A trilogy of the oculomotor system Part II - active, passive, and dissipative forces Part III - diagnostic tests.

Achilles tendon lengthening (ATL) is frequently used in the treatment of foot deformities. However, there is currently no objective method to determine the optimal muscle length during surgery. We developed an intraoperative approach to evaluate the passive and active forces of the triceps surae muscle group before and after ATL and aimed to test the following hypotheses: 1) the ankle passive range of motion (ROM) increases, 2) passive muscle forces decrease post-ATL, and 3) forces measured from patients with non-neurological and neurological conditions demonstrate different characteristics. Passive forces at various ankle joint positions were measured in ten patients (11.3 ± 3.0 years old) pre- and post-ATL using a force transducer attached to the Achilles tendon. In six patients, active isometric forces were measured by stimulating the triceps surae supramaximally. Passive forces decreased by 94.3% (p < 0.0001), and ROM increased by 89.4% (p < 0.0001) post-ATL. The pre-ATL passive forces were 70.8% ± 15.1% lower in patients with idiopathic foot deformities than in patients with neurological conditions (p < 0.001). The peak active force of 209.8 ± 114.3 N was achieved at an ankle angle of 38.3° ± 16.0°, where the passive force was 6.3 ± 6.7 N. The inter-individual variability was substantial in both groups. In conclusion, the hypotheses posed were supported. The present findings suggest that muscle passive and active force production as well as the inter-individual variability should be considered when planning further treatment.

Strips of pig bladder have been maximally stimulatedin vitro at 37°C via electrodes placed in the muscle, in order, particularly, to measure the dependence of the resulting active force on the velocity of shortening and on length changes. The active isometric force and the passive viscoelastic force are approximately, but not precisely, additive. The active isometric force, like the steady (equilibrium) passive force, is a function of the extension of the strip above its rest length, which is increased after subjection to a high passive force. The steady passive force increases quasiexponentially with this extension, of which it is therefore a measure. The active isometric force Fiso increases approximately linearly with the extension until it approaches a maximum in the region where it and the steady passive force are comparable in size. The maximum is partly obscured by rest-length changes. The dependence of the active force F on the speed of shortening of the strip has been measured in a new way, with a correction for passive viscoelastic effects. For a given strip the ratio F/Fiso is, approximately, a function of the contraction velocity only. The function is similar to that of the classical Hill equation but not identical, possibly for geometrical reasons. The results imply that a velocity parameter v*, analogous to Hill’s parameter b, is approximately constant for each strip, independent of changes of length and rest length.

Failure of stimulated skeletal muscle mainly contributed by passive force: an in vivo rabbit model

SummaryBackgroundLimb movements are generally driven by active muscular contractions working with and against passive forces arising in muscles and other structures. In relatively heavy limbs, the effects of gravity and inertia predominate, whereas in lighter limbs, passive forces intrinsic to the limb are of greater consequence. The roles of passive forces generated by muscles and tendons are well understood, but there has been little recognition that forces originating within joints themselves may also be important, and less still that these joint forces may be adapted through evolution to complement active muscle forces acting at the same joint.ResultsWe examined the roles of passive joint forces in insect legs with different arrangements of antagonist muscles. We first show that passive forces modify actively generated movements of a joint across its working range, and that they can be sufficiently strong to generate completely passive movements that are faster than active movements observed in natural behaviors. We further demonstrate that some of these forces originate within the joint itself. In legs of different species adapted to different uses (walking, jumping), these passive joint forces complement the balance of strength of the antagonist muscles acting on the joint. We show that passive joint forces are stronger where they assist the weaker of two antagonist muscles.ConclusionsIn limbs where the dictates of a key behavior produce asymmetry in muscle forces, passive joint forces can be coadapted to provide the balance needed for the effective generation of other behaviors.

The reduction of the pelvic floor muscles (PFM) strength is a major cause of stress urinary incontinence (SUI). To compare active and passive forces, and vaginal cavity aperture in continent and stress urinary incontinent women. The study included a total of thirty-two women, sixteen continent women (group 1--G1) and sixteen women with SUI (group 2--G2). To evaluate PFM passive and active forces in anteroposterior (sagittal plane) and left-right directions (frontal plane) a stainless steel specular dynamometer was used. The anteroposterior active strength for the continent women (mean±standard deviation) (0.3±0.2 N) was greater compared to the values found in the evaluation of incontinent women (0.1±0.1 N). The left-right active strength (G1=0.43±0.1 N; G2=0.40±0.1 N), the passive force (G1=1.1±0.2 N; G2=1.1±0.3 N) and the vaginal cavity aperture (G1=21±3 mm; G2=24±4 mm) did not differ between groups 1 and 2. The function evaluation of PFM showed that women with SUI had a lower anteroposterior active strength compared to continent women.

Force distribution and multi-scale mechanics in smooth muscle tissues

EMG-force relations of a single skeletal muscle acting across a joint: Dependence on joint angle

Movement of a limb is shaped by active forces generated by muscle contraction but also by passive forces within individual muscles and joints. In small animals such as insects, the contribution of passive forces to limb movement can match the active forces. However, most measurements of passive forces are limited to the femur-tibia joint in large insects. Here we take advantage of genetic tools in Drosophila to measure passive torques at multiple joints in the fly’s leg. We genetically inactivate all the motor neurons to assess passive forces. We find that the passive torques are well approximated by a linear spring, i.e., the passive torques linearly increase with angular deviation from the rest angle. The torques are much larger than the gravitational torque due to the leg itself. We estimate that the passive torques are seventy times smaller than necessary to support the weight of the animal. We also inactivated all the motor neurons in a freely standing fly and found that, as predicted from the model, the fly falls when the motor neurons are inactivated. We found that the height at which a fly stands, and, therefore the active forces vary. The fly’s height affects the time to initiate a fall. The time it takes for the fall is consistent with the active forces decaying with a time constant of ∼100 ms. Thus, although passive forces are strong and will have a large effect on limb kinematics, they are not strong enough to support the weight of the fly.

Movement of a limb is shaped by active forces generated by muscle contraction but also by passive forces within individual muscles and joints. In small animals such as insects, the contribution of passive forces to limb movement can match the active forces. However, most measurements of passive forces are limited to the femur-tibia joint in large insects. Here we take advantage of genetic tools in Drosophila to measure passive torques at multiple joints in the fly's leg. We genetically inactivate all the motor neurons to assess passive forces. We find that the passive torques are well approximated by a linear spring, i.e., the passive torques linearly increase with angular deviation from the rest angle. The torques are much larger than the gravitational torque due to the leg itself. We estimate that the passive torques are seventy times smaller than necessary to support the weight of the animal. We also inactivated all the motor neurons in a freely standing fly and found that, as predicted from the model, the fly falls when the motor neurons are inactivated. We found that the height at which a fly stands, and, therefore the active forces vary. The fly's height affects the time to initiate a fall. The time it takes for the fall is consistent with the active forces decaying with a time constant of ~100 ms. Thus, although passive forces are strong and will have a large effect on limb kinematics, they are not strong enough to support the weight of the fly.

Effects of acute experimental esophagitis on mechanical properties of the lower esophageal sphincter

Next article FreeMechanics of Formation of Arcuate MountainsWilliam H. HobbsWilliam H. Hobbs Search for more articles by this author PDFPDF PLUS Add to favoritesDownload CitationTrack CitationsPermissionsReprints Share onFacebookTwitterLinkedInRedditEmail SectionsMoreDetailsFiguresReferencesCited by The Journal of Geology Volume 22, Number 3Apr. - May, 1914 Article DOIhttps://doi.org/10.1086/622144 Views: 50Total views on this site Citations: 3Citations are reported from Crossref PDF download Crossref reports the following articles citing this article:Fabien Graveleau, Jacques Malavieille, Stéphane Dominguez Experimental modelling of orogenic wedges: A review, Tectonophysics 538-540 (May 2012): 1–66.https://doi.org/10.1016/j.tecto.2012.01.027A.J. Bull Note on the Origin of Island Arcs, Proceedings of the Geologists' Association 55, no.44 (Jan 1944): 222–226.https://doi.org/10.1016/S0016-7878(44)80003-7Sergei Obrutschew Der Bau von Nordost-Asien nach neueren Forschungen, Geologische Rundschau 25, no.66 (Dec 1934): 388–422.https://doi.org/10.1007/BF01837372

Purpose: Recent studies showed the involvement of Neuregulin (NRG)-1 in the preservation of left ventricular performance in pathophysiological conditions. Nevertheless, the role of NRG-1 in pulmonary arterial hypertension (PAH) and right ventricular (RV) failure is still unknown. Therefore, the goal of this study was to evaluate the effects of a NRG-1 chronic treatment on intrinsic myocardial properties, namely on the modulation of active and passive force of cardiomyocytes isolated from the RV of animals with PAH. Methods: Male Wistar rats (180-200g) randomly received monocrotaline (MCT, 60 mg/kg, sc) or vehicle. After 14 days, animals were randomly assigned to receive treatment with either NRG-1 (40 ug/kg/day, ip) or vehicle. The study resulted in 4 experimental groups: control (CTRL, n=16); CTRL+NRG (n=15); MCT (n=13); MCT+NRG (n=18). Twenty one to 24 days after MCT administration, samples were collected for functional studies. RV samples were mechanically disrupted and incubated in relaxing solution supplemented with Triton (0.2%). Single cardiomyocytes were subsequently attached with silicone adhesive between a force transducer and a piezoelectric motor and active and passive forces were measured. Only significant results (p<0.05) are given. Results: MCT-group isolated cardiomyocytes developed higher passive force when compared to CTRL-group cells at the sarcomere lengths of 2.0 (MCT vs. CTRL: 1.90±0.43 vs. 1.43±0.29N/m2), 2.2 (MCT vs. CTRL: 3.66±0.69 vs. 2.68±0.24N/m2), and 2.3μm (MCT vs. CTRL: 5.76±1.15 vs. 3.86±0.87N/m2). NRG-1 treatment restored passive force development to levels similar to the CTRL-group cardiomyocytes, at 2.0, 2.2, and 2.3μm (MCT+NRG: 1.28±0.25, 3.04±0.55, and 3.63±0.89N/m2, respectively). CTRL+NRG-group cardiomyocytes developed significantly less passive force when compared to CTRL-group cells (CTRL+NRG: 1.16±0.31, 2.27±0.38, and 3.05±0.54N/m2, at 2.0, 2.2, and 2.3μm respectively). In the MCT+NRG-group cardiomyocytes active force development was decreased when compared to MCT-group cells (MCT vs MCT+NRG: 14.14±5.94 vs 9.67±2.83N/m2). Conclusions: NRG-1 chronic treatment reverses the changes in both active and passive myocardial forces that occur in the presence of PAH. Interestingly, NRG-1 chronic treatment also decreases the passive force and thus myocardial stiffness of cardiomyocytes isolated from the right ventricle of healthy animals. These findings show that NRG-1 pathway regulates systolic and diastolic function at the cellular level, and suggest a potential therapeutic role of this pathway in PAH.

The purpose of this study was to choose between two popular models of skeletal muscle: one with the parallel elastic component in parallel with both the contractile element and the series elastic component (model A), and the other in which it is in parallel with only the contractile element (model B). Passive and total forces were obtained at a variety of muscle lengths for the medial gastrocnemius muscle in anesthetized rats. Passive force was measured before the contraction (passive A) or was estimated for the fascicle length at which peak total force occurred (passive B). Fascicle length was measured with sonomicrometry. Active force was calculated by subtracting passive (A or B) force from peak total force at each fascicle or muscle length. Optimal length, that fascicle length at which active force is maximized, was 13.1 +/- 1.2 mm when passive A was subtracted and 14.0 +/- 1.1 mm with passive B (P < 0.01). Furthermore, the relationship between double-pulse contraction force and length was broader when calculated with passive B than with passive A. When the muscle was held at a long length, passive force decreased due to stress relaxation. This was accompanied by no change in fascicle length at the peak of the contraction and only a small corresponding decrease in peak total force. There is no explanation for the apparent increase in active force that would be obtained when subtracting passive A from the peak total force. Therefore, to calculate active force, it is appropriate to subtract passive force measured at the fascicle length corresponding to the length at which peak total force occurs, rather than passive force measured at the length at which the contraction begins.

INTRODUCTIONThe force‐length relationship of various skeletal muscles indicates that passive force is generally much lower than active force [1]. However, a previous study showed that the whole frog tibialis anterior (TA) muscle has significantly higher passive than active forces within its normal range of motion (Figure 1) [2].It is known that titin, the giant protein within the sarcomere, is a main contributor to passive force in skeletal muscle at rest [3]. Furthermore, variations in titin isoforms have been related to different passive forces; the shorter the titin isoform, the higher the passive force [3, 4]. Therefore, the high passive force observed in frog TA muscle could result from the expression of a short titin isoform and thus a high titin‐based passive force.The purpose of this study was to investigate titin isoforms and titin‐based passive force in frog TA muscle. Titin‐based passive force was determined by testing passive force in single skinned muscle fibres in which titin is considered to be the major source of passive force [3].METHODSTitin isoforms: Titin isoforms in frog TA and rabbit psoas muscles were determined using agarose strengthened 2% acrylamide SDS‐PAGE gels.Skinned fibre experiment: Active and passive force‐length relationships were established by stretching skinned frog TA fibres (n=10) to various sarcomere lengths (2.4, 2.6, 2.8, 3.0, 3.2, 3.4 and 3.6 μm), and isometrically activating them after steady state force had been reached.RESULTSThe frog TA expresses two titin isoforms similar to those expressed by rabbit psoas muscle (3.3 and 3.40 MD).The active and passive force‐length relationships in TA skinned fibres indicate that passive force is significantly lower than active force on the descending limb of the force‐length relationship (Figure 2).DISCUSSION AND CONCLUSIONSFrog TA titin isoforms are not different from those of rabbit psoas, which are known to have relatively low passive [3, 4] compared to active force. Single skinned fibres isolated from frog TA muscle do not produce high passive compared to active forces. Therefore, it seems that titin is not responsible for the high passive force observed at the whole frog TA muscle level. It is likely that the high passive forces produced by the frog TA muscle originate from the extracellular matrix rather than structures within the fibres.The high passive forces found for the entire frog TA muscle might have implications for the function of the muscle during swimming. Since frogs have large webbed feet, a high passive force in the TA allows frogs to use their feet like human swimmers use passive fins to increase the speed and decrease the energy expenditure of swimming.Support or Funding InformationCIHR, NSERC, AIHS

Mechanical characteristics of the cat pylorus