Abstract
Skeletal muscles can be voluntary controlled by the somatic nervous system yielding an active contractile stress response. Thereby, the active muscle stresses are transmitted to the skeleton by a cascade of connective tissue and thus enable motion. In the context of joint perturbations as well as the assessment of the complexity of neural control, the initial phase of the muscle-tendon system's stress response has a particular importance and is analyzed by means of electromechanical delay (EMD). EMD is defined as the time lag between the stimulation of a muscle and a measurable change in force output. While EMD is believed to depend on multiple structures / phenomena, it is hard to separate their contributions experimentally. We employ a physiologically detailed, three-dimensional, multi-scale model of an idealized muscle-tendon system to analyze the influence of (i) muscle and tendon length, (ii) the material behavior of skeletal muscle and tendon tissue, (iii) the chemo-electro-mechanical behavior of the muscle fibers and (iv) neural control on EMD. Comparisons with experimental data show that simulated EMD values are within the physiological range, i.e., between 6.1 and 68.6 ms, and that the model is able to reproduce the characteristic EMD-stretch curve, yielding the minimum EMD at optimal length. Simulating consecutive recruitment of motor units increases EMD by more than 20 ms, indicating that during voluntary contractions neural control is the dominant factor determining EMD. In contrast, the muscle fiber action potential conduction velocity is found to influence EMD even of a 27 cm long muscle by not more than 3.7 ms. We further demonstrate that in conditions where only little pre-stretch is applied to a muscle-tendon system, the mechanical behavior of both muscle and tendon tissue considerably impacts EMD. Predicting EMD for different muscle and tendon lengths indicates that the anatomy of a specific muscle-tendon system is optimized for its function, i.e., shorter tendon lengths are beneficial to minimize the neural control effort for muscles primary acting as motor in concentric contractions.
Highlights
Skeletal muscles can provide active resistance to joint perturbations by developing protective tension
By employing the baseline experiment scenario, i.e., a 1.5 cm long muscle that is attached to a 3 cm long tendon, the computationally determined electromechanical delay (EMD)-stretch curve shown in Figure 4B is qualitatively similar to the EMD-stretch curve derived from experimental measurements of Siebert et al (2014a,b, 2016)
Beside the properties that were related to EMD within this work, experimental studies suggested that other factors such as the muscle and aponeurosis architecture or fatigue influence EMD (Nordez et al, 2009; Cè et al, 2013; Lacourpaille et al, 2013) and need to be addressed by further research
Summary
Skeletal muscles can provide active resistance to joint perturbations by developing protective tension. The active response of the muscle is delayed by sensory organs, the neural system, and the muscle’s rate of force development. EMD is defined as the time lag between the (initial) stimulation of a muscle at the neuromuscular junction and a measurable change in force output (Cavanagh and Komi, 1979). EMD is believed to depend on joint angle, motor unit recruitment, the mechanical tissue properties (of both muscle and tendon), the muscle fiber action potential (AP) conduction velocity, and the excitation-contraction coupling pathway (cf e.g., Cavanagh and Komi, 1979; Hopkins et al, 2007; Nordez et al, 2009). A better understanding of the factors influencing EMD contributes to the development of prevention, treatment, and rehabilitation strategies for ankle instability (Hopkins et al, 2009)
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