Mechanisms to think on:<p>1) Stiffening of tendon tissue via cross-linking and calification.<p>2) Loss of muscle mass and strength via all of the varied mechanisms implicated in sarcopenia, ranging from mitochondrial dysfunction to extracellular matrix disruption via cross-links and senescent cells, to fatty infiltration of muscles, diminished stem cell activity, etc, etc.<p>3) Inefficiency in blood flow to muscles, either through neurological impairment in the normal blood vessel dilation process or through cross-linking and calcification to stiffen blood vessel walls.<p>4) Dysfunction in cartilage for all the reasons implicated there, such as cross-linking, loss of stem cell function, and so on.<p>There are others, but note that all of these are secondary consequences of types of primary damage that occur as a result of the normal operation of metabolism. They are all targets for repair treatments yet to be constructed.