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Is Walking Enough?
(or, why do we over-think things)

May 28, 2016 by Dr Matthew D. Long

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Is Walking Enough?
(or, why do we over-think things)

May 28, 2016 by Dr Matthew D. Long

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Is Walking Enough?
(or, why do we over-think things)

May 28, 2016 by Dr Matthew D. Long

As clinicians we all strive to make the best decisions for our patients. To do this, we rely upon models to explain what we think is going on inside our patients. These models are also supposed to help us understand how our treatment can address these problems. However, models are always incomplete and science has a wonderful way of humbling us whenever new distinctions are made.

As chiropractors, we tend to focus upon the spine in all of its complex glory - always searching for better methods of improving its health and function. While manipulation is the most obvious approach used by chiropractors, the role of exercise is also universally acknowledged as 'a good thing'. But our general appreciation for the benefits of exercise is not matched by any widespread agreement as to what we think exercise actually

I have written about this topic previously in an article entitled ‘
Exercises, What’s the Use?’ (here). This piece questioned long-standing theories about the necessity of exercise to address theoretical muscle weakness, and therefore improve 'spinal strength’. Indeed, our simplistic models of weakness as a mechanism for recurrent spinal pain have gradually given way to a new appreciation for deficits in control of the spinal musculature. Furthermore, this control-based model has been shown to incorporate all levels of the neuraxis - from the peripheral receptors responsible for proprioception, all the way up to higher centres within the brain that are charged with overseeing complex patterns of motor integration.

The evidence is now quite convincing that spinal pain patients show significant differences in the way that they move, and the strategies they employ to maintain spinal stability. Typically this leads to increasing stiffness, as the superficial strap muscles of the spine engage to compensate for a lack of underlying
segmental muscle activity. This has been shown in both the lower back (1,2,3) and within the cervical spine (4).

But where do these changes come from?

Ultimately, all roads lead back to the brain - and to the
cortex specifically. Quite simply, patients with chronic or recurrent back pain typically express unusual patterns of cortical activity, and activate different regions of their brain to control movement than those who are healthy. The work of Moseley has been quite influential in this area of research and has inspired terms such as ‘the imprecision hypothesis of chronic pain’. Moseley and Vlaeyen (5) suggested that,
"Spatial and proprioceptive aspects of multisensory events are encoded less precisely in people with chronic pain than they are in people with acute pain or in healthy controls; the cortical representation of non-nociceptive stimuli is disrupted in people with chronic pain, a phenomenon widely termed “cortical reorganisation”; people with chronic pain have lower proprioceptive acuity, disruptions in the perceived size and alignment of body parts, and show poor ability to mentally maneuver the painful body part. Critically, these deficits are not body-wide, although they do extend to various extents beyond the region of pain, and these deficits cannot be explained by behavioral factors, tissue injury, ectopic firing of primary nociceptors, or central sensitization."
Tsao and colleagues (6) wrote a prize-winning paper entitled ‘Smudging the motor brain in young adults with recurrent low back pain’. To quote this article,
“Differential control of paraspinal muscles is compromised in LBP. In this group, paraspinal muscle fascicles tend to be recruited en masse with similar activation of iliocostalis and deep multifidus with changes in spinal curvature in sitting, and simultaneous activation of deep and superficial multifidus with trunk perturbation. The mechanisms for loss of discrete control are unclear, but one possibility can be gleaned from another painful condition associated with loss of discrete control - focal hand dystonia. In that condition, loss of discrete cortical organization of somatosensory regions associated with each finger (i.e., cortical map “smudging”) contributes to reduced ability to isolate finger movements. Changes in brain organization may underlie changes in paraspinal muscle activation.”
Tsao goes on to say,
“Motor cortex reorganization supports the notion that the nervous system adopts a new strategy for movement/stability with LBP. It has been hypothesized that in the presence of pain and/or injury, the nervous system implements new motor strategies to “protect the part” from further injury/pain. This is often mediated by increased trunk muscle activity, particularly large superficial muscles, to splint the spine."
This reorganisation of the motor cortex is then further associated with postural control deficits (7) and a generalised sensory ‘neglect’ has been suggested (8,9,10,11). Ultimately, it appears that the cortical control of spinal motor stabilisation is severely compromised and this has been documented in a number of well-performed studies (12). Interestingly, these cortical abnormalities seem to persist, even when a patient has apparently recovered from a painful episode. According to Sung et al (13),
“Patients with recurrent and chronic low back pain (LBP) present with several types of motor control impairments including altered muscle timing, changes in muscle quality, altered proprioception of trunk movements, and altered trunk stiffness. However, in some cases, interventions that were successful in improving pain and function did not affect these motor control variables.”
A number of recent papers have confirmed this observation - that patients who are ‘in remission’ from back pain often continue to harbour maladaptive strategies for spinal stability and still fail to move their spines in an appropriate fashion (14,15,16,17).

The question then arises, what can we
do about all of this?

While the role of exercise does not seem to be in dispute, the
form that these exercises should take is certainly far from clear. In recent years there has been a huge enthusiasm for tailored spinal stabilisation exercises and strategies for improving ‘core stability and strength’. But have these methods actually improved patient outcomes? Have we perhaps over-refined our approach in an effort to somehow deliver a more targeted intervention for our patients? It seems that our increasing efforts to nail down the individual dysfunctional muscles and produce a tailored solution has been an illusion, and does not reflect the way that the human body responds to normal movement and day-to-day exercise. This emphasis upon core strength was recently questioned in an excellent editorial in the Clinical Journal of Sports Medicine by Garrick (18), in which he wrote,
“'Core stability' came to my attention some 30 plus years ago with the popularization of Pilates-type exercises. It seemed logical that a stronger 'core' (trunk) would provide a more stable platform for the use of muscles of the extremities and those supporting the spine. Who knew, or cared, exactly what structures made up the 'core.' More strength and better fitness seemed unassailable goals. Then core stability took on a life of its own. In slightly more than a decade, the enhancement of core stability as treatment for, or prevention of, a myriad of problems became not only a mainstay of musculoskeletal injury management but also an accepted preventive strategy...

Thus, it seems that it is totally appropriate to examine the legitimacy of the many claims associated with core strengthening. Frustrating is the fact that there is not much there...

Earlier, the sports medicine community had embraced “stretching” as both a preventive and therapeutic “modality,” although it too had little true scientific support. Indeed, when that support was sought, the result was much like Stuber et al (19) report - not much there."

'It is totally appropriate to examine the legitimacy of the many claims associated with core strengthening. Frustrating is the fact that there is not much there...'

It is interesting to note the gradually-building voice of dissent within the physiotherapy literature, as a new realisation about the validity of core stabilisation exercises takes hold (20,21,22). Indeed, it seems that our attempts to become more specific in our exercise approach have not amounted to much at all.

But is this really surprising? I would contend that humans often have a tendency to over-think things and try to create artificial separations where none truly exist. Perhaps we should stop for a moment and just consider the whole notion of 'exercise'...

In nature, exercise is an
artificial concept. If we were still living the traditional hunter-gatherer existence I think it would be fair to say that few of us would come home after a day out foraging and try to fit in a few sets of rock-lifting before dinner. Our life would be our exercise and there would be no need to artificially supplement with extra effort. Of course, modern society has stripped much of this essential activity from our day-to-day lives and most of us are ‘malnourished’ when it comes to variable movement. For this reason I have no problem at all with the use of exercise to drive human physiology. However, when we look at the use of specifically tailored exercises to address spinal complaints, there is a growing body of evidence to suggest that less complexity is a good thing.

Recent studies have highlighted the fact that the simple act of
walking is often just as beneficial as the most rigorously tailored spinal stabilisation exercise approach. This appeals to me on an instinctive level, as walking is probably the most natural movement that humans express. Indeed, humans have populated the entire globe over thousands of years, largely by walking across its surface. Walking is what humans do. Furthermore, patients with ongoing spinal complaints frequently demonstrate abnormalities in the motor patterns associated with walking (23,24,25). According to Ghamkhar and Kahlaee (26),
"Walking is one of the most functional tasks of everyone’s activity of daily living that is of a dynamic nature. LBP is often accompanied by changes in gait, such as a decrease in comfortable walking speed, step length, stance and swing time, and changes in trunk coordination. Results of the EMG studies during walking are indicative of alterations in persons experiencing LBP. LBP patients tend to walk at slower self-selected speeds, with less typical patterns for trunk muscles. Global back extensor muscles in LBP patients exhibit higher level of activation to compensate for spinal instability."
Gombatto and colleagues (23) found that, “People with LBP displayed less lumbar region rotation than people without LBP. All subjects displayed more upper lumbar than lower lumbar region movement in the frontal and transverse planes.” In addition, Newell et al (25) found that, “LBP subjects had a slower walking velocity, smaller step length and reduced complexity (lower fractal scaling indices) compared to control subjects."

Given all of the above, we might stop for a moment to consider the role of just walking as an antidote to some of these problems. How often do we hear from our patients that an episode of lower back pain seemed to improve when they went for a walk and ‘it started to loosen up a bit’. The observation that pain decreases and stiffness reduces when walking is thought to reflect the brain’s attempts to reconfigure its motor patterns and try to normalise the delicate interplay between all of the moving parts. I tend to conceive of this process as an attempt by the brain to 'rehearse' different activation patterns as a patient walks along, trying different strategies until it settles upon one that seems to offer the best stability and efficiency of locomotion. But so many of our patients are starved of movement, and they do not walk enough to allow their brain the opportunity to work out for itself the best way of reconfiguring its motor programming. Again, this is where I think we clinicians tend to over-think the problem and try to direct the process more than it requires.

By way of an analogy, I would suggest that giving someone a glass of water does not require you to tell them where they should store the fluid within their body, or how they should go about utilising it across their physiological demands. Their body will work it out for itself. In the same way, when I eat a meal I don’t have to think about how much protein I should be diverting to the various competing structures of my body - I just assume that my body knows what to do with it and I simply have to provide the resources for the job. In a similar fashion, exercise is a very natural ‘motion nutrient’ for the body and we sometimes add a needless level of complexity to it. Asking a patient to engage more in life and to simply get up and walk can go a long way towards improving even chronic spinal complaints.

A number of studies have shown that walking is often just as effective as a muscle strengthening program for chronic LBP patients. Shnayderman (27) found that a 6 week walk training program was as effective as 6 weeks of specific strengthening exercises for the lower back. Hurley
et al (28) found similar things and concluded that,
“We found no difference in the effectiveness of a walking program, an evidence-based exercise class and usual physiotherapy for improvement in clinical outcomes for people with chronic LBP. The walking program had the highest level of adherence and the lowest mean direct health cost and mean cost per outcome at follow-up.”
Interestingly, some authors have found that over-ground walking was superior to treadmill walking for patients with chronic lower back pain (29). This makes sense if we try to maintain our ‘natural is better’ approach to exercise. After all, it is rare that the ground would move underneath us when we walk, thus a treadmill will necessarily require a completely difference balance and motor control strategy to the one required when walking on a stationary surface.

Interestingly, the pace of walking does seem to have differing effects. Overwhelmingly, studies on gait patterns in back pain patients have shown that they typically walk at a slower pace and with a shorter stride. Lee
et al (30) found that higher speed walking was significantly more effective at activating the deep intrinsic musculature of the spine than those who proceeded at a slower pace. In their 2014 study, Lee and colleagues found,
“In the present study, walking exercise is shown to activate the mid or low lumbar paraspinalis muscles. In addition, high-speed walking exercise activates the multifidus muscle more than low-speed walking. The lumbar multifidus muscle plays an important role in maintaining lumbar segmental stability because it attaches and connects each segment of the lumbar spine. In previous studies that use lumbar magnetic resonance imaging, fat infiltration and unilateral atrophy of the multifidus at the symptomatic side and level were observed. In addition, the percentage of multifidus atrophy was positively correlated with the duration of symptoms. These were most prominent at the L5 vertebral level. In another study, patients with chronic LBP had a significantly smaller percent thickness contraction at the L5 vertebral level; this reduction was not present at other vertebral levels. These observations show that the size and function of the multifidus muscle are important, especially at the L5 level. Our results showed that walking exercise activates the lumbar multifidus muscle.”
As a final thought, we should also reflect on the fact that the intervertebral discs are hugely dependent upon motion for their normal physiology and maintenance of fluid dynamics. Hedrick et al (31) discussed this in their paper, “The effectiveness of walking as an intervention for LBP; a systematic review”. They stated,
“Nutrition of the lumbar disc is dependant upon convective transport, arising from load-induced fluid movement in and out of the disc, and it is recognised that age-related disc maturation affects the ability of the disc to adapt and withstand load. Although walking provides a low compression cyclical load that may enhance disc nutrition and the ability to adapt to spinal loading, further research is required to investigate these effects.”
It makes sense to me that walking is a natural and desirable stimulus for lumbar intervertebral disc health. Indeed, there does appear to be a significant correlation between general physical inactivity and disc health. Teichtahl (32) found that, “physical inactivity is associated with narrowing intervertebral discs, high fat content of the multifidus and high intensity LBP and disability in a dose-dependent manner among community based adults.

Overall, it would appear to me that we need to take the time to rethink some of our exercise strategies for patients with spinal disorders. Our attempts to specifically target individual muscles that we deemed to be weak/tight/sluggish does not seem to improve outcomes. The human brain stores motor patterns in terms of desired functions (such as walking, signing my name, typing or swinging a golf club). As such, targeted exercises that aim to strengthen the gluteus maximus, or learn how to activate the transverse abdominus, or strengthen the ‘core’ while lying on an exercise mat, will
not help me the next time I go for a walk or bend to remove my shopping bags from the car boot. In essence, the human brain needs to practice performing real world functional movements and not the individual sub-components of a larger activity.

To conclude, there is a growing enthusiasm in the research literature for the benefits of simple functional activities as a replacement for targeted ‘specific’ back exercises. Of these, walking seems like a good place to start and you’ll probably find that most patients are relieved to hear that this may well be 'good enough' (33) to get them on the road to recovery.

Something to think about anyway...

Dr Matthew D. Long
BSc (Syd) M.Chiro (Macq)
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