Pain and Physical Activity: Friend or Foe?

Exercise is an effective treatment for various chronic pain disorders, including fibromyalgia, chronic neck pain, osteoarthritis, rheumatoid arthritis and chronic low back pain. Although the clinical benefits of exercise therapy in these populations are well established, it is currently unclear whether exercise has positive effects on the process involved in chronic pain (e.g. central pain modulation). Further, it is unclear if exercise is effective in all patients according the origin of the pain neuropathic, nociceptive or inflammation. The question remains whether exercise is recommended for all phenotype patients suffering from pain.

Exercise is frequently encountered as a central component in the treatment of patients with chronic pain, because the clinical benefits of exercise therapy in several chronic pain populations, eg. chronic low back pain, osteoarthritis, rheumatoid arthritis etc., are well known. But, on the other hand, patients often complain of pain exacerbations, post-exertional malaise, bad recovery etc.

Reduced or abnormal exercise tolerance may consequently lead to fear of movement and avoidance of certain activities. Although, kinesiophobia does not have to be related to exercise capacity, it is related to activity levels. Kinesiophobia may thus lead to further disuse, deconditioning and further lowering of exercise tolerance. This vicious circle is an important therapy barrier and compromises therapy compliance.

So the risks and dangers of exercise in chronic pain patients have to be explored and taken into account during exercise therapy.

Importantly, it is currently unclear whether exercise therapy has positive effects on the process of central sensitization. Possibly, (acute) exercise may cause further arousal of the central nervous system? It has been established that acute exercise activates pain inhibitory mechanisms in healthy subjects, resulting in increased pain thresholds. Also, in several chronic pain populations in which central sensitization is not a predominant feature, exercise seems to trigger exercise induced analgesia. But patients with central sensitization - such as fibromyalgia, chronic fatigue syndrome chronic whiplash associated disorders etc, - are unable to activate endogenous pain inhibition in response to various types of exercise, resulting in decreased pain thresholds, possibly explaining post-exertional symptom exacerbations. These patients show dysfunctioning of endogenous analgesia in response to exercise. Also local muscle contractions activate generalized endogenous analgesia in healthy, pain-free humans and patients with either osteoarthritis or rheumatoid arthritis, but result in increased generalized pain sensitivity in fibromyalgia patients.

Besides, exercise has neuro-immunological effects that are possibly not desirable in some populations. Think about the increase in nitric oxide due to exercise. Although, nitric oxide is a functional molecule, in high concentration nitric oxide can become detrimental for the body. Moreover, it is known that nitric oxide is an important player in the process of central sensitization. Exercise-induced nitric oxide release is therefore something that should be explored in more detail in order to assure safe exercise therapy in chronic pain patients. Especially, since some of these patients already have elevated nitric oxide levels.

Regarding the immune response to exercise, it is known that acute intensive exercise elicits a depression of several aspects of acquired immune function. Although not clinically immune deficient, it is possible that the combined effects of small changes in several aspects of host defence may compromise resistance to minor illnesses in an already vulnerable population.

Another issue that is becoming popular in the domain of chronic pain, is the role of Brain Derived Neurotrophic Factor (BDNF). BDNF plays an important role in neuroplasticity of the nervous system and could contribute to central sensitization. BDNF release is for instance triggered by exercise.

Finally, the stress response, which is often dampened in chronic pain patients, may be something to keep in mind when exercising chronic pain patients. Further sympathetic activation of an already exhausted stress system, may be disadvantageous.

All these (abnormal) reactions to acute exercise may give lead to bad exercise response and comprise therapy compliance or even worse, may give lead to avoidance behavior, further disuse en further deconditioning and disability. Therefore exercise induced hyperalgesia and pathophysiological responses to exercise may be a barrier we do not want to counter during rehabilitation.

On the other hand long term effects of exercise therapy are not that dramatic and it even seems that correctly tailored activity or exercise programs may be beneficial in longer term, both in terms of reconditioning and functionality as for the pain, mood, etc.

Furthermore, it is hypothesized that exercise therapy programs could be a tool to reactivate or restore endogenous pain inhibitory mechanisms. But any attempt to improve endogenous pain inhibition in clinical practice remains however speculative. At present, any treatment interfering with descending modulation is currently unavailable for clinical use in chronic pain patients. This comes as no surprise, given the lack of insight into the precise mechanisms of malfunctioning of descending pain inhibition in those with central sensitization, including during exercise. These issues should be topic of further research: how to prescribe activity programs and exercise therapy for chronic pain patients, in which above mentioned barriers are avoided and in which progressive and careful retraining of the endogenous pain system is possible.

This will lead to a risky balance exercise of tailoring the activity or exercise program. On the one hand, therapists should account for the dysfunctional response of patients with chronic pain and aberrations in central pain modulation to acute exercise, but on the other hand they should try to distract the focus of pain, as pain is not a reliable “alarm system” anymore in these patients and hypervigilance for pain should not be encouraged. This means that pain and time contingent approaches should be considered and balanced, depending on the patient and the status of the patient. In any case the patient should experience a success experience during exercise and therefore conservative, gentile, individually tailored activity or exercise programs are necessary with emphasis on prevention of symptom flares (eventually with other medical support), in order not to strengthen further catastrophic thinking about exercise and pain. So, instead of just arguing about to exercise or not to exercise, it will be the question “how to exercise”.

Mira Meeus

This was presented at the

2 ^nd World Congress on Controversies, Debates & Consensus in Bone, Muscle & Joint Diseases http://www.congressmed.com/bmjd/program/program/friday.html