George W. Woodruff School of Mechanical Engineering and School of Biological Sciences, Georgia Institute of Technology, 801 Ferst Drive, GA, USA.
Tufts University School of Medicine, Boston, MA USA.
Integr Comp Biol. 2019 Dec 1;59(6):1546-1558. doi: 10.1093/icb/icz141.
Animals can amplify the mechanical power output of their muscles as they jump to escape predators or strike to capture prey. One mechanism for amplification involves muscle-tendon unit (MT) systems in which a spring element (series elastic element [SEE]) is pre-stretched while held in place by a "latch" that prevents immediate transmission of muscle (or contractile element, CE) power to the load. In principle, this storage phase is followed by a triggered release of the latch, and elastic energy released from the SEE enables power amplification (PRATIO=PLOAD/PCE,max >1.0), whereby the peak power delivered from MT to the load exceeds the maximum power limit of the CE in isolation. Latches enable power amplification by increasing the muscle work generated during storage and reducing the duration over which that stored energy is released to power a movement. Previously described biological "latches" include: skeletal levers, anatomical triggers, accessory appendages, and even antagonist muscles. In fact, many species that rely on high-powered movements also have a large number of muscles arranged in antagonist pairs. Here, we examine whether a decaying antagonist force (e.g., from a muscle) could be useful as an active latch to achieve controlled energy transmission and modulate peak output power. We developed a computer model of a frog hindlimb driven by a compliant MT. We simulated MT power generated against an inertial load in the presence of an antagonist force "latch" (AFL) with relaxation time varying from very fast (10 ms) to very slow (1000 ms) to mirror physiological ranges of antagonist muscle. The fastest AFL produced power amplification (PRATIO=5.0) while the slowest AFL produced power attenuation (PRATIO=0.43). Notably, AFLs with relaxation times shorter than ∼300 ms also yielded greater power amplification (PRATIO>1.20) than the system driving the same inertial load using only an agonist MT without any AFL. Thus, animals that utilize a sufficiently fast relaxing AFL ought to be capable of achieving greater power output than systems confined to a single agonist MT tuned for maximum PRATIO against the same load.
动物在跳跃以逃避捕食者或打击以捕获猎物时，可以放大肌肉的机械功率输出。一种放大机制涉及肌肉-肌腱单元（MTU）系统，其中一个弹簧元件（串联弹性元件[SEE]）在被称为“闩锁”的结构固定在位时被预先拉伸，该闩锁防止肌肉（或收缩元件，CE）的功率立即传递到负载上。原则上，这个存储阶段之后是闩锁的触发释放，来自 SEE 的弹性能量释放实现了功率放大（PRATIO=PLOAD/PCE，max >1.0），其中从 MT 传递到负载的峰值功率超过了 CE 在隔离时的最大功率限制。闩锁通过增加存储期间产生的肌肉功并减少存储能量释放以驱动运动的持续时间来实现功率放大。先前描述的生物“闩锁”包括：骨骼杠杆、解剖触发、附属附件，甚至拮抗肌肉。事实上，许多依赖高功率运动的物种也有大量的肌肉排列在拮抗对中。在这里，我们研究了衰减的拮抗力（例如，来自肌肉）是否可以作为主动闩锁来实现受控的能量传递并调节峰值输出功率。我们开发了一个由顺应性 MT 驱动的青蛙后肢的计算机模型。我们模拟了 MT 在惯性负载下产生的功率，同时存在具有从非常快（10 ms）到非常慢（1000 ms）的松弛时间的拮抗力“闩锁”（AFL），以反映拮抗肌肉的生理范围。最快的 AFL 产生了功率放大（PRATIO=5.0），而最慢的 AFL 产生了功率衰减（PRATIO=0.43）。值得注意的是，松弛时间短于约 300 ms 的 AFL 也产生了比仅使用没有任何 AFL 的单个激动 MT 驱动相同惯性负载的系统更大的功率放大（PRATIO>1.20）。因此，利用足够快速松弛的 AFL 的动物应该能够实现比仅受限于针对相同负载的最大 PRATIO 进行调谐的单个激动 MT 系统更大的功率输出。
