To move or not to move: the paradoxical effect of physical exercise in axial spondyloarthritis
The verdict
Is physical exercise safe and beneficial for people with axial spondyloarthritis, or can it worsen the disease?
Exercise and physical therapy are an established cornerstone of axial spondyloarthritis management, consistently reducing disease activity, pain, and stiffness and improving function. However, preclinical evidence shows that biomechanical stress and excessive loading at entheseal sites can trigger inflammation and new bone formation, creating a paradox that remains unresolved in humans.
Mixed pictureRead paper
Primary studyLimited evidence
Key points
- Exercise reduces disease activity, pain, stiffness, and improves spinal mobility and quality of life in axSpA, especially when combined with anti-TNF therapy.
- Animal models show that both excessive mechanical loading and hind paw unloading can worsen joint inflammation and promote osteophyte formation.
- A 'Goldilocks zone' concept describes an optimal activity range; in axSpA this zone is narrower than in healthy individuals, raising the risk of entheseal damage at both extremes.
- Blue-collar workers with axSpA show greater radiographic progression than white-collar workers, suggesting physically demanding work may accelerate disease.
- One recent RCT found that high-intensity exercise improved disease activity in axSpA patients, challenging the assumption that vigorous exercise is always harmful.
How it was conducted
- Design
- Narrative review
- Search databases
- PubMed and Cochrane Library
- Date range
- 1 January 2010 to 30 March 2020
- Search terms
- axial spondyloarthritis, ankylosing spondylitis, enthesitis, biomechanical stress, microdamage, new bone formation, physical therapy, rehabilitation, exercise
- Study types included
- Preclinical studies, clinical studies, clinical trials, reviews, and meta-analyses; key abstracts from EULAR and ACR annual meetings also included
What they found
- Tail suspension (unloading) in CIA mice significantly reduced total inflammation scores compared with control mice, most strikingly around the Achilles tendon and ankle joint.
- Voluntary running in CIA mice accelerated arthritis onset after passive transfer of anti-collagen antibodies and contributed to arthritis persistence compared with controls.
- In a DBA/1 CIA mouse model, osteophytes in tail-suspended mice were significantly smaller than in control mice on both histology and micro-CT; osteophyte size correlated with inflammation severity.
- Low bone mineral density was independently associated with development of new syndesmophytes in young axSpA patients over 2 years (Kim et al).
- One RCT showed high-intensity exercise was efficacious in reducing disease burden and improving disease activity in axSpA patients.
- Supervised outpatient group physical therapy showed a tendency to be more effective than unsupervised approaches in multiple trials.
Limitations
- All mechanistic evidence linking biomechanical stress to entheseal inflammation and new bone formation comes from mouse models; direct human data are absent.
- No studies have examined the impact of exercise or physical therapy on long-term radiographic progression in axSpA patients.
- The narrative review methodology introduces selection bias; a systematic review or meta-analysis was not performed.
- Occupational studies comparing blue-collar and white-collar workers cannot exclude important confounders such as socioeconomic status, smoking, and sex-related biological differences.
Why it matters
- For patients
- Patients with axSpA should continue exercising because the evidence for benefit is strong, but they should discuss exercise type and intensity with their clinician, as very high-impact or repetitive loading may carry extra risk, particularly during active disease flares.
- For clinicians
- Until long-term radiographic data are available, exercise prescription in axSpA should follow a personalised approach that accounts for disease activity, entheseal load, and spinal stability, ideally combining supervised physiotherapy with pharmacological treatment.
- For readers
- This review highlights a biologically plausible paradox - the same biomechanical forces that exercise harnesses for benefit may also drive entheseal inflammation and new bone formation in genetically susceptible individuals - but the clinical implications remain speculative without human mechanistic or radiographic outcome data.
Source
doi:10.1136/rmdopen-2020-001480
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