The effect of intensive exercise on disease activity in rheumatoid arthritis (RA) is an interesting one.1 Although we would not dispute that such exercise does indeed have a beneficial effect on parameters of disease activity, we wish to propose an alternative hypothesis as to its mechanism. In particular, we would argue that the effect of raised intra-articular pressure on synovial blood flow during exercise is not as the authors suggest.

The intra-articular pressure in chronically inflamed joints undoubtedly rises during exercise, and exceeds capillary perfusion pressure within the synovium.2 ,3 This pressure rise occurs in joints with and without effusions. It is clearly difficult to measure intra-articular pressure during dynamic exercise, but we would speculate that the pressure rises which occur during dynamic exercise are similar to those occurring during static exercise. The study that is quoted by the authors suggests that synovial blood flow increases during dynamic exercise such as walking and cycling and was only measured in joints with effusions.4 We would argue that raised intra-articular pressure during any form of exercise not onlycompromises synovial blood flow, resulting in synovial hypoxia, but is the initiating step in reperfusion injury.5 Hypoxia-reperfusion injury is one of the mechanisms by which reactive oxygen species (ROS) are produced, including the highly toxic hydroxyl radical.6 Damage by such ROS to biomolecules and tissues within the rheumatoid joint is well documented.7 ,8 Oxidative damage to fine nociceptor nerve endings within the synovium renders the joint relatively anaesthetic9 and perhaps allows the patient to exercise the joint more vigorously. We propose therefore that intensive exercise brings about an “auto-synovectomy”, effectively reducing the amount of inflammation within the joint and thereby reducing the disease activity score.