Gray Aubrey J, Krupenevich Rebecca L, Batsis John A, Sawicki Gregory S, Franz Jason R
Joint Department of Biomedical Engineering, University of North Carolina at Chapel Hill and North Carolina State University, Chapel Hill, North Carolina, United States.
Division of Behavioral and Social Research, National Institute on Aging, Bethesda, Maryland, United States.
J Appl Physiol (1985). 2024 Dec 1;137(6):1541-1548. doi: 10.1152/japplphysiol.00377.2024. Epub 2024 Nov 7.
The mechanisms responsible for increased metabolic cost of walking in older adults are poorly understood. We recently proposed a theoretical premise by which age-related reductions in Achilles tendon stiffness (k) can disrupt the neuromechanics of calf muscle force production and contribute to faster rates of oxygen consumption during walking. The purpose of this study was to objectively evaluate this premise. We quantified k at a range of matched relative activations prescribed using electromyographic biofeedback and walking metabolic cost and ankle joint biomechanics in a group of 15 younger (age: 23 ± 4 yr) and 15 older (age: 72 ± 5 yr) adults. Older adults averaged 44% lower k than younger adults at matched triceps surae activations during isokinetic dorsiflexion tasks on a dynamometer ( = 0.046). Older adults also walked with a 17% higher net metabolic power ( = 0.017) but indistinguishable peak Achilles tendon forces than younger adults. Thus, data implicate altered tendon length-tension relations with age more than differences in the operating region of those length-tension relations between younger and older adults. In addition, we discovered empirical evidence that lesser k-likely due to the shorter muscle lengths and thus higher relative activations it imposes-was positively correlated with higher net metabolic power during walking ( = -0.365, = 0.048). These results pave the way for interventions focused on restoring ankle muscle-tendon unit structural stiffness to improve walking energetics in aging. This study provides the first empirical evidence to our knowledge that age-related decreases in k exact a potentially significant metabolic penalty during walking. These results pave the way for interventions focused on restoring ankle muscle-tendon unit structural stiffness to improve walking energetics in aging.
老年人行走时代谢成本增加的机制尚不清楚。我们最近提出了一个理论前提，即跟腱僵硬度（k）随年龄增长而降低会破坏小腿肌肉力量产生的神经力学，并导致步行过程中耗氧率加快。本研究的目的是客观评估这一前提。我们在一组15名年轻成年人（年龄：23±4岁）和15名年长成年人（年龄：72±5岁）中，使用肌电图生物反馈规定了一系列匹配的相对激活水平，量化了僵硬度（k）、行走代谢成本和踝关节生物力学。在测力计上进行等速背屈任务时，在匹配的小腿三头肌激活情况下，年长成年人的僵硬度（k）平均比年轻成年人低44%（P = 0.046）。年长成年人行走时的净代谢功率也比年轻成年人高17%（P = 0.017），但跟腱峰值力无显著差异。因此，数据表明，与年龄相关的肌腱长度 - 张力关系改变比年轻和年长成年人之间这些长度 - 张力关系的工作区域差异更重要。此外，我们发现了经验证据，即较低的僵硬度（k）——可能是由于肌肉长度较短，因此相对激活较高——与行走时较高的净代谢功率呈正相关（r = -0.365，P = 0.048）。这些结果为旨在恢复踝关节肌肉 - 肌腱单元结构僵硬度以改善老年人行走能量学的干预措施铺平了道路。据我们所知，本研究提供了首个经验证据，证明与年龄相关的僵硬度（k）降低在行走过程中会带来潜在的显著代谢代价。这些结果为旨在恢复踝关节肌肉 - 肌腱单元结构僵硬度以改善老年人行走能量学的干预措施铺平了道路。
