Hurry Up and Get Out of the Way! Exploring the Limits of Muscle-Based Latch Systems for Power Amplification

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.

Volume and intramuscular fat content of upper extremity muscles in individuals with chronic hemiparetic stroke

Stroke survivors often experience upper extremity deficits that make activities of daily living (ADLs) like dressing, cooking and bathing difficult or impossible. Survivors experience paresis, the inability to efficiently and fully activate muscles, which combined with decreased use of the upper extremity, will lead to muscle atrophy and potentially an increase in intramuscular fat. Muscle atrophy has been linked to weakness post stroke and is an important contributor to upper extremity deficits. However, the extent of upper extremity atrophy post hemiparetic stroke is unknown and a better understanding of these changes is needed to inform the direction of intervention-based research. In this study, the volume of contractile tissue and intramuscular fat in the elbow and wrist flexors and extensors were quantified in the paretic and non-paretic upper limb using MRI and the Dixon technique for the first time. Total muscle volume (p≤0.0005) and contractile element volume (p≤0.0005) were significantly smaller in the paretic upper extremity, for all muscle groups studied. The average percent difference between limbs and across participants was 21.3% for muscle volume and 22.9% for contractile element volume. We also found that while the percent intramuscular fat was greater in the paretic limb compared to the non-paretic (p≤0.0005), however, the volume of intramuscular fat was not significantly different between upper limbs (p=0.231). The average volumes of intramuscular fat for the elbow flexors/extensors and wrist flexors/extensors were 28.1, 28.8 and 19.9, 8.8 cm3 in the paretic limb and 29.6, 27.7 and 19.7, 8.8 cm3 in the non-paretic limb. In short, these findings indicate a decrease in muscle volume and not an increase in intramuscular fat, which will contribute to the reduction in strength in the paretic upper limb.

The effect of muscle-tendon unit vs. fascicle analyses on vastus lateralis force-generating capacity during constant power output cycling with variable cadence

The maximum force-generating capacity of a muscle is dependent on the lengths and velocities of its contractile apparatus. Muscle-tendon unit (MTU) length changes can be estimated from joint kinematics; however, contractile element length changes are more difficult to predict during dynamic contractions. The aim of this study was to compare vastus lateralis (VL) MTU and fascicle level force-length and force-velocity relationships, and dynamic muscle function while cycling at a constant submaximal power output (2.5 W/kg) with different cadences. We hypothesized that manipulating cadence at a constant power output would not affect VL MTU shortening, but significantly affect VL fascicle shortening. Furthermore, these differences would affect the predicted force capacity of the muscle. Using an isokinetic dynamometer and B-mode ultrasound (US), we determined the force-length and force-velocity properties of the VL MTU and its fascicles. In addition, three-dimensional kinematics and kinetics of the lower limb, as well as US images of VL fascicles were collected during submaximal cycling at cadences of 40, 60, 80, and 100 rotations per minute. Ultrasound measures revealed a significant increase in fascicle shortening as cadence decreased (84% increase across all conditions, P < 0.01), whereas there were no significant differences in MTU lengths across any of the cycling conditions (maximum of 6%). The MTU analysis resulted in greater predicted force capacity across all conditions relative to the force-velocity relationship ( P < 0.01). These results reinforce the need to determine muscle mechanics in terms of separate contractile element and connective tissue length changes during isokinetic contractions, as well as dynamic movements like cycling. NEW & NOTEWORTHY We demonstrate that vastus lateralis (VL) muscle tendon unit (MTU) length changes do not adequately reflect the underlying fascicle mechanics during cycling. When examined across different pedaling cadence conditions, the force-generating potential measured only at the level of MTU (or joint) overestimated the maximum force capacity of VL compared with analysis using fascicle level data.

Pop-Up-Inspired Design of a Septal Anchor for a Ventricular Assist Device

Heart failure (HF) is a serious condition in which the heart cannot pump sufficient blood to sustain the metabolic needs of the body. A common indication of failure is a low ejection fraction, or the volumetric proportion of blood ejected when the ventricle contracts. In end-stage HF, support from a ventricular assist device (VAD) can assume some or all of the heart’s pumping work, improving the ejection fraction and restoring normal circulation. VAD therapy options for end-stage right heart failure (RHF) are limited, with only a few FDA-approved devices available for mechanical circulatory support [1]. These devices are based on continuous flow impellers; and despite anticoagulation therapy, use of currently available VADs is associated with thrombogenic risk since the blood must contact artificial non-biologic surfaces. An implantable VAD for RHF based on soft robotic pulsatile assistance has previously been proposed [2]. This device is comprised of a contractile element that is anchored to the ventricular septum and the right ventricle (RV) free wall. The device is programmed to contract in synchrony with the native heart beat and assist in approximating the septum and free wall together in order to augment blood ejection (Fig. 1). Potential advantages of this approach include reduced risk of thrombosis, since there is no blood flow through the lumen of the device, and the possibility for minimally invasive deployment of the device under ultrasound guidance. A key component in this VAD concept is the anchoring mechanism that couples the contractile actuator to the ventricular septum. In this work, we report design, fabrication and testing of a new septal anchor design. We exploit the emerging technology of pop-up MEMS [3] in order to fabricate a collapsible anchoring mechanism. Origami-inspired engineering and pop-up MEMS manufacturing techniques have previously been used for developing disposable and low-cost medical tools and devices [4]. The pop-up anchor can be deployed into the left ventricle (LV) via a standard delivery sheath. We validate the load bearing ability of the anchor and demonstrate deployment in an ex vivo simulation.

On the System-Theoretic Passivity Properties of a Hill Muscle Model

The paper describes passivity-related input-output properties of a human muscle and tendon system given by a Hill type dynamic model. For a model having muscle contraction velocity as the input and force as the output, it is shown that the system is passive during the concentric phase. Also, it is shown that a negative strict passivity margin exists for the eccentric phase if the length and lengthening velocity of the contractile element are assumed bounded. Estimates of this margin are given by means of two alternative formulas. Further, it is shown that the mapping from contraction velocity to deviation from equilibrium force is passive in both concentric and eccentric phases. The paper discusses how these findings and the passivity theorem can be used to design controllers for a machine coupled to the muscle model by feedback interconnection. The simple case of a proportional-derivative force feedback regulator is considered as an example. A simulation example is given where the transient response of the coupled system crosses the eccentric region.

Airway smooth muscle in airway reactivity and remodeling: what have we learned?

It is now established that airway smooth muscle (ASM) has roles in determining airway structure and function, well beyond that as the major contractile element. Indeed, changes in ASM function are central to the manifestation of allergic, inflammatory, and fibrotic airway diseases in both children and adults, as well as to airway responses to local and environmental exposures. Emerging evidence points to novel signaling mechanisms within ASM cells of different species that serve to control diverse features, including 1) [Ca2+]i contractility and relaxation, 2) cell proliferation and apoptosis, 3) production and modulation of extracellular components, and 4) release of pro- vs. anti-inflammatory mediators and factors that regulate immunity as well as the function of other airway cell types, such as epithelium, fibroblasts, and nerves. These diverse effects of ASM “activity” result in modulation of bronchoconstriction vs. bronchodilation relevant to airway hyperresponsiveness, airway thickening, and fibrosis that influence compliance. This perspective highlights recent discoveries that reveal the central role of ASM in this regard and helps set the stage for future research toward understanding the pathways regulating ASM and, in turn, the influence of ASM on airway structure and function. Such exploration is key to development of novel therapeutic strategies that influence the pathophysiology of diseases such as asthma, chronic obstructive pulmonary disease, and pulmonary fibrosis.

Integration of intrinsic muscle properties, feed-forward and feedback signals for generating and stabilizing hopping

It was hypothesized that a tight integration of feed-forward and feedback-driven muscle activation with the characteristic intrinsic muscle properties is a key feature of locomotion in challenging environments. In this simulation study it was investigated whether a combination of feed-forward and feedback signals improves hopping stability compared with those simulations with one individual type of activation. In a reduced one-dimensional hopping model with a Hill-type muscle (one contractile element, neither serial nor parallel elastic elements), the level of detail of the muscle's force–length–velocity relation and the type of activation generation (feed-forward, feedback and combination of both) were varied to test their influence on periodic hopping. The stability of the hopping patterns was evaluated by return map analysis. It was found that the combination of feed-forward and proprioceptive feedback improved hopping stability. Furthermore, the nonlinear Hill-type representation of intrinsic muscle properties led to a faster reduction of perturbations than a linear approximation, independent of the type of activation. The results emphasize the ability of organisms to exploit the stabilizing properties of intrinsic muscle characteristics.

Proof of Concept: Model Based Bionic Muscle with Hyperbolic Force-Velocity Relation

Recently, the hyperbolic Hill-type force-velocity relation was derived from basic physical components. It was shown that a contractile element CE consisting of a mechanical energy source (active element AE), a parallel damper element (PDE), and a serial element (SE) exhibits operating points with hyperbolic force-velocity dependency. In this paper, a technical proof of this concept was presented. AE and PDE were implemented as electric motors, SE as a mechanical spring. The force-velocity relation of this artificial CE was determined in quick release experiments. The CE exhibited hyperbolic force-velocity dependency. This proof of concept can be seen as a well-founded starting point for the development of Hill-type artificial muscles.

The Role of SRC in Strain- and Ligand- Dependent Phenotypic Modulation of Mouse Embryonic Fibroblasts

Connective tissue fibrosis represents a significant portion of mortality and morbidity in our society. These diseases include many illnesses such as heart valve disease, atherosclerosis, macular degeneration, and cirrhosis, meaning that millions of lives are affected by these conditions each year. Fibrotic tissues form when quiescent fibroblasts activate becoming myofibroblasts, the phenotype of active tissue construction and fibrosis. During this process, the cells produce smooth muscle α-actin (αSMA), a contractile element considered to be the hallmark of cellular activation [1]. Following the production of αSMA, there is an increase in the synthesis of extracellular matrix (ECM) proteins, most notably type I collagen; this increase in ECM proteins causes the stiffening of the tissue characteristic of fibrotic disease. In non-disease states (such as wound healing or tissue development), the myofibroblasts will either deactivate, becoming fibroblasts again, or apoptose before tissue fibrosis occurs. However, when myofibroblasts persist, increased ECM protein deposition causes increased tissue stiffness and activates neighboring cells, causing the fibrosis to propagate. Currently there are no therapies to prevent or reverse fibrosis. Therefore a more thorough understanding of the dynamic mechanical environment and signaling pathways involved in the activation of fibroblasts is required to develop potential treatments.