JACM Engel Vemulpad 2011 1 1

The premise that lung function can regulate chest wall mobility is an accepted concept. Descriptions of the
primary and accessory respiratory structures do not usually include spinal components as a part of these
classifications. The case for including these components as a part of the respiratory mechanism and their role in
the development of dyspnea and chest wall rigidity in chronic obstructive pulmonary disease (COPD) is re-
viewed. Mechanical impairment of the chest wall is a contributing factor in the prognosis of COPD. Reducing
this impairment improves prognosis. Because spinal manipulation and soft-tissue therapy increase joint mobility
and decrease muscle hypertonicity, respectively, applying these interventions to the chest wall in COPD could
reduce chest wall rigidity, thereby improving breathing mechanics. Improvements in breathing mechanics re-
duce the work of the respiratory muscles and delay the onset of dyspnea. Exercise capacity is reliant on the
ability to overcome activity-limiting dyspnea, which usually occurs prior to maximum exercise capacity being
reached. Delaying the onset of dyspnea permits more exercise to be performed before dyspnea develops. Spinal
manipulation and soft-tissue therapy have the potential to deliver such a delay. Because exercise tolerance is
considered to be a strong predictor of quality of life and survival in COPD, any increase in exercise capacity
would therefore improve prognosis for the disease.

Introduction

he idea that lung function

can regulate chest wall

mobility is not a new concept.

Most descriptions of

normal respiration recognize the necessity for adequate chest
wall movements.

In the 1980s, Forkert found that the relative distribution of

inspired gas to a lung region was dependent on the mobility
of the overlying chest wall, concluding that regional lung
function was dependent on regional rib cage excursion.

More recently, O’Donnell showed that localized restriction of
the chest wall during exercise induced severe dyspnea in
otherwise healthy individuals.

The concept is not limited to

healthy individuals. For example, even in the absence of lung
or pleural disease, people with rheumatoid arthritis develop
changes in rib cage mobility, which alters breathing me-
chanics and results in a decrease in lung volume and the
development of dyspnea.

In ankylosing spondylitis, a sim-

ilar decrease in spinal mobility results in a loss of chest wall
mobility and a fall in lung vital capacity.

At the other end of the spectrum, increasing chest wall

mobility can also affect lung function. A number of studies
have shown that increasing thoracic joint mobility improves
lung function in the short term, in normal individuals.

6–8

The scenario is applicable in the presence of respiratory

disease as well. Chest percussion and vibration assist spu-
tum removal and improve lung ventilation in chronic ob-
structive pulmonary disease (COPD) and bronchiectasis.

9,10

Paraspinal muscle inhibition, rib raising, myofascial release,
and thoracic lymphatic pump have been used with some
success in the management of COPD

and pneumonia in the

elderly.

12,13

High-frequency chest wall compression im-

proves respiratory function in patients with neuromuscular
disease,

COPD,

15,16

and cystic fibrosis.

Spinal and costal

joint manipulation has some benefit for lung function and
quality of life in patients with COPD.

18–20

Department of Chiropractic, Macquarie University, Sydney, New South Wales, Australia.

Faculty of Science, Macquarie University, Sydney, New South Wales, Australia.

THE JOURNAL OF ALTERNATIVE AND COMPLEMENTARY MEDICINE
Volume 17, Number 9, 2011, pp. 797–801
ª Mary Ann Liebert, Inc.
DOI: 10.1089/acm.2010.0517

797

Following a biomechanical model, descriptions used to

explain these results include impeded inspiratory muscle
action,

2,21,22

rib cage restriction and stiffness,

4,18,20

and better

pulmonary secretion clearance resulting from improved air-
flow velocities.

Other explanations refer to the short-term

beneficial effects on breathing frequency resulting from re-
laxation exercises

24,25

and improvements in respiratory cili-

ary function following mechanical chest vibration.

Missing from these explanations is a description of the

changes that occur in some of the spinal structures that make
up the chest wall, as mobility is altered. The objectives of this
article are to review the effect of spinal manipulation, soft-
tissue therapy, and exercise on increasing lung function in
COPD, and to propose an anatomical basis for this effect.

Functional Anatomy of the Chest Wall in COPD

In healthy individuals, an increase in respiratory demand

is met by normal compensatory responses. Most descriptions
of the respiratory system, in this context, focus on the pri-
mary and secondary respiratory structures. In COPD,
breathing mechanics become distorted beyond the body’s
ability to manage respiratory demand with normal com-
pensatory responses using these structures. This results in
additional structures becoming involved. In this article, these
additional structures will be referred to as the ‘‘reserve’’ re-
spiratory structures, as they are always at hand, but not
traditionally included within the classifications of primary or
accessory respiratory structures. They include spinal mus-
cles, joints of the thoracic spine, and connective tissues as-
sociated with these structures.

Possible role of ‘‘reserve’’ respiratory structures
in ‘‘normal’’ breathing

During normal breathing at rest, the reserve respiratory

structures are not active (Fig. 1A). Under increased load
conditions, such as deep inspiration or forced expiration,
they may become active as part of normal breathing.

The configuration of the erector spinae muscle creates

multiple links between the posterior rib cage and the lumbar
spine and sacrum.

27,28

Acting as a group, contraction of the

erector spinae causes extension of the spine; individually,
subgroups have the ability to depress several ribs during
forced expiration.

The erector spinae aponeurosis is made up from tendons of

longissimus thoracis pars thoracis and iliocostalis lumborum
pars thoracis. As movement of the aponeurosis is independent
from the rest of erector spinae,

these muscles are able to act

as independent stabilizers of the posterior thoracic cage.

Multifidus is responsible for the segmental ‘‘rocking’’

component of extension in the spine.

This ability enables it to

assist in creating additional rib elevation in the later stages of
deep inspiration by creating movement in the costovertebral
and costotransverse joints through extension of the vertebrae.

The thoracolumbar fascia links the anterior abdominal wall

and the muscles of the lower back, via the lateral raphe.

This

configuration enables it to assimilate multidirectional forces
arising from the abdomen, lumbar muscles, and lumbar spine
and highlights its dynamic role in breathing.

Thoracic vertebrae articulate with more than one rib on

either side. Each rib is connected to two adjacent vertebrae
and their intervening intervertebral disc at multiple points.

As a result, each vertebra operates as the functional center of
a number of ribs. The constant distractive force created by
the intervertebral disc’s ability to resist deformation,

to-

gether with the inherent elastic nature of the ribs, produces
tension in the posterior joints of the chest wall (i.e., costo-
vertebral and costotransverse joints). These forces are bal-
anced by the capsular, sternocostal, and intra-articular
ligaments anteriorly. Together with the muscles, these
structures govern the level of chest wall recoil, or rigidity, as
the case may be.

Role of ‘‘reserve’’ respiratory structures in COPD

In COPD, there is a loss of lung elastic recoil, which results

in an increase in airway resistance, reducing dynamic

FIG. 1.

Primary, accessory, and ‘‘reserve’’ respiratory

structures involved in breathing at rest. Shaded areas rep-
resent involvement of the respective structures. A. Normal
individuals. B. Individuals with chronic obstructive pulmo-
nary disease. The proposal in (B) is tentative in that the ex-
tent of involvement of Accessory and Reserve structures is
unknown at this time.

798

ENGEL AND VEMULPAD

pulmonary compliance.

As a result, additional air is left in

the lungs at the end of expiration, leading to an increase in
end-expiratory volume. Chest wall expansion occurs, forcing
the inspiratory muscles to operate at nonoptimal lengths,
reducing their maximal contractile force.

The reduced

contractile force means the workload of these muscles in-
creases substantially during breathing. They adapt to the
situation by remodeling,

shortening in length and in-

creasing in tone.

As attempts to reduce end-expiratory volume continue,

air-trapping occurs, resulting in lung hyperinflation.

32–34

Hyperinflation pushes the sternum anteriorly and causes a
loss in thoracolumbar spine mobility, not dissimilar to what
occurs in ankylosing spondylitis or rheumatoid arthritis. The
erector spinae is stretched, pulling the aponeurosis taut,
further limiting movement of the lower ribs. As a result, the
ability of the quadratus lumborum to act as a stabilizer of
the diaphragm during deep inspiration

is compromised.

The need to recruit the abdominal muscles in order to im-
prove respiratory function increases the pull on the thor-
acolumbar fascia via the lateral raphe. This has an additional
impact on the lower rib cage’s ability to expand.

Within 4–6 weeks, the diaphragm adapts by dropping

sarcomeres and shortening its operational length.

35,36

This

restores its force-generating capacity but reduces its ability to
undergo displacement.

As a result, expansion of the lower

rib cage, which usually occurs as part of diaphragmatic
movement early in normal inspiration, is compromised. In-
spiration becomes less efficient while breathing becomes
more dependent on rib cage inspiratory muscle activity.

However, inspiratory muscle activity is already compro-
mised due to the changes brought about by hyperinflation.
In severe cases, contraction of the diaphragm produces a
decrease rather than an increase in the transverse diameter of
the lower rib cage.

39,40

Additional rib elevation is provided by multifidus. How-

ever, this action is set against a backdrop of increasing chest
wall rigidity.

Compared to normal breathing, the reserve, accessory,

and primary respiratory structures are all active in patients
with COPD, even when breathing at rest (Fig. 1B).

The role of ‘‘reserve’’ respiratory structures in dyspnea

Dyspnea is one of the main symptoms in COPD.

Its origin

is multifactorial, with part of the cause attributable to
changes in chest wall mechanics.

22,41

As hyperinflation con-

tinues, the force needed by the respiratory muscles to
counterbalance the inward recoil of the lung and chest wall
at the end of expiration becomes substantial.

This addi-

tional effort accelerates the onset of inspiratory muscle fa-
tigue and dyspnea.

42,43

Rationale for Increasing Chest Wall Mobility

Increasing chest wall rigidity reduces chest wall move-

ments during breathing. Any contribution that these move-
ments might have in promoting lung elasticity would be
diminished. As lung elasticity is a function of lung capacity,
increasing chest wall rigidity has a detrimental effect on lung
capacity. In a similar manner, decreasing chest wall rigidity
could have a beneficial effect on lung capacity. In support of
this view, the level of mechanical impairment of the chest

wall has been identified as a contributing factor in the
prognosis of COPD.

41,44

Spinal manipulation, soft-tissue therapy, and exercise

Spinal manipulation increases joint mobility while soft-

tissue therapy decreases muscle hypertonicity.

45,46

Applying

spinal manipulation and soft-tissue therapy to a single ver-
tebral joint complex would increase joint motion and de-
crease muscle tone locally. Applying these interventions at
multiple levels would alter the overall contribution the
posterior elements make toward chest wall mobility. In
the case of COPD, an increase in the mobility of any of the
posterior components of the chest wall would lessen chest
wall rigidity. The overall impact on chest wall rigidity would
be enhanced as a reciprocal flow-on effect occurred in the
anterior components of the chest wall. Decreasing chest wall
rigidity permits an increase in inspiratory muscle lengths,
improving their efficiency and reducing the level of muscle
fatigue. If independently reducing contractile respiratory
muscle effort improves dyspnea in COPD,

then decreasing

chest wall rigidity should produce a similar effect.

In COPD, exercise intolerance is considered to be a strong

predictor of quality of life and survival.

Increasing exercise

tolerance would therefore improve these outcomes. Exercise
capacity in COPD is reliant on the ability to overcome activity-
limiting dyspnea, which usually occurs prior to maximum
exercise capacity being reached.

21,22

As mentioned earlier,

spinal manipulation and soft-tissue therapy increase joint
mobility and decrease muscle hypertonicity, respectively.

45,46

Increasing chest wall mobility through spinal manipulation
and soft-tissue therapy could have a role in reducing dyspnea
levels and increasing exercise capacity, thereby improving
prognosis of the condition. This warrants further investigation.

Conclusions

When normal respiratory mechanics become compro-

mised beyond the body’s ability to manage respiratory de-
mand with normal compensatory responses, structures not
usually associated with normal breathing are recruited to
assist with breathing. These ‘‘reserve’’ respiratory structures
include spinal muscles and joints and connective tissues as-
sociated with these structures. Improving the mobility of
these ‘‘reserve’’ structures may produce a flow-on effect in
other respiratory structures, resulting in an overall decrease
in chest wall rigidity and a delay in respiratory muscle fa-
tigue. The role of spinal manipulation and soft-tissue therapy
in reducing chest wall rigidity and improving dyspnea in
COPD merits consideration and further research.

Acknowledgments

The authors would like to thank Sharyn Eaton for helpful

comments during the preparation of this article.

Disclosure Statement

No competing financial interests exist.

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Address correspondence to:

Roger Engel, DO, DC

Department of Chiropractic

Macquarie University

Balaclava Road, North Ryde, Sydney

New South Wales 2109

Australia

E-mail: roger.engel@mq.edu.au

MANUAL THERAPY AND EXERCISE IN COPD

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