Exercise as Medicine During the Course of Hip Osteoarthritis

Inger Mechlenburg; Lisa Cecilie Urup Reimer; Troels Kjeldsen; Thomas Frydendal; Ulrik Dalgas


Exerc Sport Sci Rev. 2021;49(2):77-87. 

In This Article

Mechanisms Underlying the Effects of Exercise in OA

The mechanisms underlying the positive effects of exercise in patients with OA still remain to be fully elucidated, but several potential mechanisms have been proposed including neuromuscular, periarticular, and intra-articular mechanisms.[103]

Neuromuscular mechanisms include improved muscle function, proprioception, balance and motor learning, energy absorption capacity, and stability. As an example, exercise-induced pain relief may be mediated by increased muscle strength, increased knee range of motion, or improvements in proprioception.[103,104] In addition, maximal quadriceps strength is associated with physical function in hip OA, and because of the generalized muscle weakness of the affected limb in these patients,[30] improving muscle strength is a sound target mechanism for exercise interventions. In addition, changes in muscle perfusion may play a role as this has been found to be associated with exercise-induced pain relief after a 12-wk exercise program in knee OA.[105]

Periarticular mechanisms include beneficial effects on connective tissues and bones, which may result in pain relief.[106] During gait, reduced hip range of motion, peak moments of adduction, and external rotation have been found to be associated with decreased bone mineral density of the proximal femur.[107] Importantly, exercise preserves bone mass[108] even in osteoporotic patients, with progressive resistance training being the most effective exercise type for increasing bone mineral density of the femoral neck.[109]

Finally, intra-articular mechanisms include beneficial effects of exercise on cartilage, inflammation, and joint fluid.[103] In OA, the chondrocytes of the joint tissue show greater catabolic than anabolic activity, leading to degenerative changes in the cartilage matrix and other joint tissues, including the subchondral bone and synovium.[110] In individuals with or at risk of knee OA, exercise does not up-regulate molecular biomarkers related to cartilage turnover and inflammation.[111] Although the breakdown of articular cartilage is considered the pathological hallmark of OA,[111] there is consensus that physiological mechanical loading is necessary for maintaining healthy articular cartilage, whereas insufficient or hyperphysiological loading leads to catabolism and degeneration.[31,112,113] Moreover, specific signaling pathways in articular cartilage, largely through the activation of the biosynthesis in chondrocytes, have been proposed.[110] Interestingly, chondrocytes only respond to load with increased synthesis when parameters such as frequency and loading amplitude are moderate, whereas cartilage degradation is the result of excessive, static, or sparse joint loading.[110] Mechanical loading has been found to suppress inflammatory signaling and thereby prevent cartilage degradation.[114] Figure 2 shows some of the proposed signaling pathways thought to be stimulated in articular cartilage when mechanically loaded. Clinical evidence is still sparse, but a systematic review investigated the impact of exercise on magnetic resonance imaging (MRI)–assessed articular cartilage in RCTs including individuals with or at risk of developing knee OA.[111] The results were inconclusive, with studies reporting negative, positive, or neutral between-group differences in various MRI cartilage outcomes, warranting further studies.

Figure 2.

Proposed pathways for the beneficial effect of physiological loading on articular cartilage, which can be promoted through exercise. The figure is based on findings presented by Adams et al. (2014).