Muscle Metabolism: Aerobic vs. Anaerobic

By Thomas Griner

Four different types of muscle fibers will be discussed here. However, only the aerobic slow-twitch fiber and the anaerobic fast-twitch fiber are found in human skeletal muscle. For the purpose of gaining additional insight provided by comparative study, the cardiac muscle fiber and aerobic fast-twitch fiber will also be discussed.

Aerobic means with oxygen. In body metabolism, it also means with mitochondria. The mitochondrial structure acts as a substrate to bring reactants together and catalyze reactions. The structure also helps control and neutralize the radicals, which also occur in oxidative reactions. The mitochondria also produce enzymes, which further catalyze the reactions so that they will occur at body temperature.

Three of the four fibers are aerobic, with the mitochondria in each being different from the other two. The aerobic fast-twitch fiber is really no longer a muscle, but a bag full of mitochondria with a few contractile fibers remaining. The mitochondria in this fiber are one-third the size of those in the aerobic slow-twitch fiber. These smaller mitochondria can only oxidize the components of glucose, not fatty acids or ketones as the larger mitochondria can.

The mitochondria in the cardiac muscle fibers is three times the size of the aerobic slow-twitch fiber (nine times the aerobic fast-twitch fiber) and has the added capability of oxidizing lactic acid back into pyruvic acid and pyruvate back into glucose. The only other organ which contains the largest mitochondria is the liver. The smallest mitochondria appear bright red in color like the myoglobeen, which accompanies it; the intermediate mitochondria are brownish red, and the largest mitochondria are purplish. The presence of large numbers of the largest mitochondria give the heart and liver tissues their purplish color.

The anaerobic muscle fiber contains mitochondrial fragments that produce the enzymes needed to reduce glucose to pyruvate and pyruvate to lactate. In photomicrographs of stained aerobic and anaerobic cells abutted against each other and with a capillary in the corridor between them, the mitochondria of the aerobic fibers are seen bunched near the capillary like moths around a flame, while the anaerobic fiber shows no such activity.

Comparison of aerobic and anaerobic fibers might lead to calling the aerobic ectomorphic and the anaerobic endomorphic. This is because everything other than muscle fibers is concentrated along the periphery of the aerobic fiber, but spread in the interior of the anaerobic fiber.

The mitochondria are naturally at the periphery of the aerobic fiber but are spread in the interior of the anaerobic fiber. The mitochondria are naturally at the periphery, because the oxygen they need can only come from outside the cell. The fatty acid stores are then placed near the mitochondria, because that is where they will be metabolized. The myoglobin needs to be near the periphery and the mitochondria.

Myoglobin has the same red color as hemoglobin and results in these aerobic fibers being referred to as red muscle fibers. The anaerobic fibers have no need for myoglobin since they have no mitochondria and as such are referred to as pale muscle fiber.

Aerobic fibers use large adenosine molecules as energy transporters, with AMP moving out to the mitochondria to be recharged to ATP, then lumbering back to the interior to activate calcium ion release. The mitochondria of the aerobic fibers must also serve the oxidative needs of the anaerobic fibers, so it is busy oxidizing pyruvate as well as fatty acids. (This is why the mix of the two different fibers does not vary much beyond 50/50, even though anaerobic fibers are three to six times larger than aerobic fibers.)

The fat molecular produces almost eight times the energy of a pyruvate molecule, but the mitochondria can metabolize pyruvate nine times faster than fat. In the anaerobic fibers, the large adenosine molecules are locked into the matrix of the sarcoplasmic reticular cisterns next to the calcium ion mechanisms the ATP must activate. Likewise, the glycogeneral stores are located next to the adenosine, which the glycolysis must recharge.

The mitochondrial fragments, which produce the enzymes to catalyze reactions, are also located here. Energy transport is handled by small fast creatine molecules, which can readily pass through the membranes to reach the mitochondria in the aerobic fibers. Just as the mitochondria will selectively metabolize pyruvate ahead of fat, it will also phosphorylate creatine and glucose molecules ahead of AMP.

When a runner reaches a speed of about eight and a half miles per hour, the respiratory quotient rises to one, which indicates no fat metabolism is happening. Speeds above 8.5 mph are produced only by the anaerobic fast-twitch fibers, which can contract three times faster than slow-twitch fibers (25 milliseconds versus 75 milliseconds). The fast-twitch fibers can produce a speed in excess of 25 miles per hour, which is attained in the 100 and 200-meter dashes.

It should also be clear that lower animals that don't have a 50/50 mix of aerobic slow-twitch and anaerobic fast-twitch fibers are in need of aerobic fast-twitch fibers (essentially bags of mitochondria) capable of oxidizing pyruvate from the anaerobic fibers.

The flight muscles of a bird are of necessity mostly all fast-twitch fibers. A photomicrograph shows that out of a sample of 30 fibers, 18 are anaerobic fast-twitch, with the anaerobic fibers being five to nine times larger than the aerobic fibers. If you have ever cut raw chicken or turkey breast, you will probably have noticed the tiny bright red dots located throughout the pale fibers.

The reverse situation exists in the cat soleus muscle, in that it is made up entirely of aerobic slow-twitch fibers. This allows the cat to move with incredibly smooth slow motion when in stealth mode. To provide the quick leap when pounce mode comes, the gastrocnemius is mostly fast-twitch fibers. A sample of 30 cat gastrocnemius fibers reveals seven aerobic slow-twitch fibers, 17 anaerobic fast-twitch fibers, and six aerobic fast-twitch fibers.

This heritage shows up in the human soleus being weighted slightly towards slow-twitch fibers and the human gastrocnemius being weighted slightly toward the fast-twitch, but still close to a 50/50 mix.

Glycolysis provides anaerobic energy by splitting glucose into pyruvate and hydrogen ions. These cannot be oxidized until they reach the mitochondria in the aerobic fibers. The concentration in the anaerobic fibers will rise until the hydrogen free radicals threaten to shut down the process, at which time enzymes trigger the combination of hydrogen with pyruvate to form lactate, which will level off at a concentration high enough to cause a gradient sufficient to drive the lactate into the bloodstream as fast as it is being produced.

This usually produces a 10:1 ratio in favor of lactate to pyruvate. Extremely fast activity can drive the lactate concentration high enough to shut down the process. The 10:1 ratio of lactate to pyruvate is a consequence of the slow clearing of venous blood from the fascicular arrangement of muscle fibers. The actual conversion ratio is one lactate molecule for each pyruvate molecule. The pyruvate travels across to the slow-twitch fiber to be oxidized to carbon dioxide and water. The carbon dioxide and water then become more concentrated, like the lactate waiting to be cleared from the cell.

Venous waste pickup is as important as arterial supply for muscle operation. If the venous drainage is choked down by hypertonic muscles undermining the rhythmic pumping, the arterial blood flow will divert through the shunts so that both supply and pickup will be compromised. The energy contained in the lactate is temporarily lost to the muscle cells when it is dumped into the bloodstream, but upon reaching the liver, four-fifths of the lactate is reconverted back to glucose and returned to the muscles.

When glucose enters the muscle cell, it is phosphorylated by the mitochondrial energy so that the glucose phosphate supplements the creatine phosphate in carrying anaerobic phosphate energy within the cell.

After a period of maximum exercise has depleted the oxygen and anaerobic energy stores of the muscles, only three minutes and two and a half liters of oxygen are required to recharge the creatine to creatine phosphate and AMP to ATP, and to reload the myoglobin with oxygen. However, it takes one hour and eight liters of oxygen for the liver to clear the accumulated lactate. 

Headaches and the Unresponsive Atlas Subluxation

By Joseph D. Kurnik, DC

This situation presents itself clinically as a failure to most attempts for correction. The patient presents with suboccipital pain on the left or right side. There is often radiating pain into the left or right face, especially the forehead, temple, or eye region.

Examination by static, visual and motion analysis reveals a C-1/C-2 articulation that is fixated in rotation, and lateral flexion on the left side. This means that the left side of C-1, when rotated to the right, exhibits restriction. C-1 also is restricted in lateral flexion on the left. The right side palpates freely.

When the doctor tries to adjust the atlas from the left side, nothing happens: no sound, no release, no correction, and probable increased soreness. You try again, but the atlas remains tight and unmoveable, yet clearly a hypomobile fixation. The title of this article calls this a subluxation, but it is actually a subluxation and fixation. The atlas is clearly malpositioned, as determined by static and visual analysis. To confirm this, while the patient is supine, press over the atlas lying under the SCM, bilaterally. You can feel the more anterior position and resistance of C-1 on the right side. The left side of C-1 from the anterior will palpate with less resistance.

Stop banging on the atlas and go to the right side. Do not bang on the right side of C-1, which can be very dangerous under any condition. Evaluate the ability of the occiput on the right side to rotate to the left, laterally flex on the right, and extend during rotation to the left. A common finding in these C-1 unresponsive headaches is a right-sided occipital fixation pattern. Occasionally, you may encounter a left-sided occiput rotation fixation. The most common finding with unresponsive left C-1 problems and responsive C-1 left fixations is a right-sided fixation of occiput on C-1.

You can encounter some combination of occipital problems involving rotation, lateral bending and extension. With one adjustment, you can free all the restriction problems just by incorporating correctional vectors to your corrective thrust. To rectify the extension or backward nodding problem, incorporate occipital extension in your thrust, combined with rotation. If you do not combine extension with rotation, correcting extension alone will be very difficult and can feel like you are punching the patient.

The result of correction to the occipital fixation dysfunction will be a release to atlas motion, overall cervical increased movement, and a gradual reduction in symptoms. "Migraine" type headaches often are associated with this right-sided occipital fixation pattern. Even if C-1 is responsive to adjusting on the left side, you commonly still encounter the right-sided occipital fixation. You also may encounter a simultaneous lateral bending and extension hypomobile fixation at C-2/C-3 level. You may correct this with a simultaneous contact at the occiput and C-2. The corrective thrust induces some rotation, lateral bending, and extension simultaneously. The rotation is not full, rotation and does not take C-2 to completion, which is necessary. C-2 will tend to favor rotation from right to left, and full rotation of C-2 from right to left can exacerbate the headache.

In summary, I advocate the following forms of analysis: 

• visual analysis, especially supine; observe position of SCM tissue bilaterally;
• static palpation while supine to the posterior and anterior aspects of the cervical spine bilaterally;
• static palpation of each cervical level arteriorly/posteriorly (joints and segments); extend palpation (tissue challenge); then push on tissues to feel for resistance. You will be surprised when you combine the palpation and challenge to anterior and posterior elements.
• motion palpation applied to the arterior/ posterior sides of the cervical spine in the supine position. This is easier and has more clear results than doing it seated. In this procedure, you have to bring each cervical segment and joint to tension, and beyond, with posterior and anterior contacts. There are two ways to do this, but a description of the technique has to be a separate article.
• Motion palpation to the anterior and posterior aspects of the occiput.

I guarantee that if you take the time to be more thorough in your palpatory examination of the cervical spine, you will become more accomplished in your diagnosis and understanding of cervical mechanics and patterns, including the occiput. Even beyond this, you will discover things that you have been doing wrong and must to change. You will be surprised at what you find if you force yourself to become more thorough, examining every angle of motion. You may not agree with my findings. You may say, "I've been practicing for 20 years and have had no problems, so why should I change?" Just try to be more thorough and see for yourself. 

What's Triggering That Point?

Why you should avoid random treatment of trigger points (part 1).

By Warren Hammer, MS, DC, DABCO

An orthopedic friend recently saw a patient of mine. He felt an injection of a trigger point (TP) at the upper trapezius and surrounding areas was necessary, since that was the patient's area of chief complaint and there was a tender, radiating nodule.

I told him I hoped the injection would help, but I did not feel random treatment of a local area of pain would necessarily treat the cause of the problem. After all, the word random has many synonyms including chance, haphazard, arbitraryand unsystematic.

One of the problems in dealing with local functional pain is that the area of complaint is not necessarily the causal location. The sage statement by Karel Lewit, MD, a leader in the soft-tissue movement, went something like: He who only treats the site of pain is lost. An important question is: Could this painful site be a compensation for an original problem elsewhere? Could it be that a chronic low back pain is really a compensation for a sprained ankle 10 years ago? Could a shoulder or elbow pain that occurs for no apparent reason be due to a wrist fracture that occurred when the patient was 5 years old?

Alleviating a painful point may relieve symptoms, but have nothing to do with causation; and as many of us find, the points and symptoms will recur. The pain that "appears for no apparent reason" is often the clue that should make you think of other areas.

Could a more organized method of treating these tender points help the patient for longer periods of time, or for that matter, completely cure the problem? Travell and Simons told us about these hyperirritable areas of taut bands that may radiate to particular areas. They were talking about the myofascial pain syndrome and trigger points. Of course, many of the points that have to be treated do not have to fit the definition of a TP.

Connecting TPs to Fascia

In their text, Travell and Simons offer no description of the chief connecting part of our body, the fascial system. They rarely mention TPs that may originate in fascia.¹They quote Kellgren,² who, after injecting saline solution in the fascial epimysium of the gluteus medius, realized referred pain several cm. distally. Travell identified mostly muscular areas to treat, but of course, Travell's text was written in 1983, and Killgren found the epimysial point in 1938.

The works of Travell and Simon have provided a great contribution to the world of soft tissue. They astutely reported that myofascial referred pain did not follow dermatomal, myotomal or sclerotomal patterns of innervation. Areas of referred pain can be important in our analysis of where to treat. Treating a knee area may refer to a leg area requiring treatment; it may refer to an antagonistic area requiring treatment; when it refers to the area of complaint it is regarded as a very significant possible causative area and may indicate the most important fascial chain (read below).

Connective tissue has its own system of pain referral that may or may not be tied up with the central nervous system. When mechanical load is applied to abnormal soft tissue, the area of referral is in a non-segmental pattern. There are a variety of hypotheses to explain it, such as the "connective tissue theory"³ and the "barrier-dam" theory.⁴

The latter theory states that afferent sensitive increased nociceptive peripheral nerves might become entrapped in local restrictive areas, causing hyperexcitation of nerves between the distally referred pain area and the local muscular zone of tenderness. "The primary pathogenesis of referred muscle pain is likely to be a peripheral sensitization with additionally a central modulation and not vice versa."⁴

Giamberardino⁵ states: "Referred pain / hyperalgesia from deep somatic structures is not explained by the mechanism of central sensitization of convergent neurons in its original form, since there is little convergence from deep tissues in the dorsal horn neurons." The absolute cause of non-segmental pain referral is still not entirely known. It is thought that even changes in cell shape and forces among cells can affect adjoining cells and transmit information. Stretching the fibroblast could be supplying information by way of gap junctions to other fibroblasts, transmitting information about pain and peripheral motor coordination.

Chen⁶ states that neurological (electrochemical) transmission is slower, localized and context independent compared to mechanical force distribution. Coordination by mechanical force distribution is faster, both locally and globally; and above all, occurs in a context-sensitive manner. Therefore, it is possible that stressing a specific region of the deep fascia can be transmitted over a distance by cell-to-cell communication.

Focusing on Fascial Points

Abbott, et al.,⁷ theorize that connective tissue (CT), especially fibroblasts, are part of a whole-body, cell-to-cell, communication-signaling network. They state that fibroblasts exhibit active cytoskeletal responses within minutes of tissue lengthening. Analogous cell-to-cell signaling involving calcium and/or ATP may exist within CT and may be accompanied by active tissue contraction or relaxation. "One can envisage a whole-body web of CT involved in a dynamic, body-wide pattern of cellular activity fluctuating over seconds to minutes reflecting all externally and internally generated mechanical forces acting upon the body."⁷ The chief cell in the fascia is the fibroblast.

According to the literature, it appears that treating particular related fascial points is more effective than just treating random painful sites. It was found that in treating plantar fasciitis, results were better if the gastrocnemius / soleus) trigger points and heel region were treated, rather than the heel region alone.⁸

Most of us are aware that a variety of points must be treated when using soft-tissue methods. The questions that must be answered in this regard are:

• Is there a particular sequence of points, perhaps extending, for example, from the wrist to the elbow to the shoulder to the neck?
• Are these points related in any way to our soft-tissue myofascial anatomy?

References

1. Travell JG, Simons DG. Myofascial Pain and Dysfunction: The Trigger Point Manual.Williams & Wilkins, Baltimore, 1983:19-20.
2. Kellgren JH. Observations on referred pain arising from muscle. Clin Sci, 1938;3:175-190.
3. Han D-G. The other mechanism of muscular referred pain: The "connective tissue" theory.Med Hypotheses, 2009;73:292-295.
4. Farayn A. Referred muscle pain is primarily peripheral in origin: the "barrier-dam" theory.Med Hypotheses, 2007:68(1):144-50.
5. Giamberardino MA. Referred muscle pain/hyperalgesia and central sensitisation. J Rehabil Med, 2003 May;(41 Suppl):85-8.
6. Chen CS. Mechanotransduction – a field pulling together? J Cell Sci, 2008;15(121):3285-3292.
7. Abbott RD1, Koptiuch C, Iatridis JC, et al. Stress and matrix-responsive cytoskeletal remodeling in fibroblasts. J Cell Physiol, 2013 Jan;228(1):50-7.
8. Moghtaderi A, Khosrawi S, Dehghan F. Extracorporeal shock wave therapy of gastroc-soleus trigger points in patients with plantar fasciitis: a randomized, placebo-controlled trial. Adv Biomed Res, 2014 Mar 25;3:99.

Fascial Tension Headaches

By Warren Hammer, MS, DC, DABCO

Tension-type headache (TTH) is the most common form of primary headache in the general population and like all headache complaints, requires an adequate case history to exclude other possible causes falling under the headings of cervicogenic, vascular migraine or cluster-type; organic vascular types such as subarachnoid hemorrhage, subdural hematoma, arterial hypertension, intracranial neoplasm, meningitis and infection; allergic substances; metabolic disorders; and extracranial causes such as the teeth and TMJ, among many others.¹

Tension-type headache is essentially defined as a bilateral headache of a pressing or tightening quality without a known medical cause. A tension headache is generally a diffuse, mild to moderate pain that's often described as feeling like a tight band around the head or a big weight over the head or shoulders. It is seldom pulsating unless the pain is severe.²

A non-pulsating, pressing pain is the most common complaint plus tenderness of the scalp, especially in the temporal areas. Characteristics of TTH from theInternational Classification of Headache Disorders are:³

• Episodic infrequent: < 1 day per month; episodic frequent: 1-14 days; chronic: > 15 days.
• Headache lasting from 30 minutes to seven days in duration.
• At least two of the following pain characteristics: pressing / tightening (non-pulsating) quality; mild or moderate intensity (may inhibit, but does not prohibit activities); bilateral location; and no aggravation by walking stairs or similar routine physical activity.
• Both of the following: no nausea or vomiting (anorexia may occur); and photophobia and phonophobia are absent, or one but not the other is present.

Any headache that displays a worsening pattern should raise a red flag, as should a change in characteristics such as nausea or vomiting and abnormal neurological findings.²

Both pharmacological and nonpharmacological treatments such as electromyographic (EMG) biofeedback, cognitive-behavioral therapy, relaxation training, trigger-pointtherapy, physical therapy and acupuncture have produced symptomatic results.

Currently, I am helping to edit a new text on the fascial system based on the research of Carla Stecco, MD. The book represents years of research by her on the fascial system. Dr. Stecco, who recently presented at the recent International Fascial Conference in Vancouver, writes in her upcoming text: "A common cause of cephalalgia is excessive tension of the temporalis muscle. A large percentage of the muscular fibers of the temporalis insert into the underside of the deep temporal fascia that is in continuity with the epicranial fascia. If the temporalis muscle becomes hypertonic the epicranial fascia becomes overstretched. This could activate the free nerve endings in the fascia, resulting in headache-like symptoms."

Pericranial myofascial tenderness recorded by manual palpation is a significant abnormal finding in many patients with TTH⁴ and has been recorded by pressure pain detection and tolerances in cephalic and extracephalic locations with an electronic pressure algometer.⁵ In TTH, there are also found many myofascial trigger points. It is possible that sensitization of myofascial nociceptors could be responsible for pain.

Sensitization of pain pathways in the central nervous system due to prolonged nociceptive stimuli from pericranial myofascial tissues might be responsible for prolonged pain. Significantly lower pressure pain detection thresholds and tolerances were found in all the examined locations in patients with chronic tension-type headache with a muscular disorder compared to those without a muscular disorder.⁴ It appears that disruption of cranial fascia may be causative regarding tension headaches.

Soft-tissue techniques such as fascial manipulation reduce myofascial restrictive areas by restoring normal gliding of the deep fascia with the underlying muscular fibers. This is thought to restore normal sensory stimulation and can be an effective treatment for chronic tension headaches.⁶ This may also explain the effectiveness of other types of treatment that have a fascial effect, such as Graston, active release, structural integration, muscle energy and others.

It is therefore apparent that the fascial system must be considered in TTH, and also in other types of headaches such as migraine and cervicogenic types. Current evidence that spinal manipulation alleviates tension-type headaches is encouraging, but inconclusive due to the low quantity of available data preventing a firm conclusion.⁷

A tension headache is not considered a cervicogenic-type headache. Cervicogenic headache (CH) originates from disorders of the neck and is recognized as a referred pain in the head. Freese, et al.,⁸ summarize this type of headache as follows:

"Primary sensory afferents from the cervical roots C1-C3 converge with afferents from the occiput and trigeminal afferents on the same second-order neuron in the upper cervical spine. Consequently, the anatomical structures innervated by the cervical roots C1-C3 are potential sources of CH. In normal volunteers, the painful stimulation of different anatomical structures of the neck produced headache. In CH, particular structures have been selectively anesthetized in order to identify possible sources of pain. In summary, CH can originate from different muscles and ligaments of the neck, from intervertebral discs, and, particularly, from the atlanto-occipital, atlantoaxial, and C2/C3 zygapophyseal joints. Diagnosis of CH should adhere strictly to the published diagnostic criteria to avoid misdiagnosis and confusion with primary headache disorders such as migraine and tension type headache."

Cervicogenic headache as differentiated from TTH is usually a unilateral headache of fluctuating intensity increased by movement of the head and typically radiating from occipital to frontal regions.

Finally, sometimes it is difficult to differentiate common migraine from cervicogenic headaches since there are similar symptoms, such as being often unilateral and more common in females; but for cervicogenic there is usually a reduced range of neck motion or pain with external pressure over the greater occipital C2 nerve root and possible ipsilateral shoulder / arm pain. Typical migraine symptoms include nausea, vomiting, photophobia and phonophobia, which may occur in cervicogenic headache, but are not as common.⁹

References

1. Mueller L. Tension-type, the forgotten headache. How to recognize this common but undertreated condition. Postgrad Med, 2002 Apr;111(4):25-6, 31-2, 37-8.
2. Bigal ME, Lipton RB. Tension-type headache: classification and diagnosis. Current Pain and Headache Reports, 2005;9:423-429.
3. International Statistical Classification of Diseases and Related Health Problems, 10th revision, Volume 2. World Health Organization, December 2004.www.who.int/classifications
4. Sandrini G, Antonaci F, Pucci E, et al. Comparative stud with EMG, pressure algometry, and manual palpation in tension-type headache and migraine. Cephalalgia, 1994;14:451-457.
5. Jensen R, Bendtsen L, Olesen J. Muscular factors are of importance in tension-type headache. Headache, 1998 Jan;38(1):10-7.
6. Stecco L, Stecco C. Fascial Manipulation: Practical Part. 2009, Piccin Nuova Libraria S.p.A., Padova. www.piccin.it
7. Posadzki P, Ernst E. Spinal manipulations for tension-type headaches: a systematic review of randomized controlled trials. Complement Ther Med, 2012 Aug;20(4):232-9.
8. Frese A, Schilgen M, Husstedt IW, Evers S. [Pathophysiology and clinical manifestation of cervicogenic headache.] (Article in German) Schmerz, 2003 Apr;17(2):125-30.
9. Sjaastad O, Bovim G. Cervicogenic headache. The differentiation from common migraine. An overview. Funct Neurol, 1991 Apr-Jun;6(2):93-100.

Physiological Effects of Therapeutic Massage

By Warren Hammer, MS, DC, DABCO

Many chiropractors either perform some type of massage on their patients or have a massage therapist in their office.

The term therapeutic massage (TM) is a general, nonspecific term referring to any type of massage, from superficial to deep, that may have a healing effect. Most massage therapists¹ "train in multiple programs and therapies and there is high variability in the training programs and in what therapies practitioners choose to learn."² Methods of massage include, among others, effleurage, petrissage, friction and tapotement. TM also can refer to most hands-on therapies including fascial manipulation, Graston, structural integration, active release, Swedish massage and others.

Claims regarding the effects of TM include changes in hormones, neurotransmitters, blood flow and cortisol, among others. However, as with most other mechanical pressure methods used on humans, there is a paucity of research supporting its efficacy, optimal treatment parameters and underlying physiologic responses.

Recent studies have added to the body of knowledge regarding the effects of mechanical load, showing definite physiological and clinical changes^2-3 related to TM. An important effect of TM is thought to be its effect on peripheral blood flow. While skin temperature correlates with skin blood-flow studies, skin probes and their effect on the skin are questionable.⁴ A recent study using dynamic infrared thermography² compared the effects of a 20-minute massage that included a deep muscle combination of friction, gliding (effleurage), kneading (petrissage), direct pressure and passive stretching to the neck and shoulders versus light touch (just the hands placed in contact with the skin) or a control scenario in which the patient rested quietly in the treatment position.

Light touch produced some changes in temperature, but the most significant changes occurred with the deeper massage treatment. What is most interesting is that the areas not massaged (posterior right arm, C6 to C8 dermatomes, and thoracic middle back T1 to T8 dermatomes) showed an increase in skin temperature and peripheral blood perfusion similar to the areas massaged, indicating a possible neural as well as a circulation component. The areas receiving a deeper massage showed increased temperature for 35 minutes and remained above baseline levels after 60 minutes.

One of the effects of deep massage is temperature elevation that changes hyaluronic acid molecules, which are responsible for the gel phase causing tissue restriction. The increase in temperature with associated pressure changes the gel to a fluid phase and creates the necessary tissue sliding. One study found that massage to a depth of between 1.5 cm and 2.5 cm caused changes in muscle temperature significantly greater than ultrasound.⁵

Some of the same authors of the above study submitted another significant paper on deep massage that recently appeared in Manual Therapy.³ This study compared the same three groups as the previous study: deep massage and light touch over the neck and upper trapezius areas, along with a control group. This time, the authors measured flexor carpi radialis α-motor neuron pool excitability (Hoffmann's reflex, otherwise known as the H-reflex), electromyography (EMG) signal amplitude of the upper trapezius during maximal muscle activity, and cervical ROM to help assess physiological changes and clinical effects of deeper massage compared to light touch.

The H-reflex is similar to the stretch reflex (knee jerk reflex), but differs in that it bypasses the muscle spindle and is used to assess monosynaptic reflex activity in the spinal cord. Electrical stimulation causing the H-reflex measures the efficacy of synaptic transmission as the stimulus travels along the Ia fibers, through the dorsal root ganglion, and is transmitted across the central synapse to the anterior horn cell, which fires it down along the alpha motor axon to the muscle. This measurement can be used to assess the response of the nervous system to various neurologic conditions, musculoskeletal injuries, application of therapeutic modalities, pain, exercise training, and performance of motor tasks.

In this study,³ even though the upper trapezius area was massaged, the H-reflex for this area is difficult to elicit, so the authors checked the motor neuron pool excitability in an outlying area that was not massaged: the flexor carpi radialis muscle (FCR), which generates a reliable reflex. They reasoned that massaging the trapezius and neck area would affect the cervical and brachial plexus and the median nerve, which innervates the FCR.

The H-reflex test did show a decrease in FCR α-motor neuron pool excitability compared to the light-touch and control groups. The fact that there was a decrease in neuron excitability in a non-massaged area suggests the possibility that massage was producing a centralized effect on the nervous system, affecting spinal-cord response in another area. This same neuronal possibility was expressed in the change in peripheral blood perfusion in non-massaged areas in the previous study.²

Another finding was the decrease in EMG signal amplitude in the upper trapezius muscle with deep massage, which did not occur with light touch or control. The EMG change was probably due to the decrease in -motor neuron pool activation, which has an influence on electrical activity. Additionally, compared to light touch and control, deep massage increased ROM in all cervical directions.

One caveat is that all of the studies were performed on people without known pathology, but the neurological implications of deep massage affecting circulation and the nervous system are important. The fascial manipulation hypothesis is based on the release of restricted fascia that houses mechanoreceptors and proprioceptors, thereby influencing the CNS' effect on myofascia.

Everyone who seriously uses deep massage is aware of positive changes. Science may finally be proving why there are clinical results.

References

1. Porcino AJ, Boon HS, Page SA, Verhoef. Meaning and challenges in the practice of multiple therapeutic massage modalities: a combined methods study. BMC Complement Altern Med, 2011;11:75.
2. Sefton JM, Yarar C, Berry JW, Pascoe DD. Therapeutic massage of the neck and shoulders produces changes in peripheral blood flow when assessed with dynamic infrared thermography. J Alterative & Complementary Med, 2010;16(7):723-732.
3. Sefton JM, Yarar C, Carpenter DM, Berry JW. Physiological and clinical changes after therapeutic massage of the neck and shoulders. Manual Therapy, 2011;16:487-494.
4. Pascoe DD, Mercer JB, de Weerd L. Physiologies of Thermal Signals. In: Bronzino JD, editor.Medical Devices and Systems. 3rd Edition. Boca Raton, FL: CRD Taylor & Francis, 2006:21-7.
5. Drust B, Atkinson G, Gregson W, et al. The effects of massage on intra muscular temperature in the vastus lateralis in humans. Int J Sports Med, 2003;24:395-399.

Gua Sha: Another Form of Mechanical Load

By Warren Hammer, MS, DC, DABCO

Every technique that creates compression or tensile stretch to soft tissue creates a mechanical load that is necessary for tissue change. Gua sha represents another form of mechanical load on soft tissue that claims healing results and, like all other soft-tissue methods, begs for research to prove its value.

Arya Nielsen, PhD, adjunct faculty in the Department of Integrative Medicine at New York Beth Israel Medical Center,Continuum Center for Health & Healing, and a strong proponent of gua sha, wrote an interesting article in the January 2009 issue of the Journal of Bodywork and Movement Therapies (JBMT).1 She states that often the literature incorrectly describes the results of gua sha as causing battery trauma, bruising, burns, dermatitis, pseudo bleeding and even hematoma.

Although gua means to "scrape" or "scratch" in Chinese, the skin always remains intact and there are no abrasions. Sha represents the "transient therapeutic petechiae." The extravasated blood appears as red macula and fades to ecchymosis immediately, blending into an ecchymotic patch. The scraping reveals blood stasis and its use removes blood stagnation that is considered pathogenic, thereby promoting normal circulation and metabolic processes. Gua sha lets blood from the tissue and is not let from the skin.²

This method originated in Asia and is used today in East Asian medicine and by acupuncturists. Nielsen mentions its use for colds, flu, fever, heatstroke, asthma, bronchitis and emphysema, as well as musculoskeletal problems including fibromyalgia to severe strain. Improving blood stasis and sha may even be significant in asymptomatic subjects who are considered healthy.

A recent study using laser Doppler imaging was used to make sequential measurements of the microcirculation of surface tissue before and after gua sha treatment³ in order to relieve pain. The result was a fourfold increase in microcirculation for the first 7.5 minutes following treatment and a significant increase in surface microcirculation during the entire 25 minutes of the study period following treatment. There was a decrease in myalgia not only locally but also in sites distal to the treated areas. The authors stated that the distal area of relief was not due to a distal increase in microcirculation and asserted, "There is an unidentified pain-relieving biomechanism associated with gua sha."

Recent theories based on tensegrity and the fascial continuum help to explain distal results from localized mechanical load. Ingber, who has written much on our tensegrity structure,⁴demonstrates how living cells and tissues sense and respond to mechanical stresses and in the rearrangement of the structure become mechanochemical transducers, whereby mechanical signals create chemical responses affecting local and distal parts of our structure.

Fibroblasts are the chief cell in the extracellular matrix and reproduce the extracellular matrix upon being loaded; it is thought by Langevin, et al.,⁵ that the existence of a cellular network of fibroblasts within loose connective tissue may have considerable significance, as it may support as-yet unknown bodywide cellular signaling systems. She states that fascia may serve as a bodywide mechanosensitive signaling system with an integrating function similar to the nervous system. Regarding gua sha and GT, increasing the microcirculation may stimulate platelets which release growth factors related to the healing of tissue.

Graston Technique (GT) has been compared with gua sha, and I have even heard some say that GT adopted the gua sha concept. GT was initially used on a postsurgical knee. It is extremely doubtful that the discoverers were at all familiar with gua sha, but even if they were, the GT application is significantly different. GT research has been directed toward the musculoskeletal system and its effect on various soft-tissue conditions. New studies are continually appearing demonstrating how it may be affecting soft tissue. It has its own protocol and uses instruments of different weights, shapes, and sizes to conform to the bodily contours. Its stainless-steel vibratory effect is used to detect restricted areas after functional tests are performed to determine the involved location.

While both methods can create petechiae, the stroking is not performed in the same manner. GT often achieves results without creating any petechiae at all. GT uses at least seven types of strokes, while gua sha repeats a stroke in one direction about 4-6 inches long specifically to create "therapeutic" petechiae.¹ A variety of instrument angulations and pressures may be used in GT depending upon the area of the body treated.

Doctors trained in both methods realize the vast differences. Both methods have their place and there is some obvious overlap, but the differences between the methods are significant. At present, all soft-tissue loading methods are still in their infancy regarding research as to how they affect our structure and function. Einstein referred to a unifying theory of the universe. Hopefully, there might someday be one for soft tissue.

References

1. Nielsen A. Gua sha research and the language of integrative medicine. JBMT, January 2009;13,63-72.
2. Nielsen A. Gua Sha: A Traditional Technique for Modern Practice. Edinburg: Churchill Livingstone, 2002.
3. Nielsen A, Knoblauch N, Dobos G, et al. The effect of gua sha treatment on the microcirculation of surface tissue: a pilot study in healthy subjects. EXPLORE: The Journal of Science and Healing, September 2007;3(5):456-66.
4. Ingber DE. Tensegrity: the architectural basis of cellular mechanotransduction.Ann Rev Physeal, 1997;59:575-99.
5. Langevin H, Cornbrooks CJ, Taatjes DJ. Fibroblasts form a body-wide cellular network. Histochem Cell Biol, 2004;122:7-15.

Fascial Thickening Is Responsible for Musculoskeletal Pain

By Warren Hammer, MS, DC, DABCO

An important study in the fascial world by Langevin (2009)¹ proposed that people with chronic and recurrent low back pain had 25 percent greater fascial thickness than a low back pain-free group.

Helene Langevin, MD, is a researcher at the University of Vermont who devotes a considerable amount of time studying connective tissue. She concluded her study by stating: "Increased thickness and disorganization of connective tissue layers may be an important and so-far neglected factor in human LBP pathophysiology."

She is not alone in her findings. Another study in Skeletal Radiology, 2005,² found that pathological Achilles tendonsshowed increased thickness and 89 percent were painful.

Antonio Stecco, MD, recently completed an unpublished study³ using ultrasonography on chronic (longer than 3 months' duration) neck pain patients, evaluating fascial thickness in the distal third of the SCM and scalenus medius. The deep fascia in both muscles were thicker due to the increased amount of loose connective tissue between the layers of the deep fascia (usually three layers) and the loose connective tissue between the deep fascia and the muscle.

There was a correlation between the intensity of the pain and the thickness of the fascia compared to the control patients. The dense-collagen type I fibers remained the same, while the loose connective tissue demonstrated increased GAGs and hyaluronic acid. (Figure 1) The entanglement ofhyaluronic acid (HA) molecules is the apparent cause of increased stiffness and decreased articular ROM.^4-5 (Figure 2)

According to Matteini, et al, "These chain-chain interactions were reported to be reversibly disaggregated by an increase in temperature or by alkalization." Moreover, "Recent infrared spectroscopy studies have suggested the formation of three-dimensional superstructures of HA chains stabilized by water bridges. This water-mediated supramolecular assembly was shown to break down progressively when the temperature was increased to over 40° C, in accordance with previous MRI observations."⁶

The presence of abnormal HA finally explains many of the fascial treatment explanations whereby pressure against tissue allows a "release" of the area from a gel to a solid. But to change HA entanglements, a major requirement is to increase the temperature several degrees. This might also explain an effect of moist heat. The retention of HA after exercise, as well as its endomysial location, is in accordance with the concept that HA is a substance that is present to lubricate and facilitate the movements between the muscle fibers.³

Besides the thickening of fascia beneath the deep fascia and muscle, there may be thickening between the superficial and deep fascia, and the intramuscular fascia surrounding perimysium and endomysium. According to the principles of fascial manipulation, it is essential that there be a gliding of the fascial system around and within the muscular tissue;⁷ otherwise there will be abnormal proprioception, incoordination of muscle function and pain. Graston Technique and deep friction massage are ideal methods to provide the necessary tissue compression and heat for these types of lesions.

References

1. Langevin HM,Stevens-Tuttle D, Fox JR, et al. Ultrasound evidence of altered lumbar connective tissue structure in human subjects with chronic low back pain. BMC Musculoskeletal Disorders, 2009;10:151.
2. Richards PJ, Win T, Jones PW. The distribution of microvascular response in Achilles tendonopathy assessed by color and power Doppler. Skeletal Radiol, 2005 Jun;34(6):336-42.
3. Stecco A. "Evaluation of the Role of Ultrasonography in the Diagnosis of Myofascial Neck Pain." Department of Physical Medicine and Rehabilitation, University of Padua, Italy, 2011.
4. Piehl-Aulin K, et al; Hyaluronan in human skeletal muscle of lower extremity: concentration, distribution, and effect of exercise. J Appl Physiol, 1991 Dec;71(6):2493-8.
5. Stecco A. Slide presentation on the physiology of fascia. Fascial Manipulation Seminar, Part I, Las Vegas; Feb. 17-19, 2012.
6. Matteini P, et al. Structural behavior of highly concentrated hyaluronan.Biomacromolecules, 2009 Jun 8;10(6):1516-22.
7. Stecco L, Stecco C. Fascial Manipulation Practical Part. Piccin, Padova, Italy, 2009.

Soft-Tissue Treatment Is Another Form of Exercise

By Warren Hammer, MS, DC, DABCO

Physical activity restores our body by way of mechanical loading. Mechanical loading is the crux of many methods of soft-tissue treatment.

Mechanical loading by a practitioner is a form of physical activity performed on a patient.

Mechanical loading is the principal way our body maintains itself, especially with regards to tendons, ligaments, bone, muscle and fascia. Lack of mechanical loading results in atrophy and eventual cell death. Years ago, anyone with acute lower back pain was sent to bed for a week. We now know that as soon as a patient can move with minimal discomfort, they should get out of bed and attempt the movement – i.e., mechanical loading. Thus, just rubbing someone’s skin or deeper tissues is mechanical loading that may be considered a localized form of exercise.

The literature is replete with studies on mechanical loading and its resultant effects on the extracellular matrix (ECM), especially connective tissue and its collagen, tissue structure maintenance, release of growth factors, metabolic activity, protein synthesis, cell growth and survival, circulation, and gene expression. This is only a partial list of factors related to the mechanical load created by methods such as Graston, fascial manipulation, acupuncture and others.

Cell proliferation requires cell spreading and exertion of force on the ECM. Even internally, mechanical forces associated with blood flow play important roles in the acute control of vascular tone, the regulation of arterial structure and remodeling, and the localization of atherosclerotic lesions.¹ It is hypothesized, for example, that "stress concentration" on the walls of arteries due to arterial pressure and accompanying stretch relates to the localization of atherosclerotic plaques in particular arterial areas.² So, mechanical forces that are crucial to the regulation of cell and tissue morphology and function could have both positive and negative effects (overuse, trauma, etc.)

In order for mechanical load to exert its effects, it is necessary for a process of mechanotransduction to occur, whereby stressed cells convert mechanical stimuli into chemical responses. The description as to how all this works is very complicated, but certain terminology should be part of our lexicon.³ In the field of biochemistry, a receptor is a molecule most often found on the surface of a cell, which receives chemical signals originating externally from the cell. Through binding to a receptor, these signals direct a cell to do something; for example, to divide or die, or to allow certain molecules to enter or exit.

Receptors are protein molecules embedded in the plasma membrane (cell surface receptors), or the cytoplasm or nucleus (nuclear receptors) of a cell, to which one or more specific kinds of signaling molecules may attach. A molecule that binds (attaches) to a receptor is called a ligand, and may be a peptide (short protein) or other small molecule, such as a neurotransmitter, a hormone, a pharmaceutical drug or a toxin. A ligand is a signal-triggering molecule, binding to a site on a target protein (receptor).

Numerous receptor types are found within a typical cell and each type is linked to a specific biochemical pathway. Each type of receptor recognizes and binds only certain ligand shapes (an analogy to a lock and key, with the lock representing the receptor and the key, its ligand). Hence, the selective binding of a specific ligand to its receptor activates or inhibits a specific biochemical pathway.

An important receptor is called an integrin; it connects the inner structure of the cell (cytoskeleton) with its surrounding ECM. Integrins sense mechanical forces (stretch and fluid flow) and transmit mechanical stresses across the plasma membrane into the cell. By regulating signaling pathways, they transduce physical forces into chemical signals.

Not only do integrins perform this outside-in signaling, but they also operate in an inside-out mode. Thus, they transduce information from the ECM to the cell, as well as reveal the status of the cell to the outside, allowing rapid and flexible responses to changes in the environment. Integrins are the sensors of tensile strain at the cell surface and play a crucial role in linking the ECM to the cytoskeleton. Mechanical loading creates tensile strain, among other things.

The concept of the receptor-ligand interaction is one of the most basic in all of biology. It is a key element to the functioning of all biological systems. It allows neighboring and distant cells to communicate with each other. One cell may have a receptor in its membrane and when it binds to a matching ligand on a neighboring cell, the receptor performs some action. Typically, this action is to take an existing protein and modify it in some way; to either activate or deactivate it.

It appears that the acupuncture theory of chi and "vital energy" can now be explained by the effect of mechanical load on points located in the fascial system, resulting in a receptor-ligand interaction. Both physical activity and the laying on of hands and/or instruments are stressing and exciting this cellular interaction. It remains for the clinician who uses mechanical load on soft tissue to continually improve their skill by determining – through trial and error, and controlled studies – exactly where to put their hands, and to measure whether the loading of a particular area will improve function.

References

1. Davies PF. Flow-mediated endothelial mechanotransduction. Physiol Rev, July 1995;75(3):519-560.
2. Thubrikar MJ, Robicsek F. Pressure-induced arterial wall stress and atherosclerosis. Ann Thorac Surg, 1995;59:1594-1603.
3. Description of ligand, receptor and integrin. From Wikipedia, the free encyclopedia.

The Subluxation - More Than a Single Vertebral Misalignment

By William Shepherd

The concept of a subluxation as a single vertebra out of alignment with the vertebra above and below it is well-accepted within our profession. However, it is not accurate. When stress or injury occurs in one area of the spine, the whole spine becomes involved in the process of adaptation to that injury or stress.
Muscles-from the toes to the skull-are involved in this adaptive process. This has driven us into divisiveness that should not have happened, as most researchers have concentrated on one element in this adaptive process, and found conflict with other researchers who have concentrated on other elements. We have also developed a variety of techniques that have concentrated on adjusting according to the findings their research has yielded. Thus, we have multiple techniques, with everything from Basic to Grostic being used with effectiveness. These techniques all deal with some portion of this complex total-body adaptive mechanism, and would not be in conflict if we understood this process better. My attempt here is to shed some light on this process.

My particular area of inquiry has been in the study of motion in joints; the muscles involved in that motion; how motion varies from normal when a subluxation is present. That variation from normal is, in my opinion, the only way a subluxation may be properly assessed. Any technique that normalizes motion in joints and increases muscle tone throughout the body is an acceptable technique.

The next question is, "What is the definition of normal mechanical function, and how may it be assessed accurately?" Some have defined a normal spine as one that shows no misalignment on an x-ray and little, if any, curvature. This would be true if our spines had not had to adapt to strains so severe that self-correction did not occur in a short span of time after the trauma. Unhappily, most people ignore discomfort until it becomes too painful to tolerate. During this interval, adaptation can reshape the muscles, ligaments and disc tissues to better accommodate the distress. If accommodation has been successful and pain is decreased, and nothing is done to assess the cause of the prior discomfort, the body accepts the reshaping of the spine. Thus a misalignment shows up on the x-ray, which may be very difficult (if not impossible) for a return to normal alignment.

However, many techniques do use misalignment as the way to adjust a subluxation with too much success for me to argue that it is wrong. On the other hand, we cannot x-ray patients each time they come in, so an easier and more reliable method should be found to assess whether a subluxation is present in that person on that date, and the approximate location of the subluxation. I believe this can be done with motion palpation and muscle testing.

We use the reflex neuromuscular distortion, always accompanying a subluxation, to find that it exists. This neuromuscular distortion affects the movement of the sacroiliac joints very specifically. Normal motion, when the spine bends forward, when it bends side to side, and when one leg is raised and then the other leg is raised, was established 50 years ago by Dr. Henri Gillet.

In any flexion subluxation in any vertebra in the spine, the distorted movement in the sacroiliacs is a lateral flexion distortion in which the ilia follow the lumbar spine, indicating increased muscle tension in the flexors of the lumbar spine (the iliopsoas muscles). Normal movement of the ilia is away from the lumbar spine on lateral flexion of the trunk.

Any extension subluxation in any vertebra in the spine distorts movement in the sacroiliacs, by the ishium moving toward the sacrum when the knee is bent on that side. When the other knee is bent, the sacrum moves toward the ischium on that side. Normal movement is for the ischium to move away from the sacrum when that knee is bent. When the other knee is bent, the sacrum should move away from the ischium.

Rotational subluxation in any vertebra in the spine distorts movement in the sacroiliacs, by moving the ilium toward the sacrum when the torso bends forward. The normal movement is for the ilium to move away from the sacrum on forward bend of the torso.

These three directions of subluxations - flexion, extension and rotation - are the usual misalignments found. It is true that degrees of flexion or extension can vary 180 degrees rotationally, and rotation subluxations can have degrees of flexion and extension, but the major direction of distortion will follow the distorted sacroiliac movement I have just outlined.

Lack of specific breath motion is also an indicator of the presence of subluxation. Breath motion is measured by using a goniometer with at least seven-inch prongs. With this goniometer, one degree is equal to 3mm. If the goniometer prongs are placed with one on the ilium and the other on the scapulae, the measured motion on a deep breath should be 45mm. Anything less on either side indicates a subluxation somewhere in the spine is present. There should be 6mm of breath motion between vertebrae. No breath motion of this magnitude between vertebrae is also a prime indicator that a subluxation exists. This does not indicate the position of the subluxation, because there can be many breath motion locks in many different areas of the spine from a single subluxation.

Lack of breath motion between skull bones can also be prognosticative for a variety of directional misalignments. A lack of motion between occiput and temporal bones can indicate an extension subluxation somewhere in the spine.

A lack of breath motion between the occiput and parietal bones can also indicate a flexion subluxation somewhere in the spine.

A lack of breath motion between the sphenoid and the occiput bones can indicate a rotational subluxation.

After we have ascertained the direction of the subluxation from the sacroiliac tests, we move the spine in the direction opposite the indicated movement. Reluctance in movement is found to exist from the atlas down to near the subluxation, below which the spine seems to have free movement. In this area, a vertebra will be found in either flexion, extension or rotation, depending on the direction indicated on the x-ray.

Rotation subluxations, as indicated by the sacroiliac tests, exhibit rotary reluctant movement misalignment from the atlas down to an area in the spine, and normal rotary movement below. Since rotary subluxations involve from two to four vertebrae, exact positions of the vertebrae need the x-ray to be sure of the position needing release. Palpation may sometimes be quite close to the vertebra, since rotary muscles of the spine, when unbalanced in a subluxation, will be quite tender on the spastic tendon of the rotary muscle involved. A rotary subluxation will often have shoulder blades at varying levels, which can be easily observed by placing thumbs on the spine of the scapulae.

Flexion subluxations, as indicated by the sacroiliac tests, exhibit poor extension from the atlas down to the offending injury in the spine, and normal extension below the offending injury.

Extension subluxations, as indicated by the sacroiliac tests, exhibit poor flexion from the atlas down to the injury, and normal flexion below this point.

The Derefield leg-length tests have been used for the past 40 years to indicate that a subluxation is present in the spine. When present, it is a fine indicator. We have found that it is not present in a rotary subluxation; therefore, it should not be relied upon when a rotary subluxation is primary.

Muscle strength tests have been used to assess spinal subluxation as well. We have found that weakness in muscle strength follows exactly the scenario of being opposite the bend toward which the vetebra has moved: flexion subluxations have weak extensors; extension subluxations have weak flexors; and rotation subluxations have weak rotary muscles of shoulders, hips, forearms and knees.

I have used and advocated this method of spinal evaluation for the past 40 years. I have not found it in error.