Dr. Jenny Pynt, an internationally-recognized expert on sitting ergonomics, has published a paper entitled "Rethinking design parameters in the search for optimal dynamic seating" in the Journal of Bodywork and Movement Therapies.  You can view the abstract at:  http://www.bodyworkmovementtherapies.com/article/S1360-8592(14)00128-4/abstract .  She cites research showing that current office chair designs do not promote variations of posture or muscle activity, and suggests a new definition of dynamic sitting: Sitting in which the action is provided by the sitter, while the dynamic mechanism of the chair accomodates that action.

The Core-flex chair is presented as one of four new forms of dynamic seating that promote active sitting.  Due to copyright law we cannot reproduce the article here, but we offer a review paper that Dr. Pynt has written entitled: "Dynamic sitting and the Core-flex office chair."


Dynamic sitting and the Core-flex office chair
Jenny Pynt PhD

For many years researchers have investigated the importance of movement for the health of the spine during prolonged periods of sitting. There is concurrence that active movement of muscles and joints assists spinal postural health and, as is recently being demonstrated, metabolic health. As a result designers have incorporated dynamic mechanisms that can alter the sitter’s posture from recline to incline, or vary shoulder rotation to affect forearm and wrist position, or alter sitting height, or passively move the lumbar spine through varying degrees of lordosis. This is dynamic seating design. But such design does not promote active joint or alternating muscle activity. Therefore, it does not promote dynamic sitting.

It is not surprising then that in a recent rigorous systematic review conducted by O’Sullivan and colleagues [1] dynamic mechanism chairs that relied on passive sitter operation showed no statistical improvement in modifying muscle activity when compared with static seating design. Indeed in some dynamic chairs increased static muscle activity occurred resulting in increased discomfort. In addition, in a study of 4 dynamic chairs, Ellegast et al. [2] reported that it was the task that caused bodily movement and muscle activation, not the chair design and that this muscle activity was often sustained. These authors recommended that in order to avoid sustained static postures and musculoskeletal disorders when using a standard or dynamic chair, office tasks and duties should be varied and sit/stand desks may be advisable.

This paper argues that a new approach to dynamic seating design is required; one that promotes dynamic sitting. It is proposed that for improved postural and metabolic health for those in sedentary occupations, it is the sitter who should drive activity, and it is the role of the chair to provide a compliant yet stable support as the sitter exercises the body.1 To explore this argument, discussion will focus on the manner in which:

a) sustained static sitting impacts on postural and cardio-metabolic health
b) the Core-flex chair addresses the need for movement yet differs from other dynamic seating design to promote dynamic sitting.

a) How sustained static sitting impacts on postural health
In 2001 van Dieën et al. [3] had already proposed that dynamic chairs were deficient in design. In a study of office workers carrying out repetitive desk tasks over 3 hours while seated on 2 dynamic chairs and one fixed office chair, van Dieën and colleagues reported that the trunk extensor muscles were active for 93–98% of the time. They also found it was the task, not the chair that dictated sitter movement and that task performance enforces sustained contraction of muscle groups. Sustained activity of a muscle group is unhealthy and in the spine has widespread postural health ramifications. After just 30 minutes spinal extensor muscles in a pain free sample showed fatigue even when working at a very low rate (2%) of their maximum voluntary contraction (MVC) [4]. When the spinal extensor muscles become fatigued, they relax and the spine slouches. A sustained slouched posture has been shown to have marked ill effects on the health of the viscoelastic tissues of the spine. The viscoelastic tissues impacted by static sitting are the muscles, ligaments, discs, fascia and facet joint capsules. Sustained slouched sitting causes a cascade of events in these tissues in the following manner.

Effect of sustained slouched posture on muscles, ligaments and spinal stability
Using static digital XRays of 27 subjects, Dunk et al. [5] demonstrated that when sitting in a slouched posture, the lower 3 lumbar intervertebral angles approach maximal available flexion. When intervertebral flexion angles are greater than 75% of their available range of motion, high tensile forces are generated in the posterior spinal ligaments and dorsolumbar fascia [6]. These forces are compounded by the reflex relaxation that occurs in the superficial posterior spinal muscles when the seated posture reaches mid to end range of full lumbar flexion in those without a history of low back pain [7]. When posterior spinal muscle activity ceases the anterior shear forces exerted on the discs by the ligaments are magnified [8,9]. Snijders and colleagues [10] used model calculations to demonstrate that the loss of back muscle protection that occurs in relaxed slouched sitting also permits maximal loading on the iliolumbar ligaments, stressing these ligaments to near failure. The flexion relaxation reflex also leaves the facet joints and sacro-iliac joints without the muscle protection afforded by superficial multifidi and transverse fibers of internal obliques [7,11]. As a result the lumbar spine lacks stability and is under great strain and potential pain [12].

As demonstrated in several in vivo studies, this lack of stability occurs in a surprisingly small amount of time. Those who already have a predisposition to non specific chronic low back pain (NSCLBP) from activities in flexed positions demonstrate an inability to reposition the lumbar spine in a neutral posture following just 5 seconds of sustained slouched sitting [13]. After 5 minutes of sustained flexion those without a history of low back pain are also significantly challenged in their ability to reposition the spine to neutral [14]. These researchers proposed that this lack of positional sense is reflective of trunk muscle dysfunction with resultant lack of lumbar proprioceptive awareness. O’Sullivan et al. [13] further propose that impaired motor control leading to instability of the lumbar spine significantly contributes to NSCLBP.

How sustained slouched postures elicit a neuro-muscular response
How trunk muscle dysfunction affects proprioceptive awareness is further explained by Solomonow and his school of researchers. As a response to sustained stretching from slouched sitting postures, creep and laxity occur in the posterior supraspinous spinal ligament of the lumbar spine. This ligament has sensory receptors linked to a reflex arc with the multifidus muscles. The intention of this reflex is to protect the ligaments from overload and potential damage. The creep and resultant laxity of the ligaments from sustained flexion corrupts the sensory endings in the ligament. The reflex is disrupted. The multifidus response is diminished as is its role in protecting the spine. The spine is destabilized. Hence the loss of this reflex predisposes the spine to injury [15-17].

After 2-3 hours of sustained flexion, an acute inflammation begins in the ligaments. After 6-7 hours following the cessation of sustained flexion the musculature, in an attempt to re-establish stability, exhibits significant hyperexcitability evidenced as intermittent spasms. Dependent on the length of time the lumbar spine has remained flexed, the ligamentous laxity and inhibited reflex may leave the spine at risk for 24 hours, effectively presetting the back for injury at work the following day. Thus the ligaments continue to be exposed to damage with insufficient time to repair, and a chronic traumatic disorder may begin [15-17].

Even when rest periods are instituted, this chain of neuro-muscular responses may not be avoided. After 10 minutes of sustained flexion with a light load comparable to that exerted on the spine in slouched sitting, followed by a 10 minute rest and repeated 6 times, laxity was demonstrated in the viscoelastic tissues for up to 7 hours, and multifidus activity was decreased for 3-4 hours post work. The lumbar spine remains unstable for periods up to 7 hours following sustained slouched sitting [18-20] and is particularly vulnerable to injury in this time [14,15,21].

In summary: When the protective reflex initiated by the supraspinous ligament is interrupted by sustained slouched sitting postures, trunk muscle dysfunction occurs with resultant lack of lumbar proprioceptive awareness leading to spinal instability in both those with and without episodes of NSCLBP.

Effect of sustained postures on the intervertebral discs (IVDs) and facet joints
Lack of spinal movement decreases fluid exchange and nutrition in the IVDs and causes loss of disc volume. The disc space becomes narrowed and may lead to impingement of the facet joints and compression of nerves supplying the lower limbs. Decreased IVD height can also result in diminished load carrying capacity of the spinal segment [22], particularly if the posture sustained is slouched.

If the sustained posture is slouched then the posterior surface of the IVD is impacted in the following manner. Intradiscal pressure (IDP) in a slouched sitting posture (0.83MPa), is higher than sitting erect without back support (0.55MPa) [23,24], indicating there is greater load being imposed on the IVDs in slouched than in erect sitting [25]. Claus and colleagues [26] proposed that this raised IDP in slouched sitting is caused by tension in the posterior spinal ligaments. In addition Alexander et al. [27] demonstrated with MRI that significantly more posterior migration of the nucleus pulposus occurs within the IVD in slouched sitting than occurs in lordosed sitting or standing. This migration results in bulging of the posterior surface of the IVD [27,28], increasing compressive loads in the area which is already the weakest part of the disc, thus increasing IVD vulnerability [29].

On the other hand, if the sustained posture is end of range lordosis of the lumbar spine, then the facet joints will be compressed and the load will fall substantially through them, resulting in pain. This posture can be assumed by misinformed people who believe a rigid upright posture is correct [30].

Effect of sustained postures on leg circulation and buttock pressure
Increases in venous blood flow are maintained by the pump like effect of muscle contractions. When the muscles contract intramuscular blood vessels are compressed and there is an expulsion of blood from the veins. When the compressive force is removed by subsequent muscle relaxation the venous walls are pulled open. This relaxation allows a refilling of venous segments [31]. Sitting with the legs immobile reduces blood volume flow in the popliteal vein in the leg by almost 40% [32].

The relationship between seat pressure and buttock/thigh comfort is well established in the literature [33]. Pressure is highest where the ischial tuberosities interface with the seatpan. Here even very small differences in seat pressure are easily detectable [34]. Buttock pressure in sitting beyond 50 mmHg creates sitter discomfort [33]. Buttock pressure may be more evenly dispersed through movement and by enlarging the area of seatpan contact.

Effect of sustained stationary sitting on cardio-metabolic health
Movement is also important to overall bodily health. Studies worldwide are demonstrating that sitting accounts for 51-68% of an adult’s waking day [35, 36]. Days spent at work are associated with two hours more sitting and therefore less standing and walking time than leisure days [37]. Energy expenditure during sitting is 1.0 to 1.5 METs (multiples of the basal metabolic rate). Brisk walking or running, considered moderate to vigorous activity, uses an energy expenditure of 3 to 8 METs. However the greatest part of daily energy expenditure is more often related to light intensity activities such as standing, slow walking, lifting light weights. These light activities use 1.6 to 2.9 METS. Light activities have become significantly reduced because of improvements or changes in technology that encourage prolonged sitting in the workplace as well as the home [38]. As discussed above, the use of dynamic chairs reduces active movement even more. Therefore time spent sedentary has increased markedly, while energy expenditure has decreased markedly.

The health impact of this social change is only recently being acknowledged. Research now shows a relationship between sedentary behavior and cardio-metabolic ill- health. In the short term the decreased muscle contraction that occurs with prolonged, immobile sitting slows the clearance of fat from the blood stream and decreases the effect of insulin. In the long term these effects cause obesity, type 2 diabetes, cardiovascular disease, colon cancer, and postmenopausal breast cancer [39-41].

In summary: it may be seen that sustaining an erect sitting posture requires static muscle work from the spinal extensor muscles. Even when working as low as 2% of the maximum capacity these muscles fatigue. When they fatigue the low back slouches, a neuro-muscular response ensues, and the back is left unstable and vulnerable to injury. Sustained sitting is equally harmful to cardio-metabolic health and subsequent life expectancy.

Dynamic sitting i.e. movement generated and maintained actively by the sitter, is essential to avoid sustained loads on any one viscoelastic structure, and to increase basal metabolic rate. Such seating has the potential to enhance both postural and cardio-metabolic health. However, most dynamic chairs exercise the chair but not the sitter. The following discussion reviews the manner in which a new generation dynamic chair known as the Core-flex, encourages alternating muscle activity and joint movement.

b) How the Core-flex chair promotes dynamic sitting
The Core-flex design philosophy is underpinned by research demonstrating that in standing the body has a natural medial-lateral sway controlled by the hip muscles, and an antero-posterior sway controlled by the calf muscles. It is proposed that the swaying motion of approximately 2-3 times/minute alternates muscle activity thus avoiding fatigue in any one muscle group [42].

The Core-flex chair has a longitudinally split seatpan that allows a dual flexing motion driven by active ankle plantar/dorsi flexion and a small range of alternating hip flexion/extension. The hip flexion/extension maneuver creates pelvic obliquity with concomitant lumbar spine lateral flexion. These alternating movements alternate muscular activity in the legs, between each side of the superficial trunk extensors, and between the superficial trunk extensors and flexors. In this way, active use of the Core-flex seatpan breaks the fatigue-slouch cycle that is so damaging to postural health. The Core-flex chair can also be used to ensure correct patterns of trunk muscle activity that promote a stable, yet flexible spine while sitting. This proposition is explained in the following overview of the role of the trunk muscles in protecting the spine in a controlled manner.

How the Core-flex can be used to promote trunk muscle activity and spinal stability
The trunk muscles consist of two layers of muscles that, when functioning correctly, act as a natural corset for the spine. The superficial layer (for the purposes of this discussion rectus abdominis, erector spinae, superficial multifidus) has long moment arms and provides the strength to move the spine. Rather than strength the deep layer (for the purposes of this discussion transversus abdominis and deep multifidus) requires endurance. Transversus abdominis draws in the abdominal wall and stiffens the sacro-iliac joints, it prepares the spine for perturbation and it works in coordination with deep multifidus [43]. Deep multifidus runs between vertebrae and because of the short moment arms has minimal ability to move the spine. Working together the two muscles form a deep musculo-fascial band that acts as a corset to support the spine [44]. Endurance of these deep trunk muscles enables them to work at low levels of activity for long periods without fatigue to prevent anterior slipping of one vertebra on another and maintain spinal alignment. Optimal function occurs when the deep and superficial systems work in a coordinated and harmonious manner. That is the deep system works continuously at a very low level of activity (below 2% of MVC) to control individual vertebral alignment, while the superficial system alternates activity between muscle groups to provide movement and avoid muscle fatigue [45]. Thus movement of the spine occurs in a flexible and controlled manner.

There is considerable evidence that following low back injury the deep trunk muscles become dysfunctional. In optimal function the transversus abdominis contracts, initiating deep multifidus contraction and this activity should occur prior to any spinal perturbation [43,46]. In many instances following an episode of low back pain, transversus abdominis either fails to activate in which case deep multifidus also fails to contract, or activation between transversus abdominis and deep multifidus becomes delayed and coordination is lost as patterns of recruitment alter [47-49].

There is also evidence that patterns of recruitment of the deep core muscles can be retrained to act in time and harmony with each other for sustained periods at low levels of activation [50,51] thus providing the spine with a stable but flexible base. Improving activation of deep multifidus and endurance and coordination of transversus abdominis with multifidus in turn reduces activity of the more superficial trunk muscles [52,53]. For those periods when the sitter is not activating the Core-flex seatpan, it is important to have the deep core muscles working at a low level and in harmony to reduce activity and hence fatigue in the superficial trunk muscles.

In the last few years a new avenue of research has begun into the contribution of other deep core muscles to spinal control. This research is of particular relevance to the Core-flex design. Activation of the Core-flex split seat mechanism is initiated by hip flexion, and the resultant pelvic obliquity causes lateral spinal flexion. The muscles involved in use of the Core-flex dual seat mechanism include the psoas major (hip flexion) and quadratus lumborum (lateral spinal flexion). New research is demonstrating that a) when working to flex the hip at 90 degrees, a section of psoas major also contributes to maintaining lumbar lordosis b) when working to laterally flex the spine, a section of quadratus lumborum also contributes to maintain lumbar lordosis c) different sections of these muscles are activated dependent on hip and lumbar spine positions [54,55]. Investigation into the role of these muscles in contributing to coordinated neural control of trunk muscles is ongoing. Hodges, who is a part of the research team investigating the contribution of psoas major to core control, proposes that psoas major may also act to prevent posterior translation of the lumbar vertebrae, just as deep multifidus acts to prevent anterior translation. This hypothesis is currently undergoing in vivo laboratory investigation.

How the Core-flex chair may be used to improve core muscle coordination
When considering the role of transversus abdominis in low back pain, it is changes in motor control through improved endurance and timing, not strength that are important. The Core-flex chair may be used by the sitter to improve endurance, overcome dysfunction between transversus abdominis and deep multifidus, and prevent reinforcement of incorrect movement patterns. All of these outcomes are of paramount importance to successful transversus abdominis rehabilitation. Postural training specificity is essential when training the lumbo-pelvic muscles to assist in reducing low back pain [7]. Therefore it is important to ensure activation of the deep core muscles occurs correctly. If movement is driven by the superficial rectus abdominis (which flexes the spine) without coordinated movement from the deep trunk muscles, it may lead to strain of the iliolumbar ligaments [56].

Use of the Core-flex chair to improve core muscle coordination will necessitate inclusion of instructions on how to engage the deep core muscles first, before implementing the dual seatpan mechanism. It is essential to activate the deep core muscles before beginning the flexion/extension movement of the hips, and the sitter may need instruction from a health professional in relearning this muscle pattern. Once relearned, deep core muscle activation and coordination becomes automatic and improves with practice [57]. In those with good ability to contract transversus abdominis, multifidus contraction has been demonstrated to be 4.45 times higher than those with poor contraction of TrA [47]. Once activated, the deep core muscles encourage the lumbar spine into a neutral posture and the lumbar spine is in an optimal posture for sitting.

The importance of a neutral posture in maintaining spinal postural health
In the absence of spinal anomaly or severe spinal degeneration, a neutral position of the lumbar spine is currently considered to be optimal seated posture. A neutral lumbar spine is defined as 30% off individual maximal sitting lumbar lordosis where maximum lordosis is considered 100% of lumbar range and maximum kyphosis is considered 0% of sitting lumbar range [12]. Thus there is some lumbar lordosis in a neutral lumbar posture.

A neutral posture is the least damaging sitting posture because in this position the neuromuscular system is able to control flexion, rotation and shearing without causing damaging compressive forces [58,59]. It causes less load on the spine than slouched or end of range lordotic postures. It permits ease of movement [12] such as the lateral flexion that occurs with use of the Core-flex seatpan. A neutral lumbar spine also reduces static muscle activity in the cervical and thoracic regions [60,61].

In summary: endurance of deep multifidus and transversus abdominis can be improved by activating these muscles prior to using the Core-flex mechanism and by maintaining a low level of contraction while operating the Core-flex mechanism. Engaging the deep trunk muscles as described above maintains some degree of lumbar lordosis, provides control of the spine while permitting lateral spinal movement and encouraging alternating muscle activity to avoid fatigue.

How the Core-flex may be used to increase IVD nutrition without dangerous facet loading.
Moving the spine between slouch and extension is often advocated as an exercise when sitting in order to alter intradiscal pressure and improve nutrition to the IVDs [62]. The same health effects may be generated by using the Core-flex split seatpan system. The alternating pelvic obliquity and hence spinal lateral flexion increases loads on facet joints and intervertebral discs. This increased load creates fluid exchange in the discs and is therefore beneficial to spinal health. Because the pelvic obliquity is not combined with a rotation/flexion or rotation/extension force it is not sufficient to be hazardous to the facet joint [63].

How the Core-flex may be used to increase peripheral leg circulation
It is the feet that drive the leg action and hence the hip flexion/extension movements that alter the angle of the Core-flex seatpan. Positioning the feet under the hips places the weight on the balls of the feet, improves leg muscle activation and encourages movement of the ankles and hips. The muscle pump responsible for improving venous return is more effective when muscles are lengthened and shortened [31] as occurs with the ankle movement used to initiate the Core-flex split seatpan system. Stein et al. [64] demonstrated that ankle dorsiflexion exercise in sitting increased venous blood velocity, and reduced the tendency toward venous stasis. Varying the angle of the seatpan also stimulates movement of the legs, which in turn activates venous pumps and decreases oedema caused by static sitting [65].

The lateral tilt /flexion extension mechanism of the Core-flex seatpan also alternates pressure on the ischial tuberosity and posterior thigh interface with the seatpan. However, lateral tilt of the seatpan between 10 to 20 degrees causes higher muscle, soft tissue and fat compressive deformations than occur on a neutral seatpan [66]. It must be noted that these findings were based on stationary sitting at various angles of lateral tilt. Further investigation of the effect of alternating lateral tilt with hip flexion/extension is warranted to clarify whether these findings apply to the Core-flex mechanism.

The effects of Core-flex dynamic sitting on postural and cardio-metabolic health
Researchers are demonstrating that increasing light activity by interspersing it into sitting time has a positive impact on cardio-metabolic health risks incurred from sustained sitting [67]. Dunstan et al. [38] demonstrated that 2 minutes of light activity every 20 minutes of prolonged sitting leads to significant reductions in glucose and insulin thus impacting positively on the risk of Type 2 diabetes. The light activity investigated was walking on a treadmill. While it has not yet been validated by research, increasing light activity by using the Core-flex mechanism could well have a positive effect on cardio-metabolic health. Incidental activity gained by the use of the Core-flex seatpan used to supplement incidental activity gained from standing to answer the phone and walking between offices, could well lead to even better improvement in cardio-metabolic health. A call for such research has been made by many of the leading researchers into cardio-metabolic health [38,68]. The Core-flex chair is well designed to answer this call.

The rich research potential of the Core-flex design
The dynamic sitting promoted by the use of the split Core-flex seatpan paves the way for new research. Potential research opportunities that exist include research protocols to:

1) Investigate whether those with NSCLBP who consciously use lateral sway to gain relief from their pain in standing, also gain relief using the lateral sway inducing mechanism of the Core-flex chair.
2) Measure using a wireless posture monitor, the degree of pelvic obliquity and lateral flexion that occurs with use of the Core-flex seat with subjects sitting in their neutral lumbar spine posture.
3) Compare the degree of pelvic obliquity and lateral flexion that subjects can achieve using the Core-flex mechanism with the spine in maximal slouch, maximal lordosis and neutral.
4) Investigate the effect that use of the Core-flex seatpan has on the superficial core muscles using surface EMG in both those with and without a history of NSCLBP
5) Investigate the effect that use of the Core-flex seatpan has on transversus abdominis and deep multifidus. It may be possible to track transversus abdominis contraction using Rehabilitative Ultrasound Imaging. Tracking deep multifidus will require fine wire EMG.
6) Investigate the effect that use of the Core-flex seatpan has on psoas major and quadratus lumborum and their ability to simultaneously flex the hip and laterally flex the spine respectively, while maintaining lordosis. Such studies require fine wire EMG.
7) Determine whether use of the Core-flex split system mechanism expends sufficient METS to be classified as light intensity activity.
8) Compare leg volume changes when using the Core-flex leg driven seatpan motion with the chair used by Stranden [65] where the seatpan tilt forced a reaction from the legs.
9) Compare the effect of ankle plantarflexion on venous velocity and return with the findings of Stein [64] who used dorsiflexion.
10) Determine how effective the alternating pelvic obliquity is on alternating pressure between the ischial tuberosities.
11) Determine whether buttock pressure is less than 50mmHg described by Noro et al. [33] as the “sitting buttock comfort zone”.
12) Determine how much pressure is transferred to the thighs from the ischial tuberosities by the geometry of the seatpan.

In 2011 Solomonow (p. 219) stated “The major components of stability are the properties of the external load, passive viscoelastic tissues (ligaments, discs, facet capsules and dorso-lumbar fascia) combined with the properties of the active tissues (muscles and their sensory-motor control, co-activation and associated intra-abdominal pressure) as well as the pro-inflammatory status of the tissues” [69]. The Core-flex chair addresses all of these issues by providing a design that:

  •     encourages a neutral spine posture from which movement can occur
  •     facilitates active joint movement
  •     promotes alternating activity of muscle groups
  •     can be utilized to improve patterns of muscle function
  •     encourages active sitting to prevent a fatigue-induced dysfunctional neuro-muscular response

The Core-flex chair re-defines dynamic seat design. It offers a stable base of support for low load deskbound tasks while encouraging alternating lateral movements of the lumbo-pelvic unit, promoted by active muscle involvement of the sitter. The sitter provides the dynamic momentum; the chair accommodates the movement. Past dynamic chair design has striven to avoid muscle fatigue by lessening muscle activity using posture alteration managed by weight shifting mechanisms, motors or pumps. The sitter remains a passive passenger, encouraged into relaxed slouched postures both by the mental connection of sitting and relaxation and a chair that moves for them. With the Core-flex new generation dynamic seat design, it is the sitter that exercises, not the chair.


1. O’Sullivan K, O’Sullivan P, O’Keeffe M, O’Sullivan L, Dankaerts W (2013) The effect of dynamic sitting on trunk muscle activation: A systematic review. Appl Ergon. 44: 628-635.
2. Ellegast R, Kraft K, Groenesteijn L, Ktause F, Berger H et al. (2012) Comparison of four specific dynamic office chairs with a conventional office. Appl Ergon 43: 296-307.
3. van Dieën J, Looze , Hermans V (2001) Effects of dynamic office chairs on trunk kinematics, trunk extensor EMG, and spinal shrinkage. Appl Ergon 44: 739–50.
4. van Dieën J, Westebring-van der Putten E, Kingma I, de Looze M (2009) Low-level activity of the trunk extensor muscles causes electromyographic manifestations of fatigue in absence of decreased oxygenation. J Electromyogr Kinesiol 19: 398-406.
5. Dunk N, Kedgley A, Jenkyn T (2009) Evidence of a pelvis-driven flexion pattern: Are the joints of the lower lumbar spine fully flexed in seated postures? Clin. Biomech 24: 164–168.
6. Adams MA, McNally DS, Chinn H, Dolan P (1994) Posture and the compressive strength of the lumbar spine. Clin Biomech 9: 5–14.
7. O’Sullivan P, Dankaerts W, Burnett A, Farrell GT, Jefford ET et al. (2006) Effect of different upright sitting postures on spinal-pelvic curvature and trunk muscle activation in a pain-free population. Spine 31: E707-712.
8. Callaghan JP, McGill SM (2001) Low back joint loading and kinematics during standing and unsupported sitting. Ergonomics 44: 280-294.
9. McGill S, Kippers V (1994) Transfers of loads between lumbar tissue during the flexion-relaxation phenomena. Spine 19: 2190-2196.

10. Snijders C, Hermans P, Niesing R, Spoor CW, Stoeckart R (2004) The influence of slouching and lumbar support on iliolumbar ligaments, intervertebral discs and sacroiliac joints. Clin Biomech 19: 323-329.
11. Richardson C, Snijders CJ, Hides, J, Damen L, Pas MS et al. (2002) The relation between the transversus abdominis muscle, sacroiliac joint mechanics, and low back pain. Spine 27: 399–404.
12. O’Sullivan K, O’Dea P, Dankaerts W, O’Sullivan P, Clifford A, et al. (2010) Neutral lumbar spine sitting posture in pain-free subjects. Man Ther 15: 557-561.
13. O’Sullivan K, Verschueren S, Van Hoof W, Ertanir F, Martens L et al. (2013) Lumbar repositioning error in sitting: Healthy controls versus people with sitting-related non-specific chronic low back pain (flexion pattern). Man Ther S1356-689X(13)00083-0. doi:10.1016/j.math.2013.05.005. [Epub ahead of print].
14. Dolan K, Green A (2006) Lumbar spine reposition sense: the effect of a 'slouched' posture. Man Ther 11: 202-207.
15. Solomonow M (2006) Sensory-motor control of ligaments and associated neuromuscular disorders. J. Electromyogr. Kinesiol 16: 49-67.
16. Solomonow M (2009) Ligaments: A source of musculoskeletal disorders. J Bodyw Mov Ther 13: 136–154.
17. Solomonow M (2012) Neuromuscular manifestations of viscoelastic tissue degradation following high and low risk repetitive lumbar flexion. J Electromyogr Kinesiol 22: 155-175.
18. Ben-Masaud A, Solomonow D, Davidson B, Zhou, B.H., Lu, Y et al. (2009) Motor control of lumbar instability following exposure to various cyclic load magnitudes. Eur Spine J. 18: 1022-1034.
19. Le B, Davidson B, Solomonow D, Lu Y, Patel, V et al. (2009) Neuromuscular control of lumbar instability following static work of various loads. Muscle Nerve 39: 71-82.
20. Youssef, J, Davidson B, Zhou B, Lu Y, Patel V et al. (2008) Neuromuscular neutral zones response to static lumbar flexion: muscular stability compensator. Clin Biomech 23: 870-880.
21. Beach TA, Parkinson RJ, Stothart JP, Callaghan JP (2005) Effects of prolonged sitting on the passive flexion stiffness of the in vivo lumbar spine. Spine J. 5: 145-154.
22. Owen SC, Brismée JM, Pennell PN, Dedrick GS, Sizer PS et al. (2009) Changes in spinal height following sustained lumbar flexion and extension postures: a clinical measure of intervertebral disc hydration using stadiometry. J Manipulative Physiol Ther 32: 358-363.
23. Nachemson A (1963) The influence of spinal movements on the lumbar intradiscal pressure and on the tensile stresses in the annulus fibrosus. Acta Orthop. Scand 33: 183–207.
24. Wilke HJ, Neef P, Caimi M, Hoogland T, Hoogland T, et al. (1999) New in vivo measurements of pressures in the intervertebral disc in daily life. Spine 24: 755–762.
25. Rohlmann A, Zander T, Graichen F, Dreischarf M, Bergmann G (2011) Measured loads on a vertebral body replacement during sitting. Spine J 11: 870-875.
26. Claus AP, Hides JA, Moseley GL, Hodges PW (2008) Sitting versus standing: does the intradiscal pressure cause disc degeneration or low back pain? J Electromyogr Kinesiol 18: 550-558.

27. Alexander LA, Hancock E, Agouris I, Smith FW, MacSween A (2007) The response of the nucleus pulposus of the lumbar intervertebral discs to functionally loaded positions. Spine 32: 1508–1512.
28. Nazari J, Malcolm H, Pope MH, Graveling RA (2012) Reality about migration of the nucleus pulposus within the intervertebral disc with changing postures. Clin Biomech 27: 213–217.

29. Adams MA, McMillan DW, Green P, Dolan P (1996) Sustained loading generates stress concentrations in lumbar intervertebral discs. Spine 21: 434–438.
30. O’Sullivan K, O’Keeffe M, O’Sullivan L, O’Sullivan P, Dankaerts W (2013) Perceptions of sitting posture among members of the community, both with and without non-specific chronic low back pain. Man Ther Jun 25. pii: S1356-689X(13)00108-2. doi:0.1016/j.math.2013.05.013. [Epub ahead of print]
31. Laughlin MH, Schrage WG (1999) Effects of muscle contraction on skeletal muscle blood flow: when is there a muscle pump? Med Sci Sports Exerc. 31: 1027-1035.
32. Hitos K, Cannon M, Cannon S, Garth S, Fletcher JP (2007) Effect of leg exercises on popliteal venous blood flow during prolonged immobility of seated subjects: implications for prevention of travel-related deep vein thrombosis. J Thromb Haemost 5: 1890-1895.
33. Noro K, Naruse T, Lueder R, Nao-i N, Kozawa M (2012) Application of Zen sitting principles to microscopic surgery seating. Appl Ergon 43 308-319.
34. Goossens R, Teeuw R, Snijders CJ (2005) Sensitivity for pressure difference on the ischial tuberosity. Ergonomics 48: 895-902.
35. Healy GN, Wijndaele K, Dunstan DW, Shaw JE, Salmon J (2008) Objectively measured sedentary time, physical activity, and metabolic risk: the Australian Diabetes, Obesity and Lifestyle Study (AusDiab). Diabetes Care 31: 369–371.
36. Healy G, Clark B, Winkler E, Gardiner PA, Brown WJ (2011) Measurement of adults' sedentary time in population-based studies. Am J Prev Med 41: 216–227.
37. McCrady S, Levine J (2009) Sedentariness at work; how much do we really sit? Obesity 17: 2103–2105.
38. Dunstan D, Howard B, Healy G, Owen N (2012) Review. Too much sitting – A health hazard. Diabetes Research and Clinical Practice 97: 368-376.
39. Hamilton MT, Hamilton DG, Zderic DW (2007) Role of Low Energy Expenditure and Sitting in Obesity, Metabolic Syndrome, Type 2 Diabetes, and Cardiovascular Disease. Diabetes 56: 2655–2667.
40. Katzmarzyk PT, Church TS, Craig CL, Bouchard C (2009) Sitting time and mortality from all causes, cardiovascular disease, and cancer. Med Sci Sports Exercise 41: 998-1005.
41. Owen N, Sparling PB, Healy GN, Dunstan DW, Mathews CE (2010) Sedentary Behavior: Emerging Evidence for a New Health Risk. Mayo Clin Proc. 85: 1138-1141.
42. Prado J, Dinato M,. Duarte M (2011) Age-related difference on weight transfer during unconstrained standing. Gait & Posture 33: 93-97.
43. Hodges PW, Richardson CA (1996) Inefficient muscular stabilization of the lumbar spine associated with low back pain. A motor control evaluation of transversus abdominis. Spine 21: 2640-2650.
44. Hides J, Wilson S, Stanton W, McMahon S, Keto H et al. (2006) An MRI investigation into the function of the transversus abdominis muscle during "drawing-in" of the abdominal wall. Spine 31: E175-178.
45. O’Sullivan K, McCarthy R, White A, O'Sullivan L, Dankaerts W (2012) Lumbar posture and trunk muscle activation during a typing task when sitting on a novel dynamic ergonomic chair. Ergonomics 55: 1586–1595.
46. Hodges PW, Richardson CA. (1997) Feedforward contraction f transversus abdominis is not influenced by the direction of arm movement. Exp Brain Res 114: 362-370.

47. Hides J, Stanton W, Mendis MD, Sexton M (2011) The relationship of transversus abdominis and lumbar multifidus clinical muscle tests in patients with chronic low back pain. Man Ther 16: 573-577.
48.Hodges, PW (2001) Changes in motor planning of feedforward postural responses of the trunk muscles in low back pain. Exp Brain Res 141: 261–266.
49. MacDonald D, Moseley G, Hodges PW (2009) Why do some patients keep hurting their back? Evidence of ongoing back muscle dysfunction during remission from recurrent back pain. Pain 142: 183–188.
50. Hodges PW, van den Hoorn W, Dawson A, Cholewicki J (2009) Changes in the mechanical properties of the trunk in low back pain may be associated with recurrence. J Biomech 42: 61–66.
51. Tsao H, Hodges PW (2007) Immediate changes in feedforward postural adjustments following voluntary motor training. Exp Brain Res. 181: 537–46.
52. Hodges PW (2011) Pain and motor control: From the laboratory to rehabilitation. J Electromyogr Kinesiol 21: 220–228.
53. Tsao H, Druitt TR, Schollum TM, Hodges PW (2010) Motor training of the lumbar paraspinal muscles induces immediate changes in motor coordination in patients with recurrent low back pain. J Pain, 11: 1120–1128.
54. Park RJ, Tsao H, Cresswell A, Hodges PW (2012) Differential Activity of Regions of the Psoas Major and Quadratus Lumborum during Submaximal Isometric Trunk Efforts. J Orthop Res 30: 311-318.
55. Park RJ, Tsao H, Claus A, Cresswell A, Hodges PW (2013) Changes in regional activity of the psoas major and quadratus lumborum with voluntary trunk and hip tasks and different spinal curvatures in sitting. J Orthop Sports Phys Ther 43: 74-82.
56. Snijders C, Hermans P. Niesing R, Kleinrensink GJ, Pool-Goudzwaard A (2008) Effects of slouching and muscle contraction on the strain of the iliolumbar ligament. Man Ther 13: 325-333.
57. Hides J, Stanton W, Wilson SJ (2010) Retraining motor control of abdominal muscles among elite cricketers with low back pain. Scand J Med Sco Sports 20: 834-842.
58. McGill SM, Grenier S, Kavcic N, Cholewicki J (2003) Coordination of muscle activity to assure stability of the lumbar spine. J. Electromyogr Kinesiol 13: 353-359.
59. Claus AP, Hides JA, Moseley GL, Hodges PW (2009) Different ways to balance the spine: subtle changes in sagittal spinal curves affect regional muscle activity. Spine 34: E208-214.
60. Falla D, O’Leary S, Fagan A, Jull G (2007) Recruitment of the deep cervical flexor muscles during a postural-correction exercise performed in sitting. Man Ther 12: 139-143.
61. Caneiro JP, O’Sullivan P, Burnett A, Barach A, O’Neil D et al. (2010) The influence of different sitting postures on head/neck posture and muscle activity. Man Ther 15: 54-60.
62. McKenzie R (2006) Treat Your Own Back. 6th Edition. Spinal Publications. New Zealand.
63. Popovich J, Welcher J, Hedman T, Tawackoli W, Anand N, et al. (2013) Lumbar facet joint and intervertebral disc loading during simulated pelvic obliquity. Spine J. doi:pii: S1529-9430(13)00412-9. 10.1016/j.spinee.2013.04.011. [Epub ahead of print]
64. Stein PD, Yaekoub AY, Ahsan ST Matta F, Lala MM, et a.l (2009). Ankle exercise and venous blood velocity. Thromb Haem 101: 1100-1103.
65. Stranden E. (2000) Dynamic leg volume changes when sitting in a locked and free floating tilt office chair. Ergonomics 43: 421-433.

66. Shabshin N, Ougortsin V, Zoizner G, Gefen A (2010) Evaluation of the effect of trunk tilt on compressive soft tissue deformations under the ischialtuberosities using weight-bearing MRI. Clin Biomech 25: 402-408.
67. Shiyovich A, Shlyakhover V, Katz A (2013) Sitting and cardiovascular morbidity and mortality. Harefuah. 152: 43-48.
68. Owen N (2012) Sedentary behavior: Understanding and influencing adults' prolonged sitting time. Pre Med. 55: 535–539.
69. Solomonow M (2011) Review. Time dependent spine stability: The wise old man and the six blind elephants. Clin Biomech 26: 219–228.