School of Medicine, Johns Hopkins University, Baltimore, MD, USA.
Joint Department of Biomedical Engineering, UNC Chapel Hill and NC State University, Chapel Hill, NC, USA.
J Biomech. 2023 Sep;158:111771. doi: 10.1016/j.jbiomech.2023.111771. Epub 2023 Aug 21.
The relationship between individual muscle dynamics and whole-body metabolic cost is not well established. Here we use biofeedback to modulate triceps surae (TS) activity during walking to test the following hypotheses based on basic principles of muscle physiology: (1) increased TS activity would increase metabolic cost via shorter muscle fascicle lengths and thus reduced force capacity and (2) decreased TS activity would decrease metabolic cost via longer muscle fascicle lengths and thus increased force capacity. 23 young adults walked on an instrumented treadmill at 1.25 m/s using electromyographic (EMG) biofeedback to match targets corresponding to ±20 and ±40% TS activity during push-off (late stance). B-mode ultrasound imaged the medial gastrocnemius (MG). Participants increased net metabolic power up to 85% and 21% when targeting increased and decreased TS activity, respectively (p < 0.001). At the instant of peak gastrocnemius force, MG fascicle length was 7% shorter (p < 0.001) and gastrocnemius force was 6% larger (p < 0.001) when targeting + 40% TS activity. Fascicle length was 3% shorter (p = 0.004) and force was 7% lower (p = 0.010) when targeting -40% TS activity; participants were unable to achieve decreased activation targets. MG fascicle length and activity mediated 11.7% (p = 0.036) and 57.2% (p = 0.006) of the changes in net metabolic power, respectively. MG force did not mediate changes in net metabolic power (p = 0.948). These findings suggest that changes in the functional operating length of muscle, induced here by volitional changes in TS activity, mediated changes in the metabolic cost of walking, relatively independently of force. Thus, shifts to shorter fascicle lengths (e.g., aging) may mediate activity-induced increases in metabolic cost.
个体肌肉动力学与全身代谢成本之间的关系尚未得到很好的确定。在这里，我们使用生物反馈来调节行走过程中的比目鱼肌（TS）活动，以根据肌肉生理学的基本原理来检验以下假设：（1）通过缩短肌小节长度从而降低力量产生能力，增加 TS 活动会增加代谢成本；（2）通过增加肌小节长度从而提高力量产生能力，降低 TS 活动会降低代谢成本。23 名年轻人以 1.25m/s 的速度在装有仪器的跑步机上行走，使用肌电图（EMG）生物反馈来匹配在蹬离（晚期支撑）期间目标为±20%和±40%TS 活动的目标。B 型超声成像内侧腓肠肌（MG）。当目标是增加和减少 TS 活动时，参与者的净代谢功率分别增加了 85%和 21%（p<0.001）。在腓肠肌力峰值时，当目标是+40%TS 活动时，MG 肌小节长度缩短了 7%（p<0.001），腓肠肌力增加了 6%（p<0.001）。当目标是-40%TS 活动时，肌小节长度缩短了 3%（p=0.004），腓肠肌力降低了 7%（p=0.010）；参与者无法实现减少的激活目标。MG 肌小节长度和活动分别介导了净代谢功率变化的 11.7%（p=0.036）和 57.2%（p=0.006）。MG 力并没有介导净代谢功率的变化（p=0.948）。这些发现表明，在这里通过 TS 活动的自愿变化引起的肌肉功能工作长度的变化，相对独立于力，介导了步行代谢成本的变化。因此，向更短的肌小节长度的转变（例如，衰老）可能介导了活动引起的代谢成本增加。
