Movement as Medicine: A Guide to Taming Chronic Pain Through Exercise
In our modern world, sedentary lifestyles have become so prevalent that researchers now describe the resulting health consequences as the “diseasome of physical inactivity”. This cluster of conditions includes not only cardiovascular disease and diabetes but also depression, dementia, and chronic pain (Thompson et al.2020) . Physical inactivity is now considered a major public health pandemic, with “sitting” often described as the new smoking. Whether you are living with fibromyalgia, back pain, or osteoarthritis, understanding the relationship between movement and your nervous system is the first step toward recovery (Thompson et al.2020).
How Your Brain Processes Pain: The Sedentary vs. Active State
The importance of exercise in managing pain lies in its ability to rewire the central nervous system. In a sedentary state, the brain and spinal cord can become “hyperexcitable”. This means the “pain filters” in brainstem sites like the periaqueductal gray (PAG) and the rostral ventromedial medulla (RVM) are less effective at blocking incoming signals (Coleman et al. 2022).
Research shows that regular physical activity resets these filters by:
1. Boosting Endogenous Opioids: Exercise activates the body’s natural pharmacy, releasing opioids in the brain that inhibit pain signals.
2. Modulating Serotonin: In sedentary individuals, the expression of the serotonin transporter (SERT) often increases, which clears away the serotonin needed to inhibit pain. Regular movement reduces SERT expression in the brainstem, effectively “re-tuning” the nervous system to favour pain inhibition over facilitation.
Taming the Inflammatory Fire: The Immune Benefit
Chronic pain is often linked to an elevated inflammatory status. On a cellular level, exercise helps shift the balance of your immune system. Your muscles contain immune cells called macrophages, which exist in two primary phenotypes: M1 (pro-inflammatory) and M2 (anti-inflammatory/regulatory) (Dina et al. 2011).Sedentary individuals tend to have a higher proportion of M1 macrophages, which release cytokines that activate pain-sensing nerves. Regular exercise shifts this balance toward the M2 phenotype, increasing anti-inflammatory cytokines like IL-10 that reduce nerve sensitivity (Coleman et al. 2022). For patients with conditions like fibromyalgia, even a single session of moderate cycling has been shown to decrease systemic concentrations of pro-inflammatory markers like IL-8 and cortisol, bringing them closer to the levels found in healthy individuals (Coleman et al. 2022).
Combating Pain: From Medication to Movement
The latest NICE guidelines (NG-193) represent a radical shift in how we combat chronic primary pain (Zambelli et al.2022). Because pharmacological treatments like opioids, paracetamol, and NSAIDs often provide limited relief and carry significant risks, medical experts now recommend non-pharmacological management as the first line of defence (Dina et al. 2011).
Despite these recommendations, studies show that roughly 47% of people with chronic pain are still managed with opioids. To truly combat pain, the evidence points toward:
1. Exercise Programmes: Structured aerobic and strengthening activities.
2. Psychological Therapy: Such as Cognitive Behavioural Therapy (CBT) to manage the distress associated with pain.
3. Acupuncture: Recommended for certain chronic primary pain conditions (Zambelli et al.2022)
What This Means for People Starting Physiotherapy
If you are beginning your physiotherapy journey, these findings provide a roadmap for your treatment plan:
1. A “Person-Centred” Partnership: Your treatment should be a “joint-care plan” created between you and your therapist, incorporating your preferences and specific goals.
2. Managing the “Initial Flare”: It is common for an acute bout of exercise to temporarily increase pain in people with chronic conditions. This doesn’t mean you are causing damage; rather, your nervous system is currently in a state of high sensitivity. Over time, regular participation builds a protective “analgesic” effect.
3. Overcoming Movement-Evoked Pain: To help you get started, your physiotherapist might use tools like TENS (Transcutaneous Electrical Nerve Stimulation). TENS has been shown to specifically reduce pain during movement, making it easier to participate in the exercise needed for long-term healing.
4. The “Type” Matters Less Than the “Act”: Whether it is swimming, walking, or strength training, the most effective exercise is the one you will actually do. Research suggests that aerobic activity (1–3 hours/week) and muscle strengthening (1–2 times/week) provide the most significant health and mortality benefits (Brito et al. 2017)
Breaking the Cycle of Stress and Pain
Chronic stress is a well-known exacerbator of pain. Stress activates the body’s sympathetic response, which can sensitize pain receptors (Coleman et al. 2022). In fact, in stressed states, the body can “switch” mechanisms so that standard inflammatory markers cause even more intense hyperalgesia (increased pain sensitivity).Exercise serves as a vital circuit breaker. By improving the stress-response feedback mechanism, movement prevents the over-activation of the inflammatory response that typically follows stressful experiences(Sluka et al. 2018).
Navigating the Initial Flare: Why Pain May Increase at First
One of the most common barriers to starting an exercise programme is the fear of a “flare-up.” For many living with chronic conditions like fibromyalgia or musculoskeletal pain, an acute bout of exercise can initially increase pain levels (Bote et al.2013). Research shows that a single session of fatiguing exercise can spike pain scores significantly, sometimes by as much as 3 points on a 10-point scale, in those with chronic conditions, whereas healthy individuals typically experience a decrease in pain sensitivity after movement.
The “Sedentary Gap” in Your Nervous System
This initial increase happens because a sedentary nervous system is currently set to a state of hyperexcitability. In this state, your “pain filters” (inhibition) are weak, and your “pain amplifiers” (facilitation) are highly active. When you first begin to move, the nervous system lacks the endogenous opioid tone and serotonin balance needed to dampen the signals generated by activity (Sluka et al. 2018). Essentially, your body has not yet built up its natural “internal pharmacy” that regular exercisers rely on to feel good after a workout (Sluka et al. 2018).
Rewiring for Long-Term Relief
It is vital to understand that this initial flare is often a temporary part of the “resetting” process. While the first few sessions may be uncomfortable, regular physical activity gradually shifts the balance:
1. From Excitation to Inhibition: Consistent movement increases the release of opioids in the brainstem, which eventually inhibits the nerves that were previously over-amplifying pain signals (Dina et al. 2011).
2. Normalising the Response: Over time, stimuli that the sedentary nervous system perceived as painful are no longer felt as such by the “active” nervous system.
3. Building Resilience: Regular participation builds a protective “analgesic” effect, effectively raising your pain threshold and reducing the risk of future long-term flares.
Strategies for Success
Because movement-evoked pain is a real barrier, modern physiotherapy does not just tell you to “push through it.” Instead, it uses a biopsychosocial approach to manage this transition:
1. Pacing and Preference: The type of exercise matters less than the act of doing it; choosing an activity you enjoy makes it easier to stay consistent during the early stages.
2. Supportive Tools: Your therapist may recommend tools like TENS (Transcutaneous Electrical Nerve Stimulation), which has been shown to specifically reduce pain during movement, making it easier to participate in the activities that will eventually heal your nervous system.
3. Joint-Care Planning: By collaborating on a plan that accounts for your specific triggers and goals, you can manage the initial discomfort while working toward the long-term goal of Exercise as Medicine
Reference list
Bote, M. E., Garcia, J. J., Hinchado, M. D., & Ortega, E. (2013). Fibromyalgia: Anti-inflammatory and stress responses after acute moderate exercise. PLoS ONE, 8(9), e74524.
Brito, R. G., Rasmussen, L. A., & Sluka, K. A. (2017). Regular physical activity prevents development of chronic muscle pain through modulation of supraspinal opioid and serotonergic mechanisms. Pain Reports, 2(5), e618.
Coleman, C. J., McDonough, D. J., Pope, Z. C., & Pope, C. A. (2022). Dose-response association of aerobic and muscle-strengthening physical activity with mortality: A national cohort study of 416,420 US adults. British Journal of Sports Medicine, 56(21), 1187–1193.
Dina, O. A., Levine, J. D., & Green, P. G. (2011). Enhanced cytokine-induced mechanical hyperalgesia in skeletal muscle produced by a novel mechanism in rats exposed to unpredictable sound stress. European Journal of Pain, 15(8), 796–800.
Sluka, K. A., Frey Law, L., & Hoeger Bement, M. (2018). Exercise-induced pain and analgesia? Underlying mechanisms and clinical translation. Pain, 159(Suppl 1), S91–S97.
Thompson, W. R., Sallis, R., Joy, E., Jaworski, C. A., Stuhr, R. M., & Trilk, J. L. (2020). Exercise Is Medicine. American Journal of Lifestyle Medicine, 14(5), 511–523.
Zambelli, Z., Halstead, E. J., Iles, R., Fidalgo, A. R., & Dimitriou, D. (2022). The 2021 NICE guidelines for assessment and management of chronic pain: A cross-sectional study mapping against a sample of 1,000 in the community. British Journal of Pain, 16(4), 439–449