A2 Degradation of the Elastic System

Topic

The mammalian elastic system—comprising tendons, fascia, and cartilage—functions as a mechanical energy reservoir: during the loading phase of a stride, it stores elastic potential energy, and during the subsequent propulsive phase, it releases that stored energy, drastically reducing the metabolic cost of locomotion. This elastic system degrades when the tissue's viscoelastic properties deteriorate due to aging, overuse, inflammation, or calcification; such degradation increases energy loss within the system and pathologically redistributes mechanical loads to other structures.

The mechanical behavior of the tissue forming this elastic system is modeled as a solid combining a purely elastic component—arranged in parallel—with a component that combines elasticity and viscosity in series. The former determines tissue stiffness, which dictates the amount of elastic energy that can be stored and reversibly returned, while the latter introduces time-dependent behavior that dissipates some of that energy as heat rather than returning it. As the elastic system degrades, tissue stiffness and the capacity for reversible energy storage decline, while the fraction of energy dissipated by the tissue during each loading cycle increases; this latter fraction is known as the tissue's loss factor, and its sustained rise serves as a direct mechanical signature of degradation.

At the microscopic level within the tissue, degradation progresses through material fatigue: each loading cycle causes existing micro-cracks to grow, and the rate of this growth increases exponentially with the magnitude of the mechanical stress the crack undergoes during each cycle. In healthy tissue, collagen repair mechanisms continuously offset this accumulation of damage, renewing damaged collagen at the same rate at which cracking occurs. When cyclic loading exceeds a critical threshold, the rate of fatigue damage surpasses the rate of collagen repair, and this lack of compensation leads to fatigue-induced tissue failure.

In addition to the stiffness of tendinous and fascial tissues, degradation of the elastic system also affects joint stiffness, which depends on the viscosity of the synovial fluid lubricating the joint; this viscosity increases when joint temperature drops and decreases as the hyaluronic acid in the synovial fluid degrades, meaning a joint with degraded hyaluronic acid loses the viscosity that normally cushions its movement.

The combined result of the loss of tissue stiffness, fatigue failure, and the loss of synovial fluid viscosity is a reduction in the efficiency with which the elastic system returns energy during locomotion—the very function with which this description began. Proximal joints adjacent to the degraded area compensate by bearing a larger share of the mechanical load, the elastic recoil of the system becomes less regular and exhibits greater phase variability between successive cycles, and the maximum speed the animal can sustain is reduced accordingly.

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