BUILDING STRONGER STATURES!
NHMRC Postdoctoral Research Fellow,
Curtin University of Technology WA
Honorary Fellow, Department of Medicine,
University of Melbourne, Australia
Annie Burke-Doe, PT, MPT, PhD
Associate Professor, University of St. Augustine
San Diego, California
Purpose:
To build stronger statures through research and education of effective movement training and optimal postural alignment to eliminate disability related to Osteoporosis, Osteopenia, and other process of compromised spine integrity and to improve the health and well being of individuals
* To demonstrate objective improvement in posture and other physiological factors
* To
eliminate spine fractures due to osteoporosis, osteopenia and other processes
of compromised bone
integrity
* To show evidence of improved health and well being
This year's focus of Posture Biomechanics Foundation research:
Investigate
the effectiveness and viability of specific training programs focused on
1.
Unloading the spine
2.
Realigning the spine and body
3. Endurance
strength training of the Erector Spinae, deep posture and core stabilizer muscles
* Investigate
how to safely strengthen the spine, decrease load on anterior vertebral body
* Investigate
how to load the spine within its biomechanical limits
* Discovering
how to distribute the forces within the vertebrae and throughout the
entire spine
* Investigate
how to maintain optimal alignment with all movement and activity
* Investigate
what is optimal spine curve measurement for building a stronger statures and
improving the
health of all individuals
Optimal Alignment, or posture, is a necessary component. This approach focuses on building a stronger stature for better health. In order to achieve this, it is necessary to determine optimal postural alignment. Despite the fact that current research emphasizes the importance of the three spinal curves for body support, many problems occur due to compromised spine integrity, along with abnormal compression and shear forces within and beyond the spine itself.
Review of Literature Related to PBF Research
Osteoporotic
bone loss can be characterized as primary or secondary. Primary occurs in both
genders, follows menopause in women, and occurs later in life in men. Secondary
osteoporosis occurs as a result of medications, other conditions or diseases.
The risk of fracture is primarily at skeletal sites where trabecular bone is
predominant the vertebrae being one of the main areas. Individuals who have
already had a vertebral fracture, are more likely to experience further
fractures within one year and this likelihood increases with the number of
fractures sustained. (McDonnell, et al 2006, Watts et al. 2003)
Although
measurement of bone mineral density (BMD) is the most widely used index of
skeletal integrity and bone strength, the unpredictability and risk of fracture
may be explained using several domains and their interactions. Domains recognized
in the literature as important include bone, spinal and neurophysiologic
properties. (Briggs et al 2006) Consideration of all these factors are important
components in order to understand how to safely train and load the spine, along
with possibly reversing or slowing down the process of osteoporosis, spine
deterioration and related pathologies.
BONE PROPERTIES
Bone properties encompass bone quality, microarchitecture, variation in distribution of BMD, tissue properties and levels of microdamage. All are important for bone strength. The definition of bone quality has been proposed as “the totality of features and characteristics that influence a bone’s ability to resist fractuture. (Bouxein et al. 2003) McDonnel et al 2006) This includes BMD, architecture, and intrinsic properties of the tissue that makes up the bone. Diagnostic methods do not fully account for the effect of changes on these other aspects of bone strength.
Trabecular Architecture
Vertebral
trabecular bone has a 3 dimensional architecture that consists of
interconnecting plates and rods. Vertical rods attenuate axial forces, while
horizontal plates resist shear forces from the intervertebral disc. The
resulting structure has a high porosity, but allows for relatively large
deformations under load. Local failure mechanisms are strongly influenced by
whether the structure is more plate like or more rod like. For rod like structures,
failure due to buckling and bending, followed by collapse of the overloaded
trabeculae has been observed. For plate like structures, buckling and bending
was not observed and failure appeared to instantaneously. Human vertebral
trabecular bone has a more rod like structure. (McDonnell et al 2006)
Variation in density and
architecture
The
vertebral body has an inhomogoneous density and architecture in both the
vertical and transverse (anterior-posterior) directions. Generally vertebrae are
less dense in the front and top (anteriorly and superiorly) and more dense in the back and at the bottom (posteriorly and inferiorly).
(Pollintine et al 2002)The architecture close to the endplates differs from
that in the central region; near the endplates the number is higher, the
spacing and thickness is lower. As an individual ages, there is a greater relative
loss and thinning of the horizontal trabeculae while the remaining vertical
trabeculae tend to maintain their thickness and may even increase.
(Mosekilde et al 1994, McDonnell et al 2006) This may be associated with
increased fracture risk. Ciarelli et al 2001 performed such a study and found
that fracture patients had significantly more anisotropic structure than the
controls. This suggests that for a population with similar bone volume, the
likelihood for fracture is determined by how the architecture has adapted to
bone loss. For those who have lost more transverse trabeculae, it would
appear that they are more likely to suffer a fracture. (Ciarelli et al
2001)
Vertebral
trabecular bone is lost mainly through perforation of trabeculae, rather than
general thinning. The loss of complete trabeculae results in significantly
weaker mechanical properties than an equivalent amount of thinning. Silva et al
1997 (McDonnel 2006) found that bending was the predominant mode of deformation
in the vertebral network, indicating that buckling due to loss of transverse trabecular cross-braces could
have a significant effect. This has important
implications for the treatment of osteoporotic bone loss. Treatments may
increase the thickness of remaining trabeculae, but it is not clear whether
they can replace those that are lost completely. Strength has been shown to be
in the numbers, not the increased thickness. Evidence suggests that the
architectural integrity of of the trabecular structure becomes more important
for bone strength as the bone mass decreases due to osteoporosis. (McDonnell et
al 2006)
Tissue Properties
The
mechanical properties of trabecular tissue are inhomogenous and anisotropic and
can vary across individuals and anatomic sites. Tissue properties are strongly
influenced by the bone mineral content. Mechanical testing has shown that stiffness
and hardness of bone increases with mineral content. However, the fracture
toughness of bone decreases with increasing mineral content, thus the strength
of the vertebra will directly be influenced by this aspect of bone quality. The
small size of the specimens makes it difficult to accurately and reliably
measure the tissue properties and there are conflicting views about the effect
of osteoporosis on trabecular tissue. Some researchers have proposed that
osteoporosis does not have a significant effect on mechanical properties of the
tissue material, suggesting that it is a structural
disease which is characterized by a deterioration o f the architecture
rather than by the tissue itself.
(Homming et al. 2002, McDonnel 2006 et al 2006, Ciarelli et al 2003) McDonnnell
et al 2006, examined levels of mineralization through thickness of human
vertebrae. They found no difference in mean bone mineralization levels between
fracture patients and control, but found significant difference in distribution of the mineralization
levels suggesting that those with fracture may be less capable of regulating
trabecular level stress and strain.
Microfracture and Microdamage
Damage of
trabecular bone can be divided into two categories: microfracture and
microdamage within trabeculae. Microdamage is believed to be an important
factor in bone quality and skeletal fragility. (Bouxein et al. 2003) McDonnel
et al 2006) It can occur as aresult of normal functional loading conditions,
and in healthy bone, this damage is repaired through remodeling. However,
excessive accumulation of microdamage could lead to local areas which are vulnerable
to fracture. Microdamage has been observed in various forms, such as short
linear cracks on the surface, long linear cracks extending through the
thickness, longitudinal and transverse cracks of the shear bands, and
cross-hatched microdamage. Microfractures occur less frequently than
microdamage and are the end result of excessive microdamage. Although fractured
trabeculae reduces the strength and stiffness of the trabecular structure, the
widespread accumulation of microdamage appears to be a more likely explanation
for a decrease in mechanical properties resulting in an isolated overload. Microdamage
occurs more frequently than microfracture, accumulates in bone faster than the
bone’s ability to repair it through remodeling, and happens due to fatigue at
physiologic load levels. This results in decreases stiffness, strength, and
resistence to fracture. (Wenzel et al 1996, McDonnell et al 2006)
Current
evidence indicates that once trabeculae have been perforated they cannot be
restored with therapeutic drug treatments. It has also been shown that loss of
bone strength due to perforation is much greater than the same relative amount
of general trabecular thinning. (McDonnel et al, Ding et al 2002) Studies have
shown that trabecular architecture becomes more anisotropic as bone loss
progresses, so that it can withstand normal daily loads in a cranio-caudal
axis, but is more susceptible to failure from unusual off load axis. This may
increases fracture risk as the trabecular structure adapts to compensate for
continual bone loss.
CREEP DEFORMITY Non-traumatic
With age , many people become shorter and develop a
hunched back. Some height loss is from intervertebral disc degeneration, but
most of it occurs in the vertebral bodies. This is referred to as vertebral
"deformities." Vertebral deformities are often assumed to
represent fractures, but the insidious nature of their onset and the fact that
a distinct fracture plane is not visible on radiographs, suggests that gradual
time-dependent "creep" processes may contribute to this problem.
(Pollintine et al. May 2009)
"Creep" is defined as continuing
deformation under constant load. Disc creep is entirely recoverable when the
disc is unloaded, because water is sucked back in again, but verterbral creep
deformity is largely unexplored.
Possible causes include age, vertebrae weaker and
less dense, and intervertebral
disc degeneration which concentrates loading on to the anterior/front of the
vertebral body when spine is flexed (forward bent) or in an upright position.
This is the
first study of its kind to investigate creep on whole human vertebrae. Their
hypothesis was that creep is
measurable, and is greater anterior than posterior so that affected vertebrae
develop an anterior wedge-shaped deformity. It involved spines ranging in age
from 48-91 years old with an average age 67 years old.
Bone "Creep" greater in
the front of the spine
Bone creep
deformation is greater in the anterior region of the vertebral body. This area has reduced BMD, and its trabecular architecture is often disrupted,
so the tissue is weaker and less able to resist applied loading.
Severe disc degeneration concentrates compressive loading on to adjacent annulus and onto vertebral cortex which could explain increased bone creep deformation in grade 4 discs.
CREEP HAPPENS
Persistent
residual strain after 2 hours suggests only 30-40% recovery of creep strain.
However, the underlying mechanism of bone creep is not clear, but some inferences can be
made.
The finding
that vertebral creep deformation is more rapid in the relatively weak anterior
region suggests that creep is a threshold phenomenon that becomes substantial
only when local tissue strength and BMD falls below a critical value.
Residual
strains following static and cyclic compressive loading of human trabecular
bone are similar to each other, suggesting a single underlying mechanism, and full recovery of such creep deformation
probably take 20 TIMES LONGER THAN THE PERIOD OF LOADING
This conclusion suggests that
gradual vertebral deformity observed in the experiment was mainly due to
micro-cracking of the bone matrix, which throws increased loading on to the
collagenous component of the matrix, which then creeps by relative gliding and
rearrangement of micro-fibrils!
HOW THIS RELATES TO YOU!
Living
people adopt fixed spinal postures for 30 minutes to 2 hours, for example when
driving, although it is more usual to apply cyclic (habitual) loading to the
back.
People
should be encouraged not to adopt stooped postures for "long" periods of time,
because spinal flexion increases loading of the anterior region to the
thoracolumbar vertebral bodies and could lead to anterior wedge deformity even
if spinal loading remained below the levels required to cause a fracture.
(Pollintine et al. May 2009)
Cortical and Trabecular Load Sharing
The
biomechanical role of the thin cortical shell in the vertebral body can be
substantial.
LOCAL SPINE PROPERTIES/DOMAINS
Shape, size volume
The shape of the vertbrae is designed to accept loads. The orientation and framework of the vertebral body assures that in normal circumstances, compressive load is transferred through the centrum. (Briggs etal. 2004). Fracture risk is commonly based on measurement of BMD, however bone size or cross sectional area (CSA), thickness, volume need to be considered. Several studies have shown the relationship of these factors given comparable BMD. Mazess et al (1994) found that of women with osteoporosis, those who fractured had a smaller CSA. Another study demonstrated significantly lower vertebral volume in the fracture group (Duan et al 1999) A smaller vertebral size increases mechanical stress on the spine and limiting its load capacity. By contrast , individuals with large bones and a normal BMD may obscure any deficit in volumetric bone mineral density leading to an erroneous conclusion. (Mazess et al 1994)
Intervertebral Disc Integrity and
Thoracic Kyphosis
Deformity arises from various types vertebral fracture, but the most typical is the anterior wedge fracture of the thoracolumbar vertebral body, which can occur spontaneously or after some minor incident and is seen as kyphosis. This has been conventionally explained in term of BMD. However, this cannot occur independently, nor does it explain why the anterior vertebral body should be affected so frequently. Despite regional variations in BMD being higher posteriorly than anteriorly, as previously described, there has been no explanation for this.
The vertebral body does not function independently with regards to
kyphosis. In fact, it is compressed by adjacent intervertebral discs (IVD), and
it shares with the neural arch the task of resisting compressive forces acting
down the long axis of the spine. Recent studies have shown that degenerative
changes in the IVD cause them to concentrate loading onto the anterior region
of the vertebral body when the spine is flexed. Disc degeneration has also been
shown to be proportional to thoracic kyphosis. In upright postures, degenerated
discs concentrate more load on the posterior half. Severe disc degeneration
leads to loss of disc height and a major transfer of compressive load bearing
to the neural arch whenever the spine is upright. In extreme cases, more than
80% of the compressive force acting on the spine is resisted by the neural
arches. So that the vertebral body, especially its anterior half are
substantially “stress shielded” and so lose BMD according to “Wolff’s Law” of
adaptive remodeling of bone. Spines with degenerated discs become adapted to
altered load sharing in upright postures, which are maintained for most of the
day. However, this leaves them unable to cope with flexion movements that
immediately transfer more the 50% of the compressive force onto the anterior
region of the vertebral body. In severe (grade 4) degeneration, flexion
increases the compressive force to the anterior vertebral body by 430% and the
reduced mass along with weak architecture of bone lead to less vertebral
strength.
Flexion causes similar changes in loading when discs are less
degenerated. The dangers of flexion are exaggerated by increased tension in the
back muscles, which contract to counter the forward bending moment of the upper
body. Muscle tension can increase the overall compressive force on the spine
so that in a grade 4 disc the anterior vertebral body load would increase up to
1290% compared with upright posture. This assumes that vertebral bone adapts to
forces acting in habitual postures, rather than occasional flexion movements.
In addition, old bone has a less responsiveness to mechanical stimulation. Once
formed, an anterior wedge fracture will increase spinal kyphosis and move the
center of gravity of the upper body anteriorly, so that the back muscles must
increase their activity to prevent spinal flexion. This would increase
compressive loading and cause the kyphotic deformity to progress. However,
altered load sharing after disc degeneration does not explain the initiation of
kyphotic deformity in a previously undamamaged spine. (Adams et al 2006)
GLOBAL SPINE PROPERTIES
Back Muscle Strength
Strong back
muscles contribute to good posture and skeletal support, and osteoporosis,
known as a systemic bone disease, should not affect muscle strength. However,
a study (by Sinaki et al 1996) compared back extensor strength (BES) of
osteoporotic and normal women. The findings showed that weakness in the back
extensors in osteoporotic women were specific to the back and not part of
generalized muscle weakness and thought to contribute to skeletal deformities
such as kyhphosis and other postural abnormalities associated with
osteoporosis.
Paraspinal Muscle Force affects
vertebral load
Muscles
that attach to the vertebral column produce movement and provide protection to the
spine by stabilizing its structures. Without muscle support, the spine has a
compression threshold of 2kg before buckling. The paraspinal extensor muscles
play an important role in maintaining static equilibrium of the trunk by
resisting the flexion moment imposed by gravity and any mass carried in front
of the spine. In fact, a histological study showed a predominance of Type 1
muscle fibers (slow twitch, associated with endurance) in the thoracic and lumbar
erector spinae muscle group. (Mannion et al. 1997)
However,
relative to other muscles in the body, the spinal extensors have a very short
lever arm, and are at a mechanical disadvantage. The result is higher
compressive reaction force delivered to the discs and vertebral centrum. Lever
arm length can also be affected by vertebral body size and shape. Gilsanze et
al (1995) demonstrated that women with osteoporotic fracture had smaller lever
arms resulting in increased loading in both erect stance and trunk flexion.
In a flexed
spine posture, the lever arm lengths of the erector spinae may decrease up to
13.3% (Daggfeldt et al 2003) In order to maintain the same torque, muscle force
must increase, which increases the compressive load onto the vertebral body.
The compression force may come from the body’s line of gravity shifted
anteriorly, but may also be due to the change in fiber orientation of the
erector spinae when the spine flexes. (Briggs et al 2004
Duan et al
(2001) estimates that activities associated with flexion of the upper body
resulted in approximately 10 fold increase in the compressive stress imposed on
the vertebra compared with upright standing. For any loading associated with
flexion, the majority (92-100%) of the spinal stress has been attributed to the
muscle-derived extensor moment and could be considered a significant
contributor to the incidence of vertebral fracture.
THE TERRIBLE "TRIAD"
Thoracic Kyphosis ("Poor Posture") increases Spine
Load and affects Back Muscle Strength
The shape
and design of the spine is made for efficient distribution and balance of body
mass. There is minimal spinal muscle involvement for maintaining static
equilibrium of erect stance. (Keifer et al. 1998) Changes in spinal shape,
however, are likely to alter this balance. Increased sagittal curve may change
physiologic loading through the spine as a consequence of a shift in trunk
mass, leading to increased flexion moments and compression and shear forces
imposed on spine segments. (Pearsall et al. 1991) In addition, changes in
spinal posture may compromise back extensor strength (force generating
capacity) (Mika et al. 2005) along with the normal function of paraspinal muscles. This is
thought to be due to compromised length-tension relationships, moment arm
lengths, and force vector orientations. (Briggs et al 2006 Thoracic Load)
The normal
human spine is a highly loaded structure. Compressive forces as high as 7000N are
predicted to act on lumbar vertebrae during maximum isometric trunk extension
tasks. However, in an elderly spine, body weight loading in a subject with a
thoracic vertebral strength less than 2500N would produce deformities and
compression failure with minimal strain. (Keller et al 2003) Vertebrae fail
when loads exceed their structural capacity. In osteoporotic vertebral
fractures, these loads are generally minimal trauma, and tend to occur between
T6 and T8 and at T11/12 where loads are greatest. When accounting for body
mass, physiologic loading through the spine is directly dependent on spinal
posture, since this variable determines the distribution of the mass within the
trunk. ( Briggs et al. Vert. Casc. 2006) Keller et al.( 2003) demonstrated that
postural forces can cause kyphosis deformities and are exacerbated by anterior
translation of the head and upper torso. In a severe model, a kyphosis angle of
41.7° resulted in a 25.2% decrease in spinal height, (C2-S1), an 8.6% decrease
in body weight, and produced a 15.1 cm anterior translation of C2 centroid.
This was associated with a 19% increase in compressive force, a 24% increases
in compressive stresses, and 40% increase in paraspinal extensor muscle forced
at T7-8. Deformities such as the one described are not a common occurrence, but
Cortet et al. found an average increase in thoreacic kyphosis deformities of
11° in women with radiographic evidence of fracture compared to those without.
A more recent
study established that thoracic kyphosis significantly affects spine loads and
force required by the trunk muscles to maintain an erect stance. Peak flexion
moments occurred in both high and low kyphosis groups at T8, which is not
surprising considering that T8 is likely to be the apex of curvature at the
thoracic spine. A direct relationship was demonstrated between load and kyphosis.
Net loading was greater in the high kyphosis group, due to the anterior
translation of the trunk mass associated with increased curvature. This results in increased flexion moment that
is counterbalanced by higher muscle forces, which, added to gravity, increase
both shear and compression forces. (Briggs et al 2006)
Greater net
and muscle shear loading in the high kyphosis group was thought to be due to
the decrease in verticality of the muscles line of action with more kyphosis. The
complexity of muscles and passive tissue organization in the trunk creates a
situation where an infinite number of possible force producing options are
available to balance external loads imposed on the system, in which this study
evaluated segmental loading due to gravity. (Briggs et al 2006)
Vertebral
loading due to muscle force was greater in the high kyphosis group, but muscle
loading was less than gravitational loading in terms of magnitude. It was
thought that this was due to the short lever arm of the paraspinal muscles, and
the large forces expected during functional activities. This was supported by a
study where increased cervicothoracic flexion caused an increase in myoelectric
(EMG) activity of the paraspinal muscles. It is thought that this may translate
to greater muscle force, even though EMG amplitude can be directly related to
force output. (Adams et al 2006)
In addition
to the mechanical loading implications of kyphosis, the sustained curvature
increases the likelihood of soft tissue creep, and other ligamentous strain.
Functionally, thoracic kyphosis could affect rib cage expansion, balance and cause back extensor weakness. (Sinaki et al.1996) Muscle weakness can lead to
earlier fatigue, further thoracic curvature and incrased disability. These consequences of elevated and
sustained tissue loading, due to increased thoracic kyphosis, highlight a
biomechanical rationale for treatment aimed at minimizing thoracic kyphosis.
(Briggs et al 2006)
Compression and Shear Forces
Increase with Osteoporotic Vertebral Fracture
After
sustaining an initial vertebral fracture, the risk of subsequent fracture
increases significantly within the first year (Lindsay et al 2001) One study examined the physiologic loads
imposed on the vertebrae (in those with and without vertebral fracture) to help
explain the mechanism underlying this fracture cascade.(Briggs et al 2006 Pred
Sp Load) It found that the fracture
group had significantly larger compression and shear forces as well as greater
flexion moment profile. It measured mechanical loading in a static situation in
order to directly relate to mass distribution and spinal curvature. Although no
significant difference was found in thoracic kyphosis between the groups using
standard radiographs, a comparions of intersegmental curvature profiles showed
a difference. This means that a single
vertebral fracture is not likely to change kyphosis measurement with
conventional tools. However, a single fracture is responsible for a subtle
change in curvature that significantly increases loading.
One of the more relavent findings of
this study was that shear force profiles were greater in the fracture group,
peaking at upper-mid thoracic spine and thoracolumbar junction. This supports the high fracture and subsequent fracture rate in these
areas. ( Briggs et al 2006) From a strength perspective, Keavenly et el
(2001) noted that trabecular bone properties are anistropic. Trabecular bone
has lower strength in shear force compared with compression. This is in
agreement with previously mentioned studies describing the proportion of horizontal
plates to vertical rods in trabecular architecture and its subsequent decrease in number of horizontal plates
with increasing age. Therefore,
increased shear loading in the fracture group may help to explain the risk for
subsequent fracture. This is supported by a recent study which revealed
trabulae in osteoporotic vertebrae undergo more strain in a shear like manner
than in healthy individuals. This study
suggested that interventions aimed at
restoring vertebral morphology, architecture and reducing thoracic/spine
curvature may assist in normalizing spine load profiles. (Briggs et al
2006)
NEUROPHYSIOLOGIC PROPERTIES (CENTRAL NERVOUS SYSTEM)
Paraspinal muscle control affected
by vertebral fracture
Neuromuscular
characteristics may also help to explain the aetiology of osteoporotic
vertebral fractures, because maladaptive recruitment patterns may compromise
intersegmental stability and therefore reduce the ability of the spine to
resist shear loading. This was investigated by Briggs et al (2006 ) and
involved elderly women with and without vertebral fractures. This study
provided evidence that there is a different pattern of recruitment between
individuals with and without vertebral fractures, and these changes are present
at commonly fractured levels in the mid-thoracic spine and thoracolumbar
junction. Neuromuscular postural responses of the paraspinal muscles at T6 and
T12 and deep lumbar multifidus at L4 were recorded using intramuscular EMG.
Most
notable was a delayed activation and shorter time to reach maximum amplitude of
the paraspinal muscles (at T7) compared to individuals with no history of
vertebral fracture. The different response by the Central Nervous System (CNS)
may be associated with higher loading given that muscle force was delivered
over a shorter time. The delay in recruitment of paraspinal muscles have
several implications:
1. Greater segmental loading
2. Higher static vertebral loads
3. Cyclic repetitions of this neuromuscular response may fatigue trabecular bone
and accelerate disc degeneration
4. Thereby increasing subsequent fracture risk
The shorter time to reach maximum amplitude by the fracture group,
may be a strategy by the CNS to overcome delay in activation and minimize
duration of muscle loading. The mechanism for the delayed paraspinal muscle
activity may be due to pain, while changes in thoracic kyphosis may alter
mechanical properties of the muscles. Other factors that may influence muscle
activation could be decreased mobility or even fear of falling.
Furthermore,
individuals with vertebral fracture demonstrate lower back extensor strength
compared to those without fractures. (Sinaki et al 1996) This may help to explain the reduced risk of
subsequent vertebral fractures seen after a program of back extensor
strengthening. Previous studies have established that back extensor
strengthening, orthoses and proprioceptive re-education are beneficial in
reducing the risk of osteoporotic vertebral fractures. (Sinaki et al.2002)
However, this study suggested that caution should be used when prescribing
paraspinal strengthening exercises in order to minimize compression forces through
already weakened vertebrae, and orthoses should not replace the role of active
muscles in the long-term to avoid muscle deconditioning.
REPORTED BENEFITS OF EXERCISES TO
HELP THIS PROBLEM
“Locomotion
has always been a major crieterion for human survival. Thus, it is no surprise
that science supports the dependence of bone health on weight-bearing physical
acitivities. Bone, to be maintained, needs to be mechanically strained—within
its biomechanical limits.” (Sinaki 2004)
Proper
mechanical loading can increase osteoblastic activity and the rate of bone
formation, but its mechanism is not fully understood. Preventing fracture is
the main objective of clinical intervention. This can be accomplished by more
than increasing bone mineral density. Most current medical literature focuses
on the role of exercise in improving bone mass. One study showed that
job-related physical activity correlated with bone mineral density of the
spine, where those who performed weight lifting for their job had greater bone
mineral density than those who had sedentary jobs. Other studies using similar
intervention did not show an increase. The unexpected result was thought to be
attributed to the low intensity of the exercise program, the method used,
subject’s compliance, and genetics. However, the benefit of exercise on bone
should not always be measured based on bone mineral density; the resulting
changes in bone structure are important to increasing bone strength (Sinaki et
al 2007).
Site Specificity and significance of
mechanical loading in bone health
The effect of physical activity on bone is
site-specific. This has been demonstrated in tennis players dominant humerus
and weight lifters. In general, physical activity improves the competence of
the neuromuscular structures to reduce risk of fracture. Several reports
substantiate the conclusion that bone mass is not the only factor in maintaining
bone health, muscle strength is also important. (Sinaki et al 2007)
Back Extensor Exercise: Choosing an
effective program
Before
1980, spinal flexion exercises were popular for managing back pain related to
vertebral fractures. The possible logic behind these exercises was to stretch
the paraspinal muscles that are in painful co-contraction while guarding the
painful, fractured vertebral bodies. Flexing the spine might have made
scientific sense initially, but considering that these exercise flexed and
compressed the osteoporotic spine, which was already biomechanically
compressed, made no common sense. (Sinaki et al.2007) A clinical study
clarified this and supported the fact that flexion would result in more
vertebral compression fractures. (Sinaki et al. 1984) In this study, one group
performed spinal extension, one group performed spinal flexion, one group
performed both and one group received only heat and massage with no exercise.
Comparison of baseline data showed additional fractures in 16% of the extension
group, 89% in the flexion group, 53% in flexion/extension group, and 67% in the
group that had no exercise prescribed.
This study concluded that not all
exercises affect bone and muscle in the same way, and that the type of exercise
must differ according to the various spinal deformities or skeletal challenges.
It prompted a new hypothesis that perhaps exercise to decrease vertebral
fracture should be different from loading exercises to increase bone mineral
density in the upper and lower extremities. (Sinaki et al 2007).
A subsequent
study, Sinaki et al (2002) demonstrated the effect of back-extension
strengthening exercise 8 years later in that vertebral fracture risk can be
decreased through exercise. These exercises, performed in prone (on your belly) position,
rather than vertical, may have a greater effect on decreasing the risk for
vertebral fracture without resulting in increased compressive load. Sinaki theorized
that fracture risk could be reduced through improvement of the horizontal trabeculae. Additionally, it
is thought that these exercises not only affect muscle strength, but also the
vertebral structure. Another study showed that improvement in back muscle
strength increased the level of physical activity.
In general,
physical activity increases the competence of neuromuscular structures to
reduce the risk for fracture. This is accomplished through improvement in
muscle strength, bone structure, and neuromuscular efficiency. Optimal exercise
programs differ according to an individual’s cardiovascular health, spine
integrity, and history of involvement in sports activity. Considering these
issues before recommending exercise increases the probability of adhering to a
program. Some physical activities may increase risk for vertebral fracture
rather than improve skeletal health, of these, the most well documented is
flexion. Flexion on an osteoporotic spine, even without loading the spine, may
result in vertebral fracture. (Sinaki et
al 2004)
Osteoporosis
related back pain, chronic or acute, prevents physical activity from occurring
and can result in further bone and muscle loss. After compression fracture of
vertebral bodies and induced back pain, a decrease is needed in the load over
the anterior aspect of the spine.(Sinaki 2007)
A recent
review of 20 articles evaluated specific exercise programs utilizing weights
and its affect on maintaining or increasing bone mineral density in women with
osteoporosis and osteopenia. Although the conclusion noted that weighted
exercise can help in maintaining or increasing BMD, the review did not discuss any
other possible fracture risk variables, such as fracture rate, strength gains,
activity or lifestyle changes, balance or fall frequency, and postural changes.
(Zehnacker et al 2007)
Kyphosis and Exercise
There are
very few reports of prospective studies which evaluate the effect of specific exercise
on postural alignment, yet the prevalence of kyphosis in older people is
estimated to be 20%-40%. Changes in the spinal curve cause both
physical and psychological distress due to altered balance, posture and self
image; difficulty fitting clothing, pain due to muscle spasm, tendency to fall,
and changes in the articulation of the apophysieal joint of the vertebrae. Hyperkyphosis
has been reported to predict mortality in an older community-dwelling
population (Kado et al 2004)
Understanding
the development of spinal curves provides more understanding into the pathology
of this problem. In the human upright adult spine, it is observed that there
are three superimposed curves: cervical lordosis, thoracic kyphosis, and lumbar
lordosis. Generally, it is thought that all three curves must be intersected by
the line of gravity to remain balanced. In the thoracic spine, the line of gravity
falls in front of the vertebral body, thus exerting force on the anterior
portion of the vertebrae. This creates physiological kyphosis.(Ball et al 2009)
In many
people kyphosis can be attributed to anterior vertebral compression fractures,
but there is also a high percentage of women who have hyperkyphosis without compression
fractures. (DeSmet et al 1988, and Ball et al 2009) Several other studies have
reported a high incidence of severe kyphosis without presence of vertebral
fracture. This suggests that aging of soft tissues may play a contributing role
and that improving paraspinal muscle tone may improve postural alignment. (Ball
et al 2009)
Ball et
al. 2009 assessed changes in spinal curvature, and evaluated whether exercises
designed to strengthen the extensor muscles of the spine are effective in
maintaining or improving postural alignment in aging women. It was demonstrated
that the most rapid increase in kyphosis angle occurs between 50-60 years old,
and that spinal extension exercises can prevent further kyphosis.
Functional Pathology
Changes in
posture affect the relative orientation of adjacent vertebrae, and profoundly
alter stress distribution within the apophyhseal joints and intervertebral
discs. Therefore, the precise manner in which a person sits, stands, and moves
could affect pain perception. Postural affects are exaggerated following
sustained “creep” loading, because compressive creep squeezes water from the
discs and reduces separation of vertebrae by 1-2 mm. (McMillan et al 1996)
Large stress concentrations in innervated tissues arising from relatively small
changes in posture suggest that “bad” posture could conceivably lead to spine
pain, even without degenerative changes in the affected tissue. (Adams et al
2002)
SPINE STABILITY and VERTEBRAL BODY
INTEGRITY
Spine stability and back stabilizing exercises are popular topics because of its impact on athletic, work performance, and to the rehabilitation of painful backs. The goal is to improve the trunk muscles in a way that prevents damaging the spine.
In traditional approaches to designing back exercises, the emphasis has
been on restoring a person’s motion and strength first, before gaining
stability. However, because of mixed outcomes, there has been a developing
philosophy, based on how the spine gets injured, that a spine must first be
stable…but to do it in a way without putting too much load onto on the spine.
(McGill 2001)
Spine Stability means different
things to different people and professions
1.
Biomechanics/movement specialist: A structure that becomes unstable when it reaches
a critical point
2. A
surgeon: abnormal joint motion that can become corrected by changing a body
part
3. Rehab
practitioner: patterns of muscle coordination and posture and attempt to change
on or a few of these.
Several
groups have attempted to actually quantify stability, joint motion and force
demands in order to determine how much stability we need to avoid injuring our
back.
The Injury Process
People who
report back pain also experience changes in their motor control systems at the
same time. This affects the stabilizing system. The challenge is to train the
stabilizing system during regular activities ( i.e. walking), during fast movements (i.e. walking fast or lifting a hot pot out of the
oven), to withstand sudden surprise loads (i.e. missing a step, or lifting something
heavy that a person may have thought light), or trying to catch a glass that
is about to tip over and fall off of a table.
Instability as a cause of Injury
Biomechanists
have been able to explain how injury occurs from heavy lifting, but have had a
much more difficult time figuring out how someone injures their back while
doing a task like picking up a pencil from the floor. Evidence has shown that
this is a valid injury and a result of the spine ”buckling” or demonstrating
unstable behavior. But it can also happen with far more challenging tasks, too.
Stuart McGill investigated the mechanics of power lifter spines while
they lifted extremely heavy loads. During their lifts, even though the lifters
appeared to fully bend their spines, in fact, their spines were not. The risk
of damage is very high when the spine is bent.
The most relavent part of this story is as follows: The researchers were able to see
through moving xray video an injury occur. It was the first of its kind to be
seen as far as they knew. During the incident, the semi squatting lifter had
lifted the load about 10 cm or 5 inches off the floor, only ONE joint at L2/3
briefly rotated or slid forward by only ½ of a degree, while all other vertebrae
maintained their static/stable positions. The spine buckled and broke. Studies
showed this was a motor control error where there was a short laps in one or
more of the small intersegmental muscles along the spine that would cause the
rotation or shift of just one single joint, causing injury to the muscle and
loss of stability at that place.
Stiffness versus Stability
Muscles
around the spine are designed to maintain its integrity as well as carry a
load. The spine stiffens to resist buckling. This stiffening causes more load
to the spine from the muscles and can cause injury. So how much stability is
best and how can it be achieved?
Buckling and Stiffening vs Stability
The lumbar
spine with only ligaments buckles at about 20 pounds reinforcing the critical
role of muscles to stiffen the spine against buckling. The arrangement of the
muscles around the spine, along with activation patterns, enables the spine to
handle a much higher compressive load as it stiffens and becomes more resistant
to buckling. However, this increases the load onto the spine due the stiffening
muscles activity.
Sufficient Stability
How much
stability is optimal? Not enough will make the spine unstable, but too much
overloads the spine. It is a concept that involves determining how much muscle
stiffness is necessary for stability, plus "a little extra" to have a margin of
safety. Modest muscle force results in high increase in joint stiffness so
large muscle force is rarely required. In recent papers, (Cholewickid et al
2000) it was demonstrated that sufficient stability of the lumbar spine was
achieved, in an undeviated spine, with modest levels of coactivation of the
paraspinal and abdominal wall muscles.
They
found that people, from athletes to those like you and I, must be able to
maintain stability with a low, but continuous muscle activation. This means
that stability is not compromised by lack of strength, but rather lack of
ENDURANCE. Thus, researchers are beginning to understand the validity of
endurance training for the muscles that stabilize the spine. Having strong
abdominals does not necessarily provide the effect that many people had hoped
for, but several studies suggest that endurance muscles reduce the risk of back
problems and buckling. (McGill et al 2001)
Quantifying Forces acting on the
spine
The
compressive force acting on the spine depends on body weight and internal
muscle force both of which can be increased during movement. Predictions of
spinal compression using a variety of techniques show reasonable agreement and
by implication, accuracy. However, there is scope for further biomechanics
research in this area. Relatively simple techniques are required to quantify
peak spinal loading in compression and bending, but it can vary based on muscle
recruitment strategies. Additionally, more biomechanical studies are required
to quantify forces acting on the cervical spine during normal activities,
because practically nothing is known about muscle forces acting on the neck.
The concept of functional pathology involves the relationship of poor postural
habits that could be acquired in response to back pain, and lead to a “viscious
cycle” of poor posture, muscle dysfunction and pain. (Adams et al 2002)
Further work is required to
understand spinal injury mechanisms, especially to the thoracic and cervical
regions of the spine. The large and growing problem of vertebral “osteoporotic”
fractures (in elderly people) has largely been left to bone biologists, even
though the local mechanical influences are probably as important as systemic
metabolic factors. (Pollintine et al 2004)
Any cell
based treatment for spinal disorders is unlikely to succeed unless attention is
paid to the mechanical environment of each tissue’s cell. Expert biomechanics
input into “mechanobiology” is important to ensure that normal and pathological
mechanical environments are accurately characterized.
OTHER QUESTIONS TO INVESTIGATE WITH
OBJECTIVE MEASURES
Does this specific training program:
Improve
posture measured as spine curve measures cervical through lumbar?
Improve
physiological factors like vital capacity, tissue healing, bone metabolism,
bone quality, circulation, digestion?
Preserve intervertebral
disc integrity?
Improve nutritional
capacity to vertebral body in order to improve architecture and quality?
Improve
vertebral body shape and height?
Improve
neuromuscular control measured by EMG carrying over to improved function?
Increase
height?
Improve
bone density, mass and volume?
Improve
ANSAR score for Digestive system?
Improve
recruitment pattern of ES and mulitfidi?
Improve
endurance and strength of spine extensors?
Improve
balance?
Decrease
pain at lumbar, thoracic, cervical?
Decrease
compression and shear forces and load onto anterior vertebral body?
Improve BES
of type I and II?
Increase
number of type I and/or type II muscle fibers in extensors?
Increase
overall physical activity level of individuals?
Do
specific postural cues improve after intervention of this program?
Does
the use of specified foam platforn affect recruitment of ES, deep extensors, core
stabilizers?
NEVER UNDERSTIMATE THE POWER OF POSTURE!
