Hard to beat squats and deadlifts for low impact strengthening.
After an increase in muscle strength, elastic muscles are better able to absorb shock that otherwise would be transmitted to tendons and ligaments.
Tendon and ligament strength is also usually increased with properly performed exercises like squats and deadlifts.
[Although I am quite sure that overzealous exercise can also lead to an overuse injury.]
Cartilage responds favorably to weight bearing loads - up to a point, and as long as osteoarthritis [OA] has not already occurred.
"In general, exercise and loading of joints within a physiological range appears to have beneficial effects over normal day to day activities characterised by modest movement. The anabolic changes induced by exercise appear to enhance the load bearing properties of cartilage and may help explain how lifelong physical activity protects the joint from OA during later periods in life."
["Several in vitro studies have examined the effect of physiological mechanical loading on chondrocyte function and matrix synthesis (Table 3). Indeed, stretching of cells in monolayer cultures and compression of chondrocytes in hydrogels or explants generally leads to anabolic signalling cascades and protective effects. For example, aggrecan and collagen type II gene expression was increased by cyclic pressure-induced strain, hydrostatic pressure or fluid-induced shear stress in chondrocyte monolayers [57–59]. In agarose, dynamic compression at low frequencies increased cell proliferation and proteoglycan synthesis following 2 or 21 days of stimulation [60–63]. In cartilage explants, cyclic compression at frequencies of 0.01 to 1 Hz increased proteoglycan synthesis and gene expression of extracellular matrix constituents, aggrecan, fibronectin and cartilage oligomeric matrix protein (COMP) [20, 22, 64–66]." ]
However, it is difficult to say what weight loads could lead to deletarious effects.
It is clear that in joints already suffering from osteoarthrits, heavy loads or heavy impacts can result in worsening problems, as the chondrocytes [the cells in cartilage] seem to be re-programmed to produce more inflammation.
"Normal and OA chondrocytes from diseased joints transmit mechanical signals via the α5β1 integrin, resulting in markedly different downstream signalling events. For example, mechanical stimulation of normal chondrocytes release the chondroprotective IL-4 in contrast to OA cells which produce IL-1β . It is possible that chondrocytes from OA cartilage have been reprogrammed to respond differently to their altered mechanical environment, and it may be necessary to target structural components of the cell such as the actin cytoskeleton . This may allow reversal of biomechanical changes developed during OA disease progression allowing the beneficial effects of moderate exercise to be gained at the tissue level."