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PubMed1998

Effect of exercise training on passive stiffness in locomotor skeletal muscle: role of extracellular matrix.

The purpose of this study was to evaluate the effect of endurance exercise training on both locomotor skeletal muscle collagen characteristics and passive stiffness properties in the young adult and old rat. Young (3-mo-old) and senescent (23-mo-old) male Fischer 344 rats were randomly assigned to either a control or exercise training group [young control (YC), old control (OC), young trained (YT), old trained (OT)]. Exercise training consisted of treadmill running at approximately 70% of maximal oxygen consumption (45 min/day, 5 days/wk, for 10 wk). Passive stiffness (stress/strain) of the soleus (Sol) muscle from all four groups was subsequently measured in vitro at 26 degreesC. Stiffness was significantly greater for Sol muscles in OC rats compared with YC rats, but in OT rats exercise training resulted in muscles with stiffness characteristics not different from those in YC rats. Sol muscle collagen concentration and the level of the nonreducible collagen cross-link hydroxylysylpyridinoline (HP) significantly increased from young adulthood to senescence. Although training had no effect on Sol muscle collagen concentration in either age group, it resulted in a significant reduction in the level of Sol muscle HP in OT rats. In contrast, exercise had no effect on HP in the YT animals. These findings indicate that 10 wk of endurance exercise significantly alter the passive viscoelastic properties of Sol muscle in old but not in young adult rats. The coincidental reduction in the principal collagen cross-link HP also observed in response to training in OT muscle highlights the potential role of collagen in influencing passive muscle viscoelastic properties.

Aging↗
PubMed2005

Phosphorylation of titin modulates passive stiffness of cardiac muscle in a titin isoform-dependent manner.

We investigated the effect of protein kinase A (PKA) on passive force in skinned cardiac tissues that express different isoforms of titin, i.e., stiff (N2B) and more compliant (N2BA) titins, at different levels. We used rat ventricular (RV), bovine left ventricular (BLV), and bovine left atrial (BLA) muscles (passive force: RV > BLV > BLA, with the ratio of N2B to N2BA titin, approximately 90:10, approximately 40:60, and approximately 10:90%, respectively) and found that N2B and N2BA isoforms can both be phosphorylated by PKA. Under the relaxed condition, sarcomere length was increased and then held constant for 30 min and the peak passive force, stress-relaxation, and steady-state passive force were determined. Following PKA treatment, passive force was significantly decreased in all muscle types with the effect greatest in RV, lowest in BLA, and intermediate in BLV. Fitting the stress-relaxation data to the sum of three exponential decay functions revealed that PKA blunts the magnitude of stress-relaxation and accelerates its time constants. To investigate whether or not PKA-induced decreases in passive force result from possible alteration of titin-thin filament interaction (e.g., via troponin I phosphorylation), we conducted the same experiments using RV preparations that had been treated with gelsolin to extract thin filaments. PKA decreased passive force in gelsolin-treated RV preparations with a magnitude similar to that observed in control preparations. PKA was also found to decrease restoring force in skinned ventricular myocytes of the rat that had been shortened to below the slack length. Finally, we investigated the effect of the beta-adrenergic receptor agonist isoprenaline on diastolic force in intact rat ventricular trabeculae. We found that isoprenaline phosphorylated titin and that it reduced diastolic force to a degree similar to that found in skinned RV preparations. Taken together, these results suggest that during beta-adrenergic stimulation, PKA increases ventricular compliance in a titin isoform-dependent manner.

Adrenergic beta-Agonists↗
PubMed1986

Intraoperative length and tension curves of human eye muscles. Including stiffness in passive horizontal eye movement in awake volunteers.

Intraoperative continuous-registration length and tension curves of attached and detached eye muscles were made in 18 strabismic patients under general anesthesia. For relaxed eye muscles, we found an exponential relation between length and tension. An increased stiffness was quantified in Duane's syndrome, Graves' disease, orbital-floor fracture, and superior oblique palsy. The stiffnesses of agonist and antagonist were remarkably similar, not only in uncomplicated squint, but also when only one of the two had initially become stiffer. After intravenous administration of succinylcholine chloride, the eye muscles contracted, and the exponential length and tension curve changed into a set of straight, parallel lines. In addition, we measured stiffness in passive horizontal eye movement in awake volunteers and found 0.52 to 1.26 g/degrees (other eye in 5 degrees of adduction), confirming other published results.

Adult↗
PubMed2002

Passive stiffness changes in soleus muscles from desmin knockout mice are not due to titin modifications.

Passive stiffness was found to be increased in mouse soleus muscles lacking desmin. Because titin is considered to be the major source of muscle elasticity, the stiffening might be explainable by titin adaptation. To test this, passive mechanical properties of single skinned fibres of soleus muscles from desmin knockout and control mice were analysed by using various extension tests. Titin expression was studied by SDS-gel electrophoresis. Absence of desmin did not modify either electrophoretic mobility of the titin band (3700 kDa) or optical density-unit ratios between bands for titin and nebulin (congruent with 0.3) and bands for titin and myosin heavy chain (congruent with 0.08). Elastic properties of fibres were not altered in the absence of desmin since passive tensions were similar under quasi-static (56-66 kN m(-2)) and dynamic (100-118 kN m(-2)) conditions whatever the kind of fibre. Thus, titin is unlikely to be responsible for the large increase in passive stiffness observed in whole soleus muscles when desmin is lacking.

Animals↗
PubMed2001

Passive stiffness is increased in soleus muscle of desmin knockout mouse.

The effects of an absence of desmin on passive stiffness of skeletal muscle were analyzed using soleus muscles from desmin knockout mice. Stiffness was evaluated by analyzing the passive tension induced by a ramp-and-hold extension test. This test showed that passive resistance to stretch was largely increased for muscles lacking desmin. This study could facilitate interpretation of changes in muscle mechanics observed in humans affected by desmin-related myopathies.

Animals↗
PubMed2000

Contribution of passive stiffness to ankle plantarflexor moment during gait after stroke.

OBJECTIVE: To measure the contribution of passive stiffness to the ankle plantarflexor moment during gait in subjects with hemiparesis early after stroke. The relationship of passive stiffness with gait speed was also examined. DESIGN: Cross-sectional, descriptive. PATIENTS AND OTHER PARTICIPANTS: A sample of convenience of 14 patients (54.7+/-10.9 yrs) with a hemiparesis for less than 5 months and 11 healthy controls (50.6+/-11.6 yrs). MAIN OUTCOME MEASURES: The contribution of passive stiffness to the plantarflexor moment during gait was obtained using moment-angle slope (stiffness) values. Total plantarflexor stiffness was measured during gait, and passive stiffness was measured during passive dorsiflexion imposed by an isokinetic dynamometer at velocities and ranges of movement matched with values recorded during the plantarflexor lengthening period of the stance phase. The contribution of passive stiffness was obtained by dividing the passive stiffness (dynamometer) by the total plantarflexor stiffness (gait). RESULTS: On the paretic side, passive stiffness contributed more (16.8%; range 2.9% to 49.6%) to total plantarflexor stiffness during gait compared (p<.01) with both the nonparetic side (7.3%) and control values (5.9%). This increased contribution on the paretic side resulted from a large muscle-tendon passive stiffness, a decreased active muscle contribution, or both. Although in some patients the increased passive component led to the development of a total plantarflexor stiffness that was within normal values, it did not in others either because the active component was very small or because limited dorsiflexion during the stance phase prevented the passive component tension to develop. The contribution of passive stiffness was not significantly (p>.05) related to gait speed in both the patients and the controls. CONCLUSIONS: The increased contribution of passive stiffness to total plantarflexor moment during gait likely acts as an adaptation for a defective muscle active component, helping ankle push-off at the end of the stance phase. Although this mechanism is effective in most of the patients, it cannot come into action if the dorsiflexion movement during the stance phase is prevented, for instance, by enhanced stretch reflexes.

Adult↗
PubMed2001

The Effects of Sex, Joint Angle, and the Gastrocnemius Muscle on Passive Ankle Joint Complex Stiffness.

OBJECTIVE: To assess the effects of sex, joint angle, and the gastrocnemius muscle on passive ankle joint complex stiffness (JCS). DESIGN AND SETTING: A repeated-measures design was employed using sex as a between-subjects factor and joint angle and inclusion of the gastrocnemius muscle as within-subject factors. All testing was conducted in a neuromuscular research laboratory. SUBJECTS: Twelve female and 12 male healthy, physically active subjects between the ages of 18 and 30 years volunteered for participation in this study. The dominant leg was used for testing. No subjects had a history of lower extremity musculoskeletal injury or circulatory or neurologic disorders. MEASUREMENTS: We determined passive ankle JCS by measuring resistance to passive dorsiflexion (5 degrees.s(-1)) from 23 degrees plantar flexion (PF) to 13 degrees dorsiflexion (DF). Angular position and torque data were collected from a dynamometer under 2 conditions designed to include or reduce the contribution of the gastrocnemius muscle. Separate fourth-order polynomial equations relating angular position and torque were constructed for each trial. Stiffness values (Nm.degree(-1)) were calculated at 10 degrees PF, neutral (NE), and 10 degrees DF using the slope of the line at each respective position. RESULTS: Significant condition-by-position and sex-by-position interactions and significant main effects for sex, position, and condition were revealed by a 3-way (sex-by-position, condition-by-position) analysis of variance. Post hoc analyses of the condition-by-position interaction revealed significantly higher stiffness values under the knee-straight condition compared with the knee-bent condition at both ankle NE and 10 degrees DF. Within each condition, stiffness values at each position were significantly higher as the ankle moved into DF. Post hoc analysis of the sex-by-position interaction revealed significantly higher stiffness values at 10 degrees DF in the male subjects. Post hoc analysis of the position main effect revealed that as the ankle moved into dorsiflexion, the stiffness at each position became significantly higher than at the previous position. CONCLUSIONS: The gastrocnemius contributes significantly to passive ankle JCS, thereby providing a scientific basis for clinicians incorporating stretching regimens into rehabilitation programs. Further research is warranted considering the cause and application of the sex-by-position interaction.

Journal Article↗
PubMed2006

Aging affects passive stiffness and spindle function of the rat soleus muscle.

Aging affects many motor functions, notably the spinal stretch reflexes and muscle spindle sensitivity. Spindle activation also depends on the elastic properties of the structures linked to the proprioceptive receptors. We have calculated a spindle efficacy index, SEI, for old rats. This index relates the spindle sensitivity, deduced from electroneurograms recording (ENG), to the passive stiffness of the muscle. Spindle sensitivity and passive incremental stiffness were calculated during ramp and hold stretches imposed on pseudo-isolated soleus muscles of control rats (aged 4 months, n=12) and old rats (aged 24 months, n=16). SEI were calculated for the dynamic and static phases of ramp (1-80 mm/s) and for hold (0.5-2mm) stretches imposed at two reference lengths: length threshold for spindle afferents discharges, L(n) (neurogram length) and slack length, L(s). The passive incremental stiffness was calculated from the peak and steady values of passive tension, measured under the stretch conditions used for the ENG recordings, and taking into account the muscle cross-sectional area. The pseudo-isolated soleus muscles were also stretched to establish the stress-strain relationship and to calculate muscle stiffness constant. The contralateral muscle was used to count muscle spindles and spindle fibers (ATPase staining) and immunostained to identify MyHC isoforms. L(n) and L(s) lengths were not significantly different in the control group, while L(n) was significantly greater than L(s) in old muscles. Under dynamic conditions, the SEI of old muscles was the same as in controls at L(s), but it was significantly lower than in controls at L(n) due to increased passive incremental stiffness under the stretch conditions used to analyze the ENG. Under static conditions, the SEI of old muscles was significantly lower than control values at all the stretch amplitudes and threshold lengths tested, due to increased passive incremental stiffness and decreased spindle sensitivity at L(s). The muscle stiffness constant values were greater in old muscles than in controls, confirming the changes in elastic properties under passive conditions due to aging. Aging also altered the intrafusal fibers: it increased the mean number of intrafusal fibers and the contents in the slow, neonatal and developmental isoforms intrafusal of MyHC have been modified. These structural modifications do not seem great enough to counteract the loss of the spindle sensitivity or the spindle efficacy under passive conditions and after the nerve was severed. However, they may help to maintain the spindle afferent message under natural conditions and under fusimotor control.

Aging↗
PubMed2006

Acute effects of static stretching on passive stiffness of the hamstring muscles calculated using different mathematical models.

BACKGROUND: The aim of this study was to assess the effects of static stretching on hamstring passive stiffness calculated using different data reduction methods. METHODS: Subjects performed a maximal range of motion test, five cyclic stretching repetitions and a static stretching intervention that involved five 30-s static stretches. A computerised dynamometer allowed the measurement of torque and range of motion during passive knee extension. Stiffness was then calculated as the slope of the torque-angle relationship fitted using a second-order polynomial, a fourth-order polynomial, and an exponential model. The second-order polynomial and exponential models allowed the calculation of stiffness indices normalized to knee angle and passive torque, respectively. FINDINGS: Prior to static stretching, stiffness levels were significantly different across the models. After stretching, while knee maximal joint range of motion increased, stiffness was shown to decrease. Stiffness decreased more at the extended knee joint angle, and the magnitude of change depended upon the model used. After stretching, the stiffness indices also varied according to the model used to fit data. Thus, the stiffness index normalized to knee angle was found to decrease whereas the stiffness index normalized to passive torque increased after static stretching. INTERPRETATION: Stretching has significant effects on stiffness, but the findings highlight the need to carefully assess the effect of different models when analyzing such data.

Adaptation, Physiological↗
PubMed2006

Muscle stiffness and strength and their relation to hand function in children with hemiplegic cerebral palsy.

This study compared the passive stiffness of wrist flexors and the strength of wrist flexors and extensors in three different wrist positions (30 degrees of flexion, neutral, and 30 degrees of extension) between children with cerebral palsy (CP) and typically developing (TD) comparison children. It also examined associations between these characteristics and manual function in children with CP. Eleven children with spastic hemiplegic CP (six females, five males; mean age 8y 5mo [SD 1y 8mo], range 6-11y) and 11 TD children, matched for age and sex, took part in this study. Passive stiffness of muscles was measured as the torque/angle relation during passive motion. Isometric strength tests were performed and the time needed to complete three tasks based on the Jebsen-Taylor Hand Function Test was recorded. Flexor stiffness was higher in the group with CP. Strength of flexors and extensors in the group with CP was lower with the wrist extended. No difference among test positions was found in the TD group. Moderate correlations were observed between manual function and variables related to strength and stiffness of wrist muscles in the group with CP. Children with CP showed muscle alterations coherent with the use of the wrist in flexion. Intervention on these characteristics could have a positive impact on manual function.

Age Factors↗
PubMed1996

Effects of pressure- or volume-overload hypertrophy on passive stiffness in isolated adult cardiac muscle cells.

It has been hypothesized that the changes in myocardial stiffness induced by chronic hemodynamic overloading are dependent on changes in the passive stiffness of the cardiac muscle cell (cardiocyte). However, no previous studies have examined the passive constitutive properties of cardiocytes isolated from animals with myocardial hypertrophy. Accordingly, changes in relative passive stiffness of cardiocytes isolated from animals with chronic pressure- or volume-overload hypertrophy were determined by examining the effects of anisosmotic stress on cardiocyte size. Anisosmotic stress was produced by altering superfusate osmolarity. Hypertrophied cardiocytes were enzymatically isolated from 16 adult cats with right ventricular (RV) pressure-overload hypertrophy induced by pulmonary artery banding (PAB) and from 6 adult cats with RV volume-overload hypertrophy induced by creating an atrial septal defect (ASD). Left ventricular (LV) cardiocytes from each cat served as nonhypertrophied, normally loaded, same-animal controls. Superfusate osmolarity was decreased from 305 +/- 3 to 135 +/- 5 mosM and increased to 645 +/- 4 mosM. During anisosmotic stress, there were no significant differences between hypertrophied RV and normal LV cardiocytes in pressure overload PAB cats with respect to percent change in cardiocyte area (47 +/- 2% in RV vs. 48 +/- 2% in LV), diameter (46 +/- 3% in RV vs. 48 +/- 2% in LV), or length (2.4 +/- 0.2% in RV vs. 2.0 +/- 0.3% in LV), or sarcomere length (1.5 +/- 0.1% in RV vs. 1.3 +/- 0.3% in LV). Likewise, there were no significant differences in cardiocyte strain between hypertrophied RV and normal LV cardiocytes from ASD cats. In conclusion, chronic pressure-overload hypertrophy and chronic volume-overload hypertrophy did not alter the cardiocyte response to anisosmotic stress. Thus chronic overload hypertrophy did not alter relative passive cardiocyte stiffness.

Animals↗
PubMed2006

Passive stiffness in Drosophila indirect flight muscle reduced by disrupting paramyosin phosphorylation, but not by embryonic myosin S2 hinge substitution.

High passive stiffness is one of the characteristic properties of the asynchronous indirect flight muscle (IFM) found in many insects like Drosophila. To evaluate the effects of two thick filament protein domains on passive sarcomeric stiffness, and to investigate their correlation with IFM function, we used microfabricated cantilevers and a high resolution imaging system to study the passive IFM myofibril stiffness of two groups of transgenic Drosophila lines. One group (hinge-switch mutants) had a portion of the endogenous S2 hinge region replaced by an embryonic version; the other group (paramyosin mutants) had one or more putative phosphorylation sites near the N-terminus of paramyosin disabled. Both transgenic groups showed severely compromised flight ability. In this study, we found no difference (compared to the control) in passive elastic modulus in the hinge-switch group, but a 15% reduction in the paramyosin mutants. All results were corroborated by muscle fiber mechanics experiments performed on the same lines. The fact that myofibril elasticity is unaffected by hinge switching implies alternative S2 hinges do not critically affect passive sarcomere stiffness. In contrast, the mechanical defects observed upon disrupting paramyosin phosphorylation sites in Drosophila suggests that paramyosin phosphorylation is important for maintaining high passive stiffness in IFM myofibrils, probably by affecting paramyosin's interaction with other sarcomeric proteins.

Animals↗
PubMed1997

Regulation of muscle stiffness during periodic length changes in the isolated abdomen of the hermit crab.

Reflex activation of the ventral superficial muscles (VSM) in the abdomen of the hermit crab, Pagurus pollicarus, was studied using sinusoidal and stochastic longitudinal vibration of the muscle while recording the length and force of the muscle and the spike times of three exciter motoneurons. In the absence of vibration, the interspike interval histograms of the two larger motoneurons were bimodal; cutting sensory nerves containing most of the mechanoreceptor input removed the short interval peak in the histogram, indicating that the receptors are important in maintaining tonic firing. Vibration of the muscle evoked a reflex increase in motoneuron frequency that habituated after an initial peak but remained above control levels for the duration of stimulation. Motoneuron frequency increased with root mean square (rms) stimulus amplitude. Average stiffness during stimulation was about two times the stiffness of passive muscle. The reflex did not alter muscle dynamics. Estimated transfer functions were calculated from the fast Fourier transform of length and force signals. Coherence was >0.9 for the frequency range of 3-35 Hz. Stiffness magnitude gradually increased over this range in both reflex activated and passive muscle; phase was between 10 and 20 degrees. Reflex stiffness decreased with increasing stimulus amplitudes, but at larger amplitudes, this decrease was much less pronounced; in this range stiffness was regulated by the reflex. The sinusoidal frequency at which reflex bursts were elicited was approximately 6 Hz, consistent with previous measurements using ramp stretch. During reflex excitation, there was an increase in amplitude of the short interval peak in the interspike interval histogram; this was reduced when the majority of afferent pathways was removed. A phase histogram of motoneuron firing during sinusoidal vibration had a peak at approximately 110 ms, also suggesting that an important component of the reflex is via direct projections from the mechanoreceptors. These results are consistent with the hypothesis that a robust feedforward regulation of abdominal stiffness during continuous disturbances is achieved by mechanoreceptors signalling the absolute value of changing forces; habituation of the reflex, its high-threshold for low frequency disturbances and the activation kinetics of the muscle further modify reflex dynamics.

Abdomen↗
PubMed1976

Effect of age on passive elastic stiffness of rat heart muscle.

A thick-wall spherical model for the rat left ventricle was used to deduce passive wall stiffness from diastolic pressure-volume data. This was done for rats in three age classes: young (1 mo), adult (17 mo) and old (17 mo). The model was based on finite deformation elasticity theory consistent with the magnitude of observed deformation. A least-squares procedure was used to determine elastic constants in postulated nonlinear stress-stretch relations for the myocardium. It was found that at a given level of stress, wall stiffness for ventricles in the young age class was consistently greater than wall stiffness in the other two classes. In addition, the difference in wall stiffness between rats in the adult and old age classes was found to be approximately 10%.

Aging↗
PubMed2004

Passive force, angle, and stiffness changes after stretching of hamstring muscles.

UNLABELLED: Periodic or long-term stretching programs have demonstrated changes in joint range of motion. The suggested mechanisms for these increases in range of motion are changes in the tissue properties of the muscle and more recently stretch tolerance. However, few studies have examined changes in passive resistive forces and related these changes to increases in range of motion. PURPOSE: The purpose of this study was to investigate the influence of a 6-wk hamstring-stretching program on knee extension range of motion, passive resistive forces, and muscle stiffness. METHODS: A randomized control trial with repeated measures was undertaken with 43 school-age subjects. Hamstring extensibility was assessed by a passive knee extension test using a Kincom isokinetic dynamometer. The intervention group participated in a 6-wk hamstring-stretching program. Stretches were performed 5 d x wk(-1), once per day, held for 30 s, and for 3 repetitions. The control group did not stretch over the 6-wk intervention period. Measurements of hamstring extensibility were repeated at the end of the 6-wk intervention. RESULTS: After the intervention period, significant (P < 0.05) increases in knee extension range of motion, passive resistive force, and stiffness were observed in the experimental group. No significant differences were observed in the control group's findings for the same variables. CONCLUSIONS: The findings of this study are consistent with other literature that shows periodic stretching programs over a 6-wk time frame produce significant changes in knee extension range of motion. The finding of increased stiffness in the new range of motion, gained as a result of the stretching program, provides some evidence that structural changes had occurred in the stretched muscles.

Adaptation, Physiological↗
PubMed1993

Passive motion: the dose effects on joint stiffness, muscle mass, bone density, and regional swelling. A study in an experimental model following intra-articular injury.

We studied the effects of passive motion on joint stiffness, muscle mass, bone density, and regional swelling after an intra-articular injury. Instrumentation was applied to the hindlimbs of thirty adolescent New Zealand White rabbits to allow either passive motion or immobilization of the ankle. The knee was immobilized by the locking together of Steinmann pins that had been placed within the medullary canals of the tibia and femur. An intra-articular injury was produced by drilling of the tibial pin through the ankle joint into the talus and subsequent withdrawal of the pin from the ankle joint. The rabbits were divided into five groups, and they received four, eight, twelve, sixteen, or twenty-four hours of passive motion each day during the three-week period of study. One ankle of each rabbit was moved through an arc of 90 to 170 degrees of dorsiflexion at one cycle per minute, while the contralateral ankle was immobilized in 100 degrees of dorsiflexion with an aluminum splint, which was fixed to the aluminum block that was used to stabilize the knee joint. We found that sixteen and twenty-four hours of passive motion prevented stiffness of the joint. Passive motion for shorter periods was ineffective, even harmful, and resulted in stiffness ratios that were as much as four times higher than those of the control limbs (those treated with immobilization). Swelling of the limb decreased only in the group that received twenty-four hours of passive motion. Muscle mass increased by an average of 13 per cent (range, 4 to 34 per cent), in comparison with that of the immobilized limbs in every group that was treated with passive motion. Bone density was maintained only in the limbs in which the ankle became stiff (ankles that had been treated with passive motion for twelve hours or less). An inverse relationship was noted between the duration of passive motion and the radiographic density of the distal tibial metaphysis; this relationship was statistically significant (p < 0.01). The limbs treated for twelve, eight, or four hours each day showed progressively greater bone density in comparison with those treated with immobilization or with sixteen or twenty-four hours of passive motion.

Animals↗
PubMed2002

Mechanisms of disturbed motor control in ankle weakness during gait after stroke.

This study investigated the role of paresis, excessive antagonist coactivation, increased muscle-tendon passive stiffness and spasticity in the reduced stance phase plantarflexor moment (Mmax) and swing phase dorsiflexion during gait (DFmax) in subjects with a recent (<6 months post-stroke) hemiparesis (patients). The gait pattern of the paretic and non-paretic sides was evaluated in 30 patients (aged 57.8+/-10.8 years), whereas only one side was evaluated in 15 healthy controls (aged 59.1+/-9.8 years) while walking at natural and very slow speeds. Peak plantarflexor moment (Mmax) and peak medial gastrocnemius (MG) activation during the stance phase, as well as peak dorsiflexion angle (Dfmax) and peak tibialis anterior (TA) activation during the swing phase, were retained for analysis. In addition, a coactivation index and a plantarflexor spasticity index were calculated for both the stance and the swing phase, and plantarflexor passive stiffness was evaluated on an isokinetic dynamometer. The results showed that Mmax on the paretic and non-paretic sides were both reduced compared with control values at natural speed. This reduction was combined to a low MG activation (paresis) on the paretic side. On the non-paretic side, the reduced plantarflexor moment was related to excessive coactivation levels. The swing phase Dfmax tended to be reduced (not significantly) on the paretic side of the patients compared with control values. This reduction was neither associated with excessive antagonist coactivation nor to plantarflexor hyperactive stretch reflexes, but rather to an increased plantarflexor passive stiffness. In some of the patients, however, an increased TA activation that overcame the plantarflexor passive stiffness allowed for normal DFmax values. The functional consequences of the disturbed mechanisms of motor control observed in both the paretic and non-paretic sides are discussed.

Adult↗