Exercise places widely varying biomechanical and physiologic demands upon articular cartilage. Intermittent compression tends to stimulate chondrocyte biosynthesis, which is the basis for articular cartilage adaptation. Joint motion without compression causes articular cartilage thinning, and static loading causes decreased chondrocyte biosynthesis. In vivo canine studies have demonstrated, however, that although moderate levels of running stimulate adaptation, strenuous levels can cause detrimental articular cartilage changes. Prospective studies evaluating the effect of exercise upon articular cartilage in humans have documented increased asymptomatic knee osteophytes in runners. There seem to be activity thresholds below and above which the effects are minimal or destructive, respectively. Between these thresholds, articular cartilage seems to adapt mechanically to the loads placed upon it by exercise. The adaptive ability of articular cartilage may be compromised in the injured or aged joint.