Several findings provide support for the proposed relationship between diaphragm EMG and postural control of trunk stability.
Anatomy of Diaphragm:
The diaphragmatic musculature and its fasciae imparts crucial function of respiration & postural control. The diaphragm is divided into 3 parts on the basis of these muscle fiber origins:
1. Sternal part: two muscular slips from the back of the xiphoid process.
2. Costal part: the inner surfaces of the cartilages and adjacent portions of the lower six ribs on either side, interdigitating with the Transversus abdominis.
3. Lumbar part: aponeurotic arches, named the lumbocostal arches, and from the lumbar vertebrae by two pillars or crura. There are two lumbocostal arches, a medial and a lateral, on either side.
The diaphragm is innervated by the phrenic nerve. It's a branch of C3,C4,and C5.
Crura and central tendon: At their origins the crura are tendinous in structure, and blend with the anterior longitudinal ligament of the vertebral column.The central tendon of the diaphragm is a thin but strong aponeurosis situated near the center of the vault formed by the muscle, but somewhat closer to the front than to the back of the thorax, so that the posterior muscular fibers are the longer.
Structurally the diaphragm can be compared to a round dome tent. All of the fibers originate from the ground, where the tent is staked down. The stakes in front are the xyphoid process, those in back are the lumbar vertebrae. The posterolateral stakes are the arcuate ligaments, while the anterolateral stakes are the ribs. They all insert into the central tendon, which is the top of the tent where everything comes together.
Important parts of diaphragm are:
1. Right crus: takes origin from L1-L3. It splits to enclose the esophagus, so the esophageal hiatus is (usually) entirely formed by the right crus. Fibers from the right crus intermingle with the fibers from the left crus at the aortic hiatus. (Latin, crus = resembling leg or legs)
2. Left crus: takes origin from L1-L2. It is smaller and shorter than the right crus. It sometimes contributes something to the esophageal hiatus. Fibers from the left crus intermingle with the fibers from the right crus at the aortic hiatus. (Latin, crus = resembling leg or legs)
3. Medial arcuate ligaments: thickening of psoas major fascia. Fibers taking origin from here, along with those from the lateral arcuate ligament, fill in the "gap" between the crura and the costal part of the diaphragm. They are labeled "medial lumbocostal arches" above. (Latin, arcuare = to bend like a bow)
4. Lateral arcuate ligaments: thickening of the quadratus lumborum fascia. Fibers taking origin from here, along with those from the medial arcuate ligament, fill in the "gap" between the crura and the costal part of the diaphragm. They are labeled "lateral lumbocostal arches" above. (Latin, arcuare = to bend like a bow)
Intra-thoracic & Intra-abdominal pressure changes during the diaphragm movement
The diaphragm is the primary muscle of respiration. Contraction of the fibers pulls the central tendon inferiorly, increasing the volume (and decreasing the pressure) of the thoracic cavity. This creates a pressure gradient between the inside and the outside, air rushes in to compensate. Secondary to this, the volume of the abdominal cavity is decreased, raising its pressure. During defecation or parturition diaphragm assist the abdominal wall muscles.
The diaphragm & Tr abdominis synergy:
Under normal condition diaphragm and transversus abdominis are antagonists. However, diaphragm contracts eccentrically, following the contraction of transversus abdominis and the other muscles acting on the abdomen (e.g. pelvic floor muscles). But, the length changes in either direction were relatively small, approximately 10% of initial diaphragm length (2).
Studies of trunk muscle recruitment in humans suggest that diaphragm and transversus abdominis activity, and the associated intra-abdominal pressure (IAP) contribute to the control of intervertebral motion. Elevated intra-abdominal pressure and contraction of diaphragm and transversus abdominis provide a mechanical contribution to the control of spinal intervertebral stiffness. Furthermore, the effect is modified by their muscular attachments to the spine (1).
The diaphragm & limb movement relation:
Contraction of the diaphragm precedes the onset of movement of the limb & it is hypothesized that this is a preparatory action to aid truncal stability. Diaphragmatic response requires a threshold magnitude of reactive forces resulting from the movement because studies have reported no diaphragmatic contraction with movement of the wrist, fingers or thumb while it did occur with shoulder and elbow movement.
An increase in IAP associated with arm movement is predominantly due to the contraction of the diaphragm and abdominal muscles. The diaphragm shorten initially consistent with an increase in activation but then lengthened as abdominal pressure rose.
How diaphragm controls the trunk stability:
1. Diaphragm controls the trunk stability indirectly via IAP (intra abdominal pressure): The diaphragm cannot move the trunk directly to oppose these forces, but it has been proposed that its contraction contributes to trunk stability via an increase in pressure in the abdominal cavity.
Intra-abdominal pressure mechanism for stabilizing the lumbar spine: According to a model proposed by Cholewicki & colleagues (1999) 2 distinct mechanisms were simulated separately and in combination to provide lumbar stability.
a. One was antagonistic flexor extensor muscle coactivation and
b. The second was abdominal muscle activation along with generation of IAP.
Both mechanisms were effective in stabilizing the lumbar spine. The critical load and therefore the stability of the spine increase with either increased antagonistic muscle coactivation forces or increased IAP along with increased abdominal force. Both mechanisms were also effective in providing mechanical stability to the spine when activated simultaneously.
However this model suggests that the IAP mechanism for stabilizing the lumbar spine appears preferable in tasks that demand trunk extensor moment such as lifting or jumping. This mechanism can increase spine stability without the additional coactivation of erector spinae muscles.
2. Diaphragm controls the trunk stability by maintaining the geometry of the abdominal muscles:
Diaphragmatic contraction could increase stability of the trunk by minimizing displacement of abdominal contents into the thorax, thus maintaining the hoop-like geometry of the abdominal muscles. These muscles could then increase spinal stability via tension in the thoraco-lumbar fascia (Farfan, 1973; McGill & Norman, 1987; Tesh et al. 1987).
3. Although previous animal studies have proposed that the costal and crural portions of the diaphragm may function independently (De Troyer, Sampson, Sigrist & Macklem, 1981; van Lunteren, Haxhiu, Cherniack & Goldman, 1985), the co-activation of the costal and crural portions of the diaphragm suggests that both regions of the diaphragm function together for their role in postural control.
The neural circuit for postural control via diaphragm:
Two previous human studies have provided indirect evidence of a contribution of the diaphragm to postural control.
1. Studies in decerebrate animals ware done for finding evidence of a postural role of the diaphragm. In this procedure evaluation of the response of the diaphragm to stimulation of the cerebellum (Massion et al. 1960) and stimulation of tonic cervicolabyrinthine postural reflexes (Massion, 1976), ware done.
It was found that the response in the diaphragm are preprogrammed by the CNS and initiated as part of the motor command for movement (Cordo & Nashner, 1982; Horak, Esselman, Anderson & Lynch, 1984; Bouisset & Zattara, 1987).
2. The phrenic motoneurone pool may be influenced by corticospinal pathways that do not involve pontomedullary respiratory centres both in animals (Colle & Massion, 1958; Planche & Bianche, 1972) and humans (Gandevia & Rothwell, 1987).
3. Diaphragm is activated via pathways involved in the control of postural activity associated with limb movement.
4. Co-activation of the diaphragm and transversus abdominis who have normal antagonistic function in respiration suggests that neural outputs other than those from 'classical' respiratory centres are likely to be involved in control of diaphragm movement.
5. Studies have shown that there is increase in EMG of the diaphragm which preced the onset of deltoid EMG regardless of the phase of respiration. This provides evidence that the postural function of the diaphragm interferes with the respiratory activity of this muscle.
Excluding diaphragm other respiratory muscles such as the intercostal muscles have been identified to have variation in respiratory activity due to postural changes (Rimmer et al. 1995). Contrastingly, variation in postural activity of the abdominal muscles also occurs due to changes in respiratory activity (Hodges et al. 1997).
Diaphragmatic strengthening exercises (source:http://calder.med.miami.edu/providers/PHYSICAL/resdia.html)
Diaphragm strengthening is recommended for all patients with less than normal vital capacity. Patients with lower thoracic or lumbar lesions and a fair or better grade of diaphragm strength are usually candidates for progressive resistive exercises until they regain full activity. Patients with cervical and high thoracic lesions and a less than fair grade of diaphragm strength are usually candidates for active-assistive exercises.
1. Progressive Resistive Exercises, with weights, manually, with positioning, and incentive inspiratory spriometry, for example, should allow the diaphragm to contract through its full range, to prevent altering the patient's normal breathing pattern, and should be done carefully to prevent fatiguing the diaphragm, with the patient in a lying position:
Weights - After the placing the patient in supine, the therapist places a diaphragm weight pan over the epigastric region, without the pan resting on the ribs which can prevent full excursion. The amount of weight used as resistance should allow the epigastric rise to be the same as before the weight is applied. If the diaphragm is innervated, 5 pound weights can usually be used at first. When the patient can maintain a coordinated, unaltered breathing pattern for 15 minutes, with full epigastric rise and without substituting the sternocleidomastoid muscles, the weight can be increased until the patient's strength reaches an acceptable plateau, such as vital capacity remaining the same in a subsequent evaluation, or the patient being able to tolerate full activity with early signs of fatigue.
Manually - As inspiratory capacity increases, the therapist can apply manual resistance while the patient breathes deeply. If the intercostal musculature is functional, the therapist can provide manual, visual, or verbal feedback on chest motions during inspiration to increase the ventilation of isolated lobes.
Positioning - Since resistance to the diaphragm provided by abdominal contents increases in the head-down position, resistive strengthening can be achieved by changing the patient's position. For example, a 15-degrees head-down incline supplies a resistive force equal to 10 pounds.
Incentive Spirometry - After placing the patient in the preferable supine position (the weaker the diaphragm, the greater the necessary incline), the therapist has the patient take 4 slow, easy breaths. Expiration after the first 3 breaths should be normal, but, after the 4th breath, the patient should exhale slowly until there is no more air to exhale. The patient then places the spirometer in the mouth, forms a tight seal, takes a slow, deep breath, watches the ball in the spirometer rise, maintains the rise as long as possible, removes the spirometer mouthpiece, and relaxes. This should be repeated 8-10 times and done during 3-4 sessions each day.
2. Active-Assistive Exercises are done with active-assistive devices, such as pneumobelts and corsets, after the patient with poor diaphragm strength begins to sit.
Pneumobelts - Also called exhalation belts, pneumobelts are used for patients with an initial vital capacity between 500 and 1000 cc in an upright position. They have inflatable bladders, placed over the abdomen, and connected, with a hose, to an easily adjustable positive pressure respirator. As the bladder is inflated, it pushes the abdominal contents in and up, which push the diaphragm into the optimal position for exhalation. When the patient has been upright and on an active program for 8 hours, with no signs of fatigue and/or sternocleidomastoid muscle substitution, the patient can begin to be phased off the pneumobelt, by decreasing the pressure in the bladder, first while the patient is inactive, and then while he/she is active.
Corsets - Corsets are used for patients with weak, or "less than fair" abdominal musculature, whose diaphragms therefore are in a descended position, which causes a decrease in inspiratory reserve volume. Corsets are placed just over the last two floating ribs and covering the iliac crest. They should be snug (but not too tight) to support the abdomen and displace the diaphragm to a higher resting position, with the lower buckles tighter than the upper ones. A hand should be able to be placed under the upper part of the corset. Blood pressure and heart rate should be carefully monitored for hypotension and blood pooling. If diaphragm strength improves or abdominal tone increases enough to adequately support the abdominal contents, the corset can be discontinued after the patient's vital capacity, breathing pattern, and vital signs (with the body positioned at a 45 degree incline and the head up) test the same with, and without, the corset.
1. Cholewicki J; Intra-abdominal pressure mechanism for stabilizing the lumbar spine .J Biomech. 1999 Jan;32(1):13-7.
2. Hodges P et al; Intervertebral stiffness of the spine is increased by evoked contraction of transversus abdominis and the diaphragm: in vivo porcine studies.Spine (Phila Pa 1976). 2003 Dec 1;28(23):2594-601.
3. Hodges P et al; Contraction of the human diaphragm during rapid postural adjustments. Journal of Physiology (1997), 505.2, pp.539-548