editor wrote these articles while a student at an accredited
Chiropractic Medical School. During those days, there were only
two fully Accredited Chiropractic Schools. The ACA gave permission
to reproduce this research at Chiropractic Colleges. It was
through works like this concomitant with other talented Doctor's of
Chiropractic, which helped the evolution of Chiropractic Medicine; today
Chiropractic Colleges are accredited across this nation and the globe.
THE STRAIN OF ATHLETICISM
of Chiropractic Trauma, which had eluded scientists for centuries
Part II (Published JACA
After your author had written and published part one in this series,
with a motivation of love for a profession, this soul had found a consistent set
of variables within a consistent continuum relative to patient suffering
and objective findings noted from son's of Doctor's of Chiropractic in
my class as well as my developing recognition and subsequent
investigation into the complaints, signs and symptoms of patients who
present to Doctor's of Chiropractic and why they resolve with their care
over far more radical cares offered by traditional medicine. It
was interesting that my initial theories, the "Somato-Neuro-Muscular
and Viscero-Neuro-Muscular Pathway"
and the Somato-Neuro-Muscular pathway did go
on to explain the mechanism of
pain and discomfort via direct trauma
to the spine as well as how altered joint
dynamics via spasm occured as a direct result of visceral irritation
Yet, during my research
your author discovered that both anthropologists and Doctor's of Chiropractic had noted similar albeit
uncorrelated findings. My soon to be colleagues were reporting
areas of compensatory restrictions in spinal motion or excesses in a
compensatory area secondary to a primary injured spinal area. For
example, a person with a functional scoliosis when strained,
demonstrates these types of combinations of altered joint dynamics in
their spines (e.g. their spine appears radiologically and through examination to be within normal limits and
then when strained the spine present through radiological and clinical
examination as a structural scoliosis which became a known false positive).
Thus, it was now clear
that your author needed to again investigate and report the forensic textbook sound
mechanism of spinal injury whereby a secondary spinal reaction occurs
subsequent to an overexertion injury to the spine. And why. This investigator did go on to discover the mechanism and
report the findings which were excepted universally by science and
medicine and have now stood the test of scientific and judicial review
and time. The paper was called the "Strain of Athleticism"
published in May of 1981, in the Journal for the American Chiropractic
Health care providers
from all generations have needed a therapy to aid the individual after
he had exerted himself beyond his physical conditioning.
Hippocrates said, "Get knowledge of the spine, for this is the requisite
for many diseases."1
many books on health care, including, On Setting Joints By
leverage and Manipulation and the Importance
of Good Health. Men
of his time used their muscles at work: gathering food, building or
fortifying dwellings and fighting beasts and other men.
In 1895, D.D. Palmer
rediscovered the knowledge that, when a vertebra is subluxated in
rotation or a lateral flexion-rotation, the sign was of great benefit in
making the final "total" diagnosis.
Today's person is still
likely to over-exert their muscles at work, in sports, or in situational
activities, such as changing a flat tire on their car. Because
mankind will always utilize their muscles; possibly over-exert
themselves and end up in their physician's office, it is important to
re-examine "the Strain of Athleticism."
The purpose of this
article is to combine Hippocrates' and Palmer's early concepts with
modern science and identify the mechanism of subluxations of the
vertebral column, occurring as a direct result of muscular
over-exertion, which has eluded scientists for centuries.
FORENSIC TEXTBOOK SCIENCE
When the free end of a
muscle is made to lift a weight, or to oppose a resistance held constant
during contraction; the contraction is isotonic and the work done is the
product of the distance shortened and the weight lifted by the muscle in
overcoming the external resistance. Under these isotonic
conditions, the muscle cannot shorten until the force that it develops
is greater than the load it must lift. When the force of the
muscle exceeds the load, the muscle begins to shorten.
When a muscle contracts,
as in isotonic exercise, large molecules of the resting organ break down
into many small molecules, which pass into the tissue spaces.
These metabolites can remain in considerable concentrations in the
tissue spaces for a long period and will slowly diffuse into the blood.
As the metabolites remaining in the tissue spaces are osmotically
active, they attract fluid from the blood and retain it.2
Normally this facilitates a gradual diffusion of
metabolites into the blood, owing to a difference of concentration.
However, during excessive muscular exertion, metabolites cannot be
removed from the blood quickly enough. This occurs because when a
muscle contracts, it compresses the vessel in it if it develops more
than 10% of its maximal tension. When it develops more than 70% of
its maximal tension, blood flow is completely stopped.3
Furthermore, tissue pressure exceeds pressure within small, thin-walled
vessels and even within arteries, thus causing temporary occlusion.4
The increased energy skeletal muscle output for
contraction engages the endothelium triggers as well as stimulation from
the kidney's lead to Angiotensin II direct effect on these endothelial
triggers which release endothelan-1 and prostanoids further causing
combined with a concomitant fight/flight situation, the adrenal glands
will release epinephrine and norepinephrine into the blood stream.
Both of these amines main effect on vascular beds is vasoconstriction
(In low releases, epinephrine can cause vasodilatation).
Thus the metabolites tend to accumulate during exercise and increase with
each additional contraction. In other words, local blood flow
spurts and ceases with cyclic contraction and relaxation and these
spurts of blood are not equal to the normal circulation, thus allowing
toxic metabolites to accumulate. During high-intensity static
exercise, such as weight lifting, or a sudden trauma of equivalent
overexertion, blood vessels are compressed by the skeletal muscle, thus
increasing vascular resistance and decreasing blood flow
(Opposite of dynamic, endurance exercise where there is a 20% increase in
blood flow in exercising skeletal muscle due to vasodilators such as
adenosine, carbon dioxide, and lactic acid which overcome the increased
sympathetic outflow stimulation of alpha receptors which would otherwise
cause the sympathetic (vasoconstriction) effect in skeletal muscle
causing a "metabolic vasodilation of arterioles). Hence, during muscular activity,
(decrease in vascular resistance.)
the weight of the muscle increases by 20% due to the increased amount of
retained fluid and metabolites. This swelling of the muscle may
cause the muscle stiffness, which follows extreme exertion.5
During the first few minutes of maximal isotonic
contraction, or excessive exercise, anaerobic energy is sometimes needed
until the acceleration of O2 debt mechanism in
association with maximal utilization of the aerobic mechanism.6
The myoglobin-rich, capillary-rich,
mitochondria-rich muscles of man offer the luxury of maximal utilization
of aerobic energy mechanisms with a ready reserve anaerobic energy
able to yield energy when needed. The energies released by
anaerobic mechanisms due to
lactic acidosis (increased anion-gap
metabolic acidosis with tissue hypoxia/
are extremely important in maximal work, where they
permit a man to expend energy far in excess of his capacity for carrying
on oxidative metabolism.7
This process is limited by the individual's tolerance for acidosis
resulting from accumulation of lactic acid in the muscles, which is an
end product of anaerobic glycolysis.8
One of the suggested causes of pain in ischemia is accumulation of large
amounts of lactic acid in the tissues.9
Potassium ions now
are considered important vasodilator metabolites, which have the
task of dilating arterioles in the exercising muscle. The
increased blood flow is due to potassium ions' general effect to inhibit
smooth muscle contraction.10
Potassium ions are also one of the suggested
causes of pain in ischemia.11
activity, sweat glands can be stimulated by the sympathetic system.
These sweat glands secrete a proteolytic enzyme called kalikreins into
the tissue where it acts on alpha2-globulin (or A2)
to split the polypeptide to lysyl-bradykinin when in tissue and to
bradykininn when in plasma. Ischemia also ruptures the tissue and
the proteolytic enzyme is released. Once formed, the bradykininn
exists for only a matter of minutes because it is digested by the enzyme
The actions of kinins causes visceral smooth muscle contraction,
relaxation of vascular smooth muscle, increased capillary permeability,
lowers the threshold of pain in the area and causes severe pain.13
also accumulate in the tissue spaces. Adenosine and Co2 for that
matter cause vasodilation.
Increased hydrogen ions
accumulate in muscles contracting in the absence of oxygen.14
And finally, Lewis originally hypothesized that sustained muscle contractions are painful
because the muscle becomes ischemic, and a substance which stimulates
pain endings accumulates (Factor P).15
Histamine is an
autacoid present at high levels in the lungs, skin, and the
gastrointestinal tract and is released from mast cells and
basophiles by type 1 hypersensitivity reactions, drugs, venoms and
trauma. Through the activation of H1 receptors Histamine increases
activation of peripheral nociceptive receptors and thus increase pain
and pruritus. Thus histamine alone can cause the classic symptoms
of pain and pruritus.
Thus, it is easy to
envision that increased contraction of arterial blood vessels, ischemia,
increased trapped noxious metabolites in the interstitial space (lactic
acid, P Factor, bradykininn, potassium, hydrogen ions, histamine and metabolite
products of muscle catabolism), increased tissue oncotic pressure,
over-stimulation of nerve endings by the presence of metabolites,
increased fluid in the interstitial space, temporary local soft tissue
acidosis as a result of lactic acid, all yield muscle stiffness,
muscular spasticity and pain as a result of muscular overexertion.
over-exertion has ended, yet a deep paravertebral muscle (e.g.
unilateral rotator, multifides, etc) remains strained, stiff and spastic
(primary muscle spasticity), the muscle may pull a vertebra into
subluxation or a state of altered joint dynamics. As the vertebra
becomes subluxated, ligaments associated with it become stretched.
This stimulates the "Somato-Neuro-Muscular Pathway," which results in
increased general ipsilateral paravertebral muscular spasticity and
However, as the strained, stiff (primary spasticity) paravertebral
muscle causes a subluxation (primary subluxation), the muscle also pulls
on various muscle spindles (which detect muscle length) and golgi tendon
organs (which detect muscle tension), as well as on neighboring joints.
The proprioceptors circuit impulses to the cerebellum via anterior and
posterior spino-cerebellar tracts.17
The cerebellum is concerned with coordination of somatic motor
activity, the regulation of muscle tone and mechanisms that influence
and maintain equilibrium.18
Fixating muscles which fix neighboring or even distant joints must be
compensated by complex reciprocal innervation for coordinated control of
the spinal equilibrium. Thus, as the stiff, spastic muscle pulls
the vertebrae into subluxation or a "state of altered joint dynamics",
associated proprioceptors stimulate the cerebellum to send impulses from
the dentate nucleus through the superior cerebellar peduncle to synapse
in the contralateral thalamic nucleus. From here the neuron
travels to the motor cortex as the thalamocortical fibers. In this
manner, the influence of motor neuron activity in the cerebral cortex is
Hence, impulses travel from the motor cortex via the corticospinal tract
to anterior horns at spinal levels coordinated by the cerebellum and
cerebral cortex. From the anterior horns, lower motor neurons
travel to associated paravertebral muscles. This innervation
increases muscle tonus (secondary muscular spasticity), which pulls
neighboring and distant vertebrae into compensation subluxation
(secondary subluxation). These compensation subluxation may occur
for many reasons. One hypothesis is to allow some mobility for the
biped as fighting the painful muscle spasticity and gravity. A
correlate is to maintain the eyes at near the horizontal.
Unfortunately, a distorted gait or some antalgic position may result.
cerebellum also activates the extra-pyramidal system via a circuit
beginning in the deep cerebellar nuclei. From these nuclei the
neurons continue through the superior cerebellar peduncle to synapse in
the centromedian nucleus of the thalamus. The stimulus from the
thalamus continues to travel via thalamostriate fibers to the basal
ganglia. The basal ganglia sends the impulse via the lenticular
fasciculus, through the prerubral field to synapse with the red nucleus.
The red nucleus sends out two signals. The first travels through
the ventral tegmental decussation via the ruberospinal tract to synapse
at motor centers at the level of the upper cervicals.
provides precise muscle tone for stabilization of movements and
maintenance of normal body orientation in space.20
second signal to leave the red nucleus travels through the substantia
nigra to have an inhibitory effect on the reticular formation located in
the midbrain tegmentum. The effect will inhibit the reticulospinal
and reticulobulbar tracts.21
These tracts synapse with motor nuclei. In this manner smooth
hypermyotomia is maintained and not that of multiple twitch-like
actions. However, the inhibition is not enough to inhibit the
overworked muscles and balance the compensatory spasticity.
It is now
clear that progressive muscular over-exertion may cause increased
contraction of arterial blood vessels, ischemia, metabolites (lactic
acid, P Factor, bradykininn, potassium ions, hydrogen ions and
metabolites formed by the breakdown of muscle) to accumulate in the
tissue spaces, resulting in increased interstitial fluid colloid osmotic
pressure, increased muscle fluid in the interstitial space, increased
muscle stiffness, over-stimulation of nerve endings by the presence of
trapped metabolites, temporary soft tissue acidosis resulting from
lactic acid, pain, muscular spasticity, primary vertebral subluxations
or areas of altered spinal joint dynamics, increased energy through the
cerebellum, thalamic relay, cortical, pyramidal, extra-pyramidal and
reticular systems, general hypermyotomia, neighboring or distant
secondary areas of altered spinal joint dynamics
(secondary subluxations), thus a multi-subluxated vertebral column. This
cyclic system describing subluxations resulting from over-exertion will
be called the "Physio-Somato-Neuro-Somatic System."
D.D. Palmer and H.G. Wells all
were men of great vision. H.G. Wells
wrote of men who would travel to the moon. Almost a century later, man
did walk on the moon. Like Wells, both Hippocrates and
Palmer wrote of concepts that were controversial in their time,
but have become real experiences of people today.
"Physio-Somato-Neuro-Somatic System" describes primary vertebral subluxations occurring as the result of over-exertion.
Furthermore, the system describes the occurrence of primary vertebral
subluxations and their associated secondary compensatory subluxations
which are the direct result of muscular strain and spasticity.
This system is just one more small step among the many giant steps left
in communicating our chiropractic experience in the scientific language
of the 1980's. Of course the future may bring new language, but
we, as professionals, must change, accept new corrections and bend as
the wisdom of science bends in the currents of new knowledge.
1. Chiropractic Health Care, 2nd, Ed, The Foundation for Chiropractic
Education and Research, 1977, P. 14
Samson Wright; Applied Physiology. 10th Ed, Oxford University Press,
1961, p. 19.
Ganong: Medical Physiology, 8th Ed, Lange Medical Publications, 1977, p.
Vernon B. Mountcastle: Medical Physiology 13th Ed, Volume 1, 1974 p.
Wright; Applied Physiology. 10th Ed, Oxford University Press, 1961, p.
6. Vernon B.
Mountcastle: Medical Physiology 13th Ed, Volume 1, 1974 pp 1279-1284
Ibid: p. 1280
edition, W.B. Saunders Company 1976, pp 665
11. Ganong: Medical
Physiology, 8th Ed, Lange Medical Publications, 1977, p. 80.
12. Guyton: 5th edition, W.B.
Saunders Company 1977, p. 262.
i. Best and Taylor; Physiological Basis of Medical Practice, 10th
Ed, Williams & Wilkins Company, 1978, p. 3-216
ii. Vernon B.
Mountcastle: Medical Physiology 13th Ed, Volume 1, 1974 pp 951-952.
iii. Guyton: 5th edition, W.B.
Saunders Company 1976, pp 664-665.
Samson Wright; Applied Physiology. 10th Ed, Oxford University Press,
v. Orten and Neuhaus: Human Biochemistry, 9th Ed, C.V. Mosby
Company, 1975, p. 765.
14. Samson Wright; Applied Physiology. 10th Ed, Oxford University Press,
1961, p. 209
15. Lewis, T.; Pain, The MacMillan
Co., 1943, p, 99
Scott D. Neff: "Neuroanatomy of Vertebral Subluxations, "The ACA Journal
of Chiropractic, Volume 17, No 4, April 1980, p. s-55.
17. Carpenter: Human
Neuroanatomy, 7th edition, Williams and Williams Company, pp .249-252,
Ibid: pp 420 and 430
Ibid: p. 434
Ibid pp 261-264; Figures 10-17, 384-386, 496-511 and 512-514.
Ibid: pp 393-397, 501-503
D. Neff, DC DABCO CFE DABFE FFABS FFAAJTS
shall know the truth, and the truth shall make you free.”John, viii, 32
For Part 1 the Neuroanatomy of Vertebral Subluxation hit this link