The primary sensory nerve endings of the muscle spindle wraps around the center nuclear bag and nuclear
chain regions and is called the annulospiral ending. The secondary sensory nerve endings branch into many
smaller fibers onto the intrafusal fibers and these are called the flower spray endings. The motor endings to
the muscle spindle also innervate the intrafusal fibers and are called the gamma efferent endings.
The muscle spindle runs parallel among the extrafusal muscle fibers. It inserts from tendon to tendon or
may attach to one tendon and to a muscle fiber on its other end. The gamma efferents adjust the length of
the muscle spindle by contracting or relaxing the intrafusal fibers and in this way maintain the spindles
comparative length relationship to the extrafusal fibers.
The afferent receptor sites of the muscle spindle are sensitive to stretch. When a muscle spindle is
stretched, the result is contraction of the muscle. Namely, stretch of a muscle will also stretch the inherent
muscle spindles; if the fibers are not "reset" in proportion to the stretch of the extrafusal fibers, then
mechanical deformation of the spindles receptor site will occur. Action potentials will then be generated
along the afferent sensory endings. The impulses travel through the dorsal root of the spinal nerve trunk into
the spinal cord where a monosynaptic connection occurs within the anterior horn of the gray matter. The
motor neuron (and the impulses) then travels through the ventral root of the spinal nerve trunk to innervate
the specific motor unit of the muscle in which the impulse originated. The extrafusal fibers of the motor
unit will respond with contraction. Contraction of the extrafusal fibers surrounding the muscle spindle can
then shorten the muscle; the spindle length is decreased and the action potentials from the receptor site
cease. This is called the stretch reflex. This reflex occurs in response to passive longitudinal stretch of the
muscle. For this reason the muscle spindle is referred to as a stretch receptor.
Gamma efferent stimulation will cause contraction of the intrafusal fibers; this will also stretch the receptor
site and cause subsequent extrafusal contraction to occur (this process is responsible for the tone of skeletal
muscle). In this way, the brain can set the spindles at various lengths, allowing and gauging movement and
causing the reflex contraction to occur at predetermined lengths.
The nuclear bag region of the receptor site is concerned with the dynamic stretch reflex: strong opposition
(contraction) to passive movement of a joint while the movement is still occurring. The nuclear chain
region is concerned with the static stretch reflex: prolonged opposition (contraction) to undesirable
movement of a joint after stretch has already occurred. The static reflex adds only minimal contraction to
the muscle, so that voluntary movement can be superimposed over the reflex contraction. This prolonged
reflex contraction can be maintained very efficiently for long periods of time (perhaps indefinitely). In fact,
posture is maintained for long periods with little or no evidence of fatigue. This is the feature of tonic
contraction; its economy in the expenditure of energy. It is thought that there are active groups mingled
with inactive groups, scattered throughout the muscle. Alternating periods of rest and activity of muscle
groups (or motor units) explain the ability of tonic contraction to be maintained for so long without
showing fatigue.
The misalignment becomes a static condition in which certain muscles are stretched and therefore working
for correction (as we have described) and in which opposing muscles are shortened. These shortened
muscles may become "acquainted and content" with this chronic malposition. Stretch receptors in these
muscles would then be reset to accommodate the deranged posture of this vertebra. In this way, fixation
may be due to strong muscle opposition to lengthening via gamma efferent "sensitization" of the muscle
spindles of specific segmental muscles. The shortened muscles would not be active, except to exhibit
natural tone, similar to the surrounding musculature. Any dynamic movement, toward correction of the
misalignment would elicit the contractive reflex of the muscle (or muscles); again this would discourage the
natural correction of the misalignment, guarding the fixation. Note that while the vertebra remains static
(without the addition of natural forces of correction, such as movement, etc.), this muscle occupies its
resting tone. As the adjustive thrust is introduced, this muscle may momentarily oppose the correction of
the vertebral subluxation, because this would disturb the muscle from its newly attained posture. Realizing
that the anatomy and actual length of the muscle's structures had not changed, it seems likely that the
muscle would now be reset to maintain its original resting length (being the proper juxtaposition of the
vertebra). In any case, the contralateral muscle that had been working for correction of the vertebral
misalignment, would now be satisfied and begin to assume the function of "sentinel rather than combatant."
Traumatic or chronic misalignment would discourage stability of the vertebral motor units because of
viscoelastic and scarring changes of the connective tissues and of the muscles themselves. Nociceptive
aberrant reflexes due to mechanical and chemical irritation of the spinal ligaments (including the joint
capsules), the disc and other sensitive joint tissues, also contribute to recurrent misalignment patterns. Such
nerve interference reduces the threshold of afferent firing even further if left uncorrected and can therefore
be self perpetuating, activating muscular imbalance through polysynaptic pathways. Hypomobility which is
by definition a component of the misalignment, decreases mechanorecptor afferent stimulation of the cord
and thus diminishes proper neuromuscular responses.
The muscles that are shortened with the change of structural relationships, upon vertebral misalignment, we
will label antagonists, because it is these that oppose the action of the working muscles. The new
physiologic range of motion during the misalignment may well be due to the of the antagonist muscles,
limiting motion to altered boundaries of "protection." The muscles are primed and are safeguarding against
further structural threat. Areas of the brain amplify the gamma efferent discharge; the intrafusal fibers are
slightly contracted, stretching the center nuclear bag region of the muscle spindle. The preshortened spindle
is stimulated sooner (and to a greater degree) when the muscle is stretched. In this way, the threshold of the
stretch receptors can be shifted to meet the needs of postural control.
Perhaps joint and tendon receptors and the Golgi tendon organs (G.T.O.), play the role of informing the
subconscious nuclei of the brain that the misalignment has been corrected. This is highly likely because of
an immediate burst of impulses to the brain centers upon joint movement and succeeding slow and steady
impulses thereafter. Graphically, let us apply this to our theory:
The joints require intelligent positioning, while muscle function relies upon the maintenance of constant
tension and will adapt when it is "desirable" to different lengths.