A12 Elastic / Tendon Failure

Topic

This tendon, along with the muscle's own elastic component, generally functions to store and subsequently return mechanical energy during each movement cycle of the organism. Consequently, an elastic failure occurs precisely when the tendon—or that elastic muscle component—loses some of this capacity to store and return mechanical energy, whether due to chronic tissue degeneration, a partial structural rupture, or reflex inhibition that reduces the load ultimately reaching it.

In the case of tendinosis, however, the tendon's collagen undergoes chronic degeneration, thereby reducing both the tendon's modulus of elasticity and its stiffness; this reduction increases the tendon's deformation under a given load and slows the speed at which force is transmitted along the degenerated tendon. Consequently, the degenerated tendon loses a greater proportion of mechanical energy during each loading cycle, and its elastic recovery coefficient drops from a relatively high normal value to a considerably lower one. Further chronic degeneration of the tendon's collagen causes this elastic recovery coefficient to drop even lower.

Conversely, a partial rupture reduces the tendon's cross-sectional area—following the same proportional reduction in maximum tolerable force established by another model in this set regarding the functional cross-section of a torn muscle. This reduction in cross-sectional area lowers the maximum force the tendon can withstand before complete rupture, thereby increasing the risk of a total rupture. A more extensive partial rupture further reduces the tendon's maximum tolerable force, thereby further increasing the risk of complete rupture. This reduction in the stiffness of the degenerated tendon alters the natural frequency of the spring-mass system—formed by the tendon and the body mass it supports—thereby decoupling the tendon's stretch-shortening cycle from the organism's optimal locomotor rhythm. The fact that the tendon's stiffness is even lower causes the system's natural frequency to diverge further from that optimal locomotor rhythm.

Consequently, given the model's capacity to store and return mechanical energy, tendinitis in this tendon triggers pain capable of activating the same reflex inhibition seen in models of neuromuscular dysfunction in injured muscles; this reflex inhibition reduces neural activation of the associated muscle, thereby lowering the final load that muscle transmits to the inflamed tendon. The tendon's pain threshold under repetitive cyclic loading determines the maximum training level it can tolerate during rehabilitation. A lower pain threshold further restricts the tolerable training level, thereby protecting the tendon's capacity to store and return mechanical energy.

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