PT on the Net Research

The Core - Part 2

Abdominal Bracing vs Abdominal Hollowing

Perhaps a good analogy here is a car. If you imagine abdominal bracing as holding the brake pedal down in a car to stabilize it, then you have a stable car. Undoubtedly, this is the best way to stop a car rolling away. You can still move the car using a jack (legs) or a crane (arms during a pull up), but you cannot do what is most efficient for a car and “roll it” (walk/run). Figure 1: Abdominal Bracing? Or abdominal hollowing? In terms of a strategy for what to use, and when, abdominal bracing may be useful in squatting or for doing chin-ups, but it would be counterproductive for gait-based activities as it would compromise the efficacy of the spinal engine. Aside from the debate on whether to brace or to hollow, the most important consideration is motor sequencing. Based on this, the transversus and other inner-unit muscles should co-contract prior to contraction of the outer-unit muscles – even in a squat or a chin-up. This reduces wear and tear on the passive subsystem, minimising firing of mechanoreceptors that otherwise would be stimulated and result in a neurally mediated inhibition of outer unit musculature. Hence, clients whose inner unit does not pre-contract (in the correct sequence) will suffer with decreased performance and increased risk of injury.

Similarly, if you brace the abdominal wall at too high a level, then it’s like applying the brake fully in a car – the superincumbent body can be moved by the legs (as in a squat), but it cannot be moved in an efficient manner. For a full review of this, see Gracovetsky’s Spinal Engine. Richardson et al compared the effect of abdominal hollowing against abdominal bracing in sacro-iliac joint stabilisation efficacy. They found that both techniques significantly reduced movement at the SIJ, but hollowing increased the stability significantly more than bracing, suggesting that hollowing is both more functionally effective and more energy efficient. Abdominal hollowing, using predominantly TVA contraction, leaves the prime movers of trunk rotation (the IO and EO) free to mobilise the trunk in the rotary fashion we see so commonly in sports and daily activities. To throw another spanner in the works, McGill states that during abdominal bracing (which linguistically would seem to imply a near-maximal contraction), only requires approximately a one to three percent MVC during activities of daily living, or only 10 percent MVC during more vigorous activities. The ability of anyone to consciously engage any muscle at one to three percent, no matter what their level of motor skill, is likely to be poor. The subtlety therefore of the difference between the hollowing described by the Richardson group and the bracing described by McGill could all be down to a matter of semantics.

Figure 2a Figure 2b Figure 2c

Figures 2a, 2b and 2c: Rotation is used for most explosive sports situations where power generation is required. These sporting rotary actions are metaphorical representations of actions that were critical for survival – such as a) kicking away or b) clubbing a potential predator, or c,d) throwing a spear or rock. As such, these explosive actions would have created the greatest adaptive stress on the body and consequently the greatest developmental impact on the natural plasticity of human anatomy.

Favouring the abdominal hollowing hypothesis is the concept that the deeper-seated muscles have a higher level of slow twitch muscle fibres, and the research suggesting that the transversus pre-contracts, supporting the visceral fulcrum theory. This would provide a good explanation for how the abdominal wall works in a closed-to-open chain environment where transverse plane motion of the trunk, such as hitting, kicking, throwing, running and walking, are involved. In more static, closed chain activities, such as squatting and bending, where the feet remain planted on the ground, a bracing strategy is likely to be more effective for force generation – as the trunk is not required to move in the transverse plane. Add to this the knowledge that the abdominal wall and the intercostals literally form from one sheet in utero, almost artificially dividing this abdominal sheet of tissue into obliques and “intercostals,” and you begin to realise that the concept of the trunk as a cylinder extends beyond the abdomen and into the thorax, and therefore naturally into the upper limbs via the pectoral or spino-scapulo-humeral musculature. Vleeming et al, Van Wingerden, Gracovetsky and Lee describe this in some detail from the posterior aspect of the body, whilst Lee describes it from the anterior aspect of the body.

However, Wallden has also identified a sling from the posterior aspect of the lower limb to the anterior aspect of the upper limb (see Figure 3 below) – this has a great deal of significance in spinal mobilization and in its dynamic stabilisation, as functionally, it correlates with the interlimb coupling we see in gait and other powerful movement patterns. It also is important from the point of view that this deep postero-anterior sling acts as a brake to decelerate movement through eccentric contraction. In any fast-twitch or survival movement, such as a sprint, a hit, a throw or a kick the contractile field or muscle chain that is of most significance is not the power generator but the decelerator of the movement pattern.

Just like the Ferrari with the Volkswagen Beetle brakes, for self-preservation the body will only accelerate as quickly as it can decelerate; otherwise the integrity of its passive control system structures (ligaments/joint capsules etc) is jeopardised (see Figure 5). In this way then, the decelerating muscle sling is analogous to a rate-limiting enzyme in a metabolic pathway.

Figure 3: The deep posterior-anterior sling runs from the soccer player’s right biceps femoris, via his sacrotuberous ligament and thoracolumbar fascia, into his left internal oblique. From here, the internal oblique wraps up around the trunk and via the abdominal aponeurosis fuses with the right external oblique/intercostals. Right-sided external intercostal fibres (and the sternum itself) fuse with the pectoralis muscles to translate the elastic forces into the right shoulder complex. In maximal extension.

The deep anterior-posterior sling of the body draws on the anatomical findings of Vleeming et al, van Wingerden et al and Willard showing that the long head of biceps femoris, in particular, is often continuous with the sacrotuberous ligament which connects into the thoracolumbar fascia. This may seem of little relevance to sports, until you realise that the part of the thoracolumbar fascia that the ligament runs in to is the deep lamina of the superficial layer, the same part of the thoracolumbar fascia that connects to the internal oblique.

The idea that abdominal hollowing is more effective at stabilising the lumbo pelvic region, and in particular the sacro-iliac joints, is one that has been investigated by Richardson. In her research it was found that TVA contraction was more effective in sacro-iliac joint stabilisation than full abdominal bracing. This may reflect the morphology of the abdominal obliques, being better sited both to mobilise (and therefore create shear, compression and torsion through the lumbo-pelvic joints) and having the physiology to primarily generate a powerful, short duration contraction due to a higher preponderance of fast-twitch fibres. Furthermore, research has demonstrated that under normal circumstances, only an extremely minor contraction (10 to 15 percent MVC is the suggested level in Richardson et al of the TVA is necessary to create force closure and stability of the SIJs.

This low level of TVA MVC is of relevance to the discussion regarding the likelihood of TVA contraction to create a knock-on internal oblique contraction through stimulation of the spindle cells (see Figure 8 in Part 1). It may be that the 10 percent MVC described as the most appropriate level of contraction for achieving lumbo-pelvic stability is just the appropriate level of contraction to create stability using the TVA without invoking a stretch reflex in the OU musculature*. Sure enough on the EMG studies of Richardson et al, it is demonstrated that engagement of the TVA is followed by engagement of the IO, and then the EO sequentially; this correlates with:

It may be that the 10 percent MVC described to effectively engage the inner unit, is the amount of firing that truly allows independent TVA contraction without stimulation of the muscle spindles in the IO and EO; this then allows them to be worked dynamically in the specific movement pattern the brain chooses. Any more than 10 percent and you get more of an abdominal bracing situation. Both strategies are useful to the body but in different environments and under different loads.

NB: The internal oblique is often cited as a transitional muscle (functioning both as an inner and outer unit muscle), which makes sense given its morphology. However, much of the research that describes it as an IU muscle is derived from information gathered from the infra-umbilical portion of the internal oblique and may be inappropriate or irrelevant to the function of the spinal (supra-umbilical) portion that, biomechanically, demonstrates more of an outer unit function.

Hollowing Bracing
Early couch/floor based rehabilitation Static holds
Motor sequence retraining e.g., statice lean/static lifts
e.g., prior to twist e.g., deadlift, squat
Gait related stabilisation High-level stability training
Multi directional training Perturbation training
Sports specific training Impact resistance (martial arts/fighting sports)

Table 1 (above): Examples of where hollowing strategy and bracing strategy may have their merits.

Back to the Future

Sometimes, to move forward, we have to look backward. Looking back to both how our structure developed phylogenetically as a species, and how our structure developed embryologically, casts a great deal of light on our function.

Although this topic will be covered in far greater detail in a forthcoming publication, the evolutionary and embryological anatomy essentially shows us that both the transversus abdominis and inner unit came before the outer unit system, and that the upper and lower abdominal walls are very distinct entities.

In a nutshell, a single celled animal only has the capability to radially contract – similar to the action of the TVA. A multi-cellular creature has the ability to radially contract sequentially. This is what we have all observed in the locomotion of worms and should be aware of with regard to the peristalsis of our own gut tubes. As the body walls of such creatures became more specialised, so too did the neuromusculoskeletal system, allowing for the lateral flexion motion we see in fish. As fish moved to land, so the vertebrate spine began to develop axial torque and finally flexion-extension.

Therefore, it is of little surprise that the research to date has shown that functionally, the TVA and inner unit should pre-contract before the outer unit muscles.

Logically, this research has demonstrated that the TVA is important in stabilising the lumbo-pelvic region, that the internal oblique is also implicated to a lesser extent, and that the external oblique is primarily a mobiliser. This layering of function is not dissimilar to the way the brain has developed in layers – reptilian, mammalian and neocortical. This topic will also be discussed in more depth in an upcoming publication.

TVA Dysfunction

So now you know some more about the origins of the TVA, we need to know what may cause so-called “TVA dysfunction.”

One thing that the Australian group has demonstrated quite conclusively is that in healthy subjects, the transversus abdominis activates before both conscious (intentional) or reflexive (unexpected) movement of the upper or lower limb. In chronic low back pain sufferers this is not the case; they find that this early contraction of the core muscles in general – not just the transversus abdominis - occurs after the peripheral muscles of the limbs activate.

This means that in people with low back pain, their spine is actively unstable, creating shear on the passive elements. This, in turn, means over time it will become both passively unstable (resulting in stress on pain sensitive structures), and therefore will be neurally unstable as the body will be attempting to shut down certain muscles (inhibition) and up-regulate other muscles (spasm/hypertonus/facilitation).

Figure 4: When all three elements are functioning harmoniously about a joint, that joint will be stable and functional. It only takes one of these factors to disrupt joint function and create instability, leading to decreased performance and increased likelihood of injury (adapted from Panjabi).

So it seems that those with chronic low back pain are caught in a vicious cycle where the muscles that support the back are inhibited to reduce compression, stiffness or intra-abdominal pressure aggravating the pain, yet simultaneously, this means that they have a vastly reduced active support system. This can surely only lead to further strain on the passive structures – such as discs, ligaments, joints, joint capsules creating further pain and further neurological dysfunction. In fact, according to Hides et al, as soon as an individual suffers with low back pain, they will incur inner unit inhibition, and this inhibition will not automatically correct when the pain is gone. It is for this reason that movement re-education is essential in any client with any history of low back pain, and this is where the personal trainer’s expertise and referral network is essential.

How can you train the TVA if it’s being inhibited by pain?

Firstly, the client will often consciously be able to overcome their nervous system’s inhibition of their TVA – so cognitive training of both appropriate levels of contraction, as well as appropriate sequencing of contraction should be encouraged until the point that activation of the TVA is automatic.

Figure 5: Cognitive rehearsal of motor sequencing will, over time, result in that motor skill becoming more autonomic and less cognitive (adapted from Lederman, 1997). In such instances, this is a classic case of not "practice makes perfect" but "perfect practice makes perfect."

Secondly, having access to a network of skilled therapists will help you to optimise your results. A skilled manual therapist can help to minimise muscle spasm, joint restriction and tissue congestion through techniques such as soft-tissue therapy, neuromuscular technique and rhythmic mobilisations. A good naturopath or nutritionist will be able to advise on nutritional intervention, hydrotherapy techniques and other natural intervention to assist in natural pain relief and therefore decreased inhibition of the TVA.

Research presented at the World Congress on Low Back & Pelvic Pain in 2001 suggested that lactose intolerance may be a risk factor for developing chronic pelvic pain after pregnancy. While it’s accepted that there may be biochemical causes for ongoing pelvic pain associated with lactose intolerance, it is also pointed out that any form of repetitive irritation to the gut such as a food allergen is likely to result in central sensitisation and a reflexive inhibition of the lower abdominal wall and pelvic floor. Given that Timmins suggest that gluten intolerance is somewhere in the region of 40 to 60 percent for the Caucasian population, and lactose intolerance is not far behind, it is not surprising that so many of our clients have a dysfunctional lower abdominal wall and/or low back pain.

Figure 6: The naturopathic triad, or the triad of health. Similar to the joint stability model described above, this model has been used by naturopaths for many years (Newman-Turner, 1990). Again, a good balance is required across all three areas to achieve and maintain stability of your health.

Inner versus outer unit, or upper vs. lower abdominal wall? Research flaws?

Most of the discussion in the literature thus far has focused on TVA function, versus oblique function, or inner unit versus outer unit. However, when we consider literature from the fields of embryology and neurology, as well as applied anatomy, it would seem pertinent to also discuss upper abdominal wall versus lower abdominal wall function.

The upper abdominal wall is clearly designed – from a biomechanical, morphological, and physiological point of view – to have a mobilizer dominance, as revealed through the following:

  1. Its effect on the spine/role in transducing force from lower limb girdle to upper limb girdle
  2. Fibre direction and association with the lower limb slings
  3. EMG activity – as demonstrated by Urquhart et al 

Clinically, the lower abdominal wall also commonly tests (through standing observation, muscle testing, symptomology and orthopaedic testing) in a manner disparate from the upper abdominal wall. The oblique and transverse sections of the lower abdominal wall are clearly designed to have a stabiliser dominance (see research below by Urquhart, Hodges & Story)*. This part of the abdomen is commonly inhibited during clinical examination without concomitant upper abdominal wall dysfunction.

Figure 7: Photograph showing a female client with an inhibited lower abdominal wall and a well-toned upper abdominal wall. In the left-hand picture, the lower abdominal wall has been covered to demonstrate how the tone of the upper abdominal wall is good, even "athletic" looking. But when we look at the lower abdominal wall, we see a very different picture.

This is not to say that the lower abdominal wall isn’t a prime mobilizer in some key movement patterns. Certainly sprinting and possibly even kicking could be argued to be essential for survival. In both these instances, the lower abdominal wall is a primary mobilizer.

Much of the previous research into the function of the abdominal wall has involved fine-wire electromyography (which in itself has many flaws as described by the researchers). Other known flaws of fine-wire electrode research are tabulated below, but before you read them, it is important to know that the way electrical activity is tested in a muscle group is by measuring the electrical current between two separate wires or “electrodes” in the same muscle belly. We have to be careful not to take at face value these inherently limited research protocols, and we should be cognizant of  the many potential legitimate flaws with the research. All technologies are attempts to reproduce what good clinicians have already demonstrated through their own skills and abilities with the ultimate tool: him or herself.

Flaws associated with electromyography research:

Although the information presented above may seem very negative and anti-EMG, the evidence produced in most of the published EMG research is compelling. The flaws of such work should not detract from the value of it, but rather should help to remind us of its limitations. Despite these limitations, currently EMG assessment is probably the best objective tool we have to evaluate dis-synergic firing patterns within muscle.

Moreover, if we take a look at the methodology employed, we also see that these researchers had considered “the abdominal wall” as a whole, and have therefore used vantage points to access the specific layers without consideration of the fact that both structurally and functionally the abdominal infra- and supra- umbilical portions are clearly delineated.

Figure 8: Adapted from Ng, J. Kippers, V. & Richardson, C (1998) Muscle fibre orientation of the abdominal muscles and suggested surface EMG electrode positions. Electromyogr. Clin. Neurophysiol., 38, pp 51-58. Note the two points for placement to measure EO activity are both supra-umbilical, while the IO placement is only infra-umbilical. The RA has two suggested sites; one supra- and one infra- umbilical. The yellow line depicts the level of the umbilicus.

Subsequent research from the same group has demonstrated a functional disparity between the upper and lower abdominal wall. Urquhart, Hodges & Story studied the effect of rapid arm movement on the TVA using fine-wire electrodes in several different portions of the TVA. They concluded that the lower fibres appeared to have a greater role in spinal control, while the upper fibres may have a greater role in trunk rotation.

So what is of greater significance clinically – the inner-outer unit debate, or the upper-lower abdominal wall debate?

Firstly we should clarify the point that the terms inner unit and outer unit are mainly useful descriptors to help categorise function; they are not real entities. If one part of the system is dysfunctional, the whole system is crippled. For example, if your client is not eating well (i.e., too many grains*, too little nutrient density in their food, micro-waved or genetically modified foods, alcohol), it will create inflammation in their gastro-intestinal tract. This will result in abdominal inhibition via viscero-somatic neural phenomena. So no matter how “scientifically correct” their motor re-education program, they will not make the gains that someone with a functional GI tract would. Quite aside from the neural implications, there will be poor tissue health and repair due to depleted nutrient availability.

*The myth that all athletes should “carbo-load” – which often involves predominantly grain-based foods - could be a major factor in back and other injuries in sports people, due to inhibition of their lower abdominal wall. It has been touted as ridiculous that “even elite athletes” should need to condition their cores, but it is extremely common that top athletes do have poor core function. This is frequently due to misguided nutritional advice resulting in gastro-intestinal inflammation, and to excessive levels of machine training, which encourages recruitment of prime-movers without stabiliser activity and sedates the neural drive to stabiliser musculature.

The inner unit and, in particular the lower abdominal wall, must function synergistically to provide stability to the lumbo-pelvic region. The understanding that the upper and lower abdominal wall can function both independently and synergistically is important in your assessment protocols and subsequent exercise prescription. Being able to competently assess for this through postural and functional protocols is of paramount importance, determining how much success you will have; firstly in rehabilitating an injured client, and secondly, in preventing injury/maximizing the potential of your non-injured clients. As with any dysfunction, the area that requires work should be first isolated, worked upon, and then integrated back into the functional system.

“Movement emanates from the core…”

What does the term, “movement emanates from the core”, mean? Well, it is based on the research work originating from Richardson’s group in Australia in the early to mid 1990s. This research showed that before there was contraction of any part of the periphery of the body (arms or legs), the core of the body needed to be stabilised. Sure enough this is what was found when assessing TVA contraction, with it engaging 30 to 60ms before arm movement or 110ms before leg movement. This then became a very exciting new concept as it fitted with earlier work produced by Gracovetsky in 1988 in his book “The Spinal Engine”. Gracovetsky demonstrated through mathematical modeling and evolutionary rationale that the legs are driven forward by the spine not the inverse.

Some confusion arises; in the vast majority of gait and biomechanical analysis the focus has remained fixed on the idea that the legs propel the body forward and that the arms are more or less passive slaves that move as a result of leg movement. In fact, as recently as 1999, Lees – a professor of biomechanics - suggested that the arms are primarily used to counterbalance the motion of the legs in running and may also create some lift during a sprint. This may have some truth, but misses much of the relevance of inter-limb coupling in force generation and dampening. A literature search in 2000 identified a total of zero published papers suggesting that the trunk or upper limbs played any significant role in locomotion. Gracovetsky’s research and the work from Australia turned this thinking on its head.

Another miscomprehension arose in the fitness and biomechanical community with the supposition that the new researchers were suggesting that the legs were no longer important in force generation. Of course this is not the case. The fact is that both ways of looking at the body are correct, but force generation in the periphery must be preceded by stabilisation of the core – otherwise the body is jeopardising its very integrity. Again, looking at the evolutionary rationale for the primary action of the core in movement of the organism, Gracovetsky has detailed the development of gait from our vertebrate ancestral line. In summary, Gracovetsky shows that the primary locomotive generation in fish (early vertebrate ancestors) was not through the movements of their fins, but moreover through lateral flexion of the core – their trunk muscles. As fish moved into swamp environments and required greater peripheral strength to clamber over debris, such as fallen trees, weeds and branches, their fins developed greater strength. The next logical step was for these creatures (through survival pressures) to develop the ability to survive for periods out of water – either to escape predators, or to take advantage of the plentiful supply of food in the form of plant life, or the rife insect life at that time.

Figure 9: Gracovetsky’s diagram of what a sprinter would look like, if the legs were all that drove the trunk forward during gait. Clearly this is not the case.

As such, the locomotor apparatus at that time consisted of slightly strengthened, pectoral and pelvic fins that were only able to move the organism forward via lateral flexion of the trunk – like many existing lizards today. However, once again through survival pressures, the ability to lift these modified fins off the ground to circumnavigate objects and lift the limbs over obstacles, an axial torsion (rotation) of the spine would have become an advantage. Therefore this axial torsion became a feature of vertebrate spines, but equally would have required the ability to induce rotation and to control it. It is a known mechanical concept that when you take a rod-like shape, like the spine, any rotation combined with a lateral flexion will result in a flexion-extension of that rod. A couple of hundred million years on, the facet joint arrangement in our spines still reflects that coupling pattern. In fact, our ability to rotate has become even more significant since the initial function of circumnavigating ground-lying obstacles, as demonstrated in the sporting examples above. Sports, of course, are simply metaphorical hunting/survival rituals.

Pain and Core Function

Pain will inhibit action of the TVA and other supporting musculature of the lumbar spine. The TVA is thought to support the lumbar spine through raising the intra-abdominal pressure creating a traction effect upward through the diaphragm which co-contracts with the TVA and pelvic diaphragm. With an increase of intra-abdominal pressure, the viscera move upward, creating pressure on the diaphragm. Because the crura of the diaphragm attach to the anterior vertebral bodies of L2 and L3, the increased IAP against the stabilising contraction of the diaphragm results in a decompressive force on the second and third lumbar vertebral bodies, ultimately resulting in some level of decompression in the region of the spine most commonly injured.

The multifidus also co-contracts with the transversus-pelvic/respiratory diaphragm, which stiffens the lumbar spine through compression. If, as described by Kapandji, the nucleus pulposis of the disc is the true centre of rotation of the organism which would make sense embryologically and phylogenetically, then the multifidus would need to co-contract with the transversus-pelvic/respiratory diaphragm complex to allow effective rotation of the trunk via the obliques (see Figure 6 above).

Note that if the multifidus did not contract, the action of the obliques would create a sufficient flexor moment on the thoraco-lumbar spine disrupting the instantaneous axis of rotation of the thoraco-lumbar spine, inhibit the joint range of motion, jeopardise the posterior annulus of the disc and therefore the central nervous system and consequently inhibit the potential power generation of the obliques. The brain will reflexively avoid any stress to the central nervous system if at all possible by altering muscle tone.

Figure 10: Spinal flexion. How a flexion moment through the spine (large black arrow) will result in reciprocal posterior migration of the nucleus of the disc (small black arrow) thereby stressing the posterior annulus. Such a flexion moment would be generated if the transversus-pelvic-respiratory diaphragm complex contracted without the co-contraction of the multifidus. Thus, with repetitive stress and posterior annular weakening, the integrity of the spinal cord (or cauda equina) would become jeopardised. Adapted from Kapandji (1974).

Why does low back pain inhibit the very muscles that support the back?

The natural response of the body to pain is known as the “red light posture,” the startle response or “the flexor response.” This posture correlates with a return to the foetal position; and as anyone with an interest in the psychology of success will know, people either move forward into the unknown, or backward into safety. This is true of people who are in pain – they tend to move back toward safety, and foetal life is the very epitome of safety. What occurs neurologically in any painful situation is that reflexively the body goes into a flexor response (this is akin to treading on a pin, the hip flexors and knee flexors both engage to draw the foot away from the painful stimulus). In order for this to occur efficiently, the extensors must be inhibited. Technically, the TVA is an extensor of the spine, so it is little wonder that it becomes inhibited in a pain state; besides which, the red light posture, startle response and flexor response all suggest the body should move into flexion when it is in pain.

It just so happens that the most common causes of low back pain, such as facet irritation, disc degeneration and spondylosis, spondylolysthesis (see O’Sullivan) can all be aggravated by compression and raised intra-abdominal pressure. It is not surprising therefore that the body would reflexively inhibit these muscles – altering breathing patterns and movement patterns. Pain itself is a significant stressor to the body, inducing sympathetic response and therefore a faulty breathing pattern, meaning the accessory muscles of respiration become overactive. The subsequent atrophy of the local system (inner unit) musculature found by the Australian researchers is a natural sequela of under-use and inhibition.

TVA dysfunction causes a compensatory strategy to be used by the body leading to over-recruitment of the outer unit whilst in pain. This may, in part, be due to the vegetative, almost autonomic nature of the inner unit muscles, and the increased sensory and cognitive awareness of the outer unit musculature.

Because pain re-writes motor programs in the brain quicker than any other stimulus, a body in pain will efficiently rewrite its new compensatory, and therefore faulty, movement patterns, replacing the older more functional movement patterns. Of course, during rehabilitation, and under the influence of pain medication, the learning of more “functional” movement patterns is not so quickly realised as there isn’t the advantage of the pain motivation.* The upshot of this process is ongoing use of outer unit musculature to stabilise which, across time, creates increased shear and compression through joints and greater joint degeneration. This is the vicious cycle of the chronic low back pain sufferer.

***Ironically, both paracetamol-based medications and non-steroidal anti-inflammatories can cause inner unit inhibition due to the fact that the former commonly cause constipation and the latter are well known to create GI inflammation. Both will potentially result in a viscero-somatic inhibition of the lower abdominal wall.


Therefore to suggest, as some authorities have, that the transversus abdominis can be compensated for by the other abdominal wall musculature is somewhat flawed on many levels:

Why does the average person have to learn TVA activation when it’s reflexive?

So the question, “Why does the average person have to learn TVA activation when it’s reflexive?” should have been answered above, but in case you missed the answer, it is because:

  1. more than 80 percent of Westerners will suffer from a debilitating bout of low back pain in their lives; the research shows that just one episode of this will inhibit the inner unit muscles.
  2. Conservative estimates suggest that 40 to 60 percent of Caucasians suffer with gluten intolerance, which in the medium and longer term will inhibit the abdominal wall. Gluten is just one source of food allergen, dairy, soya, rice, nuts, strawberries, many of the food additives, microwaved food and genetically modified food will often create similar irritation to the GI system.
  3. 47 percent of women at the mean age of 38.5 have a stress incontinence problem indicating dysfunction of their inner unit.
  4. Clinical testing suggests that more than 80 to 90 percent of people have a parasitic infection in their digestive system, which will in many cases create a level of underlying repetitive GI tract inflammation and subsequent abdominal wall dysfunction. The same figure is true in Westerners of those tested for fungal infection of the gastro-intestinal tract.
  5. Premenstrual syndrome is prevalent in Western populations (and almost unheard of in native populations), resulting in abdominal wall dysfunction.
  6. Adrenal stress is more common than ever in the current nutritionally depleted, glycaemically challenged, stressed living and work environments many people survive in (adrenals reflex to same region of thoracolumbar cord as TVA). Just like the stressed, caged, diseased animals we often eat, we too are placing ourselves in similar living conditions, with similar impact on our health. The rise in adrenal exhaustion and fatigue-related conditions such as post-viral fatigue and ME are testament to just such conditions. Physiologically it is likely that repetitive exposure to these conditions creates sensitisation of the thoracolumbar cord and may therefore contribute altered recruitment of muscles supplied by nerves from this level.

The list above is in no way exhaustive of the kind of pain and visceral conditions that can reflexively inhibit the inner-unit – leave aside from the deconditioning we observe in society as a whole and the use of non-functional, fixed-axis exercise equipment in those who do actually exercise.

In understanding the back-ground neurophysiology and having a clinical appreciation of the incidence of associated conditions, it should be transparent that, far from it being the exception to have to re-educate the use of the inner-unit, in Western society, it is the rule.


  1. Ahlberg, P. (2000) Personal communication. Professor of Evolutionary Organismal Biology, Uppsala University, Sweden.
  2. Attfield, S. (2000) Personal communication. Elite systems engineer, Derby Royal Infirmary, Derby, England.
  3. Barber, B. (2004) How common are parasites? Genesis Health Products.  Accessed: 17th March 2004.
  4. Beach, P. (2003) Personal Communication. Lecturer: British College of Osteopathic Medicine, British School of Osteopathy.
  5. Bogduk, N. & Twomey, L. (1991) Clinical anatomy of the lumbar spine (2nd Ed) Churchill Livingstone pp102-103
  6. Brady, Mayer & Gatchel (1994) Physical Progress and Residual Impairment Quantification After Functional Restoration – Part 2: Isokinetic Trunk Strength Spine vol:19 no:4 pp 395-400
  7. Chek, P. (1996) Awesome Abs! The gut-busting solution for men and women. Pub Robert Kennedy’s Muscle Mag International
  8. Chek, P (1999) Advanced Program Design, Correspondence Course, C.H.E.K. Institute, San Diego, USA
  9. Chek, P (2000) Movement that matters, Pub: C.H.E.K. Institute, pp19-24
  10. Chek, P (2001) Abs in or out? Article:
  11. Chek, P (1993, 2002) Scientific Back Training, Correspondence Course, C.H.E.K. Institute, San Diego, USA
  12. Comerford, M. Mottram, S (2001) Functional stability re-training: principles and strategies for managing mechanical dysfunction. Manual Therapy 6(1)pp3-14
  13. Cresswell, A. Grundstrom, H. & Thorstensson, A. (1992) Observations on intra-abdominal pressure and patterns of abdominal intra-muscular activity in man. Acta Phusiologica Scandanavia 1992, 144, pp409-418
  14. Edwards, S. (2000) Neurological Physiotherapy – a problem-solving approach Pub: Churchill Livingstone, pp6-7
  15. Granath, A. Mellström, D. & Hellgren-Wangdahl, M. (2001) Lactose Intolerance – a risk factor for developing longstanding pelvic pain after pregnancy? In “Proceedings of 4th Interdisciplinary World Congress on Low Back & Pelvic Pain” pp 460-462
  16. Gracovetsky, S. (1988) The Spinal Engine. Pub:Springer-Verlag/Wien pp9-16
  17. Gracovetsky, S (1997) Linking the spinal engine with the legs; a theory of gait in Movement Stability & Low Back Pain. Churchill Livingstone
  18. Gracovetsky, S. (2003) Personal communication. Professor Emeritus, Concordia University, Canada
  19. Hanna, T. (1988) Somatics – reawakening the mind’s control of movement flexibility and health. Perseus Books pp49-59
  20. Hides, J. Richardson, C. Jull, G. (1996) Multifidus muscle recovery is not automatic after resolution of acute, first episode low back pain. Spine 21:2763-2769
  21. Hodges, P. & Richardson, C (1996) Inefficient muscular stabilisation of the lumbar spine associated with low back pain: a motor control evaluation of transversus abdominis. Spine Vol. 21, No. 22, pp2640-2650
  22. Hodges, P. (1999) Is there a role for the transversus abdominis in lumbo-pelvic stability? Review Article. Manual Therapy 4 (2) pp74-86
  23. Hodges, P. Heijnen & Gandevia (2001) Postural activity of the diaphragm is reduced in humans when respiratory demand increases. Journal of Physiology, 537.3, pp999-1008
  24. Holstege, G. (2001) Emotional Motor System, in “Proceedings of 4th Interdisciplinary World Congress on Low Back & Pelvic Pain” pp160-177
  25. Kapandji, I. (1974) The Physiology of the Joints, Volume 3: The Trunk and the Vertebral Column. Pub. Churchill Livingstone.
  26. Kelly, B. Cooper, L. Kirkendall, D. & Speer, K. (1997) Technical considerations for electromyographical research on the shoulder. Clinical Orthopaedics and Related Research. No. 335, pp140-151
  27. Kuchera (1997a) Treatment of Gravitational Strain Pathophysiology, in Movement, Stability and Low Back Pain – the essential role of the pelvis, Ed.s Vleeming, Mooney, Dorman, Snijders & Stoeckart. Pub: Churchill Livingstone, pp477-499
  28. Kuchera (1997b) Osteopathic considerations in diagnosis and treatment / Postural considerations in the sagittal plane, in Foundations for Osteopathic Medicine, Pub: American Osteopathic Association pp970, 999-1001
  29. Lederman, E. (2003) Osteopathic Neuromuscular Rehabilitation. Lecture, March 2003, British College of Osteopathic Medicine.
  30. Lederman, E. (1997) Fundamentals of manual therapy. Churchill Livingstone pp73-74, 103-122
  31. Lee, D (1997) Instability of the sacro-iliac joint and the consequences for gait, in Movement, Stability and Low Back Pain – the essential role of the pelvis, Ed.s Vleeming, Mooney, Dorman, Snijders & Stoeckart. Pub: Churchill Livingstone, pp231-233
  32. Lee, D (1999) The Pelvic Girdle. Pub: Churchill Livingstone, pp52-66
  33. Lee, D. (2001) An integrated model of joint function and its clinical application, in proceedings of 4th Interdisciplinary World Congress on Low Back & Pelvic Pain pp137-152
  34. Lees, A. (1999) Running in "Functional Human Movement" Eds: Durkward, Baer & Rowe Pub:Butterworth Heinemann chpt 8 pp122-133
  35. Leibenson (1999) Motivating pain patients. Journal of bodywork and movement therapy Vol.3 No.3 Pp143-146
  36. Levin, S (1997) A different approach to the mechanics of the human pelvis: tensegrity, in Movement, Stability and Low Back Pain – the essential role of the pelvis, Ed.s Vleeming, Mooney, Dorman, Snijders & Stoeckart. Pub: Churchill Livingstone, pp157-167
  37. Lewit, K (1999) Manipulative Therapy in Rehabilitation of the Locomotor System (3rd Edition). Butterworth-Heinemann. pp27-28
  38. McGill (2002) Low Back Disorders – evidence based prevention and rehabilitation Pub: Human Kinetics
  39. McGill, S (2001) Achieving spinal stability: blending engineering and clinical approaches. In “Proceedings of 4th Interdisciplinary World Congress on Low Back & Pelvic Pain”, pp203-210
  40. Mayer, Tabor, Bovasso & Gatchel (1994) Physical Progress and Residual Impairment Quantification after Functional Restoration – Part 1: Lumbar Mobility Spine vol:19 no:4 pp389-394
  41. Myers, T. (1998) Kinesthetic Dystonia (Part 2). Journal of Bodywork and Movement Therapies. Vol.2, No.4, pp231-247
  42. Myers, T. (1999) The Anatomy Trains. Pub: Churchill Livingstone
  43. Newman-Turner, R. (1990) Naturopathic Medicine – treating the whole person. Pub: Thorsons pp26
  44. Ng, J. Kippers, V. & Richardson, C (1998) Muscle fibre orientation of the abdominal muscles and suggested surface EMG electrode positions. Electromyogr. Clin. Neurophysiol., 38, pp51-58
  45. Norris, C. (2000) The muscle designation debate: the experts respond. Journal of bodywork and movement therapies, Ed. Leon Chaitow, 4(4) pp232-235
  46. O’Sullivan, P. Twomey, L. & Allison, G. (1997) Evaluation of specific stabilising exercise in the treatment of chronic low back pain with radiologic diagnosis of spondylosis or spondylolishthesis. Spine Vol.22, No.24, pp2959-2967
  47. O’Sullivan, P (2000) Lumbar segmental ‘instability’: clinical presentation and specific stabilising exercise management. Manual therapy 5(1) pp2-12
  48. Proctor, B. (2003) The Freedom Series. Bob Proctor Life Success Productions.
  49. Panjabi, M (1992) The stabilising system of the spine. Part 1 Function, dysfunction, adaption and enhancement. Journal of Spinal Disorders 5:383-389
  50. Richardson, C., Sniijders, Hides, Damen, Pas & Storm (2001) The relationship between the transversus abdominis muscles, sacro-iliac joint mechanics and low back pain. In proceedings of 4th Interdisciplinary World Congress on Low Back & Pelvic Pain, pp132-133
  51. Richardson, C. Jull, G. Hodges, P. and Hides, J (1999) Therapeutic exercise for spinal segmental stabilization in low back pain – scientific basis and clinical approach. Churchill Livingstone.
  52. Rizk, N. (1980) A new description of the anterior abdominal wall in man and mammals. Journal of anatomy 131 pp373-385
  53. Schmidt, R. & Wrisberg, C. (1999) Motor control and performance. Pub. Human Kinetics pp89-99
  54. Siff, M. (2003) Transversus Abdominis Revisited.
  55. Timmins, R (2000) Personal communication. Founder of Biohealth Diagnostic Laboratories, San Diego, California.
  56. Tulloch, S. (1993) The Readers Digest Oxford Complete Word Finder. Oxford University Press.
  57. Urquhart, Hodges & Story (2001) Regional variation in transversus abdominis recruitment, in Proceedings of 4th Interdisciplinary World Congress on Low Back & Pelvic Pain, pp358-359
  58. van Wingerden, Vleeming, A. Kleinrensink, Stoeckart, R. (1997) The role of the hamstrings in pelvic and spinal function in "Movement, Stability & Low Back Pain - the essential role of the pelvis" Ed:Vleeming et al Pub:Churchill Livingstone pp207-210
  59. Vleeming, A. Stoeckart, R. & Snijders, C. (1989) The Sacrotuberous Ligament: a conceptual approach to its dynamic role in stabilising the sacro-iliac joint Clinical Biomechanics vol 4 no 4 pp201-203
  60. Vleeming, A. Snijders, C. Stoeckart, R. & Mens, J. (1997) The role of the sacroiliac joints in coupling between spine, pelvis, legs and arms. In "Movement, Stability & Low Back Pain - the essential role of the pelvis" Ed:Vleeming et al Pub:Churchill Livingstone pp53-71
  61. Wallden, M. (2000) Lumbo-pelvic associations with hamstring strain in professional footballers. MSc dissertation, British College of Osteopathic Medicine (formerly British College of Naturopathy and Osteopathy)
  62. Wallden, M. (2003) Understanding the interactions between our food and inhibition of the abdominal wall. CHEK Report. CHEK Institute, San Diego, CA, USA pp10,11&16
  63. Willard, F. (1997) The muscular, ligamentous and neural structure of the low back and its relation to back pain, in "Movement, Stability & Low Back Pain - the essential role of the pelvis" Ed:Vleeming et al Pub:Churchill Livingstone
  64. Willard, F. (1999) Human Axial Anatomy: Lumbar Spine and Pelvis (BCNO presentation/personal communication) British College of Naturopathy & Osteopathy. Nov 1999
  65. Williams, P. (1995) Skeletal Muscle, (Muscle - Chpt 7), in Gray’s Anatomy 38th Edition. Churchill Livinstone pp739-764