perfection, point your face to the floor and trace an imaginary
circle on the floor with your NOSE, first counterclockwise, then clockwise.

Now give your right arm a well-deserved break and repeat the nose-tracing
procedure while your LEFT ARM takes up the polishing chore. The movement of
your dominant hand should interfere more with the nose-tracing performance
than the motion of your non-dominant hand, even though the neck muscles that
move your nose in an arc are thought to be controlled equally by both sides
of the brain. Neuroscientists haven’t determined precisely why this happens,
but one plausible explanation is that dominant regions of the brain (the left
motor cortex, if you’re right-handed) take up more neuronal resources than
non-dominant areas and therefore are more inconsiderate neural neighbors.

Researchers examining these and other intra-brain interference effects hope
that a better understanding of the relationships between neighbouring regions
of gray matter will provide important insights into how the brain creates a
whole which is greater than the sum of its parts.

—————-

These basic experiments tell us more about how much more we need to learn
about the nature of “specificity” and intertask transfer of learning.
Other Supertrainers might like to share similar basic experiments which yield
us some insights into the nature of neural programming – over to you!

Mel Siff

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Mel Siff Discusses Periodising Psychological Skills

Posted by: Mel Siff Blog  :  Category: Mel Siff Mind/Brain Stuff, Periodisation

One member of the Supertraining Yahoo group asked Mel Siff;

<I am currently writing a research paper and am wondering if anyone has any
literature or references regarding the periodization of mental skills
training (psychological skills periodization). Any input would be greatly
appreciated.

*** In writing any research paper, it is vital to introduce the study by
providing some of the salient background, history, science and definitions.
In the case of your project, the entire concept of exactly what is meant by
“periodisation” needs to be summarised first in the “Introduction”.

Let’s begin with a point of technical pedantry. While it is possible to
refer to the periodisation of physical skills of all types, it is more
appropriate to refer to the organisation and programming of mental or
psychological drills or skills. This is because periodisation was conceived
as a method of long-term planning of sports training based upon fluctuations
in one’s physiological state, as I described in Ch 6 of “Supertraining”
(which also offers a great deal of information on many different types and
models of “periodisation” and “planning”).

Nobody has shown that cognitive processes follow some naturally varying
physiological (or psychophysiological) scheme, even though variations in
certain psychophysiological processes such as reaction time, arousal and
kinaesthetic sensitivity have been observed (e.g. see Fogel in
“Biotechnology” and other texts on ergonomics). However, these are not
cognitive in nature. Thus, depending on one’s individual abilities,
capabilities, training history and level of overall fatigue, one can execute
as many cognitive mental drills as is desired, presuming that the necessary
time is available to master them.

A fundamental characteristic of all periodisation models is the planning of
training to ensure that certain peaks in performance are achieved in specific
major competitions. Since mental skills do not change in a comparable way as
do physical quantities such as strength, power, speed and endurance, they
cannot accurately be periodised. That, of course, is why you will struggle
to find any valid research information on that topic. Before you can even
think of writing about mental periodisation, you need to find research which
validates any hypothesis that mental events fluctuate and reach peaks over a
prolonged period.

Maybe you would care to elaborate on the objectives and scope of your
intended project, so that some of us can better guide you in your labours.

Dr Mel C Siff

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Strength and Neural Drive – Part 2

Posted by: Mel Siff Blog  :  Category: Mel Siff Mind/Brain Stuff, Weight Training

EMG:

Previous investigations have reported training-induced increases in EMG
amplitude after concentric isokinetic training. The results of the present
study and those of Komi and Buskirk, however, indicated that concentric
isokinetic strength training did not result in significantly greater EMG
amplitude values. The reason for the discrepancies between the results of the
present investigation and those of others examining EMG responses to
concentric isokinetic training may be a function of differences in the
procedures used to analyze and quantify the EMG signal.

The lack of a significant change in EMG amplitude in the present study (Fig 3
) indicated that increased PT in the trained limb was not associated with
increased neural drive to the vastus lateralis. The reason for the increase
in PT in the absence of increased EMG activity is unknown; however, previous
investigations have provided plausible hypotheses:

(a) changes in neural drive to the other muscles or muscle groups involved in
the performance of leg extension, and

(b) muscle adaptations independent of EMG activity.

Changes in Neural Drive to Other Muscles or Muscle Groups

When performing leg extensions, many muscles in addition to the vastus
lateralis are involved. These muscles include (a) muscles of the stabilizing
muscle groups, (b) muscles of the antagonistic muscle groups, and/or (c) the
other muscles of the quadriceps femoris. Stabilizing muscle groups involved
in leg extension, such as the back, abdominal, shoulder, and arm muscles, are
essential for maximum peak torque production because they stabilize the upper
body and prevent flexion at the trunk .

Rutherford and Jones have suggested that the ability of the quadriceps
femoris to generate torque may be limited by the lack of coordinated
activation of these muscles. These investigators reported that an improvement
in PT of the leg extensors after isometric training did not occur until new
neural pathways that coordinated the actions of stabilizing muscle groups
were established. It was suggested that during muscular training,
coordination of the muscles that aid in the performance of leg extension are
involved in a learning process and that more complex movements may require a
longer learning process. Thus, it is possible that the training in the
present study increased the coordination of the stabilizing muscle groups,
which resulted in increased PT production.

Another group of muscles that may “learn” to aid in the expression of leg
extension torque are the muscles that are antagonistic to the quadriceps
femoris. Recent evidence indicates that the levels of antagonistic
cocontraction are modifiable with training. Carolan and Cafarelli measured
the EMG activity in the vastus lateralis and hamstrings after isometric
training of the leg extensors and reported that there was no change in vastus
lateralis EMG activity, but there was a decrease in hamstring EMG activity. A
training-induced decrease in hamstring coactivation in the present
investigation may have provided less opposing torque to the contracting
quadriceps femoris and resulted in increased PT production.

This hypothesis is not in accordance with the findings of Tyler and Hutton ,
who have suggested that since antagonistic coactivation reduces the neural
drive to the agonists through reciprocal inhibition, a training-induced
reduction in antagonistic coactivation would allow greater activation of
agonists. If the suggestion of Tyler and Hutton is correct, a
training-induced reduction in hamstring coactivation in the present study
would have resulted in greater activation and, therefore, greater EMG
amplitude in the vastus lateralis.

Measurements of EMG activity in the present study were made only for the
vastus lateralis. It is possible that there may have been changes in neural
drive to the other muscles of the quadriceps femoris, which could have
resulted in an increased ability to produce torque. Narici et al attributed
differences in the hypertrophic responses of the individual muscles of the
quadriceps femoris to differences in muscle activation after concentric
isokinetic training at a velocity of 120° per sec. These authors observed
preferential hypertrophy and greater EMG activity in the vastus medialis and
rectus femoris when compared with the vastus lateralis. Thus, there may have
been increased neural activation of the other muscles of the quadriceps
femoris, which resulted in preferential hypertrophy and increased PT
production.

Muscular Adaptations Independent of EMG Activity in the Trained Limb

Hypertrophic Factors:

As individual muscle fibers enlarge, their positions under surface electrodes
are altered. Therefore, it is possible that hypertrophy alone could have
influenced the EMG signal. Garfinkel and Cafarelli, however, hypothesized
that if electrode placement is constant, then the electrodes are detecting
EMG over the same area of muscle membrane and, therefore, hypertrophy would
not alter the EMG.

If the hypothesis of Garfinkel and Cafarelli is correct, hypertrophy of the
vastus lateralis could have occurred in the present study without directly
influencing the amplitude of the EMG signal. In addition to the vastus
lateralis, other muscles involved in leg extension (i.e., stabilizing muscle
groups, rectus femoris, vastus intermedius, vastus medialis, and other
muscles) may have hypertrophied as well.

It is possible that architectural factors that cause or are a result of
hypertrophy of these muscles, yet are independent of muscle activation, may
have contributed to PT production. Such factors include (a) increased
contractile protein content, (b) increased pennation angles, and/or (c)
changes in tendinous attachments.

Garfinkel and Cafarelli examined the EMG responses of the vastus lateralis to
isometric training and reported that there was no change in the EMG activity
but a 28% increase in PT production. It was proposed that the increase in
contractile proteins that accompanies muscle training could result in greater
PT simply because each hypertrophied muscle cell is able to form a greater
number of cross-bridges for any level of activation.

Another architectural factor that is important in the production of PT, yet
is independent of EMG activity, is the pennation angle. Recent studies have
shown that trained or hypertrophied muscles have pennation angles greater
than those in untrained or atrophied muscles. It has been suggested that an
increase in pennation angles would allow attachment of a greater amount of
contractile tissue to the tendon, which may result in increased PT
production.

It is also possible that the increased collagen synthesis that has been
observed during training-induced muscular hypertrophy may alter connective
tissue attachments. Jones and Rutherford have suggested that if new
attachments were made intermediately between sarcomeres in series and the
tendon, the tension would not only be transmitted through sarcomeres in
series, but also through intermediate sarcomeres, thereby, increasing torque
production. Thus, it is possible that muscle hypertrophy, either in the
vastus lateralis or other muscles involved in leg extension, occurred as a
result of the maximal isokinetic training and resulted in increased PT
production that was independent of EMG activity.

Nonhypertrophic Factors

Previous investigations have reported that there may be qualitative changes
in muscle fiber protein expression (i.e., fast fiber type conversions from
Type IIb to Type IIa) as a result of resistance training. Although it is not
known how these changes may affect strength, it is possible that the
intramuscular remodeling could contribute to strength gains in the absence of
changes in the EMG….

———————-

Mel Siff

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