Narici Marco V, Maganaris Constantinos N
Institute for Biophysical and Clinical Research into Human Movement, Manchester Metropolitan University, Cheshire, UK.
J Anat. 2006 Apr;208(4):433-43. doi: 10.1111/j.1469-7580.2006.00548.x.
Senile sarcopenia, the loss of muscle mass associated with aging, is one of the main causes of muscle weakness and reduced locomotor ability in old age. Although this condition is mainly driven by neuropathic processes, nutritional, hormonal and immunological factors, as well as a reduction in physical activity, contribute to this phenomenon. Sarcopenia alone, however, does not fully account for the observed muscle weakness, as the loss of force is greater than that accounted for by the decrease in muscle size. As a consequence, a reduction in the force per unit area, both at single fibre and at whole muscle level, is observed. We recently suggested that at whole muscle level, this reduction in intrinsic force is the result of the combined effect of changes in (1) muscle architecture, (2) tendon mechanical properties, (3) neural drive (reduced agonist and increased antagonist muscle activity) and (4) single fibre-specific tension. Whereas several studies support the role of the last two factors in the loss of intrinsic muscle force with aging, alterations in muscle architecture and in tendon mechanical properties have also been shown to contribute to the above phenomenon. Indeed, sarcopenia of the human plantarflexors, represented by a 25% reduction in muscle volume, was found to be associated with a 10% reduction in fibre fascicle length and 13% reduction in pennation angle. These architectural alterations were accompanied by a 10% decrease in tendon stiffness, attributable to alterations in tendon material properties, as suggested by a 14% decrease in Young's modulus. Most of these changes may be reversed by 14 weeks of resistive training; both fibre fascicle length and tendon stiffness were found to be increased by 10 and 64%, respectively. Surprisingly, however, training had no effect on the estimated relative length-tension properties of the muscle, indicating that the effects of greater tendon stiffness and increased fascicle length cancelled out each other. It seems that natural strategies may be in place to ensure that the relative operating range of muscle remains unaltered by changes in physical activity, in old age.
老年肌肉减少症是与衰老相关的肌肉质量流失，是老年人肌肉无力和运动能力下降的主要原因之一。虽然这种情况主要由神经病变过程驱动，但营养、激素和免疫因素以及身体活动的减少也促成了这一现象。然而，仅肌肉减少症并不能完全解释所观察到的肌肉无力，因为力量的损失大于肌肉大小减少所导致的力量损失。因此，在单根肌纤维和整个肌肉水平上，都观察到单位面积力量的降低。我们最近提出，在整个肌肉水平上，这种内在力量的降低是以下因素变化综合作用的结果：（1）肌肉结构，（2）肌腱力学特性，（3）神经驱动（主动肌活动减少和拮抗肌活动增加）以及（4）单根肌纤维特定张力。尽管多项研究支持后两个因素在衰老导致的肌肉内在力量损失中的作用，但肌肉结构和肌腱力学特性的改变也被证明促成了上述现象。事实上，以肌肉体积减少25%为代表的人类跖屈肌肌肉减少症，被发现与肌纤维束长度减少10%和羽状角减少13%有关。这些结构改变伴随着肌腱刚度降低10%，这归因于肌腱材料特性的改变，如杨氏模量降低14%所表明的那样。这些变化大多可通过14周的阻力训练逆转；肌纤维束长度和肌腱刚度分别增加了10%和64%。然而，令人惊讶的是，训练对肌肉估计的相对长度 - 张力特性没有影响，这表明更大的肌腱刚度和增加的肌束长度的影响相互抵消了。似乎存在自然策略来确保老年人身体活动的变化不会改变肌肉的相对工作范围。
