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Energy dissipation in mammalian collagen fibrils: Cyclic strain-induced damping toughening and strengthening

机译：哺乳动物胶原蛋白原纤维的能量耗散：循环应变诱导的阻尼增韧和增强

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摘要

As the fundamental structural protein in mammals, collagen transmits cyclic forces that are necessary for the mechanical function of tissues, such as bone and tendon. Although the tissue-level mechanical behavior of collagenous tissues is well understood, the response of collagen at the nanometer length scales to cyclical loading remains elusive. To address this major gap, we cyclically stretched individual reconstituted collagen fibrils, with average diameter of 145±42 nm, to small and large strains in the partially hydrated conditions of 60% relative humidity. It is shown that cyclical loading results in large steady-state hysteresis that is reached immediately after the first loading cycle, followed thereafter by limited accumulation of inelastic strain and constant initial elastic modulus. Cyclic loading above 20% strain resulted in 70% increase in tensile strength, from 638±98 MPa to 1091±110 MPa, and 70% increase in toughness, while maintaining the ultimate tensile strain of collagen fibrils not subjected to cyclic loading. Throughout cyclic stretching, the fibrils maintained a steady-state hysteresis, yielding loss coefficients that are 5–10 times larger than those of known homogeneous materials in their modulus range, thus establishing damping of nanoscale collagen fibrils as a major component of damping in tissues.
机译：作为哺乳动物中的基本结构蛋白，胶原蛋白传递的循环力是组织（例如骨骼和腱）的机械功能所必需的。尽管已经很好地了解了胶原组织的组织水平的机械行为，但是在纳米级尺度上的胶原对循环负荷的响应仍然难以捉摸。为了解决这一主要差距，我们在60％相对湿度的部分水合条件下，将平均直径为145±42 nm的单个重构胶原纤维循环拉伸为大小菌株。结果表明，周期性加载会导致较大的稳态滞后，该滞后在第一个加载周期后立即达到，此后有限的非弹性应变累积和恒定的初始弹性模量。高于20％应变的循环载荷可使抗张强度从638±98 MPa升高70％，达到1091±110 MPa，而韧性提高70％，同时保持不受循环载荷作用的胶原原纤维的最终拉伸应变。在整个循环拉伸过程中，原纤维保持稳态磁滞，其模量范围内的损失系数比已知均质材料的损失系数大5-10倍，从而将纳米级胶原原纤维的阻尼作用作为组织阻尼的主要组成部分。

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