Recent clinical trials have shown that strengthening exercises
of muscles remote to the knee (isolated hip muscle
strengthening) caused reductions in knee OA pain over
8 –12 weeks (9,10). One suggested mechanism behind the
clinical effects of exercise is biomechanical optimization;
however, in a number of studies no effects of exercise on
knee biomechanics have been reported (9,11–14). Another
possible mechanism is that exercise leads to widespread
adaptations in the central nervous system, resulting in
reduced pain sensitivity. Joint nociception may cause sensitization
of pain mechanisms in the central nervous system
(15). In addition, peripheral sensitization includes
structural and functional changes in the peripheral nociceptors,
e.g., caused by inflammation (15). In systemic
low-grade inflammatory diseases (e.g., diabetes mellitus),
antiinflammatory effects of regular exercises have been
suggested (16), which in turn may lead to reduced peripheral
sensitization. In healthy young volunteers, a single
bout of resistance exercise is capable of modifying the
sensation of experimentally induced pain (17). However,
the long-term effects of regular exercise therapy on sensitization
in knee OA are unknown. A deeper understanding
of the mechanisms involved in the pain-relieving effects of
therapeutic exercises in patients with knee OA is imperative
to optimize the exercise paradigm in OA research and
clinical management