DOSAGE! It is a subject that is not often discussed but may make a HUGE difference in the success of using movement and exercise during rehab. Perhaps MORE than the exercise itself!

Article at a glance

 

  • Dosage is a big deal
  • Intensity, volume and frequency all affect dosage.
  • Both over and under dosing are issues.
  • Try to find minimal effective dose. It can always be progressed.
  • Shared decision making helps find tolerable/effective dose.
  • Define what the right dosage should feel like.
  • Give a regression and progression.
  • Offer support to manage dosage.

 

Doctor holding heap of drugs in a hand

What is dosage?

 

Simply put, it is intensity, volume and frequency!

Intensity will be affected by the amount of weight we used or how fast we move the weight; both will affect the amount of force applied to a tissue and this is simply expressed as F = MA. The individual measure of intensity will be moderated by someone’s current tolerance.

The amount of repetitions and sets defines the volume. This can be manipulated and will have an affect on the overall overload.

Frequency is another aspect. You could have the most applicable exercise but if we do it 10 times a day (you have all had THAT person) that could be TOO MUCH of a good thing. So an exercise focused on changes in movement skill or quality (whatever that is!) could be done MORE frequently potentially than an exercise focusing on tissue load where you need time for POSITIVE adaptation to occur at a cellular level.

We can manipulate all three to achieve the desired response. Much more than 3 sets of 10 I am sure you will agree! The reasoning process behind movement/exercise is as important as any other aspect of rehab but not always considered.

This could be increasing intensity and decreasing volume, or increasing volume while decreasing intensity, or leaving those the same and changing frequency. There are a whole bunch of ways that dosage can be manipulated for large or smaller changes in overload.

Smaller changes can be REALLY important to get positive affects as large changes in dosage could have the opposite negative outcome. I have ballsed up a few times by changing the intensity in terms of load and not decreasing volume and have had negative outcomes.

Under dosing

 

If we under dose then potentially we will get no real adaptation. If you are looking for a change in whatever targeted aspect you are aiming for, lets say strength or load tolerance, if your manipulation of the variables is not on point then you won’t get much adaptation.

The caveat here is maybe there is no need to change the targeted aspect. Many studies have shown NO change in kinematics, posture, ROM or strength but a change in pain.

The caveat to the caveat might be that we don’t often measure the long term trajectory of injuries meaning that although we have a short term successful outcome in changes in pain that show up in studies many people often still suffer longer term with reoccurrence of an injury. This is different to chronicity because it may not be continuous and hence why it is often hard to simply define painful problems as acute or chronic. Perhaps we need some adaptation to affect these things longer term, but I am just thinking out loud.

Perhaps we are altering things we don’t or cannot measure such as local physiology, cellular adaptations, neurophysiology (nociceptive apparatus) or central changes such as can happen in the cortex with sensory and motor representations.

Under dosing could be frustrating as it is less likely to have an effect on the problem and not speed up (if we ever do!) the process of feeling better. This is potentially why we have seen a rise in the use of strength training as with a greater load we are less likely to under dose.

Over dosing

 

The opposite end of spectrum is giving too great a dose. To a sensitized system this could most definitely be an issue and cause an adverse response and could be why many therapeutic exercises are quite low in the overload stakes using minimal body weight or therabands.

Making someone’s pain worse can have a real effect on how they perceive the care you are giving, your competence and therefore the therapeutic relationship and trust bond. It is also really quite frustrating for them, people want to be able to get back to the activities they enjoy, they want hope and this is often fostered by progression.

Unfortunately it is very difficult to gauge what someone’s response maybe. Much like pain itself this will be dependent on many factors occurring in someone’s life at the this precise moment in time from stress to sleep to their emotional state.

Everybody has managed to make someone worse with a really minimal dose and also thought they have may have crossed the line with too great a dosage to find out that the person handled it just fine.

In reality we never really know where that line is!

Minimal effective dose

 

A minimal effective dose simply is trying to find a dosage that you think will cause an overload on whatever you are trying to effect but minimizes any potential for side effects. Remember you can always incrementally increase or decrease dosage later.

20 ibuprofen would get rid of your headache but would also expose us to other potential complications. So 2 tablets, or 200mg, is deemed a dosage that is effective but reduces complications.

Unfortunately the biochemistry of medication seems to be more generalizable across the population OR has been more widely studied with large clinical trials. Exercise dosage is still something that needs to be better quantified in the research base.

We could do this through looking at the person’s previous history such as chronicity or frequency of the same injury, the amount of a stimulus that may aggravate their problem such as time or load and then how long it takes to settle down after it rears its ugly head. If you flair your back up when picking up a biro and it takes 3 days to calm down then the dosage should reflect this, especially initially.

We can then adapt the intensity it terms of weight, speed or reps or the frequency of how often they do the exercise(s).

How can we make our dosing more effective?

 

Firstly we should think about shared decision making and discussing the potential outcomes of the variables being manipulated.

This helps people be better informed, and able to rationalize, what is happening to them especially if we explain WHY they may be feeling what they are feeling and what this ACTUALLY means for them. This hopefully avoids any uncertainty to be filled in by misinformation or investigation on the internet.

Explain that rehab is not a linear process and we don’t always know what the correct dosage should always be, hence why they need to be an active participant in the process.

All of this hopefully adds up to a greater internal locus of control.

Actually perform the dosage, or new dosage, with them and find out how it feels and how comfortable they are with it. If we are adapting a dosage then ask if they feel more comfortable increasing intensity, volume or frequency. Sometimes they maybe more willing to add more load than more reps or sets and sometimes the other way around, maybe they are happy now to do them daily rather than every other day.

Secondly the ability to independently manipulate dosage can be a really big deal. Often there are weeks between contacts so a dosage that is ineffective or aggravating could go unchecked for quite a while.

Here are my 5A's of self management.

5as

Even in the face of increasing pain many folk STILL keep going with their exercises. They blindly believe that it will still make them better, hence if we arm people with some knowledge about what they should be feeling they could limit or adapt what they are doing and minimizing adverse effects.

Part of any exercise prescription (I hate THAT word BTW in relation to exercise) should be the ability to regress or progress based on an agreed level of discomfort, e.g. exercise soreness or actual pain. This could be based on a VAS score or some other personal measure.

If an exercise really hurts, both immediately or 24hr response, could you regress to an isometric? Or if already an isometric could you regress to a lower level of effort or frequency?

If it is not having much of an overload, perhaps gauged by muscle soreness, then could you add in more weight or reps and sets or how often it is performed? Again this offers people a greater internal locus of control.

Offering people support BETWEEN appointments could also be another way to better manage dosage and done via phone or email.

Conclusion

 

  • Dosage is a big deal
  • Intensity, volume and frequency all affect dosage.
  • Both over and under dosing are issues.
  • Try to find minimal effective dose. It can always be progressed.
  • Shared decision making helps find tolerable/effective dose.
  • Define what the right dosage should feel like.
  • Give a regression and progression.
  • Offer support to manage dosage.

 

 

 

 

 

 

Please click on the large image of all the cards below to download the FREE pain flash cards. You will be redirected to a drop box link containing all 6.

This is a resource aimed at anyone who has an interest in pain and some of the science (what we have looked at so far!) behind the way it works.

Please feel free to share with anyone who you think would benefit.

Subjects covered:

  • Pain
  • Pain & stress
  • Nociception
  • Central sensitisation
  • Descending inhibition
  • Peripheral inhibition

Each one contains approx 500 words on each subject split into:

  • Complex bit
  • Simple bit
  • Simple story to use
  • Reading list

pain-cards-montage

Why do I still hurt?

Why is it not going away this time?

Why am I so sensitive?

Why does it keep happening?

why

People want answers

 

These are all questions that people regularly ask regarding their pain and injuries and they want to know a reason why. The bottom line is people want answers and in the absence of satisfactory answers will often jump to the worst possible conclusion.

Perhaps questions like these are indicators for the need for a different type of explanation beyond the pathoanatomical model?

Uncertainty

 

Uncertainty can be present in both acute and chronic pain. Mishel first proposed this in the “theory of uncertainty of illness” HERE. Uncertainty is a cognitive stressor and can be at its height during the diagnosis phase. This was defined as “an inability to determine illness related events”, the sufferer is unable to estimate what the issue is and unable to accurately predict what the outcome will be.

Mishel outlined 3 major points in the “theory of uncertainty of illness”:

    1. Antecedents of uncertainty- Things that occur previously to the illness. These can affect the patient's thinking such as pain, prior experiences and perception.
    2. Appraisal of uncertainty- Procedure of placing a value on the uncertain situation.
    3. Coping with uncertainty- Activities that are used in dealing with uncertainty.

 

Uncertainty has been linked with increased pain sensitivity, increased psychological distress and maladaptive coping HERE. Higher levels of disability and depression were found in LBP patients who felt their pain was due to diagnostic uncertainty HEREHERE we see experimental data on uncertainty having an effect on the pain people experience.

Getting an answer

 

The perception can often be an answer or a diagnosis hopefully provides us with a pathway of what to do next and a fix, solution or a cure. Answers are often quite abundant, they are given out by all manner of therapists, trainers, medical doctors and of course everybody’s favorite doctor….doctor google. A key aspect in the expectation of recovery, a very important factor in actual recovery HERE, is a diagnosis and part of this includes diagnostic imaging HERE. Unfortunately we also know that it is not as simple as that HERE.

Without a clear diagnosis we may see expectations of recovery also diminish. We do as well as we think we will do! HERE.

Increasing stress and pain have a negative relationship, uncertainty can increases psychological stress and therefore potentially leads to increased pain levels too. Higher levels of acute pain have been cited as a risk factor for the development of chronic pain HERE.

Unfortunately there is lots we still don’t know and may never do, many painful situations have an unclear cause and diagnosis, and symptoms can be unpredictable.

Potentially this is why we have so many theories and syndromes that try and fill the gaps by supplying us with information about our postures being ‘bad’, joints being out of place or having dysfunctional movement patterns. In situations where people demand answers it is easy to reel off a basic, simple but often untrue explanations. Read more HERE and HERE.  Although uncertainty maybe reduced it can be replaced by negative beliefs that cause more stress or negatively modify behaviours such as the avoidance of movement or reliance on being ‘put back into place’ by their therapist.

Maybe the answer, in part, with the scenarios that arise from these types of questions lies in understanding more about the myriad of changes that can occur within the systems that are involved with the experience of pain itself. In the absence of a plausible explanation the myths that pervade about the human body can continue to flourish and fill the void that people desperately want filled. The premise of pain education in essence is separating the pain someone experiences from the state of their bodies and not simply being reflective of the state of the tissue. Pain not being a measure of increasing harm.

This reconceptualization of what the problem might be really is a tough thing to be able to do. The question is are simple metaphors enough? How far does our knowledge have to go to really help people?

That of course may depend on the person, their education level and how much they really want to know. For some the science may baffle and bemuse and be counter productive as we often see in response to scan reports. Others may need the level of detail to high to make it believable and plausible. Finding the balance between being potentially too superficial and metaphorical and too heavy and science based is important but tough.

Whatever the route you take it is unlikely to be quick or simple with epiphanies all over the place.

Einstein told us “if you can’t explain it simply you don’t know it well enough” but also left us with “ make it things as simple as possible but no simpler”. Maybe these quotes sums up explaining pain quite well. Sometimes it needs to be simple and other times complex things must remain complex.

einstein

Perhaps we need layers to how we explain complex things like pain. Superficial metaphors and stories to help with concepts and backed up by a deeper knowledge of changes that can occur at multiple levels from the periphery, dorsal horn, spinal cord and up in the brain too.

Maybe this is why we have more recent problems with some of the issues surrounding the idea, or mantra as some have described it, that ‘pain is in the brain’ and the negative influence that that can have if the recipient misconstrues it as a purely psychological issue HERE. There are very physical and biochemical changes that can occur and discussing these as well as psychological factors might help fulfill some of the more uncertain aspects.

Armed with knowledge and how to get it across

 

The key to reassurance, a most powerful pain killer –Gifford, and that there really is nothing serious maybe the ability to perform a good clinical exam and being able to speak from a position of confidence that everything is likely to be ok.

Louw et al discuss the need for a good clinical exam in their recent paper HERE. Making sure that this base is covered before moving and finding out if someone is “interested in finding out why they still hurt”.

We have to appreciate that people may not need or want to know more about why they hurt. This aspect should not be seen as standalone or sufficient for recovery in the majority of situations but instead part of a multidimensional approach to care. Education seems to be more effective when combined with other stuff. Does this suggest that pain is not "in the brain"?

But if it is required is the key to reconceptualising also to have a similar level of knowledge and confidence about the subject that you are espousing on?

Wijma et al HERE look at classifying the type of pain to be then able to give a more detailed diagnosis of the source. They look at classifying pain as being mechanism based, the classification being based on history and sensation as nociceptive, neuropathic or central sensitized. This allows a pathway to explain the mechanisms involved in the pain rather than a more traditional pathoanotomical model of damage or alignment driven pain.

Nijs et al wrote a great paper HERE and also Lotze & Moseley HERE on the subject.

A criticism of research is bridging gap between academia and therapist and then between the therapist and person and being able to provide applicability. This can prove challenging in the area of pain with topics such as the level of complexity of the biochemistry and there may not be a substitute for having a decent grasp of the underpinning science.

The point of the blog is that people want a thorough explanation. Is don’t worry about pain enough?

Pain is an alarm!

Pain is in the brain!

It’s a perception!

Pain is helps us to protect!

Sometimes it goes a bit wrong!

Someone will always ask why?

So we have to be able to explain how and why it might be amplified. The mechanisms underpinning the plastic changes that happen peripherally to terminal endings and previously silent receptors, changes at the dorsal horn with receptive fields and available synapses and supra spinally to with increased attention to incoming information, changes in the sensory cortex and strengthening of neural connections.

Stress can come from another conflicting piece of information making the situation uncertain again. Finding the right place on the continuum between simplicity and complexity for the individual maybe the key. This can be tough if the knowledge base lends itself to the simple end.

Another challenge is can you make it FUN. People probably switch off with any boring explanation. How we get things across is probably MORE important than actually what is said!

The use of visual representations and diagrams can help. We could show multiple layers of processing in the CNS or more open doors in the dorsal horn quickly with a basic picture. It is no different from the model of the knee or back used in clinics the world over.

These are some basic tips for the practical application of pain science HERE

Individualising

 

Rather than trotting out the same old patter each time it maybe good to use peoples experiences to individualize the interaction. Can we find part of someone’s history or story that lends itself to highlighting the unclear or trajectory nature of pain. This could be in contrast to scan results that can remain relatively unchanged over extended periods of time.

Does their pain correlate with periods of extreme stress or ease over the weekend or on holiday?

Have previous treatment methods aimed at the diagnosis helped over the longer term? Can we explain HOW they may have helped in the short term?

Why did picking up a biro cause their back pain to flare up but going to the gym did not?

Did their back pain flared up without any apparent stimulus or adverse event?

Key points

 

      • People WANT an explanation or diagnosis
      • Uncertainty is a stressor
      • Expectation of recovery is a big deal
      • Misinformation fills the gaps very nicely
      • Simple explanations can be good and bad
      • A Good grasp of the science is ALWAYS good
      • Individualising helps

 

 

There are a few muscles in the body that are often thought of as ‘magic’.

These ‘magic muscles’ seem to act differently from the other muscles in the body and we need to get them working at all cost by prodding and poking or performing bizarre exercises to ‘fire’ them up so that we can avoid ‘dysfunction’ and the inevitable contribution to pain from ‘sub optimal’ activation.

Witch doing her dirty tricks

Examples of these muscles and their related ‘dysfunctions’ are the TvA and back pain, the rotator cuff and shoulder pain and the glutes and well every pain going from the knee to the lower back and shoulder.

Sometimes (this means often) we just blame the muscle automatically without even bothering to perform ANY kind of test.

Simply stating “Your back pain is because your TvA is not firing”

We have some wonderful theories about how and when ‘magic’ muscles should activate and what role they perform at a joint such as are they movers or stabilizers.

It has been suggested some deep muscles should activate first and independently of the movement being performed to provide stability rather than help move the body such as the TvA and rotator cuff whilst the glutes should activate first before other more superficial muscles of the hip to be the ‘prime mover’.

It has also been hypothesized that muscles may have specific jobs because of their fibre type. Muscles with a predominance of slow twitch fibres mean that they are better suited to a postural or ‘stabilizer’ role rather than movers witch have been proposed to contain a greater proportion of type 2 fibres. Sometimes we call them local and global or even fancier…..tonic and phasic.

This influences a whole bunch of what people do, both therapeutically and in gym settings. Do we have much evidence beyond the theory to support these common practices?

This gives us three questions to answer in this blog in relation to this line of theory about muscles and if it contrasts with what has ACTUALLY been studied?

• Do ‘magic’ muscles have specific firing patterns or onset times?

• Do ‘magic’ muscles act independently to carry out specific roles such as stabilization?

• Do ‘magic’ muscles display a distinct dominance of fibre type that mean they have specific roles such as moving or stabilizing?

 

Muscle ‘firing’

 

Glutes

How many times have you heard someone say “They told me my glutes weren’t firing”. The glutes not firing or ‘activating’ first have been blamed for lower back pain, SI pain, knee pain and my personal favourite, opposite shoulder pain (its true……myofascial slings baby) amongst other things.

There are a few purported reasons for this lack of 'firing'.

• ‘Inhibition’ of the muscle after injury.

• Excessive sitting causing inhibition

To determine if there should be a specific firing order it is important to look objectively at how healthy people activate their muscles. We can then see if there is a specific pattern or level of activity we should to try to aim for to be healthy and if there is inhibition OR the theory is incorrect.

The prone hip extension test has always been a favourite way of doing this. You know the one, get people to lie on their fronts and then the therapist or trainer pretends that their fingers are EMG machines and can tell which muscles activates first! This is known as the prone hip extension (PHT) test.

So, if pain was a consistent inhibitor of the glutes then we should see DECREASED EMG (with a proper machine) output from people who have had a previous injury during the PHT. This paper *HERE* actually found that the participants who had suffered a previous injury (in this case hamstring) had a GREATER EMG output. This was also the case here *HERE* where the chronic LBP group had a GREATER EMG signal in the PHT compared to those without. In fact any muscle ‘inhibition’ seems to resolve quite quickly *HERE* after injury.

As far back as 1990, so we really have ‘known’ this for a while, *HERE* they found that muscle firing was pretty variable in the PHT. Twenty healthy subjects each made 30 prone hip extensions with EMG used to measure the onset times of the right glute, biceps femoris, eractor spinae and left erector spinae. They found no significant difference in onset times between the muscles and variability in muscle activation within and between subjects. So the same person can perform the action differently and different people also perform it differently. This makes it really tough to have an objective firing order to base ‘dysfunction’ from.

This paper *HERE* DID find an objective order of muscle firing. They state very nicely their rationale for the need for the research.

“The development of low back pain is ascribed to changes of the muscle firing order in prone hip extension. There appeared to be no normative data on muscle firing order of the lumbar and hip musculature to provide a basis for recognizing variations”

They had healthy fifteen subjects and had a very similar testing procedure with a slightly different set of muscles around the hip but found the glute max actually activated LAST rather than first.

This was finding was supported *HERE* with a much greater sample size of fifty participants, 30 with back pain and 20 without. They looked at both onset time and amount of activation and found that glute activity was delayed significantly in both the symptomatic AND asymptomatic groups. Their conclusion being that the PHT was not able to discriminate between those with and without back pain.

They also made the great point that it is also tough to generalize what happens prone to standing or walking. This paper *HERE* found that changes in hip abduction altered the activation order and amount of activation (EMG amplitude) of the hip musculature. With 15 or 30 deg of hip abduction the glute max firing time was advanced with 0 deg delayed relative to the hamstring.

So slight alterations in hip position when prone changed firing order! What would happen with changes in body orientation (prone, supine, standing) or actually moving and at different speeds. Different terrains may influence hip width *HERE* and this would probably change firing order based on leg orientation.

In the Lieberman study looking at glutes during walking and running *HERE* we see alterations in timing and substantial activation changes between the two activities. This suggests that a single test is probably not transferable across multiple activities that may require different timings and activation levels.

As far as I am aware glute inhibition with prolonged sitting has not been studied. This is quite amazing considering how prevalent the theory is so it is tough to corroborate it. However WITHOUT evidence to support it and as we see delayed firing in those WITHOUT pain then we have to wait for more evidence before we can support this claim.

There is also the small point of can you really feel micro second differences in muscle activation with your fingers and if they are pretty minute do they matter anyway?

Although the 'glutes aren’t firing’ line sounds like an alluring and simple explanation for someone’s problems the actual SCIENCE really does not support such a simple answer.

TvA

The TvA is often a muscle that is blamed for not firing and inadequately stabilizing the spine leading to back pain. Although there certainly has been some early research showing delayed firing there is certainly not a well-defined causal link between delayed onset and lower back pain. Later work using both EMG and M mode ultrasound *HERE* have shown variable firing in healthy individuals and back pain sufferers with delayed onset not being a consistent finding for LBP patients.

Vasseljen et al state “Within and between subject variations need to be acknowledged in future studies” This paper found no association between changes in onset timing of the deep abdominal muscles and LBP.

This was finding was mirrored by Mannion et al *HERE*They found no association between the ability to activate the TvA both before or after training and a good clinical outcome.

Much like the glutes, the onset of TvA muscular activity has been shown to be variable between tasks so generalizing what happens with a muscle in one research piece using a specific movement such as rapid arm movement cannot be used to create a generalized muscular model for human function.

Morris et al *HERE* found the role of the TvA to be more function specific with muscular activation to being dependent on direction and magnitude of an action being performed. It has previously been hypothesized that the TvA acts independently (not function dependent) like a corset to stabalize the spine and it does this bilaterally. The original research only looked at the contralateral (to the arm motion) TvA but extrapolated this to bilateral activity.

Morris et al reported that no one (in the admittedly small sample size of seven) used a bilateral activation strategy in response to unilateral arm movements, the TvA acted both reciprocally and asymmetrically and the authors suggested that training the TvA to act bilaterally may actually INHIBIT normal movement.

Again we see that it is just not that simple and giving a muscle a specific job with a timing strategy is a potentially problematic line of reasoning when we dig a bit deeper than the theory.

Rotator cuff

The rotator cuff (RC) has also be given the job of stabilizing the gleno-humeral joint with a hypothesized earlier onset time and co contraction to provide joint stability. This systematic review of the stabilizing characteristics of the rotator cuff *HERE* found only in 4 out of 10 of the tested movements that the RC onset time was earlier than more ‘global’ muscles around the shoulder joint. Co-activation was also not consistent across different movements.

The authors concluded here that there is no clear evidence for seeing the RC muscles as simply stabilizers but instead acting in a direction specific manner. This was supported by more co contraction between the supraspinatus and infraspinatus than between either muscle and the subscapularis. The stabilizing role of the RC maybe the limiting of translation within the joint in a direction specific manner.

This is supported by this paper *HERE* that found that the subscapularis being more active in shoulder extension and the supraspinatus and infraspinatus more active in shoulder flexion. Interestingly the level of external load did not alter muscular activation level! It was also supported *HERE* with different variations of shoulder exercises influencing the muscles role.

Boettcher et al *HERE* helpfully put their conclusion in the title of their paper “The role of shoulder muscles is task specific”. They wanted to see if the RC muscles displayed distinct rotator or stabilizer function and although the title somewhat suggested this was not the case this was confirmed in the paper with a task specific activation being apparent.

Muscle fibre type

 

The predominant fibre type of muscles has been cited as a reason behind why a muscle should be classified as a ‘stabilizer’ or a ‘prime mover’. A stabilizer would have a much greater amount of type 1 fibres whilst a prime mover a greater amount of type 2 and type 2A.

But do we see a predominance of fibre types within muscles?

Trunk muscles are often theoretically split into ‘inner’ and ‘outer’, the inner unit involving the deeper muscles that should have a much greater concentration of type 1 fibres. As we have looked at previously the inner unit muscles don’t appear to have a reflexive and independent activation or movement strategy. So what about their fibre type, is this more suited to stabilization?

This study *HERE* used bioposy to study the rectus abdominis, TvA and Obliques. They found large variation BETWEEN people but little difference between the individual muscles, in fact their words were “minor or non-existant”. They concluded that the muscles actually have a SIMILAR functional capacity.

This paper *HERE* looked at 36 muscles in a relatively young sample size. They found that “Most of the muscles studied were known to fulfil both tonic and phasic functions, however, and showed no striking preponderance of either fibre type.”

In an older population in the rotator cuff, this paper *HERE* also showed a mixed fibre with a maximum of a 60/40 split between type 1 and 2. This was also apparent in an older paper *HERE* looking at back muscles with around a similar split between type 1 and 2. Certainly not enough to warrant classifying muscles into specific roles.

A more recent systematic review paper *HERE* also suggests that there is little inter (between) or intra (within) differentiation of fibre types in either healthy people or LBP patients in the multifidus and erector spinae muscles.

Two muscles *HERE* that DO APPEAR to have a much greater predominance of type 1 fibres are the soleus and tibialis anterior that have around 80% of fibres being more ‘postural’ although we don’t seem to talk about these muscles in the same way but obviously they do a lot of endurance type work!

Conclusion

 

What does the research tell us?

• Muscle firing patterns do not appear to fit theories that are often discussed and that influence exercise prescription.

• Muscle firing, when looked at over repeat trials, seems to be variable within and between individuals and does not support a specific muscular strategy to base ‘dysfunction’ from.

• Muscles appear not to simply have ‘roles’ that are independent of the action being performed and can be consistently defined.

• Co contraction levels appear not to be consistent enough to support a singular role of stabalistation to a joint.

• Generalising activation patterns in one task to beyond that task appear unfounded.

• Fibre types although not a perfect 50/50 split do not really show a dominance of fibres that allow us to categorise muscles into postural or movers. Movement data also does not support this.

Knowledge about pain science is rapidly growing with articles and blogs aimed at everybody from personal trainers to doctors and surgeons springing up on the topic. It could be argued that anyone who deals with the body should have a basic understanding of how pain works.

We have criticism that we still have not gone far enough in this field and others seeing the pendulum as having swung far to far already!

Whilst it is important to digest this barrage of information, we also need to think about the real world application of the academia to the end user, e.g. the person you are trying to help understand all this information, and often this is the bit people find hard.

1. Pain science can help us to understand what NOT to say, but not what TO say.

 

At the very LEAST a better understanding of pain science should influence us to know that what we say can have a profound affect on the way someone perceives themselves and their current state. Unfortunately words that hinder rather than help can often easily trip off the tongue as they have been used so many times before!

Just staying away from certain words may help to not create detrimental nocibo effects.

• Rip
• Tear
• Instability
• Damage
• Degeneration
• Chronic
• Out of place

These words have the potential to alter people’s perceptions of their capabilities, beliefs and expectations for recovery. ‘Thought viruses’ is a catchy term regarding negative beliefs and how they can be generated and passed between people.

What should we say? Well that is an infinitely harder question to answer and will vary between individuals, there are certainly are no recipes here.

Hence why learning what NOT to say is often a great start!

2. Learn more about the subject!

 

A criticism of our current educational processes is that they do not teach much about the mechanisms behind the experience of pain at undergraduate level or in many courses that deal with injury.

While it is a start to watch a few videos or read a few blogs, using the concepts of modern pain science should be underpinned by a good working knowledge of how pain works. A few buzz words or analogies probably aren’t quite enough to get it across to the target audience, especially when they have a habit of asking tricky questions.

Here are some questions it may just be worth knowing the answer to or how to explain:

What is pain?
How does nociception work?
What is central sensitisation?
What is peripheral sensitisation?
What are the supra spinal mechanisms involved in the pain experience?
What are descending inhibition & facilitation?
Why do stress, context & emotion have an effect on the pain experience?

3. Explanation of a complex subject like pain takes practice.

 

Everything is hard before it is easy - motivational slogan on a clipboard with a cup of coffee

People can feel under pressure to be able to ‘explain pain’ like an expert. Firstly you need the basic science then you need to learn how to articulate it and this does not happen over night.

As Einstein says, “If you can’t explain it simply you don’t know it well enough”.

Complexity and confusion during an explanation may lead to confusion and uncertainty in someone’s understanding and actually increase rather than dampen down someone’s pain experience.

Perhaps it is something than should be practiced away from a ‘live’ environment to build your own confidence and communication skills? Fuck it up a few times, learn from this and be ready to roll it out when you need it.

All the best presenters practice after all!

4. You may need more than one analogy.

 

Analogies have been promoted as a great way to get across complex subjects such as pain. As we use analogy so much in everyday life this makes a lot of sense but it is good to keep in mind always that these things depend on the person receiving the analogies previous experiences, cultural factors and education level.

SO if it aint working then switch it up.

5. Challenge concepts and not people.

 

A great way to ruin rapport, which can be vital to the success of what you are trying to achieve, is to tell people they are wrong or make them feel stupid. Beliefs can be like superglue and adding confrontation into the mix can make things go downhill quickly. If it is not working STOP, maybe you can come back to it later or drip feed in over time.

6. Always find out how someone has perceived what you have told them.

 

This is vital, it maybe the information you have presented is perceived in precisely the way that you did not mean it to be! Prof Kieran O’Sullivan promotes a most sensible course of action by asking “What would you tell your friends and family about what I have told you”.

This means any miscommunications can be (hopefully) remedied before they turn into ‘thought viruses’ such as “they told me the pain was all in my head”.

7. There are no recipes or protocols - It is about the individual.

 

What works for one person may not work for another. Perhaps a plus for pain science is it points towards being person centered rather than having a specific protocol across humans such as more protocol based approaches do.

Strategies that have been promoted from the fields of psychology involve techniques such as exposure therapy and expectancy violation. We have to be careful that the patient/client identifies the specific fears and beliefs to be addressed, and hopefully inhibited, and this is not seen as a general concept.

8. Changing beliefs is not an instantaneous process, an exact science or even always possible.

 

As discussed in point 5, beliefs can be sticky and contagious between friends, family and work colleagues (even more so with Dr Google!). Rarely do people walk out from chatting with their therapist or trainer and suddenly change their outlook and opinion on themselves or beliefs they hold.

It could be a slow and laborious process (likely!) or in fact never happen at all!

9. People often have their OWN epiphanies away from you.

 

Reconceptualising can happen in mysterious ways with mysterious triggers, a bit like an apple falling on your head! You may have to wait for someone to come to their own realisations about the information you are giving them rather than expecting an epiphany in front of your eyes.

10. You can’t talk tolerance into a tissue.

 

One of the major parts of the BPS model is the B for biological. Just because you can help someone understand they are not fragile does not mean they suddenly develop an enhanced capacity for moving. The less you move the less likely you are to be robust at moving, that’s the SAID principle in action.

Someone once said “you can’t talk tolerance into a tissue” a very true statement. But you may have to talk to someone first to get them to do that work and get the tolerance!

11. BPS model is still in the minority away from social media.

 

For the eagle eyed yes it did say 10 and this is number 11!

It may feel like social media is awash with pain science from every angle to the delight of some and not to others! Go out into the wider world of the internet and shock, horror the actual real world and it feels like the information being delivered in the medical and training world regarding pain is still pretty traditional with structural and biomechanical factors being promoted.

Lower back pain is a real BIG DEAL for a lot of people and with all the opinion and dogma that gets attached to various exercise types surrounding it I thought I would take a little look at the EVIDENCE base to try and get some clarity on what really is the BEST exercise for low back pain (LBP).

We are in luck here too. The good folks of academia have blessed us with a plethora of studies to choose from, not just looking at if a certain type of exercise is effective for LBP but also comparison studies to find out if they are MORE effective than something else!

The evidence

 

Lets start off looking at one of the most popular methods touted to resolve chronic back pain…..Pilates. This study *HERE* looked at Pilates in comparison to a stationary bike program over 8 weeks. The results indicated that at a 6 month follow up, an important time measure for CHRONIC pain, there was no between group differences, both were effective for reducing pain, disability and catastrophising.

Interestingly at 8 weeks the Pilates group was performing significantly better than the stationary bike group but NOT at the six month follow up. Could this be due to receiving an exercise method PERCEIVED to be the most clinically relevant treatment and influencing the short term measure?

This result was also replicated with a larger look at the data in a meta analysis of core stability exercises versus general exercises for chronic back pain *HERE*. The authors concluding that core stability training out performed general exercise in the short term but not in the longer term.

This paper found that a successful outcome for lower back pain using core based exercises was not associated with improved abdominal muscle function *HERE*. A positive effect of stability exercises has been postulated to be due to central mechanisms unrelated to abdominal muscle function. One reason could be the expectation being met of receiving the most PERCEIVED relevant treatment hence the shorter term success in the outcome measures. An expectation being met may activate mechanism’s such as the reward analgesia system.

Another systematic review with meta analysis provides the ‘coup de grace’ *HERE* concluding unequivocally:

 "There is strong evidence stabilisation exercises are not more effective than any other form of active exercise in the long term. The low levels of heterogeneity and large number of high methodological quality of available studies, at long term follow-up, strengthen our current findings, and further research is unlikely to considerably alter this conclusion”

Next up we have a walking program compared to specific back strengthening exercises *HERE*Both were performed twice a week for six weeks and a number of measures were taken. Again both groups improved but without much difference between them. It is important to note here that the participants were all sedentary to begin with so a take away maybe that the ACTIVITY here was the most important factor for those who do not do very much of it rather than the SPECIFICS of the activity.

Athletic woman warming up doing weighted lunges with dumbbells workout exercise for butt legs at home healthy lifestyle sport bodybuilding concept.

Conventional wisdom may have us believe that a specific intervention, due to its targeted nature, should out perform the more general one and not just a bit but significantly. That does not seem to be the case however. Much more general exercise WITHOUT the need for specific instructions or exercise experience and expertise seems to be just as effective.

A classic ‘moan’ from the sycophantic supporters of failed treatments is “they did not do it right” shifting the blame over to the person. The good thing with a more general program is that we can say with a degree of certainty they are just as effective but without so much that can be done in the ‘wrong’ way.

This randomised control trial *HERE* looked at a higher loading exercise program versus a lower loading ‘motor control’ program for patients with ‘mechanical’ lower back pain. Here the lower load group outperformed the high load group in some measures but at the 12 & 24 month follow up *HERE* there was no significant difference in the outcome measures. So again we see no real differences between two quite distinct exercise programs with both making improvements.

There are some caveats here. Both groups received education about pain mechanisms and, gulp, non alignment and optimal movement (whatever that is). As both groups shared this, it could have been an influence on the outcome. The low load group also did a greater variety of movements rather than just the deadlift performed by the higher load group. There is data, that we will get to later, that suggests reduced variability could be a factor in cLBP hence a healthy dollop of variation of movements performed could have had a positive effect.

A comprehensive paper “Exercise interventions for the treatment of chronic low back pain: a systematic review and meta-analysis of randomised controlled trials” found beneficial effects for exercise over thirty nine RCTs with a small but SIGNIFICANT effects on lower back pain for both strength/resistance AND coordination/stabalisation programs. The largest effect size was seen with exercise programs that focused on the WHOLE body which tended to be strength/resistance based. The important take home here is that exercise interventions were deemed more beneficial than other treatments.

The EVIDENCE of ANY real superiority of one type of exercise over another seems to be lacking here. Anyone who tells you they have a SUPERIOR ‘method’ maybe over egging the pudding!

What does that mean? Well exercise that gets DONE will probably be the most effective. Some questions worth considering are:

  • What activities do people ENJOY?
  • How easy is it for them to do?
  • How relevant is it to their functional outcome measures?
  • Are they easily able to access the necessary equipment or need specialist instruction?

I discuss the effect of environment and access *HERE*.

A focus on the HUMAN BEING doing the exercise rather than just their back might be just the ticket!

A good rehab program should be well rounded and encompass lots of factors associated with human function rather than trying to find the magic bullet of one type of exercise. Imagine if athletes only ever practiced one type of exercise! A combined approach to physical rehab could be beneficial incorporating variation in movements, high and low loads and specific and more general components.

An approach to lower back pain that considers lots of different aspects around movement is by Nijs et al *HERE*. It fits all my biases of people’s individual relationships with movement/exercise therapy for their back pain and the multiple factors to be considered across both the cognitive and physical realms.

It is also important to think about other factors associated with LBP and not just get hung up on exercise *HERE* and *HERE* 

Deconditioning

 

So it makes sense that if exercise works for lower back pain then it maybe due to the fact that people need to get a bit stronger or some more endurance and that performing exercise helps with this.

Like lots of things that seem to make sense in regards to the body it is not so clear cut when we delve in a bit deeper. This systematic review *HERE* concluded that the positive effects from exercise for LBP were NOT directly attributable to things such as strength, mobility or endurance.

Deconditioning has often been linked to lower back pain and hence the idea of reconditioning as a cure for lower back pain. This did not seem to be the case in this study *HERE* that looked at physical deconditioning in the first year following the onset of back pain.

Perhaps this adds to the argument that the DOING of exercise in more important than the type or the targeted physical aspects e.g. strength. The potential for the PSYCHOLOGICAL effects to be as important, or even more so, than the physical seems highly plausible and is certainly food for thought.

Being physically active is often touted as both prevention AND cure for LBP. This paper *HERE* suggests that it is not that clear cut, surprise surprise, looking at it as being more of a U shaped relationship. They found a moderate increase in cLBP risk with both a sedentary lifestyle OR excessive activities so more does not simply equal better when it comes to exercise.

This systematic review with meta analysis *HERE* DID find, although no discussion of the bottom and top ends, low to very low evidence that exercise alone reduces incidences of LBP and moderate evidence that combing education with exercise also helps.

As usual the deeper we delve the less clear it becomes and why we should be wary of simplistic answers and cures that are usually based around doing the one BEST thing such as activating a muscle or correcting a pelvic tilt.

Are there any physical ‘deficits’ or characteristics we see with LBP?

 

Laird et al looked at lumbo pelvic MOVEMENT in people with AND without back pain *HERE*. Their systematic review found, in comparison to those NOT in pain, reduced proprioception (15 studies), slower movement (8 studies) and reduced range of movement in all directions (26 studies)

Nourbakhsh and Arab *HERE* DID find that muscle endurance and weakness WERE associated in their sample size of 600. This however does not imply that these factors were a cause of LBP especially with the type of the study performed.

Both papers also looked at some structural factors and their association with LBP. NEITHER paper could find an association between lumbar lordosis angle or pelvic tilt angle. Nourbakhsh and Arab also investigated the association of leg length discrepancy and abdominal, hamstring and hip flexor length with LBP and found none.

This paper *HERE* looked at the spine loading characteristics of those with and without back pain. They found INCREASED spine loading for those with LBP and significant increases in all of the 10 muscles studied using EMG data. They also found the LBP group had severely restricted motion in a free lifting task. They concluded that the increase in spinal loading was due to INCREASED muscular co-activation.

Trunk stiffness in this study *HERE* was related to fear of movement in those suffering from LBP. Greater kinesaphobia fear of movement) resulted in greater trunk stiffness.

So we have kinematic and muscular data suggesting that those suffering from LBP have GREATER muscle activation and co activation and REDUCED movement around the lumbopelvic area. This makes sense if we see muscular responses to pain as being PROTECTIVE in nature and aiming to minimise movement in this area due to pain or the perceived THREAT of pain.

Here is a bit of opinion based on the data.

How do exercise strategies that promote core stiffness such as many popular approaches for LBP affect this? Could they perpetuate the problem rather than solve it? High loading strategies may also promote increased stiffness, could this have the same negative effect?

Could a key be being able to ‘turn off’ muscles as much as we are trying to ‘turn them on’? Potentially choosing the right amount of muscular activation and stiffness for the task is the sign of ‘healthy’ movement rather than just increased ‘activating’, ‘firing’ or whatever you choose to call it. Reduced movement may not be under activation of a muscle but increased activation of another to stiffen the joint.

Freedom of movement, both physically and psychologically, should be an aim for those working with people suffering from lower back pain.

 

Variability

 

As it’s my blog I get to indulge in some my biases! One of those is movement variability. There is a reasonable amount of data in my opinion that suggests decreased movement variability is associated with LBP.

This first paper supports some of the kinematic changes we see around the trunk discussed in the section above. The authors *HERE* looked at the coordination patterns between the trunk and the pelvis during running and walking comparing different groups. As loads increased during running, variability in pelvis and thorax rotation decreased on a continuum between the no LBP group, one bout of LBP and then the chronic LBP group. The decrease in variability could be due to the increased trunk STIFFNESS noted in other papers.

Lamoth et al *HERE* found a more rigid, less flexible pelvis-thorax coordination variability (counter rotation) as walking velocity, and therefore demand, increased. This decrease in thorax to pelvis motion was also present in a study by Van Den Hoorn *HERE* and also attributed to increases in trunk stiffness.

Falla et al found reduced ranges of motion in a free lifting task with the LBP group in their study *HERE*

As well as looking at the kinematics they also explored INTRA (within) muscular activity using EMG. They found significant higher values for EMG activity for the LBP group, consistent with other studies, to accompany the reduced kinematics of the spine indicating a stiffer strategy.

The LBP group also displayed decreased variability in muscular strategy, not displaying the shift in activity to different muscular regions that the pain free group did. This repetitive muscular strategy was accompanied by an increase in LBP, reduced lumbar movement and increased pressure pain sensitivity.

Decreases in variability have also been linked to chronicity in back pain *HERE*

 

What does this variability stuff all mean?

 

Well it could be that simply decreasing trunk stiffness may automatically increase variability. It may also be that focusing on decreasing stiffness through more relaxed movement across a variety of tasks, such as gait, could be a treatment strategy for LBP sufferers.

Could this increase in stiffness and decrease in variation also play into intra muscular metabolism? This could potentially increase ongoing sensitivity via mechanisms such as changes in local tissue PH and excitation of acid sensing ion channels in afferent neurons.

Whilst looking at variability is a promising avenue, and worthy of exploration in my opinion, I do discuss some of the limitations currently present here in this line of research *HERE*

Conclusion

 

  • Lots of different types of exercise have a positive effect on LBP.
  • No one type seems to be superior.
  • Focus on the HUMAN BEING not just the back.
  • Exercise that people enjoy and is easy for them to do will probably get done and hence have a positive effect.
  • Consider a rehab program combining different exercise variables e.g. high and low load and types rather than one singular type or exercise method.
  • Deconditioning is not clearly associated with LBP.
  • Positive effects from exercise for LBP may NOT be directly attributable to things such as strength, mobility or endurance.
  • Increased trunk stiffness and decreased ROM and speed of lumbar movement ARE associated with LBP.
  • Structural factors such as lumbar lordosis, pelvic tilt, leg length discrepancy and muscle length are NOT likely to be associated with LBP.
  • Kinematic AND intramuscular reduction in variability is associated with LBP.
  • Decreasing stiffness and promoting freedom and variability of movement maybe a good goal in rehab, especially with those displaying kinesiophobia.

 

I have to give a hat tip to my mate Todd Hargrove for getting me thinking about the subject of environment and the effect it can have on movement behaviours. Here is a link to his recent blog piece "The environment for movement"

It is really important that we think about the environment that people will be using for increased activity or the exercises we have asked them to perform. The environment around them will affect the outcome of the activity or the exercises and we can help shape this environment for them to be successful in the tasks we want them to perform.

A question I ponder more and more is how many failed rehab or fitness programs are because of a lack of consideration of ENVIRONMENT and NOT the person or the program?

We have to consider the HUMAN BEING doing the exercise. You can discuss the relative evidence base or sets, reps and % of MVC of whatever exercise bias you hold. It really does not matter IF IT AINT GETTING DONE and the environment can directly affect that.

Our ENVIRONMENT can act as a constraint to either INCREASE exercise & exercise compliance or DECREASE it. Movements and actions will emerge based on the constraints placed upon them. When we are dishing out exercises this should be at the forefront of our minds, as these constraints will dictate how much of the exercises are performed and the way in which they will get done.

Child hand sticking out from plastic bottles garbage - environmental disaster concept, copyspace

The environment could affect the AMOUNT of movement such as EVEN doing an exercise in the first place to manipulating the environment OF an exercise and the specific outcome.

My son and swimming

 

A personal example of the emergence of movement happened shortly after reading Todd’s blog. I went on holiday and fortunately we had a very shallow and warm swimming pool right outside our room. My son, who is 4, with a bit of cajoling managed to teach himself to swim! Cue proud dad moment.

The fact we had a shallow and warm (important when you are 4) pool meant my son was able with great confidence to get in the water without his arm bands. He was also able to push off the pool floor and touch down if needed. This aided his practice enormously.

The environment of having a shallow pool with no deep parts enabled AND contributed to his learning process. The location meant he could go any time he wanted and hence increased his practice time. The depth improved his confidence at not having an external aid and also acted as a safety net to make mistakes in learning non lethal : )

The ENVIRONMENT acted as a direct catalyst to confidence, compliance and outcome. A question we should all ask ourselves is “Does my treatment or fitness program do this?”

Are you self limiting?

 

It could also affect someone’s whole treatment or training approach!

How many therapists work out of rooms that you could not swing a cat in? If a treatment couch dominates the room then it will probably dominate the therapeutic approach too! This environment does not lend itself to the performance of exercise and coaching cues etc.

A trainer in a busy commercial gym may be affected via the amount of space or the equipment available to them. Hence their exercise programming may be limited to using small spaces and fixed resistance machines.

External & internal constraints

 

We have a number of different EXTERNAL constraints acting on us such as the environment someone is operating in, the task being performed, the instructions they are given and the equipment they use.

We also have INTERNAL constraints. These would be things like confidence, fear (of movement, reinjury etc) and movement skill (ability to perform a task). If your task is beyond any of these internal constraints there is more likely hood of it not getting done! A complicated lift, in a rehab or training context, for someone with low confidence, body awareness and movement skill may prove far to challenging and hence affect the outcome.

Then we may have Internal constraints such as confidence in using the equipment, body image and fear of getting it wrong and making things worse. A focus on fitting exercise/exercises in with the person and involving them rather than just dictating to them may have a profound impact on if they actually get done or not! In fact it could be more important than the exercise itself in many cases.

The concept of exercise itself may need to be reframed for someone with poor associations with exercises, we could regard this as an internal constraint, and many failed attempts to integrate exercise into their lives. Can we create fun movement tasks or activities to help movement emerge? Can we tie these in with physical activities they do enjoy and are more likely to perform?

Environment & an LBP example

 

An example could be getting someone with lower back pain that is sedentary more active as part of a rehab plan. If you say you have to do a specific type of exercise program in a gym then that may present external environmental problems. Someone has to be a member of a gym, get to the gym, the gym they are able to get to also has to have whatever equipment you have suggested they use. All of these factors may present barriers and hence must be considered and addressed. In contrast a walking program in a local park may yield better results for some with a much lower barrier to getting it done based on their location, preference and confidence.

Rather than just shoving an exercise down someone’s throat…..

Find out what activities they enjoy and feel capable of. Are they a regular exerciser or gym goer to begin with?

  •  Explain the exercise/movement or activity, why they are doing it and the importance of it to their problem or goal.
  •  Ask what is their opinion/perception of what you have asked them to do and their confidence in doing it.
  •  Help set out when in their schedule would be best for them to realistically do it.
  •  Making sure they have good instructions of what to do. A short video clip using a video phone can help.

At a recent course I ran the class brainstormed ways of creating loaded training without having to attend a gym. This can be a barrier for many people with this aspect of rehab or training.

Ideas included:

  •  Sand bags
  •  Bags filled with books
  •  Bags of compost (they come in 20kg bags!)

Much as we aim to ‘meet the person where they are at’ with an educational approach to reduce barriers we should also do this with exercise to increase compliance.

In part two of this blog we will look at how factors such as environment and the other constraints that we have lightly discussed here will affect movement outcomes such as variability and skill development.

If you have been any where near social media over the last few years it cannot have escaped your attention that pain is seen as a much more complicated entity than had been previously thought.

We have to see pain as a SUBJECTIVE experience that can be modified by many varying elements such as emotional, sensory and cognitive factors. One of the most studied aspects of the modulation of the pain experience is the placebo and the placebo effect.

Here is a great comment on what the study of the placebo effect is.

“The study of the placebo effect, at its core, is the study of how the context of beliefs and values shape brain processes related to perception and emotion and, ultimately, mental and physical health” - Benedetti *HERE*

Placebo 1

Multiple factors

 

We could perhaps split any therapeutic interaction into two components:

• Specific/active biological
• Contextual/psychosocial

I think it is fair to say the Specific/active biological part is probably thought about much more than the Contextual/psychosocial part, certainly during my educational process.

External contextual factors

External contextual factors such as visual stimulus, smells, size and colour of tablets have all been shown to exert an effect on the sensation of pain. Here we see a noxious stimulus when associated with the colour red as being perceived as hotter and hurting more than when associated with the colour blue *HERE*

Internal contextual factors

Internal contextual factors such as previous experiences, beliefs and expectations and positive or negative emotion have also been shown to modulate the outcome of a treatment.

So it sounds like this placebo and its effects thing should be pretty important right? Yep but unfortunately one of my least favourite words is…… Placebo!

Here are a couple of definitions of what a placebo is.

"a substance or procedure... that is objectively without specific activity for the condition being treated" - Shapiro

“An intervention designed to simulate a medical therapy that at the time of use is believed not to be a specific therapy for the condition for which it is offered” - Brody

We are presented with a paradox here. If something is without specific activity or is inert then how can it have an effect? This paradox presents a problem as it casts the placebo and its effect in a negative light.

Here are some words that have been associated with placebo and the placebo effect.

• Deception.
• Ineffective.
• Unethical.
• Fake
• Unintended

Here is a great paper from the main man on the subject, Fabrizio Benedetti “Mechanisms of Placebo and Placebo-Related Effects Across Diseases and Treatments” who explains it all much better than me!

A much better term

 

A much better term in my opinion is CONTEXT.

Regardless of what you do with the human body from being a trainer to a physio or even a doctor, it is important to recognise that the CONTEXT you create in your interaction with your clients and patients has a very real effect on the outcome you are trying to achieve. We could even go as far as saying that being a good car salesman has similarities in this regard.

Now we could see this as unethical if someone were to manipulate CONTEXT to create a positive effect whilst knowing that the intervention they were using had NO real evidence of effect. But if we can SPECIFICALLY create the most advantageous context coupled with best practice then surely this has to be the overriding goal? This is suggested here with regards to manual therapy *HERE*   

Potentially EVEN more important could be that a negative context could influence a well evidenced treatment and reduce its effect. The influence of negative context appears to be more powerful than the influence of a positive context *HERE*

Simply avoiding creating a negative context could be a big deal for the overall outcome. A classic paper from Darlow *HERE* highlights the impact of what is said on the attitudes and beliefs of patients with lower back pain. It has been suggested that the variable of a negative context or nocebo is scarcely considered in a clinical setting. In fact peoples satisfaction is not influenced only by the treatment outcome but also but interaction with the therapist and the PROCESS of care itself. The magic is not just in the technique as many believe! *HERE*

Think about the negative influence of potentially NORMAL scan results. This may not only create a short-term negative influence but can go on to change behaviours and expected outcomes over the longer term. This study found early imaging for acute back pain actually increased long term disability *HERE* . A potential reason maybe the negative contexts that MRI’s can create. Simply rewording MRI reports had a positive effect on aspects associated with creating a positive context *HERE*

The complicated bit

 

A lot of study into placebo and the placebo effect has focused on the neuroanatomical and biological aspects such as the brain areas involved and chemicals produced. This is exceptionally important in my opinion as it provides a clear link between thoughts and emotions and chemical influences on the experience of pain. Rather than being a mysterious enigmatic creation of the mind, positive context becomes a real event with real chemical mechanisms.

Top down modulatory systems are activated in both positive and negative context. This excellent paper explores these mechanisms. “Different contexts, Different pains and different experiences”

Positive context activates key neurotransmitters such as:

• Endogenous Opioid
• Cannabinoids
• Dopamine
• Oxytocin

These are are all involved in analgesia.

Negative context activates

• Cholecystokinin (anti opioid)
• Opiod/dopamine deactivation
• Cyclooxygenase-prostaglandins (pro inflammatory) pathway

Brain areas such as:

• Anterior cingulate cortex,
• Amygdala,
• Dorsolateral prefrontal cortex
• Periaqueductal gray
• Rostral ventromedial Medulla
• Hypothalamus

Screen Shot 2016-07-09 at 09.15.49

Are all involved in the placebo effect.

There are some fantastic papers on the descending inhibitory systems. I would advise anyone with an interest in pain to read these.

Descending Inhibitory Systems

Central modulation of pain

What we can learn by looking at context and its effect on these modulatory systems is that the effects are VERY REAL and backed up by a large body of scientific literature. Hence the context we create should be a very real consideration rather than a side effect or something to be hoped for from an ineffective treatment.

Reward analgesia

Pain that is coupled with a positive context via reward is another example of pain modulation. The coupling of positive context of reward has been shown to significantly increase pain tolerance through the activation of the opioid and cannabinoid systems.

This experiment *HERE* used ischemically induced pain and we can potentially apply this to the old fitness saying ‘Feel the burn’ that ties an uncomfortable sensation into a positive context to drive us on to achieve exercise targets.

Dopamine is also linked with reward analgesia and involves the Nucleus accumbens (NAc) that pumps out the neurotransmitter dopamine. Both cocaine and opiates (there is a rumour they make you feel good!) stimulate dopamine release from the NAc.

Conditioning effect

We also have an effect of preconditioning and associative learning. If we have previously had a good experience from a treatment we are more likely to have another good experience with the same treatment EVEN if the treatment potentially is ineffective or implausible.

We may associate a person with a specific outcome such as “My therapist has magic hands”, this belief and expectation goes some way to making a positive outcome more likely to happen again. Expectation of decreased pain was looked *HERE* 

Previous experiences shape our future expectations and when the expectations are met they reinforce future belief leading to an even greater relationship. We could potentially apply this model of belief expectation and conditioning to repeated treatments that give people short-term relief.

Predicted expectation and outcomes of treatment have been shown to have a relationship for a number of conditions.

This is a great paper from Bialosky.
“Individual Expectation: An Overlooked, but Pertinent, Factor in the Treatment of Individuals Experiencing Musculoskeletal Pain” 

Pain facilitation

We have to also remember that pain perception can be facilitated or ‘turned up’ as well. The rostral ventromedial medulla (RVM) has both ‘off’ (inhibitory) and ‘on’ cells (facilitatory) that will influence pain perception. The two papers linked above on descending modulatory mechanisms go into this process in more detail.

During periods of acute injury this may provide a powerful biological protective mechanism but may also be involved in the maintenance of chronic pain.

The title of this paper is fantastic, “Bad news from the brain”  It describes mechanisms of descending facilitation linked into cognitive and emotional aspects.

The critical bit

 

My only caveat is the literature is still dominated by the concept of nociception and I would be interested to understand the effects of context on less nociceptively driven pain mechanisms too, especially in light of our changing understanding of pain! Does this model work better with chronic pain driven by sensitization of the periphery, spinal cord and brain stem driving nociception (from potentially previously non nociceptive stimulus) rather than supra spinally?

The simple bit

 

CREATE A POSITIVE CONTEXT!

Make people feel positive about you, themselves, the issue they have, the process they are about to go through and the outcome of it all!

Start by listening and actually hearing. We are ALL guilty of formulating a reply in our heads while someone is still talking. This probably means you are not listening! Listening and concentrating is a real skill in my opinion and one I am constantly struggling with.

Helping reconceptualise someone’s current experience and the meaning of what they are experiencing might just get some of these complicated neurobiological systems going.

The practical bit - Ways in which we can affect context

 

This recent paper “Enhance placebo, avoid nocebo: How contextual factors affect physiotherapy outcomes” explores ways of creating the best context during a therapeutic encounter.

Communication is a key aspect to providing a positive context and being “person centered”

These are some key communication points from the paper:

 

  • Be optimistic during the consultation and regarding the dysfunction
  •  Explore the patient's disease and illness, request and trust the patient's opinion
  •  Encourage questions, answer queries from the patient, deliver positive feedback
  • Investigate expectation, preferences and the patient's previous experiences
  •  Be warm, confident, friendly, relaxed and open during the clinical encounter
  •  Use verbal expressions of empathy, support, sympathy and language reciprocity
  •  Use positive messages associated with treatment for pain relief;
  •  Use eye contact, smiling, caring expressions of support and interest
  •  Use affirmative head nodding, forward leaning and open body posture

This was another interesting recent paper that provided a self assessment tool for dealing with patients in healthcare “Dealing with patients in healthcare: A self-assessment tool” 

Example bit

 

My bias is using movement as a tool to help.

The question I ask myself is “How can I create a positive context around moving?”

This means that I can hopefully get the positive physical biological and the contextual biological parts of an interaction.

We may have to overcome negative context surrounding the physical aspect first to actually get to the physical aspect! We can often pathologise movement that may create entirely the opposite effect regardless of someone’s positive intentions.

  • Avoid negative language around moving or a movement and use positive language and examples
  • Explain simply, including basic science, why moving may help
  • Listen to any fears someone has around moving or a specific movement (predicted outcome)
  • What movements/type of moving does someone enjoy?
  • Ask what a specific negative outcome might be and discuss this.
  • Shared decision making in how far (ROM), how heavy, how long (duration), how fast?
  • Set small achievable targets that provide reward
  • Reinforce positive outcomes and reinforce any violation of negative expected outcomes through discussion
  • Discuss any potential side effects such as muscle soreness and what this may mean.

1. Thinking there was one way to move.

 

I used to have a magic blueprint of what I thought was ‘correct’ movement but the more I looked at movement data, now a (boring) hobby of mine, and also anecdotally, the more I realize how differently we all move.

Movement research can often average the data from different subjects and multiple reps of the same movement from the same subject. This can hide that individuals generally move very differently from each other and also the same individual will move differently each time they repeat a movement, especially during cyclic activities. Bernstein described this eloquently as “repetition WITHOUT repetition”

We have a whole bunch of theoretical models of ‘correct’ movement, often with little underpinning data, but can they all be right? That we have so many differing models of what is ‘correct’ may inherently reflect that there is not a singular correct way.

Why should we all move the same given we have different anatomies and different movement experiences? It is madness, in my opinion, to expect that we would or should.

2. That we had defined that one way to move.

 

If you are happy for someone to suggest that they know an ‘optimal’ or ‘normal’ or ‘efficient’ way to move without much rationale why, then that of course is your prerogative. It was once something I was happy to do but now not so much and this may depend on what you require in terms of hard data.

A recent favourite of mine that I read on social media was “90% of people do X wrong” (The proposed issue has been omitted to protect the guilty!). If this was true then the test is probably wrong as if most people do X in a certain way then it is probably just normal!

Motor theories based on modern movement data and ideas are more inclined to define a wide parameter of what is considered ‘optimal’ in which we see a fair amount of normal variation rather than a rigid criteria based model.

Movement often changes when someone is fatigued or in pain making it even harder to define an 'optimal'

3. Thinking deviations from ‘optimal’ movement caused pain.

 

Again we often see this touted but with very little data to support it. “Micro trauma” is a classic example from damaging “micro movements”. Do we have data to suggest this? Signs such as inflammatory markers to suggest damage is occurring? I am open to any evidence highlighting that specific defined ‘micro movements’ are related to measures of ‘micro trauma’.

If we have macro movements that the body can adapt to then why are micro movements so problematic?

Also how the F**k do you know? We are often only seeing people's movement post pain so have no idea what it looked like pre pain.

Mistake at work

4. Pain was due to a single movement problem.

 

The likely hood is it is not. We could move in the best way imaginable but do it too much or too much too soon. The external load applied or the rate at which it is applied to the body could be much more important than any internal load occurring from ‘faulty’ movement. Equally the opposite could be true.

Pain is multi factorial, which has to negate the idea that a movement ‘issue’ is the sole cause of someone’s pain.

5. Getting a positive result was via attaining the ‘correct’ way to move.

 

There are many reasons why someone may feel better that have nothing to do with the specifics of what you have done to them.

  • They could have faith in you.
  • They like you.
  • Feel they are being listened to.
  • Getting relevant help.
  • Simply getting moving.
  • Moving at a tolerable dosage.
  • Getting a new novel input.
  • Time.

In fact anything that has altered input may affect the output of pain. Expectations and contexts can also profoundly alter someone’s experience.

6. Thinking I know what is happening internally.

 

For some it is getting the ‘correct’ muscle firing patterns, for others the right arthrokinematics and postures. For me the right biomechanical reactions. If someone improved it was because I had changed them!

In reality there is just no way of knowing what is happening internally within someones body without expensive lab equipment, which 99% of people in their day to day working environments do not have access to. Trying to define such things has proven to be elusive and also changes often bear little relation to a positive outcome when studied

7. Not appreciating Moving MAY be more important than the result of that movement.

 

Can we really attribute people feeling better to ACTUAL changes in their movement? Does everybody measure this pre and post? Are our measures really reliable? Does it matter?

It is a bit like ‘strengthening’. We often don’t know how strong people were previously to attribute any therapeutic effect to actual changes in strength. It could just be as pain subsides people regain their strength and movement.

It could be getting people moving provides input to the brain that decrease inhibition or creates local physiological effects rather than actually permanently changes motor output from a pre pain level. We just don’t know. There has been evidence to suggest getting better from back pain using exercise has nothing to do with the aim of the exercise e.g. increasing strength or flexibility

8. Having to find a movement problem.

 

I used to scratch my head like Stan Laurel if I could not find a problem. Now I realise movement 'tests' can also be used to highlight positives or break down previous beliefs especially when someones movement is really good.

If I thought my movement is ‘faulty’ and may lead to more harm and pain then I might just move less, especially if someone with perceived wisdom has told me so. This could mean my level of tolerance to movement drops and I become deconditioned and sensitive. As Louis Gifford reminded us, reassurance is a powerful painkiller and hopefully an activity inducer too.

Framing movement positively such as “you move really well you may just need to do a bit more of it” could impact profoundly on how someone perceives the act of moving and the amount of it they perform. Also shifting away from an exercise based paradigm to an activity based one can be useful especially if people have bad associations with exercise and potentially performing exercises badly causing more harm.

9. Ignoring the psychological impact of movement.

 

It is huge!

How we perceive a movement or moving from a specific area of the body maybe much more important than the reality of how we achieve that movement, especially if it stops me from doing the movement in the first place! Highlighting the difference between the belief and actual outcome is vital for changing the belief and even more powerful if we can do that physically through movement experiences.

Helping people understand the relevance of a movement/moving/exercise to their problem is also a huge help in getting them to actually do it and benefit from the more physical effects if this is a major part of your intervention.

10. Movement training has to be rigid and ‘correct’.

 

Attaining proper form or targeting the right tissue or mechanics through micro management of someone’s movement is often a staple of those that are ‘movement’ focused.

If I was to take notice of my previous 9 mistakes it probably leads me to understand using movement, especially therapeutically, should be varied and fun, have some relevance attached, has an appropriate dosage, is framed positively and contains a dash of novelty and challenge instead of just a rigid set of instructions.

Anyone who has read my blog will know that the concept of movement variability fits my biases very nicely. But as time goes by and I delve deeper and deeper into the subject I find myself being forced to challenge those biases as the information does not always fall as nicely into place as I once hoped it would!

‘Movement variability’ seems to have become a bit of a buzzword like ‘functional’ and ‘neuroplasticity’ before it.

Both those terms have merit when applied with the right dose of science and context but have had their validity eroded by poorly reasoned blanket usage. We end up with ‘XXX works because of…..variability’ which is simply a sentence not a mechanism or explanation.

shrugging

What NOT to do!

 

Where the concept of movement variability has been most enlightening is to help us learn what NOT to do, not always a reason TO DO something. We see the same with pain science that helps us understand what NOT to say not always what to say. Research into core stability has helped us to understand the probabilities are stacked against it being the answer to back pain but in many cases not what the actual answer is.

Understanding that movement is variable helps us to recognize that models that define ‘good’ and ‘bad’ movement are perhaps less valid than we previously thought. We have proposed models of ‘optimal’ movement that blame any deviation for micro trauma when in fact biological adaptation to tolerable dosages is much more likely to occur.

When we look at movement data for asymptomatic people we see a huge variation in the way that they move. So different people move differently and have different ways of achieving the same task and then the same individual may also have multiple ways of achieving that same task. So movement has both inter and intra individual variation.

This means that deviations from an ‘optimal’ (within safe anatomical range) ARE NOT problems just variations or resource for problem solving. We always have to consider the potential harm of labeling movements as ‘dangerous’ or having the potential to damage and how that affects someone’s desire to move for fear of injury or re injury and even if this information has ‘truth’ to it!

End point vs Coordinative

 

There are a couple of ways we can look at movement variability and increase our understanding.

The traditional view of variability would be to analyse the ‘end point’ or the execution of a skill, an example would be a throwing action or a stride when running. We would want to keep the amount of variability fairly stable here as to much variability would make it hard to execute a skill repetitively, so just doing random stuff and justifying it by calling it variable does not really fit the bill here but enough variability around a general movement template is good! In more reactive functions we may see the need for greater inter and intra movement variability.

Another way to look at variability is ‘coordinative variability’. This is looking at the inter limb relationship during the action or how the 'end point' is physically organized between the functional muscle & joint linkages that comprise the human movement system. The knee and hip coupling in running would be an example of this, the stride may look no different externally but the internal couplings maybe organized subtly differently temporaly each time. Much of the research into variability has looked at coordinative variability.

Skilled movers often display reasonably low ‘end point’ variability or skill execution, higher for reactive scenario’s than rehearsed, with higher ‘coordinative variability’ potentially to decrease repetitive loads which could help avoid overuse type injury and fits nicely with Bernstein’s great quote of “repetition without repetition”

So is movement variability an important concept to apply practically?

 

As always the answer comes down to “it depends”.

Movement is variable and being able to move in variable ways and having the ability to so is no bad thing, especially the more you require this bio motor ability for sport or health. If you already have a lot then it is probably not such a big deal. If you don’t have a lot then it likely becomes more of a big deal. We must be careful to not confuse variations around relevant movements with just moving in as many random ways as possible.

Perhaps where I have changed my view point most is the idea that pain ALWAYS = reduced variability. It is likely to be a little bit more complex than that. Sometimes we see the two factors correlate and other times not so much. Pain and motor patterns are both outputs of a complex system that may work independently or interdependently.

Here is a cool quote from "Neural representations and the cortical body matrix: implications for sports medicine and future directions"

“Pain and motor control are outputs of primary neurotags, intimately linked but not hierarchically differentiated”

We also have to separate acute from chronic pain states here as during a painful episode it has been postulated that the motor system is searching for non painful ways to move and therefore may become more variable find pain free solutions. A chronic problem maybe characterised by maladaptive protective stiffness with the net result being reduced variability. We need to carefully interpret who is being studied and the nature of their pain when using the information from these studies.

This paper maybe an example of this "Coupling angle variability in healthy and patellofemoral pain runners" where we see an increase in variability correlated with an increase in pain. A uniform response in variability, that would make thing sooo much simpler, is also not observed which given what we know about humans is unsurprising.

Movement variability likely to be very important for those that have their variability reduced after a painful episode but we cannot say with certainty that this will be everybody and that pain has a consistent effect on variability. But for those that DO have their variability reduced it may play a role in the transition to chronicity as previously discussed by Moseley and Hodges.

 “In summary, the findings show that when pain induces a loss of normal variability in the postural strategy, then normal strategy does not return, which is important because non resolution of the strategy probably increases the likelihood of further back trouble” Mosely and hodges

We have to be aware that motor system adaptations, we are learning, are highly individual and certainly not stereotypical as we may have been led to believe by many ‘models’ of movement and movement ‘dysfunction’. It has been postulated by some that having higher variability in movement maybe protective against the development of chronic pain complaints.

How do we use this information clinically or for training?

 

That is a great question and one with no clear answer. The vast majority have no access to expensive lab equipment such as 3D video analysis that would allow them to objectively collect the kind of data to answer this question. My opinion is that we can apply movement challenges or tasks that require variability in position, range, speed, balance etc that may highlight the adaptability of someone to variable stimuli.

We could define a problem of posture in a similar way. Applying movement challenges to ascertain if someone can move away from their postural start position may help decide if the posture is actually an issue or not.

We could do this to specific areas of the body or within relevant tasks that are problematic or you feel are relevant generally or relevant functionally. As we have so many relevant tasks and ways to achieve them it is hard to have objective data to work with for such a vast array of movements and their variations.

The question is do we need objective data here?

 

It is always preferable but probably unrealistic for most clinicians or trainers & coaches.

Perhaps we need a process that fosters inherent variability within the system and focuses more on the task and its constraints rather than solutions to a task such as an inflexible template to adhere to as we see with most exercises. Instead helping people to explore multiple solutions via experimentation with movement patterns and also developing coordinative segmental relationships.

Non linear pedagogy fits the bill nicely here. It moves away from providing a criteria or template led approach that allows the emergence of self organization and inherent variability to occur via the constraints imposed on the task.

You can read more here Chow (2013)

Task constraints could be:

Environment – The space around us.

Instructions – External or internal cues that provide variability

Equipment – Different objects will provide alternative stimulus

An example for a LBP sufferer.

Relevant Task – Bending over to pick something up.

Environment – Placing objects in differing positions to pick up requiring larger or smaller movements or movements in different planes or combination of planes.

Instructions – Sit bum back, bend or straighten the knees or reach left or right to vary the way in which the task is performed.

Equipment – A Power bag would provide the need for an alternative strategy than a barbell as an example. A more functionally relevant everyday item that is problematic could also be used.

Just as variability is probably not THE answer, neither I suspect is the current trend of ‘just load it’. Putting aside the complex multi dimensional nature of many problems, when it comes to a physical stimulus why do we have to choose only one of these concepts?

We may just need two exercises but that provide DIFFERENT stimulus, one that provides a variable movement stimulus, and one that provides a load based stimulus for strength and load tolerance adaptations.

Give exercises with different aims instead of a number of exercises that provide a similar stimulus such as the classic printed therapist sheet!