The physiological reduction in flexibility and elasticity of connective tissues, primarily collagen and elastin, that occurs as a natural consequence of chronological aging. This systemic decline impacts joint range of motion and arterial compliance, contributing to reduced physical performance and increased cardiovascular risk over time. Clinically, it is a key marker of biological age that reflects the progressive accumulation of advanced glycation end products (AGEs) and structural protein cross-linking. Understanding this stiffness is vital for developing targeted longevity interventions.
Origin
The concept arises from gerontology and biomechanics, focusing on the measurable changes in the viscoelastic properties of biological tissues. Its clinical relevance is deeply rooted in rheumatology and cardiovascular physiology, where tissue rigidity is directly linked to disease pathology. The term synthesizes the observable physical changes with their underlying biochemical etiology, making it a functional descriptor of age-related decline.
Mechanism
Mechanistically, the stiffness is driven by non-enzymatic glycation, where sugars spontaneously bind to proteins, forming irreversible AGEs. These cross-links rigidify the collagen matrix in tendons, ligaments, and vessel walls, thereby decreasing their inherent elasticity. Furthermore, chronic, low-grade inflammation, or inflammaging, contributes to the breakdown and inefficient repair of the extracellular matrix. Hormonal shifts, such as the decline in estrogen and testosterone, can also impair collagen synthesis and turnover, accelerating the stiffening process.
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