The multifidus muscle
- biomechanical considerations
- is there a role for the modulation
of inflammation?
by Martin Krause (2008)
The multifidus muscle gained
notoriety in the mid 1990's when researchers at Queensland University
first demonstrated gross muscle atrophy using real-time ultrasound.
Previously Lance Twomey and Nikolai Bogduk had remarked on the
close anatomical nature of the multifidus to the capsule of the
Zygapophysial joint and suggested that it may act similarly to
the rotator cuff muscles of the shoulder. Moreover, they suggested
that the angle of pull of these muscles and their relative shortness
would make these muscles more likely to have a proprioceptive
function working together with the oblique abdominals to sense
rotation in the lumbar spine. Further support for this hypothesis
came from additional evidence demonstrating that the multifidus
had a higher concentration of annulospiral endings than other
muscles.
The function of the multifidus
then became implicated with Transverse Abdominus function, as
it's tendonous fascia placed tension on the fascia of the multifidus.
Many EMG, US, MRI, CT and PET/functional MRI investigations followed.
Indeed, the transverse abdominus is anatomically uniquely positioned
to act as a stabiliser in the horizontal and transverse planes
of motion for not only the L/S but also the SIJ's. Although it
would seem obvious that synergistic muscle contractions would
be superior to isolated ones, for about a decade, physiotherapists
were statically stabilising the lumbar spine with Transverse Abdominal
contractions under dynamic US, whilst the external obliques and
rectus abdominus were detrained. This seemed a curious notion
as the multifidus was supposed to be a sensor for the oblique
muscles. Furthermore, the natural postural swaying mechanisms
in the saggital plane suggest rectus abdominus : erector spinae
rhythm which in turn would control extensor torques on the lumbar
spine as well as reduce excessive force closure. Additionally,
the 4 point "happy cat" exercise results in rhythmical
oscillations between the serratus anterior, external oblique and
multifidus muscles whilst "the needle" encourages T/S
rotational mobility whilst enlongating and stabilising the abdominal
region using the external obliques.
The entire concept of detraining
any muscle must be a fallacy as the better trained a muscle, the
less likely it is to become overloaded, shortened and suffer both
metabolic and mechanical failure. If a muscle can only lift 1kg
and the Activities of Daily Living (ADL) require that muscle to
lift 0.8kg then it will very quickly fatigue creating abnormal
movement patterns, insecurity and a loss of form. If that muscle
is trained up to lift 5kg, then the 0.8kg load becomes insignificant.
Yet, even as recently as 2004, arguements raged as to the importance
of low loading regimes for the treatment of low back pain (LBP).
On the other hand, Stuart McGill, using investigations on highly
trained weight lifters, was suggesting that maximal loading was
best. Common sense dictates that the spectrum of loading is required
for ADL.
Beyond the multifidus and
the transverse abdominus, it has become recently clear (2007)
that the pelvic floor is immensely important in the stability
of the lumbar spine. Here I would agree that these postural muscles
require low loading since high loading will induce external oblique
contractions which can place pressure on the bladder leading to
incontinence. On the upper side of the barrel the other endurance
muscle which requires long low lateral loading is the diaphragm.
Previously, people were taught diaphragmatic breathing by stretching
their stomach out. Yet, again this is counter-intuitive as it
reduces the ability for transverse abdominus and internal oblique
muscles to contract. Through lateral breathing, the lower 6 ribs
can expand, placing an elongating contracting (eccentric) influence
on the external obliques, whilst elongating the connections between
the sympathetic ganglia. Also, by emphasising the slow 10 second
breath (6 breaths per minute) it discourages hyperventilation
which can lead to respiratory alkalosis and hence metabolic acidosis.
Yet, all things aside, the multifidus muscle clearly
has a crucial role to play. Each day when I examine MRI's and
CT's of the lumbar spine I see huge white areas of scar tissue
or total blackness around the areas where the multifidus is supposed
to be. This seems to be more prominant in the low lumbar spine,
which in turn has significant bearing on the nutation of the sacrum
as well as the propriocetive functions already described. The
pelvic floor contraction on it's own will result in counter-nutation
of the sacrum, which intuitively can be balanced by multifidus
contractions on the sacrum.
Beyond these biomechanical considerations, what
role can a muscle such as multifidus have in the regulation of
inflammation? In October 2005 I presented a paper in Rome on the
importance of muscle mass on immune function. This was partially
based on a paper I wrote in 2003 on Sarcopenia
which is characterized by the reduction in muscle mass and may
contribute to immunosenescence.
Here, I argued that the muscles represent an important reservoir
of protein required for immune function. (Rome
presentation). In 1995, I argued for the importance of the
dorsal root ganglia (DRG) in the regulation of inflammation and
repair in my treatise
on mechanical traction. Late in 2007, 5 chapters (of 23) in
DeLeo, Sorkin & Watins : Immune and
Glial Regulation of Pain. IASP publication were devoted
to the DRG and astrocyte-glial immune function in hyperalgesia
and allodynia. Importantly, it was argued that retrograde signalling
from the periphery and anterograde signalling from the DRG created
a response by glial cells and astrocytes in the CNS. I had argued
previously (1995) that such a mechanism should incorporate descending
modulation by the sympathetic nervous system.
Hence, wouldn't it be interesting to generate a
hypothesis, whereby exercising muscles innervated by the nerve
affected by pathology would enhance immune-metabolic function
not only of the muscle but may in turn help 'fine tune' the immune-metabolic
function of the astrocytes and glia of the CNS? The electron transport
chain (ETC) has been implicated in neuropathic pain. Similarly,
the glutamine-glutamate energy systems have also been considered
to be depleted in the cells of the DRG. The production of cytokines
are also upregulated or downregulated depending upon the appropriatness
of the response. Muscles can be trained to more successfully deal
with oxygen free radicals (ROS). Since, muscle contractions involve
glutamate, ETC and the balance of cytokine production, then it
may be interesting to speculate that, the multifidus being the
organ closest to the DRG may be optimally located for a CNS priming
function???
Although, a lot of emphasis has been placed on motor
control, perhaps the cognitive behavioural properties of motor
control and their affect on the sympathetic nervous system are
of primary importance when treating LBP and multifidus dysfunction????
Exercise and Growth Hormone
Bed rest can have deleterious effects on muscle
function. Researchers have recently described a direct muscle
afferent-pituitary axis whereby bio-assayable growth hormone (BGH)
regulation is tightly coupled with muscle function rather than
muscle fibre type. Unlike, exercise-induced increases in
plasma immuno-assayable growth hormone (IGH), whose concentration
peak occurs during or after longer duration aerobic or resistance
exercise involving larger muscle mass, BGH is released after a
brief series of isometric contraction (McCall et al 2001).
The BGH response is absent , despite the maintenance of normal
torque output and pre-exercise plasma BGH and IGH, when leg musculature
is chronically unloaded, as after 2 days bed rest or space flight.
They hypothesised that this was due to chronic alterations in
proprioceptive inputs (McCall et al 2001). These responses
normalised within approximately 8 days of ambulatory recovery.
Furthermore, they suggested that BGH stimulates bone growth and
that low threshold fibre activation through electrical stimulation,
exercise and /or vibration may ameliorate the effects of chronic
unloading (McCall et al 2001). Moreover, this
is direct evidence for the existence of a muscle-pituitary functional
pathway in the absence of inflammation. It also
highlights the need not to underestimate the effects of bed rest
when recommencing a training regime after a period of illness
or trauma. Furthermore, it would appear that low threshold
isometric contractions, as occur during the application of muscle
energy techniques, may stimulate this growth hormone.
see :
Neuro-immune
and cognitive behavioural responses
Motor
Learning and Orienteering
