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Biomedical subjects

S Nadeau

Publications and source records attributed to S Nadeau.

At least 19 recordsLinked to original sources
PubMed2002

Handling missing marker coordinates in 3D analysis.

The use of mathematical formulations to retrieve missing data is not usually implemented as an automated computer procedure. The purpose of this paper is to present a simple mathematical formulation that can be used to retrieve the coordinates of markers hidden during a task. A strategy based on the smoothness of the variation of distance between points is devised, which leads to an automated computer procedure for retrieving hidden skin markers or missing joint coordinates (missing 3D points). This approach has the advantage of not being restricted to the usual rigid-body assumption.

Algorithms↗
PubMed2001

Effects of muscle strengthening and physical conditioning training on temporal, kinematic and kinetic variables during gait in chronic stroke survivors.

The purpose of this study was to evaluate the impact of a combined program of muscle strengthening and physical conditioning on gait performance in subjects with chronic stroke, using a single group pre- and post-test design. Thirteen subjects were recruited for the 10-week program (3 days/week), which consisted of warm-up, aerobic exercises, lower extremity muscle strengthening and cool-down. Data from cinematographic film and a force plate obtained during multiple walking trials were used in a four-segment kinetic model to yield spatiotemporal, kinematic and kinetic variables. Gait analysis revealed that the 10 week training resulted in significant increases in gait speed associated with improvements in walking patterns as determined by increases in selected kinematic and kinetic measures. After training, subjects were able to generate higher levels of powers and demonstrated increases in positive work performed by the ankle plantar flexor and hip flexor/extensor muscles.

Aged↗
PubMed2000

Role of microglial-derived tumor necrosis factor in mediating CD14 transcription and nuclear factor kappa B activity in the brain during endotoxemia.

Systemic injection of the endotoxin lipopolysaccharide (LPS) upregulates the gene encoding CD14 early in the circumventricular organs (CVOs) and later in the brain parenchyma. The present study tested the hypothesis that the parenchymal production of the proinflammatory cytokine tumor necrosis factor alpha (TNF-alpha) by microglial cells is responsible for triggering CD14 transcription in an autocrine/paracrine loop-like manner. In a first set of experiments, Sprague Dawley rats were killed 1, 3, 6, and 12 hr after an intracerebroventricular administration of recombinant rat TNF-alpha or vehicle solution. Second, anti-rat TNF-alpha-neutralizing antibody or vehicle solution was administrated into the lateral ventricle 10 hr before an intraperitoneal injection of LPS. Central administration of the cytokine caused a strong induction of IkappaBalpha, TNF-alpha, and CD14 mRNA in parenchymal microglial cells. The hybridization signal for these transcripts was localized to the edge of the ventricles and the site of infusion. The time-related expression of each mRNA suggested that TNF-alpha has the ability to trigger its own production followed by the transcription of the LPS receptor; the signal for IkappaBalpha, TNF-alpha, and CD14 peaked at 1, 3, and 6 hr, respectively. The genes encoding TNF-alpha and mCD14 were also induced in the CVOs and within microglial cells across the brain parenchyma in response to intraperitoneal LPS administration. This induction in parenchymal cells of the brain was prevented in animals that received the anti-TNF-antisera intracerebroventricularly 10 hr before the systemic treatment with the endotoxin. The present data provide the evidence that microglial-derived TNF-alpha is responsible for the production of the LPS receptor CD14 during endotoxemia. This autocrine/paracrine stimulatory loop may be of great importance in controlling the inflammatory events that take place in the CNS during innate immune response as well as under pathological conditions.

Animals↗
PubMed2000

How the blood talks to the brain parenchyma and the paraventricular nucleus of the hypothalamus during systemic inflammatory and infectious stimuli.

There are exciting new developments regarding the molecular mechanisms involved in the influence of circulating proinflammatory molecules within cells of the blood-brain barrier (BBB) during systemic immune challenges. These molecules, when present in the circulation, have the ability to trigger a series of events in cascade, leading to either the mitogen-activated protein (MAP) kinases/nuclear factor kappa B (NF-kappaB) or the janus kinase (JAK)/signal transducer and activator of transcription (STAT) transduction pathways in vascular-associated cells of the central nervous system (CNS). The brain blood vessels exhibit both constitutive and induced expression of receptors for different proinflammatory ligands that have the ability to stimulate these signaling molecules. Depending on the challenges and the cytokines involved, the transduction signal(s) solicited in cells of the BBB may orient the neuronal activity in a very specific manner in activating the transcription and production of soluble factors, such as prostaglandins (PGs). It is interesting to note that cytokines as well as systemic localized inflammation stimulate the cells of the BBB in a nonselective manner (i.e., within both large blood vessels and small capillaries across the brain). This nonselectivity raises several questions with regard to the localized neuronal activation induced by different experimental models of inflammation and cytokines. It is possible that the selectivity of the neuronal response is a consequence of the fine interaction between nonparenchymal synthesis of soluble mediators and expression of specific receptors for these ligands within parenchymal elements of different brain nuclei. This review will present the recent developments on this concept and the mechanisms that take place in cells of the BBB, which lead to the neuronal circuits involved in restoring the body's homeostasis during systemic immunogenic challenges. The induction of fever, the hypothalamic-pituitary adrenal (HPA) axis, and other autonomic functions are among the physiological outcomes necessary for the protection of the mammalian organism in the presence of foreign material.

Animals↗
PubMed1999

Conduction aphasia and the arcuate fasciculus: A reexamination of the Wernicke-Geschwind model.

Wernicke, and later Geschwind, posited that the critical lesion in conduction aphasia is in the dominant hemisphere's arcuate fasciculus. This white matter pathway was thought to connect the anterior language production areas with the posterior language areas that contain auditory memories of words (a phonological lexicon). Alternatively, conduction aphasia might be induced by cortical dysfunction, which impairs the phonological output lexicon. We observed an epileptic patient who, during cortical stimulation of her posterior superior temporal gyrus, demonstrated frequent phonemic paraphasias, decreased repetition of words, and yet had intact semantic knowledge, a pattern consistent with conduction aphasia. These findings suggest that cortical dysfunction alone may induce conduction aphasia.

Aphasia, Conduction↗
PubMed1999

Muscle strengthening and physical conditioning to reduce impairment and disability in chronic stroke survivors.

OBJECTIVE: To evaluate the impact of a program of muscle strengthening and physical conditioning on impairment and disability in chronic stroke subjects. DESIGN: A randomized pretest and posttest control group, followed by a single-group pretest and posttest design. SUBJECTS: Thirteen community-dwelling stroke survivors of at least 9 months. INTERVENTION: A 10-week (3 days/week) program consisting of a warm-up, aerobic exercises, lower extremity muscle strengthening, and a cool-down. MAIN OUTCOME MEASURES: Peak isokinetic torque of the major muscle groups of the affected lower limb, quadriceps and ankle plantarflexor spasticity, gait speed, rate of stair climbing, the Human Activity Profile (HAP), and the Nottingham Health Profile (NHP) were recorded twice for the treatment group and three times for the control group. RESULTS: Significant improvements were found for all the selected outcome measures (HAP, NHP, and gait speed) for the treatment group (p < .001). In terms of overall training effects, the 13 subjects demonstrated increases in strength of the affected major muscle groups, in HAP and NHP profiles, and in gait speed and rate of stair climbing without concomitant increases in either quadriceps or ankle plantarflexor spasticity. CONCLUSIONS: The 10-week combined program of muscle strengthening and physical conditioning resulted in gains in all measures of impairment and disability. These gains were not associated with measurable changes of spasticity in either quadriceps or ankle plantarflexors.

Activities of Daily Living↗
PubMed1999

Plantarflexor weakness as a limiting factor of gait speed in stroke subjects and the compensating role of hip flexors.

OBJECTIVE: To determine, using the Muscular Utilization Ratio (MUR) method, whether plantarflexor weakness is among the factors preventing stroke subjects from walking at faster speeds. Potential compensations by the hip flexors were also examined. DESIGN: A convenience sample of 17 chronic stroke subjects in a context of a descriptive study. BACKGROUND: Gait speed is correlated with the residual strength of the muscles involved in gait in stroke subjects. However, it has not been established if this residual strength limits gait speed. METHODS: Kinetic and kinematic data for comfortable and maximal gait speeds were collected on the paretic side, and were used to determine the moments in plantarflexion (mechanical demand: MUR numerator) during the push-off phase. The maximal potential moment (MUR denominator) of the plantarflexors during gait was predicted using an equation derived from dynamometric data collected with a Biodex system. The MURs of the plantarflexors were then calculated at every 1% interval of the push-off phase. The pull-off phase of gait and the hip flexor strength were also examined. RESULTS: Ten subjects of the sample had a MUR value between 80 and 150% at maximal gait speed. These subjects produced the lowest peak torques in plantarflexion. Each of the four fastest subjects of this group had a large hip flexion moment during the pull-off phase of gait and produced high hip flexion torque values on the dynamometer. Each of the seven remaining subjects had a MUR value under 70% when they walked at maximal speed. CONCLUSIONS: Weakness of the plantarflexors should be considered as one factor limiting gait speed in 10 hemiparetic subjects. Some subjects with weak plantarflexors could walk rapidly because they compensated with the hip flexors. For the remaining stroke subjects, factors other than weakness of the plantarflexors have to be considered in order to explain the reduction in their gait speed.

Adolescent↗
PubMed1999

Effects of circulating tumor necrosis factor on the neuronal activity and expression of the genes encoding the tumor necrosis factor receptors (p55 and p75) in the rat brain: a view from the blood-brain barrier.

Tumor necrosis factor is a potent activator of myeloid cells, which acts via two cell-surface receptors, the p55 and p75 tumor necrosis factor receptors. The present study describes the cellular distribution of both receptor messenger RNAs across the rat brain under basal conditions and in response to systemic injection with the bacterial endotoxin lipopolysaccharide and recombinant rat tumor necrosis factor-alpha. Time-related induction of the messenger RNA encoding c-fos, cyclo-oxygenase-2 enzyme and the inhibitory factor kappa B alpha was assayed as an index of activated neurons and cells of the microvasculature by intravenous tumor necrosis factor-alpha challenge. The effect of the proinflammatory cytokine on the hypothalamic-pituitary-adrenal axis was determined by measuring the transcriptional activity of corticotropin-releasing factor and plasma corticosterone levels. Constitutive expression of p55 messenger RNA was detected in the circumventricular organs, choroid plexus, leptomeninges, the ependymal lining cells of the ventricular walls and along the blood vessels, whereas p75 transcript was barely detectable in the brain under basal conditions. Immunogenic insults caused up-regulation of both tumor necrosis factor receptors in barrier-associated structures, as well as over the blood vessels, an event that was associated with a robust activation of the microvasculature. Indeed, intravenous tumor necrosis factor-alpha provoked a rapid and transient transcription of inhibitory factor kappa B alpha and cyclo-oxygenase-2 within cells of the blood-brain barrier, and a dual-labeling technique provided the anatomical evidence that the endothelium of the brain capillaries expressed inhibitory factor kappa B alpha. Circulating tumor necrosis factor-alpha also rapidly stimulated c-fos expression in nuclei involved in the autonomic control, including the bed nucleus of the stria terminalis, the paraventricular nucleus of the hypothalamus, the central nucleus of the amygdala, the nucleus of the solitary tract and the ventrolateral medulla. A delayed c-fos mRNA induction was detected in the circumventricular organs, organum vascularis of the lamina terminalis, the subfornical organ, the median eminence and the area postrema. The paraventricular nucleus of the hypothalamus exhibited expression of corticotropin-releasing factor primary transcript that was associated with a sharp increase in the plasma corticosterone levels 1h after intravenous tumor necrosis factor-alpha administration. Taken together, these data provide the evidence that p55 is the most abundant tumor necrosis factor receptor in the central nervous system and is expressed in barrier-associated structures. Circulating tumor necrosis factor has the ability to directly activate the endothelium of the brain's large blood vessels and small capillaries, which may produce soluble molecules (such as prostaglandins) to vehicle the signal through parenchymal elements. The pattern of c-fos-inducible nuclei suggests complex neuronal circuits solicited by the cytokine to activate neuroendocrine corticotropin-releasing factor and the corticotroph axis, a key physiological response for the appropriate control of the systemic inflammatory response.

Animals↗
PubMed1999

Regulation of the gene encoding tumor necrosis factor alpha (TNF-alpha) in the rat brain and pituitary in response in different models of systemic immune challenge.

Tumor necrosis factor (TNF)-alpha is usually referred to as a proinflammatory cytokine that plays a central role in initiating the cascade of other cytokines and factors for an appropriate immune response to infection. Like systemic phagocytes, recent studies have reported that specific cellular populations of the CNS have the ability to express and release the proinflammatory cytokine in response to peripheral administration of the bacterial endotoxin lipopolysaccharide (LPS). Whether such phenomenon represents a general mechanism of systemic immunogenic stimuli and how the severity of the challenge may influence TNF-alpha transcription in the brain has yet to be defined. Adult male rats were sacrificed 1, 3, 6, 12, 24 and 48 hours (h) after intraperitoneal (IP) injection of LPS (25-250 microg/100 g) or intramuscular (IM) injection of turpentine. Brains and pituitary glands were removed, cut, and TNF-alpha mRNA assayed by in situ hybridization using a full-length rat cRNA probe. The results show no positive signal under basal conditions or following sterile inflammation into the left hind limb. Systemic LPS caused a profound increase in the expression of the gene encoding TNF-alpha in the leptomeninges, choroid plexus (chp) and all sensorial circumventricular organs (CVOs). Interestingly, a migratory-like pattern of TNF-alpha-positive cells became apparent around the sensorial CVOs at 3 h, while a ubiquitous-like positive signal was found throughout the brain 6 h after the injection with the highest dose of LPS. The IP LPS injection also stimulated TNF-alpha transcription in the anterior pituitary lobe; the signal was maximal 1 h after the injection and returned gradually to basal levels at 12 h, whereas the mRNA encoding the cytokine was detected later in the neurohypophysis, i.e. 3 and 6 h post challenge. Dual-labeling procedure provided the evidence of an LPS-dependent induction of TNF-alpha in different phagocytic cellular populations of the brain, including parenchymal microglial cells during severe endotoxemia. The fact that these myeloid-derived cells have the ability to express the LPS receptor CD14 in the brain may well explain the transcriptional activation of the cytokine in response to the bacterial endotoxin, but not to systemic localized inflammation.

Animals↗
PubMed1999

Droperidol lengthens cardiac repolarization due to block of the rapid component of the delayed rectifier potassium current.

INTRODUCTION: Torsades de pointes have been observed during treatment with droperidol, a butyrophenone neuroleptic agent. Our objectives were (1) to characterize the effects of droperidol on cardiac repolarization and (2) to evaluate effects of droperidol on a major time-dependent outward potassium current involved in cardiac repolarization (I(K)r). METHODS AND RESULTS: Isolated, buffer-perfused guinea pig hearts (n = 32) were stimulated at different pacing cycle lengths (150 to 250 msec) and exposed to droperidol in concentrations ranging from 10 to 300 nmol/L. Droperidol increased monophasic action potential duration measured at 90% repolarization (MAPD90) in a concentration-dependent manner by 9.8+/-2.3 msec (7.3%+/-0.7%) at 10 nmol/L but by 32.7+/-3.6 msec (25.7%+/-2.2%) at 300 nmol/L (250-msec cycle length). Increase in MAPD90 also was reverse frequency dependent. As noted previously, droperidol 300 nmol/L increased MAPD90 by 32.7+/-3.6 msec (25.7%+/-2.2%) at a pacing cycle length of 250 msec but by only 14.1+/-1.3 msec (13.6%+/-2.3%) at a pacing cycle length of 150 msec. Patch clamp experiments performed in isolated guinea pig ventricular myocytes demonstrated that droperidol decreases the time-dependent outward K+ current elicited by short depolarizations (250 msec; I(K)250) in a concentration-dependent manner. Estimated IC50 for I(K)250, which mostly underlies I(K)r, was 28 nmol/L. Finally, HERG K+ current elicited in HEK293 cells expressing high levels of HERG protein was decreased 50% by droperidol 32.2 nmol/L. CONCLUSION: Potent block of I(K)r by droperidol is likely to underlie QT prolongation observed in patients treated at therapeutic plasma concentrations (10 to 400 nmol/L) of the drug.

Action Potentials↗
PubMed1999

Thioridazine lengthens repolarization of cardiac ventricular myocytes by blocking the delayed rectifier potassium current.

Proarrhythmia has been observed with the antipsychotic agent thioridazine (THIO). The mechanisms underlying these effects are unknown. The objectives of this study were 1) to characterize the effects of THIO on cardiac repolarization and 2) to determine whether lengthening of the Q-T interval could be explained by blocking major K+-repolarizing currents. Isolated, buffer-perfused guinea pig hearts (n = 32) were stimulated at various pacing cycle lengths (150-250 ms) and exposed to THIO at concentrations ranging from 300 nM to 3 microM. THIO increased monophasic action potential duration at 90% repolarization (MAPD90) in a concentration-dependent manner from 14.9 +/- 1.8 at 300 nM to 37.1 +/- 3.2 ms at 3 microM. Increase in MAPD90 was also reverse frequency-dependent; THIO (300 nM) increased MAPD90 by 14.9 +/- 1.8 ms at a pacing cycle length of 250 ms, but by only 7.7 +/- 1.2 ms at a pacing cycle length of 150 ms. Patch-clamp experiments demonstrated that THIO decreases the time-dependent outward K+ current elicited by short depolarizations (250 ms; IK250) in a concentration-dependent manner. Estimated IC50 for IK250, which mostly underlies IKr, was 1.25 microM. Time-dependent outward K+ current elicited in tsA201 cells expressing high levels of HERG protein was also decreased approximately 50% by 1.25 microM THIO. On the other hand, THIO was less potent (IC50 of 14 microM) to decrease time-dependent K+ current elicited by long pulses (5000 ms; IK5000). Under the latter conditions, IK5000 corresponds mainly to IKs. Thus, these results demonstrate block of K+ currents and lengthening of cardiac repolarization by THIO in a concentration-dependent manner. This may provide an explanation of Q-T prolongation observed in some patients treated with THIO.

Action Potentials↗
PubMed1998

Cold effect on oxygen uptake, perceived exertion, and spasticity in patients with multiple sclerosis.

OBJECTIVE: To determine the effect of a cold bath (24 degrees C) on oxygen consumption and perceived exertion during ambulation and on spasticity in individuals with mild to moderate multiple sclerosis. DESIGN: A repeated-measures design with random assignment of experimental and control conditions. SETTING: Outpatient physical therapy department associated with an academic institution. PATIENTS: Fourteen individuals with clinically definite multiple sclerosis exhibiting spasticity and capable of ambulating at 0.7 m/sec on a motorized treadmill without handrail support. MEASUREMENT: Assessment of oxygen uptake, heart rate, and perceived exertion occurred during two 10-minute walks interspersed with a 30-minute rest on 2 separate days. Measurement of spasticity occurred three times during each session. RESULTS: Oxygen consumption and perceived exertion were unchanged. Spasticity was higher immediately (p < .05) after the cold bath. CONCLUSIONS: Increase in spasticity was statistically significant, but unlikely to be of any clinical importance. Contrary to our hypothesis, a cold bath (24 degrees C) for 20 minutes did not reduce oxygen consumption or rating of perceived exertion during ambulation.

Adult↗
PubMed1997

Lexical-semantic deficits in two patients with dominant thalamic infarction.

Two patients with dominant thalamic infarction, one in the tuberothalamic artery territory, the other in the paramedian artery territory, demonstrated language impairment limited to word retrieval difficulties in spontaneous language and structured naming tasks. Using a cognitive neuropsychological model of lexical processing developed in the study of patients with cortical lesions. We carried out a detailed investigation of their lexical abilities. Both patients demonstrated impairment restricted to oral and written picture naming and oral naming to definition and spared performance on tasks of lexical comprehension, oral word reading, and writing to dictation, as well as syntactic comprehension and production. Naming impairment disproportionately affected lower frequency words, and word substitutions often corresponded to objects that were semantically-related to target words. We propose that our patients' word retrieval impairments reflect a failure of thalamic input to effectively engage the cortical networks subserving lexical semantic processing, leading to degraded levels of activation as the semantic system interfaces with subsequent stages of lexical processing.

Aphasia↗
PubMed1997

Relationships between torque, velocity and power output during plantarflexion in healthy subjects.

This study investigated the relationships existing between torque, velocity and power output during plantarflexion. Using a Biodex dynamometric system, 15 healthy subjects performed three maximal dynamic tests, ranging from -12 degrees (-0.209 rad) of dorsiflexion to +47 degrees (+0.818 rad) of plantarflexion and one static test (test 4) at an angle of +10 degrees (+0.174 rad). The dynamic assessment included a 30 degrees s-1 (0.52 rad s-1) concentric isokinetic test (test 1) preceded by a 2-sec maximal pre-loading contraction. The other two dynamic tests were performed using the isotonic mode of testing with a selected torque of 27 N m; one of these tests was executed with pre-loading (test 2) while the other was performed without pre-loading (test 3). The results indicated that the dynamic peak torque, the peak power and the peak velocity were obtained in test 1, test 2 and test 3, respectively. These peak values, as well as the values of torque (test 1 and test 4), power (test 2) and velocity (test 3) obtained at a constant angle +10 degrees (+0.174 rad), were selected for the correlation analyses. The results showed that the torque, velocity and power output during plantarflexion were linearly related to one another with significant correlations (0.71 < r < 0.92; p < 0.01). This finding suggests that a common factor of muscular performance is assessed. Furthermore, these results indicated that the maximal torque produced by a subject can be predictive of his or her maximal velocity and power. Consequently, a stronger subject can generate higher velocity and power than a weaker subject when tested with the same load during maximal effort.

Adult↗
PubMed1997

Dynamometric assessment of the plantarflexors in hemiparetic subjects: relations between muscular, gait and clinical parameters.

The aims of this study were to investigate, in 16 subjects with hemiparesis, the plantarflexor muscle performance of the paretic side and to determine the level of the relationships between muscular parameters, clinical measures and gait performance. A Biodex dynamometric system was used to evaluate static and dynamic torques, power and maximal rate of tension development of the plantarflexor muscles. The clinical measures included the Fugl-Meyer assessment (FMA), the "Up & Go" test and an evaluation of ankle muscle tone. Velocity, cadence, stride length and gait cycle duration were determined for each subject at both comfortable and maximal safe speeds using foot contacts and videographic data. Results indicated that dynamometric values produced by the hemiparetic subjects were reduced in comparison to those reported for healthy subjects. Their torque-angle curves had a curvilinear shape which indicated pronounced decrease of torque for plantarflexion efforts at the beginning of the movement. Torques produced at different velocities of testing did not demonstrate significant differences (MANOVAs: p > 0.05) but power values were significantly different. Results also showed that all the selected muscular parameters (torque, power and maximal rate of tension development) were moderately to highly interrelated (0.65 < r < 0.94; p < 0.01) suggesting that a common factor of muscular performance was assessed. Furthermore, the dynamometric data were significantly associated with some of the clinical measures (sensation and lower limb motor control scores of the FMA) but were not related to the gait variables (Pearson's r < 0.45; p > 0.05). This last finding suggests that the relationship between plantarflexor strength and the level of gait performance in adults with stroke is complex. The relationship may be influenced by other factors such as muscular compensations within and between limbs and motor control impairments.

Adolescent↗
PubMed1996

Preloading and range of motion effect on plantarflexor muscle performance.

OBJECTIVE: To determine the effects of maximal preloading and range of motion (ROM) on the mechanical parameters of the plantarflexor muscles obtained while using the isotonic mode of testing of a Biodex dynamometer. DESIGN: A convenience sample of healthy subjects in the context of a descriptive comparative study. SETTING: Research laboratory in Canada. SUBJECTS: Fifteen volunteered subjects without history of injury or disorder to the right lower extremity. MEASUREMENTS: Four maximal isotonic tests were performed against a selected load of 27Nm. For the first two tests, the movement at the ankle ranged from -12 degrees (dorsiflexion) to +32 degrees (plantarflexion); one of these tests was preceded by a 2-second maximal preloading contraction, while the other was performed without preloading. For the other two tests, the ROM at the ankle was increased by 15 degrees of plantarflexion and thus ranged from -12 degrees to +47 degrees; again one of these tests was executed with preloading and the other without preloading. RESULTS: The four tests showed differences in the mechanical parameters (MANOVA p < .05). At angles of -10 degrees and +5 degrees, subjects produced higher torque and power but lower velocity values for the two tests preceded by a maximal preloading. The effect of ROM was demonstrated at +20 degrees where tests performed in a small amplitude reached a lower velocity than the corresponding tests performed in a larger amplitude. Based on the velocity profiles, the results also revealed that maximal preloading changed the selected isotonic movement of the Biodex dynamometer to an isoaccelerative movement characterized by high torque and power production. CONCLUSIONS: Isotonic assessment using the Biodex dynamometer provides different values of torque, velocity, and power depending on the testing conditions used. In clinical settings, it would be important to control these testing conditions.

Analysis of Variance↗
PubMed1996

A mechanical model to study the relationship between gait speed and muscular strength.

This study proposes a mechanical model to investigate the relationship between gait speed and strength of the ankle plantarflexor muscles. The model calculates the muscular utilization ratio (MUR) of the plantarflexor muscles during gait by comparing the plantarflexion moment used while walking to the maximal moment of the plantarflexors estimated from dynamometric measurements. To verify the model, MURs of the plantarflexor muscles were calculated for five healthy subjects and one hemiparetic subject walking at different speeds (slow, self-selected, and fast). Generally, the results of the healthy subjects revealed that MURs increase with an increasing gait speed: average (+/-SD) peak values of MUR reached 58.8% (+/-18.5), 65.6% (+/-17.2) and 71.0% (+/-17.8) for the slow, self-selected, and fast speeds, respectively. The average peak value of MURs at the self-selected speed corresponds to values reported in electromyographic studies of the plantarflexor muscles. At self-selected gait speed, the hemiparetic subject presented a higher peak MUR (80.5%) of the plantarflexors and a lower gait velocity when compared to healthy subjects. For the hemiparetic subject, peak values of MUR of the plantarflexor muscles at maximal walking speed reached 100% suggesting that full activation of the plantarflexors had been reached preventing him from walking faster. From these preliminary results, it appears that MURs calculated by the proposed model are sensitive to the mechanical demands imposed on a group of muscles during a task (eg., increase in gait speed) and to change in the maximal plantarflexor's strength (eg., weakness). The proposed model seems to have the potential to demonstrate whether muscle weakness limits maximal gait speed in hemiparetic subjects. However, considering the complexity of gait speed regulation in hemiparetic patients, the model should be tested on a large number of hemiparetic subjects.

Adolescent↗