The Physiology and Proposed
   Hypothesis of Working Muscles

Spinal musculature comprises a stabilizing system for the vertebrae, among its other functions.  Upon vertebral subluxation, juxtaposition is not maintained and the muscles that attach directly to the osseous processes are affected.  A muscle that is stretched from the misalignment will respond by contracting; this response is called the stretch reflex.

Within each muscle (particularly within the postural muscles) is contained specialized fibers that differ from the ordinary contractile fibers in that these special fibers are neuromuscular in their structure and function.  They have been labeled muscle spindles and come under the category of mechanoreceptors.

Each muscle spindle is made up of small bundle or "fascicle" of muscle fibers, two to ten in number (per muscle spindle).  These are called the intrafusal fibers, whereas "ordinary" muscle fibers are known as extrafusal fibers and they make up the bulk of each muscle belly.

The extrafusal fibers are responsible for the "mechanical" contraction of the muscle.  The intrafusal fibers (within each muscle spindle) add little to the contraction of the entire muscle and therefore are not directly involved with joint movement (in reference to actively drawing insertion towards origin).  The intrafusal fibers from either of the spindle ends, meet in the center to form a unique bag or chain region in a specialized receptor arrangement with the intrinsic nerve endings.

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 spindle’s 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 spindle’s 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 stretch reflex is essential to postural control and equilibrium.

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.

Thus, different muscle groups contract in relays with only a portion in active contraction.  Similarly, the vertebral subluxation being so minute as to only elicit a partial response.  In view of these things, it is clear why the muscle spindles have frequently been called "misalignment detectors," telegraphing the distance between intended and actual movement to the central nervous system.

Our theory in brief:

  • one vertebra misaligns from juxtaposition lengthening certain muscles attached to the vertebra.
  • the muscle spindles within these muscles are stretched and afferent transmission is stimulated.
  • the spinal cord transmits motor impulses to the involved motor units (this is a very local reflex).
  • subtle resiliency is encountered upon palpation of these working muscles!

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:

  • misalignment occurs (working muscles are initiated).
  • the joint receptors fire, informing the brain of the independent position and compromise of the vertebra.
  • muscles are activated via the stretch reflex to "work" (physical work is not actually accomplished until movement occurs).  Segmental activity produces a distinct paravertbral muscular pattern of tension.
  • an adequate and utilizable force is introduced to the vertebra and correction of the misalignment begins.
  • Intrafusal fibers of working muscles are resetting to meet the demands of brain centers, serving to maintain muscle tone (and therefore maintain sensory awareness) as the muscles shorten during the correction.
  • the antagonistic muscles respond with dynamic contraction (the strong phasic reflex to stretch while movement is still occurring).
  • the Golgi Tendon Organs detect the extreme "antagonist" tension, due to muscle lengthening and contraction occuring simultaneously.
  • the G.T.O. fires, inhibiting muscle contraction and therefore avoiding soft tissue damage.
  • the antagonist muscles relax allowing the adjustment to occur.
  • mechanoreceptors in the joint capsules quickly send the brain of the desired movement.
  • the Intrafusal fibers of the antagonistic muscles could then be reset via gamma efferent transmission and return the muscle to tone.

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.