Viscoelastic Behavior of Plantar Flexor Muscle-Tendon Unit at Rest

Abstract

A s most biological tissues, skeletal muscle and its tendon behave as viscoelastic materials in that they develop higher tension in response to increasing stretch velocity rates (1,6,32,33). This strain rate dependence in skeletal muscle is of nonreflex origin and likely related to a relaxation process defined as a decrease in muscle stiffness when it is stretched and maintained at a fixed length (l7,32). A low stretch velocity would allow more relaxation to take place, resulting in a lower resistance to passive movements than with a higher stretch velocity (32).Velocity-sensitivity or strain rate dependence of nonreflex components was first studied in animals. During passive sinusoidal displacements of the limb at frequencies ranging from 0.25 to 12.5 Hz, velocity-sensitive responses in the cat muscle were found only at frequencies over 5 Hz (24). Taylor et al (32) showed that passive elongation up to 10% of the muscle resting length of rabbit extensor digitorum longus and tibialis anterior muscles (in vivo) led to higher tension and energy absorp tion with increasing stretch velocities (0.1-10 cm/sec).While very few studies have established the strain rate dependence of skeletal muscles in humans, many assume the latter behavior and dissociate, using mathematical models, the resistance to passive movements into viscous and elastic stiffness (9,ll-13, 22,35). Lehmann et al (15) found an increased stiffness of the plantar flexor muscles with increasing sinusoidal stretch frequencies (3-12 Hz) of 5" amplitude in normal ( N = 13) and also in spastic ( N = 13) subjects with nerve blocks. Price et al (23), using similar passive movement parameters, also observed that the nonreflex stiffness of the plantar flexors was velocity-sensitive in normal groups of adults ( N = 10) and children ( N = l l ) . In contrast to the above studies, Hufschmidt and Mauritz (lo), in a study with normal ( N = 20) and spastic ( N = 21) subjects, did not observe any increase in

Measurement of passive ankle stiffness in subjects with chronic hemiparesis using a novel ankle robot

“…Torque was assigned a polarity consistent with the direction of the movement that it would generate (e.g., dorsiflexion torque was taken as positive). Each perturbation was made at a constant velocity of 5°/s so as to not evoke stretch reflex (Saripalli and Wilson 2005;Hufschmidt and Mauritz, 1985;Lamontagne et al 1997;Lorentzen et al 2010). The passive movement of the ankle occurred with nominal controller settings (robot torsional stiffness and damping) of 100 N·m/rad and 2 N·m·s/rad.…”

“…This affirms that our ankle position and torque data yielded a "near-true" estimate of passive ankle stiffness. 3) We also considered elicitation of stretch reflex: we used a slow-perturbation velocity to prevent evoking stretch-reflex activity (Saripalli and Wilson 2005;Lamontagne et al 1997;Lorentzen et al 2010). The decision to set 5°/s as the perturbation velocity in this protocol was, in part, based on previous work that has shown that stretch velocities of this magnitude do not evoke stretch reflex in both healthy (Saripalli and Wilson 2005;Lorentzen et al 2010) and stroke (Hufschmidt and Mauritz 1985;Lorentzen et al 2010) subjects under similar experimental conditions.…”

“…Although many studies report passive ankle-sagittalplane-stiffness measurements in healthy older adults to afford comparison against their neurologically impaired test subjects (e.g., Rydahl and Brouwer 2004;Lamontagne et al 1997;Chung et al 2004;Lorentzen et al 2010), few studies have reported data on young healthy individuals. Moreover, estimates of passive ankle stiffness vary greatly between studies because of differences in experimental conditions: 1) Posture, e.g., upright stance vs. supine, flexed vs. extended knee (Riemann et al 2001;Saripalli and Wilson 2005;Morasso and Sanguineti 2002), 2) perturbation type, e.g., active vs. passive, magnitude and waveform (Riemann et al 2001;Morasso and Sanguineti 2002;Kearney et al 1997;Casadio et al 2005), 3) physiological conditions, e.g., elicitation of maximal muscle contraction or joint ROM vs. submaximal activation conditions (Riemann et al 2001;Morasso and Sanguineti 2002;Rao 2006), 4) population characteristics, e.g., age (Lark et al 2003), sex (Padua et al 2005;Cammarata et al 2007;Lephart et al 2002;Granata et al 2002), 5) time postlesion (Mirbagheri et al 2007), and 6) location of lesion, e.g., cortical vs. subcortical, have all been shown to be important determinants of passive ankle stiffness.…”

“…They defined passive stiffness to be the applied torque recorded at the slowest stretch velocity (8°/s) at which no stretch-reflex response was elicited. Others have used passive perturbations generated by force plates (e.g., Rydahl and Brouwer 2004) or dynamometers (e.g., Lamontagne et al 1997) to measure the resultant angular displacement. Using system-identification techniques and assuming linearity, ankle inertia, damping, stiffness (and other dynamic factors) can be approximated for various perturbations at different ankle angles and for different levels of muscular activation (Kearney and Hunter 1990).…”

“…Whereas the passive ankle stiffness has been estimated and reported extensively, both for healthy and neurologically impaired human subjects, nearly all those measurements have been made in the sagittal plane, i.e., the dorsi-plantarflexion degree-of-freedom (DOF) (Rydahl and Brouwer 2004;Lamontagne et al 1997, Chung et al 2004, Sinkjaer et al 1988Harlaar et al 2000;Singer et al 2002;Lorentzen et al 2010). In contrast, with the exception of only a few studies (e.g., Zinder et al 2007), very little information is available on the ankle-joint stiffness in healthy individuals in the frontal plane, i.e., eversion-inversion DOF.…”