Exercise is widely recommended for painful conditions, but many people in pain don’t respond well to exercise and we have no idea why. Through this blog, I explain that we know very little about how exercise works for pain. I will summarise the theories that have been proposed and raise an important point; we know almost nothing about how psychological variables fit into this puzzle.
Exercise, however, is a high-value, evidence-based treatment for pain (Ref). There are also established long-term benefits of remaining active, like improved cardiovascular, bone, metabolic and mental health (Ref). In our sedentary and overweight society, these benefits should be promoted far and wide for everybody, not just people in pain.
Part of the problem is that the response to exercise is extremely variable for people who have pain. Exercise also can’t be measured against a sham situation, which makes the effects difficult to unpack. In pain-free individuals, exercise has potent effects on nociception, but this doesn’t work for everyone. Exercise temporarily increases the pain experience in many people (Ref). This short-term pain flare-up may make it an unattractive proposition to continue with.
How exercise might work
I will limit this discussion to theories of how one bout of exercise (not prolonged ‘training’) might work on pain and compare the effect in people without pain to people with pain. And I will also combine all exercise modalities, but will attempt to differentiate where possible.
Descending Systems theories
We are endowed with our own pain relieving systems. Throughout this portion, I will refer to our own ‘pain relief’ for simplicity; however, it would be much more accurate to say ‘nociception alteration’ as these systems predominantly alter the message, or the pathway before the brain makes pain. There are three main systems and they function to either:
Proactively flood the brain and body with our own supply of ‘pain relief’ (endogenous opioid system)
Change receptor sensitivity in the brain and spinal cord (non-opioid systems) or
Alter the traffic that is sent up the spinal cord to the brain (Conditioned pain Modulation or descending inhibition).
In people with pain, these systems normally function to alter the pain response after exercise and cause exercise induced hypoalgaesia (EIH). When people already have pain, though, it doesn’t seem to be so clear.
1. Endogenous Opioid System
This theory states exercise will trigger a release of our endorphins from the hypothalamus and pituitary regions in the brain, through an increase in blood pressure. These endorphins act centrally and peripherally to activate the same receptors that opioid medication acts on (yes, opioid receptors) (Ref). These receptors change the threshold to nociception (the signals that can help create pain).
In people without pain, there is some support for this hypothesis through administering opioid antagonist, and a lower analgesic response from exercise (Ref). This response does not seem to replicate well, so it’s complicated (Ref).
In people with pain, their endogenous opioid systems are dysfunctional and the normal analgesic response following exercise is impaired (Ref). Some people experience an increase in pain following a single bout of exercise, and this is similar for resistance exercise (mainly isometric) and aerobic (Ref). Unfortunately, this tells us nothing about how this works, only that the normal analgesic response to exercise is altered.
2. Non-opioid systems
One reason for increased interest in non-opioid systems in exercise induced analgesia is that pain-free individuals have a variable response when opioid antagonists are administered before exercising (Ref). So there must be other things going on. One of the explanations for this is the endocannabinoid system, which involves lipids released in the brain and spinal cord to either increase or decrease synapse excitability (Ref). For exercise induced analgesia to occur, synapsis in the spinal cord would be inhibited.
When people without pain have their blood taken before and after exercise, there is some evidence to show increase release of endocannabinoids may work in concert with the opioid system to produce analgesia after exercise (Ref).
There is one pre and post-test study investigating the mechanism of non-opioid systems in women with shoulder pain (Ref). Pain increased during a series of arm movements and along with this came a release of endocannabinoids (Ref).
3. Conditioned Pain Modulation
Previously called ‘Diffuse Noxious Inhibitory Control’, conditioned pain modulation is well trodden territory in pain research (Ref). This is because this system can be theoretically ‘hi-jacked’ to peddle all manner of unscrupulous treatments for pain like scraping skin with a spoon and ‘opening a window of opportunity’. The messages that eventually turn into the pain experience travel up the spinal cord, and are ‘turned up’ or ‘turned down’ at each level (Ref). Two structures in the brainstem represent large switchboards for these messages travelling towards cortical areas responsible for the sensation of pain. They send ‘diffuse’ descending inhibition, which allows a painful stimuli somewhere to be ‘muted’, when another more pressing novel stimulus comes along (Ref).
In people with pain this system may have a hard time ‘turning down’ the nociception that travels up the spinal cord, and dysfunction in this system could explain the altered response to exercise (Ref). As yet there is no good evidence to support this theory in exercise interventions (Ref).
Aside from boosting our immune systems across our lifespan, exercise immediately changes immunity. Within 1-2 hours of exercise, immune cells are dramatically redistributed to peripheral tissues reflecting a heightened state of immune surveillance and regulation (Ref). An immune response to exercise can increase excitability of the central nervous system (Ref).
In people with pain, particularly chronic widespread pain, immune function may be heightened and a single session of exercise may aggravate this and result in a pain flare (Ref).
Autonomic Nervous System
Exercise normally activates our stress response, which results in a flood of stress hormones (Ref). These hormones also happen to have analgesic effects at the brain and spinal cord (Ref). Autonomic nervous system activity can be indirectly measured through heart rate variability, with greater variability indicating better parasympathetic tone (Ref).
People with chronic wide-spread pain may have lower parasympathetic activity at rest, which could theoretically reduce the normal ‘fight or flight’ and thus analgesic effect of exercise (Ref). There is currently no evidence to support this theory (Ref).
The great unknown
Exercise is not just a physical stressor, although most research to date has considered it as such - particularly with pain research. Positive outcomes from painful conditions are known to be mediated by psychosocial factors (Ref). But we know almost nothing about the psychological mechanisms of exercise for pain.
Self-efficacy is a pivotal mediating factor for pain outcomes and we are just starting to shed light on how this model fits into exercise. Allowing painful exercise may alter the outcome expectation for individuals and change their perception of what’s possible (Ref).
The fear avoidance model has long been used to model how patients may become avoidant of certain movement or exercise (Ref). But there is a paucity of research investigating the role of fear in the analgesic effects of exercise (Ref).
We should prescribe for psychological variables
Although psychological variables like self-efficacy, fear, locus of control and mood are key factors that explain pain outcomes there is next to no evidence showing how they work in exercise treatment. It may be likely that these factors explain a large proportion of the effects observed in exercise treatment.
We tend to prescribe exercise based on the physical capacities we observe and the physical outcomes we want to achieve. But how much of these outcomes are based on the physical effects of exercise? We should at least prescribe based on psychological variables in concert with physical variables (and I think eventually we should consider psychological variables first not last in exercise).
With basic science, we have proposed some theories about how exercise might work on pain, but we don’t have much good evidence. The elephant in the room is that we can’t actually test exercise against a sham situation, so we’re just not sure how much of the effect of exercise is due to the exercise itself. These ‘extra’ effects from exercise may be predominantly explained by psychological, emotional and social factors. For people without pain, there are so many benefits of exercise beyond the physical. These emotional, affective and social factors are key reasons why people enjoy and continue exercising. We need to understand more about these factors in order to optimise the effect of exercise for those in pain.