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PubMed1975

A three-element model describes excised cat papillary muscle elasticity.

The three-element model for skeletal muscle has been widely applied to cardiac muscle. It consists of an active contractile element (CE) that represents the muscle's response to stimulation, in series with an elastic element (SE) and the CE and SE in parallel with another elastic element (PE). There have been problems in interpreting experimental data on muscle elasticity using this model. Data seem to indicate that SE force depends not only on instantaneous length, but also initial length; it is not only elastic. Recent experiments seem to indicate that the SE has time-varying properties; it is not passive. This paper formulates a three-element model in which phi(x) = alpha[e beta(x-x*)-1] governs the elastic elements, where phi = force, alpha, beta = spring constants, x = length, and x* = rest length, which avoids these problems. The SE and PE have the same properties. (Typical values: alpha approximately equals .045 g/mm2, beta approximately equals 5.9 mm-1 for cat papillary at 29 degrees C.). By accounting for the nonlinearity of the SE-PE interaction, this three-element model leads to predictions that agree with published data on excised papillary muscle's elastic properties.

Animals↗

PubMed1976

Series elasticity of urinary bladder smooth muscle.

Loops of rat bladder were stretched between pins in vitro, supported by a clamp that could be suddenly shortened by activation of a solenoid to achieve a quick release of tension. The series elasticity measured in this fashion was found to follow an exponential course and to be modified by the rate of release, indicating a minor viscous component. Tissue length decreased and series elastic stiffness appeared to increase with muscle contraction, but no alteration in series elasticity was evident when the data were related to the tension existing in the tissue at the moment of quick release. Inactivation of the contractile system by removing calcium ion with ethylene glycol-bis-(beta-aminoethylether)-N,N'-tetraacetate (EGTA) similarly did not alter series elasticity when it was related to the tension existing in the tissue. Series elasticity during the stress relaxation following a stretch, and during the contracting and relaxing phases of rhythmic contractions, was also determined by tissue tension. The conclusion drawn is that contractile cross bridges do not contribute to the series elasticity measured in bladder tissue.

Animals↗

PubMed1989

Influence of muscle activity on the elastance of the upper airway of rabbits.

This study sought to assess the effect of variations in upper airway muscle activity on upper airway pressure-volume properties. Upper airway elastance, closing pressure, and reserve volume were measured in the isolated upper airways of anesthetized rabbits under control conditions and after administration of gallamine (2 mg/kg iv) or after 10 min of spontaneous respiration of 7% CO2 in O2. Administration of gallamine to seven animals was associated with a fall in reserve volume from 0.94 +/- 0.24 to 0.69 +/- 0.17 (95% confidence interval) ml (P less than 0.01) and of closing pressure from -7.53 +/- 0.23 to -5.75 +/- 1.05 cmH2O (P less than 0.01), but airway elastance did not change significantly. Hypercapnia in seven animals was associated with a rise in elastance from 7.06 +/- 0.91 to 7.67 +/- 0.86 cmH2O/ml (P less than 0.001) and in reserve volume from 0.68 +/- 0.06 to 0.86 +/- 0.13 ml (P less than 0.05). Closing pressure also changed from -5.88 +/- 0.94 to -7.92 +/- 1.85 cmH2O. This change was correlated with the change in reserve volume but not with the change in elastance. In three animals exposed to hypercapnia, return to room air breathing was associated with return of elastance, reserve volume, and closing pressure to control levels. It is concluded that muscle activity in the upper airway affects both the size and elastance of the airway, but the dominant mechanism by which upper airway muscles increase the resistance of the upper airway to collapse is by increasing airway volume.

Airway Resistance↗

PubMed1996

Alterations in structure of elastic laminae of rat pulmonary arteries in hypoxic hypertension.

The effect of hypoxic hypertension on the remodeling process of the elastic laminae of the rat hilar pulmonary arteries (PAs) was studied by electron microscopy. Rats were exposed to hypoxia (10% O2) for periods of 0.5, 2,6,12,48,96,144, and 240 h. Changes in the structure of the PA elastic laminae were examined and analyzed with respect to changes in the PA wall tensile stress. The PA blood pressure increased rapidly within the first several hours of hypoxia and reached a stable level within 2 days, whereas the PA wall tensile stress increased initially due to elevated blood pressure and then decreased after 48 h due to vessel wall thickening and returned to the control level after 4 days. In association with these changes, the elastic laminae, which appeared homogeneous in normal control rats, changed into structures composed of randomly oriented filaments and edematous contents with an increase in the volume during the early period of hypoxia and regained their homogeneous appearance and normal volume after 4 days. The changes in the elastic laminae were correlated with changes in the tensile stress. These changes were associated with a transient decrease in the stiffness of the PAs. In hypoxic rats given nifedipine, no change was found in the blood pressure, the tensile stress, or the structure of the elastic laminae of the PAs despite continuous exposure to hypoxia. These results suggested that altered tensile stress in the PA wall played a critical role in the initiation and regulation of structural changes in the elastic laminae and that these changes might contribute to alterations in the mechanical properties of the PA in hypoxic hypertension.

Animals↗

PubMedDate not supplied

Different effects of ageing on elastic and muscular arterial bifurcations in men.

In a previous study we have shown that the wall of the elastic carotid artery bifurcation (CAB) stiffens inhomogeneously with increasing age, the carotid artery bulb being most affected. In the present study the effect of ageing on the elastic properties of the wall and the strain the wall is exposed to along the muscular femoral artery bifurcation (FAB) was investigated using the CAB for comparison. The study was performed with 10 young (aged 20-30 years) and 10 old (50-60 years) presumed healthy volunteers. Distensibility along the bifurcation was determined by measuring noninvasively the maximum relative diameter changes of the artery during systole (peak delta d/d.100%), which is also a measure of strain, at various sites along both bifurcations by means of a vessel wall moving detector system. This system also makes the assessment of (end-diastolic) diameter possible. At all levels along the CAB, the diameter was significantly larger in the old than in the young. In the FAB, the diameter was only significantly larger in the old than in the young in the common and superficial femoral arteries. At all levels in the CAB, peak delta d/d.100% was significantly lower in the old than in the young, the carotid artery bulb being more affected than the common carotid artery (CCA), while in the FAB this parameter was lower in the old than in the young only in the common femoral artery (CFA). Peak delta d/d.100% was similar in the CCA and in the bulb in the young, but significantly higher in the CCA than at all levels in the bulb in the old. In the FAB, in the young peak delta d/d 100% was significantly higher in the CFA than at both levels in the deep and superficial femoral arteries, while in the old no significant differences in peak delta d/d.100% along the FAB could be detected. These findings indicate that the loss of wall elasticity with increasing age is different in the muscular and elastic arterial bifurcations investigated. The homogeneous distribution of wall elasticity in the elastic CAB at a younger age becomes inhomogeneous at an older age, while the opposite is observed in the muscular FAB. The changes in strain the different parts of the bifurcations are exposed to with increasing age are different in the CAB and the FAB. Differences in distensibility along bifurcations will make them deform inhomogeneously during the cardiac cycle.

Adult↗

PubMed1996

Age-related changes in elastic fibers of human heart.

The effects of age on the human heart elastic fibers were studied by light and electron microscopy. Studies were done on 15 hearts from male subjects 42 days to 87 years of age. Using specific staining procedures, the length of elastic fibers was determined by morphometry in the parenchyma of right and left ventricles. These studies suggest that the length of elastic fibers per unit heart volume is present early in life, possibly at birth, and thereafter remains constant until adulthood. Average fiber length increases significantly beyond the third decade of life which can be interpreted as a continuous formation of new fibers and a continuous apposition of elastic-type material to these fibers. Electron microscopy confirmed the presence of mature elastic fibers at birth, since they contained amorphous substance (elastin) surrounded by numerous microfibrils. In the adult hearts, the amount of amorphous substance has increased and the number of microfibrils has decreased. With advancing age the amorphous substance forms areas of rarefaction and the microfibrils have disappeared. Whether or not such morphometric modifications could influence the elastic properties of the ventricular myocardium requires further study.

Adult↗

PubMed1988

Human right ventricular end-systolic pressure-volume relation defined by maximal elastance.

This study was undertaken to determine 1) whether a combined radionuclide-hemodynamic technique could define the right ventricular end-systolic pressure-volume relation (RV ESPVR) in the clinical setting, 2) whether the human RV ESPVR defined by maximal elastance is linear and responsive to inotropic interventions, and 3) whether more easily measured modifications of the ESPVR are reliable substitutes as an index of RV function. Eight patients with normal RV function were studied with simultaneous micromanometer RV pressure measurements and radionuclide ventriculography to construct RV pressure-volume loops. Data were collected at baseline and after at least two alterations in loading conditions with nitroglycerin, phenylephrine, or saline. End systole was defined by maximal elastance (E(t) = P(t)/[V(t) - V0]). Data were also obtained during administration of dobutamine in four patients and after atrial pacing tachycardia in one patient. The RV ESPVR defined by maximal elastance was highly linear (r = 0.988-0.999) throughout the range of pressures and volumes tested. Furthermore, the linear correlations were significantly higher (p less than 0.005), and the linear regression standard error of the estimate (SEE) was significantly lower (p less than 0.005) for the RV ESPVR defined by maximal elastance compared with modifications of the ESPVR with the ratio of pulmonary artery-dicrotic notch pressure or RV peak pressure to end-ejection volume. Dobutamine or atrial pacing tachycardia produced a leftward shift of the entire RV pressure-volume loop, and in each patient (five of five), the point of maximal elastance fell outside the 95% confidence interval defined by the baseline ESPVR. However, because of the larger SEE, the leftward shift with modifications of the ESPVR was not statistically significant in any patient by the pulmonary artery-dicrotic notch pressure: end-ejection volume ratio and was significant in only one of five patients by the RV peak pressure: end-ejection volume ratio (p less than 0.03). Therefore, it appears that the steady-state RV ESPVR defined by maximal elastance in patients with normal RV function is responsive to alterations in inotropic state and is more sensitive to alterations in RV function than the frequently used, more easily measured modifications of the RV ESPVR.

Blood Pressure↗

PubMed1980

The elastic modulus of canine aortic valve leaflets in vivo and in vitro.

Aortic valve leaflets undergo extraordinary flexion due to the complete reversal of their curvature during billions of cardiac cycles. The flexion stresses in the leaflet depend on its elastic modulus which we investigated in vivo and in vitro. In six dogs, we placed radiopaque markers on an aortic leaflet. Leaflet length was calculated from the marker positions recorded fluoroscopically. Aortic and ventricular pressures were recorded. Dogs were killed and leaflet stress-strain curves determined in vitro. Leaflet length in vivo decreased 10.4 +/- 4.7% from diastole to systole in each cardiac cycle. Using the law of LaPlace, pressure gradients across the leaflets were converted into the stresses in the leaflets. The leaflets had an initial "elastic phase" of low modulus in systole followed by an "inelastic phase" of high modulus in diastole. The elastic modulus was 2.4 +/- 0.7 x 10(6) dynes/cm2 in systole and 5.2 +/- 1.7 x 10(7) dynes/cm2 in diastole. These results were similar to those obtained in vitro. Since flexion rigidity is proportional to (elastic modulus) x (thickness)3, the lower modulus in systole greatly reduces flexion stresses in the leaflet and increases leaflet longevity. The higher elastic modulus in diastole prevents excessive bulging or prolapse of the leaflet while it is subjected to the diastolic pressure gradient. We conclude that a natural or prosthetic leaflet which is thickened or has a high elastic modulus throughout the cardiac cycle will have a greater flexion stress that could cause early failure.

Animals↗

PubMed1993

Assessment of smooth muscle contribution to descending thoracic aortic elastic mechanics in conscious dogs.

Early investigators found contradictory evidence that vascular smooth muscle activation reduces the elastic modulus of the arterial wall under isotonic conditions but increases it under isometric conditions, concomitant with increased pulse-wave velocity. We examined the individual contributions of aortic constituents to the elastic modulus of the aortic wall to determine if isobaric analysis produces an accurate assessment of vascular smooth muscle activation. We used a modified Maxwell model assuming an incremental elastic modulus (Einc) composed of the elastic modulus of elastin fibers (EE), the elastic modulus of collagen fibers (EC) affected by the fraction of collagen fibers (fC) recruited to support wall stress, and the elastic modulus of the vascular smooth muscle (ESM) according to the following formula: Einc = EE+EC x fC+ESM.Einc was assessed in eight conscious dogs using descending thoracic aortic pressure (microtransducer) and diameter (sonomicrometry) measurements. Stress-strain relations in the control state and during activation of smooth muscle by continuous administration of phenylephrine (5 micrograms.kg-1 x min-1) were obtained by transient occlusions of the descending aorta and inferior vena cava. Results were as follows: EE was 4.99 +/- 1.58 x 10(6) dynes/cm2 (mean +/- SD), and EC was 965.8 +/- 399.8 x 10(6) dynes/cm2, assessed during the control state. Phenylephrine administration increased the theoretical pulse-wave velocity (Moens-Korteweg equation) from 5.25 +/- 1.03 m/s during the control state to 7.57 +/- 2.53 m/s (P < .005). Active muscle exhibited a unimodal stress-strain curve with a maximum stress of 0.949 +/- 0.57 x 10(6) dynes/cm2 at a corresponding strain value of 1.299 +/- 0.083. The maximum value observed corresponded, on the pressure-diameter curve of the active artery, to a pressure of 234.28 +/- 46.6 mm Hg and a diameter of 17.94 +/- 1.6 mm. The maximum ESM derived from the stress-strain relation of the active muscle was 8.345 +/- 7.56 x 10(6) dynes/cm2 at a strain value of 1.283 +/- 0.079. This point was located at 208.01 +/- 40.8 mm Hg and 17.73 +/- 1.41 mm on the active pressure-diameter curve. During activation of vascular smooth muscle, Einc decreased (P < .05) when plotted against internal pressure but increased (P < .05) when plotted against strain, over the operative range.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1995

Arterial wall mechanics in conscious dogs. Assessment of viscous, inertial, and elastic moduli to characterize aortic wall behavior.

To evaluate arterial physiopathology, complete arterial wall mechanical characterization is necessary. This study presents a model for determining the elastic response of elastin (sigma E, where sigma is stress), collagen (sigma C), and smooth muscle (sigma SM) fibers and viscous (sigma eta) and inertial (sigma M) aortic wall behaviors. Our work assumes that the total stress developed by the wall to resist stretching is governed by the elastic modulus of elastin fibers (EE), the elastic modulus of collagen (EC) affected by the fraction of collagen fibers (fC) recruited to support wall stress, and the elastic modulus of the maximally contracted vascular smooth muscle (ESM) affected by an activation function (fA). We constructed the constitutive equation of the aortic wall on the basis of three different hookean materials and two nonlinear functions, fA and fC: sigma = sigma E + sigma C + sigma SM + sigma eta + sigma M = EE. (epsilon - epsilon 0E) + EC.fC.epsilon + ESM.fA.epsilon + eta. [equation: see text] + M.[equation: see text] where epsilon is strain and epsilon 0E is strain at zero stress. Stress-strain relations in the control state and during activation of smooth muscle (phenylephrine, 5 micrograms.kg-1.min-1 IV) were obtained by transient occlusions of the descending aorta and the inferior vena cava in 15 conscious dogs by using descending thoracic aortic pressure (microtransducer) and diameter (sonomicrometry) measurements. The fC was not linear with strain, and at the onset of significant collagen participation in the elastic response (break point of the stress-strain relation), 6.02 +/- 2.6% collagen fibers were recruited at 23% of stretching of the unstressed diameter. The fA exhibited a skewed unimodal curve with a maximum level of activation at 28.3 +/- 7.9% of stretching. The aortic wall dynamic behavior was modified by activation increasing viscous (eta) and inertial (M) moduli from the control to active state (viscous, 3.8 +/- 1.3 x 10(4) to 7.8 +/- 1.1 x 10(4) dyne.s.cm-2, P < .0005; inertial, 61 +/- 42 to 91 +/- 23 dyne.s2.cm-2, P < .05). Finally, the purely elastic stress-strain relation was assessed by subtracting the viscous and inertial behaviors.

Animals↗

PubMed1992

Risk factors for the degradation of lung elastic fibers in the ventilated neonate. Implications for impaired lung development in bronchopulmonary dysplasia.

In order to evaluate the risk for proteolytic destruction of lung parenchymal elastic fibers in ventilated premature infants, the concentrations of elastase were determined in tracheal aspirates of 65 infants from whom we obtained a total of 327 sequential samples. Elastase was detected at least once in 39 of the 65 infants studied. Eleven of these infants were ventilated with greater than 60% oxygen for greater than 5 days. In 19 infants, the presence of elastase was associated with positive bacterial and/or viral cultures and/or elevated ratios (greater than 0.22) of immature neutrophils to total neutrophils. Elastase was not detected in the lung secretions of 26 infants ventilated with greater than 60% oxygen for less than 3 days, suggesting minimal risk for elastic fiber destruction in the intubated infant who neither has pneumonia nor requires prolonged hyperoxic ventilation. The risk for elastic fiber destruction was further evaluated by analyzing sequential urine and tracheal aspirate samples for the presence of an elastolytic degradation product of elastin (desmosine). The biochemical data indicated a potential risk for proteolytic destruction of elastic fibers in association with infection and/or prolonged hyperoxic exposure. In addition, autopsy specimens obtained from three of the infants revealed structurally abnormal lung parenchymal elastic fibers. Because elastic fibers are believed to provide the structural support for alveolar septal development, proteolytic degradation of these fibers may be a significant factor in the impaired lung development that occurs in infants with bronchopulmonary dysplasia.

Bronchopulmonary Dysplasia↗

PubMed1997

Repair of elastase-digested elastic fibers in acellular matrices by replating with neonatal rat-lung lipid interstitial fibroblasts or other elastogenic cell types.

Disruption of elastic fibers is a major factor in the pathogenesis of pulmonary emphysema. Elastic fibers in culture, injured by exposure to elastase, undergo repair in the presence of elastogenic cells that restores the fibers toward normal as determined by biochemical and ultrastructural methods. The repair appears to be the result of both salvage and de novo repair mechanisms. The evidence for salvage repair is that hot-alkali resistance, lost as a result of elastase treatment, is restored to previously radiolabeled elastic fibers. This repair mechanism has been shown in aortic smooth muscle cell cultures. In order to determine the potential relevance of this mechanism for elastic fiber repair in the lungs, experiments were carried out using neonatal rat lung lipid interstitial fibroblasts (LIF). Treatment of the LIF cultures with elastase, in the absence of serum, caused solubilization of 12% of elastin; however, 81% of the elastin protein and 80% of the elastin-associated radioactivity (EAR) were solubilized by subsequent hot-alkali treatment, indicating that most of the elastin was retained in the matrix but was damaged. Ultrastructurally, the elastic fibers were frayed. After 6 additional wk in culture, hot-alkali resistant elastin protein and EAR were restored to 88 and 62% of control values, respectively, and the ultrastructural appearance of elastic fibers was restored to normal. We calculate that about 42% of the restored elastin represented salvage repair; the remainder was new elastin. No repair occurred in matrices rendered acellular by azide treatment; however, when acellular matrices were replated with LIF, repair was complete at 6 wk. No repair was seen when acellular matrices were replated with a transformed mouse macrophage cell line. We conclude that lung LIF are capable of mounting a robust repair process after elastolytic injury of elastin and that the repair is the result of both salvage and de novo repair mechanisms.

3T3 Cells↗

PubMedDate not supplied

Elastic buckling of multiwall carbon nanotubes under high pressure.

This paper studies elastic buckling of individual multiwall carbon nanotubes under radial pressure. The analysis is based on a multiple-elastic-shell model in which each of the concentric tubes of a multiwall carbon nanotube is described as an individual elastic shell. According to their radius-to-thickness ratios, the multiwall carbon nanotubes discussed here are classified into three types: thin, thick, and (almost) solid. The critical pressure for elastic buckling is calculated for examples of all three types. It is found that a thin N-wall nanotube (defined by a radius-to-thickness ratio larger than 4) is approximately equivalent to a single-layer elastic shell whose effective bending stiffness and thickness are N times the effective bending stiffness and thickness of single-wall carbon nanotubes. Based on this result, an approximate method is suggested for replacing the problematic multiwall nanotube of many layers with a multilayer elastic shell of fewer layers. In particular, the critical pressure predicted by the present model is in good agreement with known experimental results.

Compressive Strength↗

PubMed2001

Arterial elastance and wave reflection augmentation of systolic blood pressure: deleterious effects and implications for therapy.

Systolic and pulse blood pressures are stronger predictors of stroke, coronary heart disease, myocardial infarction, heart failure, end-stage renal disease, and cardiovascular mortality than diastolic pressure. Furthermore, diastolic pressure is inversely related to coronary heart disease and cardiovascular mortality. Increased elastance (or stiffness, inverse of compliance) of the central elastic arteries is the primary cause of increased systolic and pulse pressure with advancing age and in patients with cardiovascular disease, including hypertension, and is due to degeneration and hyperplasia of the arterial wall; diastolic pressure decreases as arterial elastance increases. As elastance increases, transmission velocity of both forward and backward (or reflected) traveling waves increases, which causes the reflected wave to arrive earlier in the central aorta and augments pressure in late systole. These changes in arterial wall properties cause an increase in left ventricular afterload and myocardial oxygen consumption and a decrease in myocardial perfusion pressure, which may induce an imbalance in the supply-demand ratio, especially in hypertrophied hearts with coronary artery disease. Also, an increase in systolic pressure increases arterial wall circumferential stress, which promotes fatigue and development of atherosclerosis. Vasodilator drugs have little direct active effect on large elastic arteries but can markedly reduce wave reflection amplitude and augmentation index by decreasing elastance of the muscular arteries and reducing pulse wave velocity of the reflected wave from the periphery to the heart. This decrease in intensity (or amplitude) and increase in travel time (or delay) of the reflected wave causes a generalized decrease in systolic pressure and arterial wall stress and an increase in ascending aortic flow during the deceleration phase. The decrease in systolic pressure brought about by this mechanism is grossly underestimated when systolic pressure is measured in the brachial artery.

Adult↗

PubMed1993

The effects of hypoxic acidemia on left ventricular end-systolic elastance in fetal sheep.

Using the conductance catheter technique, we measured the effects of hypoxic acidemia on left ventricular end-systolic elastance in anesthetized, 133-d gestation, in utero fetal sheep (n = 7). Conductance and Millar catheters were introduced into the left ventricle through a carotid artery cutdown. Fetuses were rendered progressively hypoxic and acidemic by placental embolization with repeated injections of 5 x 10(5) 50-microns plastic spheres every 15 min via a catheter placed in the fetal abdominal aorta. We recorded pressure-volume data and arterial blood gases at 15-min intervals. End-systolic elastance was computed using a single-beat method of extrapolating maximum isovolumic pressure. A mean of five boluses was required to cause fetal death. Placental embolization caused progressive fetal acidemia. Mean baseline fetal arterial pH was 7.32 +/- 0.06 (mean +/- SD) and gradually decreased with embolization (p < 0.0001). A linear relationship was found to exist between elastance and pH with a mean decrease of 0.46 kPa/mL per 0.1-unit drop in pH (r = 0.96; p < 0.0001). Despite the decrease in end-systolic elastance, stroke volume and left-ventricular output were maintained due to a parallel decrease in afterload. The decrease in end-systolic elastance was gradual and extended over the entire clinically important range of pH, rather than being a terminal event. This study, which, to our knowledge, is the first to use the conductance catheter to measure fetal left ventricular function demonstrates that hypoxic acidemia adversely affects myocardial contractility assessed by end-systolic elastance.

Acidosis↗

PubMed1996

Elastic and length-force characteristics of the gastrocnemius of the hopping mouse (Notomys alexis) and the rat (Rattus norvegicus).

The aim of this study was to compare the contractile and series elastic properties of terrestrial mammals that use bipedal versus quadrupedal gaits. The gastrocnemius muscle of the hopping mouse (body mass 30.2 +/- 2.4 g, mean +/- S.D.) and the rat (313 +/- 10.7 g) were compared with data from the literature for the wallaby and the kangaroo rat to distinguish scaling effects and locomotion-related effects on muscle properties. Contractile length-force properties and series elastic stiffness were measured in situ during maximal tetanic contractions. The rat had a larger muscle-fibre-to-tendon-length ratio. The rat and hopping mouse showed similar normalised length-force characteristics of the gastrocnemius. Normalised stiffness in the hopping mouse was higher. The hopping mouse showed a higher capacity to store elastic energy per unit of contractile work capacity, as well as per unit of body mass. Accounting for body size differences, the rat had a smaller relative muscle mass and thus smaller work capacity than the three hopping animals considered. This is an agreement with a quadrupedal versus bipedal locomotion style. The differences in contractile and elastic properties of the gastrocnemius of the rat and hopping mouse seem to be closely related to locomotion patterns. Small animals seem to be able to utilise the storage and release of elastic energy to a far lesser extent than larger animals. However, even in animals as small as hopping mice, the storage and utilisation of elastic energy during locomotion is of functional significance and probably depends on locomotor behaviour.

Animals↗

PubMed1996

Mechanical efficiency and efficiency of storage and release of series elastic energy in skeletal muscle during stretch-shorten cycles.

The mechanical energy exchanges between components of a muscle-tendon complex, i.e. the contractile element (CE) and the series elastic element (SEE), and the environment during stretch-shorten cycles were examined. The efficiency of the storage and release of series elastic energy (SEE efficiency) and the overall mechanical efficiency of the rat gastrocnemius muscle (N = 5) were determined for a range of stretch-shorten contractions. SEE efficiency was defined as elastic energy released to the environment divided by external work done upon the muscle-tendon complex plus internal work exchange from the CE to the SEE. Mechanical efficiency is external work done by the muscle-tendon complex divided by the external work done upon the muscle-tendon complex plus work done by the CE. All stretch-shorten cycles were performed with a movement amplitude of 3mm (6.7% strain). Cycle frequency, duty factor and the onset of stimulation were altered for the different cycles. SEE efficiency varied from 0.02 to 0.85, mechanical efficiency from 0.43 t 0.92. SEE efficiency depended on the timing of stimulation and net muscle power in different ways. Mechanical efficiency was much more closely correlated with net power. The timing of muscle relaxation was crucial for the effective release of elastic energy. Simulated in vivo contractions indicated that during rat locomotion the gastrocnemius may have a role other than that of effectively storing elastic energy and generating work. Computer simulations showed that the amount of series elastic compliance can affect the internal energetics of a muscle contraction strongly without changing the muscle force generation dramatically.

Animals↗

PubMed1999

Direct measurement of inter-doublet elasticity in flagellar axonemes.

The outer doublet microtubules in ciliary and flagellar axonemes are presumed to be connected with each other by elastic links called the inter-doublet links or the nexin links, but it is not known whether there actually are such elastic links. In this study, to detect the elasticity of the putative inter-doublet links, shear force was applied to Chlamydomonas axonemes with a fine glass needle and the longitudinal elasticity was determined from the deflection of the needle. Wild-type axonemes underwent a high-frequency, nanometer-scale vibration in the presence of ATP. When longitudinal shear force was applied, the average position of the needle tip attached to the axoneme moved linearly with the force applied, yielding an estimate of spring constant of 2.0 (S.D.: 0.8) pN/nm for 1 microm of axoneme. This value did not change in the presence of vanadate, i.e., when dynein does not form strong cross bridges. In contrast, it was at least five times larger when ATP was absent, i.e., when dynein forms strong cross bridges. The measured elasticity did not significantly differ in various mutant axonemes lacking the central-pair microtubules, a subset of inner-arm dynein, outer-arm dynein, or the radial spokes, although it was somewhat smaller in the latter two mutants. It was also observed that the shear displacement in an axoneme in the presence of ATP often took place in a stepwise manner. This suggests that the inter-doublet links can reversibly detach from and reattach to the outer doublets in a cooperative manner. This study thus provides the first direct measure of the elasticity of inter-doublet links and also demonstrates its dynamic nature.

Animals↗