Breathing control is a topic close to the hearts of most physiotherapists. My recollection is that respiratory care in general was never a particularly popular speciality in my time as a rotational physiotherapist and I am not sure much has changed.
However, there was a temporary resurgence of interest in musculoskeletal applications of respiratory assessment over a decade ago with the evolution of core stability research. Don’t worry – we’re not going to get into another laborious discussion on the merits of core control here!
For those whose memories are short, part of the theoretical modelling of mechanisms of core control as proposed by Hodges and Jull was the synergic interaction of four muscle groups which formed an internal cylinder within the trunk. (see thoracolumbar fascia for review) These muscle groups consisted of:
The anterolateral abdominal wall.
The deep spinal musculature and associated thoracolumbar fascia.
The pelvic floor
The conceptual model was that the diaphragm generated a base line level of resting tone to provide mechanical resistance to stiffen the internal muscle cylinder comprised of the synergic muscles listed above and thereby facilitate spinal support. Superimposed upon this diaphragmatic postural function was the intermittent phasic contraction associated with the respiratory cycle. This fitted in nicely with the much described muscle activation model (Bergmark) of sustained tonic low level activation with superimposed bursts of phasic activity related to functional demand.
This became relevant to physiotherapists because of the common observation of breath holding when executing exercises aimed at core muscle activation. In fact many exercises, both rigorous, high load and fine dexterous tasks, are often associated with temporary breath holding simply associated with concentration on the task. However, from an instructional perspective, it was deemed important that physiotherapists recognise breath holding as a potential compensatory strategy to artificially achieve core stability, with the obvious disadvantage of not being sustainable for any longer than the period of breath holding.
Around this time also, in the field of occupational medicine, it became evident from EMG studies that prolonged sitting and typically in poor posture, compromised diaphragmatic excursion (simply as a consequence of the mechanical restraints of the thorax and ribcage) and thereby potentiated a compensatory strategy of inhibiting / relaxing the anterolateral abdominal wall as the path of least resistance relative to superior diagrammatic excursion into the restricted chest cavity.
Superimposed upon this sustained static loading scenario, was the frequent clinical observation of elevated / rounded shoulder girdles whether habitual, stress induced, ergonomic or breathing compensation induced, which all fed into a cycle of musculoskeletal compensation.
For some years, well known American physiotherapist Peter Edgelow, has been highlighting the merits of specific breathing control in treating thoracic outlet disorder’s (That well known clinical hot potato at which so many different therapies get thrown). Edgelow’s contention, also substantiated by the opinions of Travell & Simons’ in the myofascial world, contended that scalene hyperactivity associated with respiratory dysfunction had the potential to either change thoracic outlet dynamics by virtue of their rib attachments, or simply by increasing muscle tone and reducing the diameter of the thoracic outlet and hence the potential for neural irritation. Coupled with the adaptive changes in this area were potential tightness of the Pectoralis minor and a protracted shoulder girdle all increasing the likelihood of anterior compression.
I have always found teaching breathing control challenging in the clinical situation, partly because of the difficulty in achieving patient compliance and also because of the difficulty in proving direct association with the clinical features. With this in mind I was interested to see some recent developments in this area, which I intend to explore further.
The first is the work of a Canadian physiotherapist Laurie McLaughlin who presented at the 3rd international conference on movement dysfunction in Edinburgh a couple of years ago. She is using some interesting techniques to evaluate breathing function and her work is outlined in more detail if you follow the link.
The second factor, (which partly initiated this post) was a recent notification from Human Kinetics on a book publication entitled ‘Breath Strong, Perform better’. This looks an interesting one and is certainly on my ‘to read’ list.
For those who are interested in this subject the work of Simon Gandevia (who incidentally was a collaborator with Paul Hodges’ original work) has been a significant contribution in this field. There is a concept in the sports science literature known as ‘respiratory entrainment’, which studies the pattern of respiratory activity in association with limb and body position. This has been studied in cyclists and rowers in particular, with the view to attempting to understand mechanisms and also determine whether limb / body position and repetitive movement dictate the respiratory pattern or visa versa.
In the context of the recent Wimbledon Tennis tournament, the much talked about grunting and groaning of female tennis players has achieved it’s usual amount of attention but also appears to be associated with these breathing control / mechanical force output requirements.
So perhaps as musculoskeletal physiotherapists it is time to reconsider our attitude to breathing control and to evaluate the multitude of variables which impinge upon this function from a musculoskeletal perspective,
Let us know if you have any useful clinical strategies or experience in dealing with this type of caseload.
Enjoy the clinical challenge.
DavidGHTime Code(s): nc
The typical research methodology examining cervical muscle function in neck pain involves strength and endurance testing using various forms of dynamometry devices. Deficits in isometric strength and endurance have been consistently documented for the cervical flexors, the cranio-cervical flexors and the cervical extensor muscles. Importantly, neck pain sufferers exhibit a poorer steadiness of contraction at low load (20% of MVC) compared to controls, which may reflect other muscle fatigue manifestations such as muscle tremor.
In accordance with the general theories of muscle imbalance the theoretical model suggests an impairment of deep cervical muscle function produces a secondary overload in synergic muscles – which appears what we frequently observe clinically. This would appear to correlate with patient subjective reports of difficulty in sustained postures, classically keyboards, reading and driving.
More subtle forms of investigation into muscle function attempt to explore the efficiency of motor control. This relates more specifically to the timing and intensity of synergic muscle function and the appropriateness of activation for a given functional task. One of the fundamental principles of an efficient motor control is the efficiency of motor recruitment whereby there is:
1) minimal extraneous muscle recruitment for the task in hand.
2) optimal force generation specific to the task at hand
3) sequencing of motor unit activation in accordance with the level of demand and
4) deactivation / switching off of the activated groups following execution of the task.
In clinical practice the analyses of these variables is not always possible to explore in depth so we are left extrapolating information from the results of more primitive strength/endurance/alignment/length-tension relationships.
One of the biggest challenges that we face clinically is evaluating the contribution of the axioscapular musculature as a contributory mechanism to cervical pain. This is compounded by the fact that frequently patients report exacerbating activities that involve the simultaneous challenge of the neck and use of the arm i.e. reading, keyboards and driving and therefore the challenge clinically is to determine which mechanism is the dominant driver. The conventional wisdom is to view the most superficial muscles of the posterior neck as prime axio-scapular muscles i.e. trapezius and levator scapula and to evaluate their function in the context of efficiency of scapular/arm control on the basis of a separate intrinsic muscular control system for the neck. This of course is a hypothetical construct (originally discussed in Bergmarks paper postulating local and global muscle function) but one, which seems to have some relevance clinically, at least to provide a guiding framework for intervention.
Because the timescale to improve muscle function both around the neck and the scapular area is likely to extend over weeks rather than days it becomes a management priority to determine the most legitimate target to treat. I find kinesio tape to be of great assistance in this regard because it is straightforward to apply a supportive taping technique to either the cervical spine or scapular and assess the response on the next patient review. This is what the renowned Australian Physiotherapist Bill Vicenzino calls a “treatment direction” test and is very worthwhile applying in the clinical setting.
It is also much easier to achieve patient compliance with specific (often subtle) corrective therapeutic exercise if it can be demonstrated that their symptoms are eased by changing the pattern of muscle activation artificially and therefore provide an incentive to comply with the rehabilitation regime to reinforce this.
Enjoy the clinical challenge.
Integrating core stability into functional movement has long been one of those un-talked about subjects where the assumption is that prerequisite loading in other non-functional positions is then transferred into a loaded environment. The model used to explain this is the classic model of motor learning described by Posner & Fitt’s in the late 1960’s, which describes three stages of motor learning:
The Cognitive phase
The Associative phase
The Autonomous phase
This model repeatedly surfaces in the physiotherapy rehabilitation literature as an framework for the sequential loading working towards functional tasks. It should be pointed out that there are several other theories of motor learning which do not necessary follow this paradigm, but it also serves a dual purpose in the clinical environment, as interventions at the early phases using this strategy tend to be low load and therefore minimal risk / reduced likelihood of provocation.
However, there is an equally strong argument for the massive sensory bombardment, which occurs from using functional positions as a way to stimulate specific muscle activity. Historically, the difficulty in clinical practice is to ascertain whether the target muscle groups are actually being recruited as part of a global functional movement pattern. This undoubtedly remains the significant clinical challenge.
Some of the recent trends in athletic training involve the use of functional exercise programs, which try to replicate functional demands. If we look at the frequent reports of symptom provocation from patients, there are some very familiar aggravating factors, which I think we would all recognise.
Sweeping & Hoovering
Walking the dog
Accessing car boots
Working in overhead positions
Twisting or reaching
It is clear from evaluating these positions that there is a change in the relationship between the thorax, the pelvis and the intervening lumbar spine and therefore some degree of mobility must accompany the necessary “stability” to counteract loading.
Because segmental rotation in the lumbar spine is very limited (estimated at 2º – 3º in each direction per segment) it would appear biomechanically that the majority of rotation must occur from the thoracic spine and the hips. It is tempting to speculate that any impaired mobility in these areas maybe a significant driver to rotational pressures through the lumbar spine causing tissue sensitivity.
If we look at control of the lumbar spine during function from that perspective, the role of the oblique musculature (both abdominal and spinal) could be considered as “anti-rotation” muscles whose role is to minimise the stresses distributed to the Lumbar segmental structures. In that situation the limbs and torso become the external “drivers” forcing load on the core..
Using this model to replicate function there are two key principles of loading.
1) Asymmetrical stance
2) Altering the loading segment (driver).
In reality this means that evaluating trunk stability needs to be assessed in conjunction with asymmetric limb loading which is more akin to normal activities of daily living.
Clinically, this means using positions such as:
Single leg stance
as variations in the start position and combining this with variations in the loading force (driver), either using arms, torso or legs. The degree of difficulty, hence risk of injury, is related to the magnitude of load with arms being the lowest, legs being second and torso being highest.
Whilst visual observation is how most of us rely on accessing the quality of movement there is certainly a limit to what can be achieved. The big clinical decision is whether we can use load or speed of motion as the next level of exploration/provocation to see if we can elicit a breakdown in control. Obviously this needs to be weighed up against the vulnerability of the pathology.
So from a practical perspective it is quicker and easier to initiate functional rehabilitation strategies as the prime intervention for low back pain patients unless their level of irritation contra-indicates or they do not tolerate the level of loading associated with function. Patients in that category may then self-select for lower loading regimes as an intermediate stage.
The alternative, and one which has become pervasive in recent years, is to work through a multitude of phases which may not particularly challenge the patient in a way that is relative to function, although appear deficient from the perspective of musculoskeletal control and ideal movement patterns. The well known phrase “Paralysis from Analysis” springs to mind.
Enjoy the clinical challenge.
As clinicians we often use these terms interchangeably to describe the phenomena of altered limb sensation or control. However, researchers classify each component separately on the basis that there are different physiological mechanisms underlying each component.
– is considered the cumulative neural input to the CNS from mechano-receptors located in the joint capsules, ligaments, muscles, tendons and the skin. Other terms that are often used synonymously with proprioception include ‘kinaesthesia’ and ‘balance’.
– is the conscious awareness of joint position and movement resulting from proprioceptive input to the CNS.
– refers to the ability to maintain the centre of gravity over the base of support without falling. The ability to maintain balance requires the integration of proprioceptive input from the periphery and afferent information from the eyes and vestibular apparatus in the inner ear.
Appropriate use of this terminology is important among clinicians to enhance communication and understanding in this area.
In the last decade clinicians have been increasingly interested in the use of closed chain exercises on the basis of their enhanced proprioceptive value. This is partly on the basis of the similarity to functional loading and the presumption that the total proprioceptive input is more likely to activate the appropriate neural pathways. Closed chain exercise results in the simultaneous motion of all joints in the extremity, which thus requires co-ordinated muscle activity to control all the segments in the limb.
Here lies the challenge for us clinicians because the attraction of such a massive sensory of bombardment is obvious, but the trade off is the inability to accurately quantify the contribution of individual muscles and the specific area of breakdown. If we take ‘single leg squat’ as an example and look at the typical areas of breakdown as determined from observational analysis we might observe some of the following:
1) Increased pronation.
2) External tibial rotation (out toeing).
3) Valgus knee.
4) Medial femoral rotation.
5) Adducted femur.
6) Laterally displaced pelvis.
7) Pelvic drop or elevation (trendelenberg or disguised trendelenberg)
8) Pelvic rotation.
9) Trunk deviation.
10) Balance reactions using the upper limbs.
The challenge as clinicians is to determine the zone of breakdown and the compensatory mechanisms. The dilemma of functional loading is to stimulate proprioceptive input where the sensory feedback is usually far less distinct than isolation of a specific region in a non-functional position. Treatment strategies therefore involve some element of “aspiration” that there will be transfer of muscle recruitment and position sense from specific exercise positions into functional situations. Therein lies the challenge – to go specific or go general.
There certainly appear to be a group of patients where any physical stimulation is sufficient to activate some level of useful muscle function and significantly impact symptoms.
There also appear to be a group of patients who are reasonable active but present with more specific muscle imbalance issues related to patterns of activation.
There are also patients who are systemically hypermobile with a pre-disposition to low tone. They are dependent on specific stimulation to maintain status.
And then there are those who are stiff, who are usually structurally more robust, appear to have better intrinsic tissue characteristics and can be less vigilant about maintaining muscle tone. They may however require more of a flexibility focus.
Such is the tapestry of life but worth remembering as it influences the nature of our patient management and the type of advice given – very important if we are to be credible messangers.
Enjoy the clinical challenge.
The acknowledgement of quadriceps inhibition as a complicating factor in knee joint pathology is pretty much unquestioned in routine clinical practice. This is evident by the standard prescription of inner range quadriceps exercises as part of any post operative knee regime and also cases of knee pathology that do not require surgical intervention. My views on the appropriateness of inner range quadriceps as a primary strategy for quadriceps re-education are well known and have been discussed in previous posts (see Terminal Knee Extension) but suffice to say that I am not a big fan as I think there are more superior choices of exercise.
Compensatory Movement Patterns
In this discussion I want to review some of the compensatory movement patterns observed clinically which appear to be the result of poor quadriceps functioning:
1. Impaired terminal knee extension
- is the most obvious example and needs no further expansion here.
2. Compensatory hamstring hyperactivity
– this can be indicated by a persistence of hamstring tightness even when routinely stretched, indicative of an increased recruitment strategy. It may appear paradoxical but the literature is full of detail on quadriceps / hamstring co-activation (particularly the ACL rehabilitation literature). Not surprisingly the reciprocal activation of hamstring / quadriceps recruitment is not an on-off mechanism but a graded degree of simultaneous tension – consistent with all joint requirements for stability. It may be that the compression produced by hamstring activity is a compensatory strategy for compromised quadriceps contribution?
3. Hamstring dominance in active straight leg raise test
– the active straight leg raise test has been utilised as a measure of pelvic and groin dysfunction can also yield useful information regarding hamstrings / quadriceps activation.
I modify this test by bringing the patient into a straight leg raise position just short of hamstring tension and then request an active hold in this position.
Therapists can then observe two things:
A). A loss of terminal knee extension when under active control or
B) Determining the site of predominant muscle activity (asking the patient to report their predominant area of perceived effort) which in this situation will often point to the hamstrings.
Because the position of the test is short of full hamstring tension one cannot deduce that this perception of increased hamstring tension is due to a lack of elasticity.
4. Compensatory trunk flexion
in an attempt to maintain the length / tension relationship of the quadriceps. This is usefully measured in sitting with the establishment of a lumbar lordosis in an upright-seated alignment, feet off the floor. The patient is then asked to extend the knee. The frequent observation in this test is for the pelvis to posteriorly rotate producing trunk flexion.
In order to determine if this is a result of hamstring restriction or lack of active quadriceps control the therapist should try to passively extend the knee at the point at which the pelvis starts to posteriorly rotate. Increased mechanical resistance indicates posterior leg tightness; greater passive range indicates inner range quadriceps inhibition compensated by posterior pelvic rotation.
5. The hamstring – gastroc paradox
– this is a concept we have touched on before and one not frequently discussed in clinical circles – although sometimes alluded to in gait analysis. The crux of this theory is that the gastroc soleus complex acts with reversed origin / insertion activity with the ankle as the fixed point. Gastrocnemius contraction coupled with that of the hamstring produce a combined force, which tends to extend the knee.
In biomechanical terms this is the old ” parallelogram of forces” rule where two muscle groups crossing a joint from above and below act in a combined manner to extend the joint. This again can be tested clinically by utilising a stance position superimposing a ¼ – ½ range squat on the front leg. Palpation of dominant muscle activity is one way to try to determine predominant muscle activity and of course verbal feedback on dominant site of perceived effort is another.
In a previous discussion’s on extensor chain function we looked at the interaction between hip extension, knee extension and ankle plantar flexion as part of the basic propulsive mechanism. Obviously disturbances in the synergies of these primary muscle groups will compromise the efficiency of this movement pattern. The clinical challenge is to determine the site of increased stress and the mechanism of overload within the system. So many patients we see demonstrate an “Apropulsive (without propulsion) gait due to compromise of the extensor chain. As clinicians we need to be alert to recognise these mechanisms.
what observational gait parameters would give us clues about lack of propulsion in walking?
Enjoy the clinical challenge.