In a person with no structural patholgy of the IT Band it seems logical to suggest that lengthening of the IT band will be due to improvements in the physiological range e.g. stretching the TFL and Glute Max. The component limiting the lengthening of the IT band itself is primarily collagen whose principal and mechanical properties include elasticity, viscoelasticity and plasticity. Of these plasticity is the property that allows for permanent change and deformation. When the IT band (& TFL) is stretched the collagen will respond by elongating and if its yield point is not reached it will recover its normal length (via its elasticity). Although microtears will occur up to the yield point these are probably insignificant with regards to function, functionally significant changes will probably only occur at the yield point which is followed by gross failure and in structurally similar ligaments, injury. Muscle, when appropriately stretched, will respond by increasing the number of sarcomeres to maintain optimum function. Neurophysiological mechanisms can also result in reflex relaxation and subsequent muscle lengthening (of a muscle in spasm etc).

Where structural patholgy is present that has resulted in contractures or adhesions of the IT band to surrounding tissues, there will be a higher rate of collagen turnover and newly deposited type 3 collagen. The type 3 collagen has fewer cross bridges that are relatively easily reduced, and if it is these that are causing the IT band "tightness", hence the IT band itself can be stretched. This is similar to some of the primary goals of mobilization techniques, to stretch ligamentous tissue and break adhesions.