Increment Of Stiffness Research Articles

Effects of isometric training at different knee angles on the muscle–tendon complex in vivo

The purpose of this study was to investigate the influences of isometric training at different joint angles on the muscle size and function of the human muscle-tendon complex in vivo. Furthermore, we tried to gain a better understanding of the mechanisms involved in angle specificity after isometric training from the aspect of neuromuscular adaptation and the changes in the properties of the muscle-tendon complex. Nine males completed 12-week unilateral training program (70% of maximal voluntary contraction (MVC) x 15 s x six sets) on the knee extensors at 50 degrees (shorter muscle length: ST) and 100 degrees (longer muscle length: LT). The internal muscle force (mechanical stress) is higher at 100 degrees than at 50 degrees because of the difference in the moment arm length, although there were no difference in the relative torque level, contraction and relaxation times, and repetition between ST and LT. Before and after training, isometric strength at eight angles and muscle volume were determined. Tendon elongation of knee extensors was measured by ultrasonography. There was no significant difference in the rate of increment of muscle volume between the protocols. Tendon stiffness increased significantly for LT, but not for ST. Although significant gain was limited to angles at or near the training angle for ST, increases in MVC at all angles were found for LT. These results suggest that only mechanical stress (internal muscle force imposed on muscle and tendon) contributes to adaptation in the tendon stiffness, although metabolic (relative torque level, etc.) and mechanical stress relate to muscle hypertrophy. Furthermore, increment of tendon stiffness for LT might contribute to increase torque output at smaller angles other than the training angle.

Effects of glucose intolerance on myocardial function and collagen-linked glycation.

In experimental diabetes, diastolic dysfunction of the left ventricle has been associated with collagen-linked glycation. To determine whether less severe hyperglycemia may have similar effects, we gave alloxan to mongrel dogs (group 2) to induce impaired glucose tolerance (IGT) for comparison with normal subjects (group 1). After 6 months, hemodynamic studies were performed in the anesthetized animals. Basal heart rate, aortic pressure, and ejection fraction were comparable in the two groups, but calculated chamber stiffness was increased in group 2, associated with a reduced end diastolic volume and increased pressure. During infusion of dextran, the volume and pressure responses were similarly abnormal in group 2. In the myocardium, the collagen concentration rose with an increased interstitial distribution histologically. To assess glycation, collagen was extracted, digested with collagenase, and measured for fluorescence. Advanced glycation end products were increased in group 2 to 10.6 +/- 1.6 vs. 6.9 +/- 0.7 fluorescent units (FU)/mg collagen in group 1 (P < 0.01). To assess whether this could be pharmacologically prevented, we administered enalapril to inhibit ACE during the 6 months of glucose intolerance to group 3. This resulted in normal glycation and significant reduction in chamber stiffness increment. We gave group 4 animals aminoguanidine daily for 6 months, which prevented abnormal collagen glycation and chamber stiffness. Thus, in animals with IGT, collagen-linked glycosylation appeared to be a major factor affecting diastolic function and was shown to be amenable to pharmacological intervention.

Novel attributes of an androgenic steroid-mediated increase in cardiac end diastolic stiffness in rats.

Although cardiac early and mid-diastolic stiffness constants are well accepted as being modulated by alterations in myocyte active processes, increments in left ventricular end diastolic (LVED) stiffness (LVED k; g x cm(-2)) in classical pathological models of a reduced LVED k (e.g., diabetes mellitus (DM) and hypertension) are determined largely by the properties of the myocardial extracellular matrix (ECM). As such, increases in LVED k in the latter cardiac pathologies are insensitive to acute changes in cardiac load, heart rate, and contractility. We examined whether the same attributes that apply to changes in LVED k in DM and in spontaneously hypertensive rats (SHRs) also apply to an androgenic steroid (nandrolone decanoate; 5 mg x kg(-1) biweekly) induced increase in LVED k. Myocardial collagen (ECM) characteristics and the capacity of acute verapamil-mediated changes in cardiac dynamics to impact on LVED k were evaluated after 3 months of steroid treatment to rats, 4 months of DM in rats, and in 45-week-old SHRs. Chronic steroid administration increased LVED k (steroid = 42 +/- 4, control = 25 +/- 2; p < 0.01). An acute infusion of verapamil to steroid-treated rats decreased LVED k to values not different from controls (29 +/- 3; p < 0.05 as compared with LVED k at baseline). Measures of myocardial collagen concentrations, phenotype ratios, and cross-linking were unchanged following steroid administration. Verapamil failed to alter the increased LVED k that occurs in either rats with DM or in SHRs, despite similar effects on cardiac dynamics as those noted in steroid-treated rats. The increased LVED k in the former animal models was associated with alterations in the ECM. In conclusion, the unique lack of association of the androgenic steroid-induced increase in LVED k with alterations in the myocardial ECM and the novel sensitivity of the steroid-mediated increment in LVED k to acute alterations in cardiac dynamics further supports the notion that changes in LVED k should not be considered to be a reflection of ECM characteristics in all cardiac conditions.

Pharmacologic myocardial protection during percutaneous transluminal coronary angioplasty by intracoronary application of dipyridamole: Impact on hemodynamic function and left ventricular performance

The aim of this study was to investigate whether intracoronary infusion of dipyridamole represents a suitable tool for preventing deterioration of left ventricular performance and hemodynamic function during percutaneous transluminal coronary angioplasty (PTCA). Coronary angioplasty represents a suitable model for establishing myocardial ischemia in humans. Balloon inflation is usually accompanied by significant deterioration in left ventricular systolic and diastolic properties. A brief episode of ischemia followed by reperfusion, termed preconditioning, has been identified as a mechanism for rendering the myocardium more resistant to ischemia. Adenosine is considered an important mediator of preconditioning. Dipyridamole is an important drug that interferes with myocardial adenosine metabolism by inhibiting its cellular reuptake. In 20 patients undergoing elective coronary angioplasty of a major vessel, assessment of angiographic left ventricular performance and hemodynamic variables was performed before, during and after PTCA. Patients were randomly allocated to pretreatment with intracoronary infusion of dipyridamole before percutaneous transluminal coronary angioplasty (10 patients) or conventional pretreatment without dipyridamole (10 patients). Dipyridamole pretreatment resulted in significant preservation of systolic and diastolic left ventricular performance during percutaneous transluminal coronary angioplasty, as documented by an unaffected global ejection fraction (vs. a deterioration of 29.2% with conventional pretreatment, p < 0.01) and an increment in diastolic stiffness of only 12.7% (vs. an increment of 57.3% with conventional pretreatment, p < 0.01). Apart from one instance of coronary steal phenomenon, no significant side effects of dipyridamole infusion could be detected. It is concluded that intracoronary application of dipyridamole may result in the induction of myocardial preconditioning by improving systolic and diastolic ventricular performance during percutaneous transluminal coronary angioplasty, thereby potentially reducing the risk of the angioplasty procedure.

A psychophysical evaluation of manual stiffness discrimination

One possible explanation for the poor reliability of clinical judgments of spinal stiffness is that humans do not possess a good ability to discriminate stiffness stimuli. This study sought to investigate this hypothesis by conducting stiffness discrimination tests on 72 subjects, using a mechanical device to provide the stiffness stimuli. The relative increment in stiffness needed so that two stimuli could be differentiated 75 per cent of the time was found to be 11 per cent when the pisiform grip was used to assess stiffness of stimuli in the range from 6 to 11 N/mm. Thus, by inference, other factors are more likely to be the cause of the poor reliability of clinical judgments of spinal stiffness.

Optimization of Vibration Reduction on the Mast by Active Stay System

An investigation of vibration reduction at the top of the mast by active control system is presented. Two typical external excitations, impact and random dynamic load, are considered. For each type of load, a cost function is defined and its optimal law is solved. Besides, an active stay system is designed to offer an active force on the mast.By comparing the direct stiffness increment and fixed stay auxiliary methods, it is shown that the active stay system has the fastest decay property among these methods for impact induced motion. For random exciting load, it has superior effect of peak suppressed in spectral density response than other two methods and its standard variations much lower than other cases compared. In addition, the lateral translation and slope accelerations at the top of the mast reduced by the active stay system is also the most effective. Numerical examples demonstrate that the active stay system with optimal law is a powerful and feasible scheme for mast vibration reduction.

Weakly attached cross-bridges in relaxed frog muscle fibers

Tension responses due to small, rapid length changes (completed within 40 microseconds) were obtained from skinned single frog muscle fiber segments (4-10 mm length) incubated in relaxing and rigor solutions at various ionic strengths. The first 2 ms of these responses can be described with a linear model in which the fiber is regarded as a rod, composed of infinitesimally small, identical segments, containing one undamped elastic element and two or three damped elastic elements and a mass in series. Rigor stiffness changed less than 10% in a limited range, 40-160 mM, of ionic strength conditions. Equatorial x-ray diffraction patterns show a similar finding for the filament spacing and intensity ratio I(11)/I(10). Relaxed fibers became stiffer under low ionic strength conditions. This stiffness increment can be correlated with a decreasing filament spacing and (an increased number of) weakly attached cross-bridges. Under low ionic strength conditions an additional recovery (1 ms time constant) became noticeable which might reflect characteristics of weakly attached cross-bridges.

The role of preparation in tuning anticipatory and reflex responses during catching

The pattern of muscle responses associated with catching a ball in the presence of vision was investigated by independently varying the height of the drop and the mass of the ball. It was found that the anticipatory EMG responses comprised early and late components. The early components were produced at a roughly constant latency (about 130 msec) from the time of ball release. Their mean amplitude decreased with increasing height of fall. Late components represented the major build-up of muscle activity preceding the ball's impact and were accompanied by limb flexion. Their onset time was roughly constant (about 100 msec) with respect to the time of impact (except in wrist extensors). This indicates that the timing of these responses was based on an accurate estimate of the instantaneous values of the time-to-contact (time remaining before impact). The mean amplitude of the late anticipatory responses increased linearly with the expected momentum of the ball at impact. The reflex responses evoked by the ball's impact consisted in a short-latency coactivation of flexor and extensor muscles at the elbow and wrist joints. Their mean amplitude generally increased with the intensity of the perturbation both in the stretched muscles and in the shortening muscles. We argue that both the anticipatory and the reflex coactivation are centrally preset in preparation for catching and are instrumental for stabilizing limb posture after impact. A model with linear, time-varying viscoelastic coefficients was used to assess the neural and mechanical contributions to the damping of limb oscillations induced by the ball's impact. The model demonstrates that (1) anticipatory muscle stiffening and anticipatory flexion of the limb are synergistic in building up resistance of the hand to vertical displacement and (2) the reflex coactivation produces a further increment of hand stiffness and viscosity which tends to offset the decrement which would result from the limb extension produced by the impact.

Is the SII portion of the cross-bridge in glycerinated rabbit psoas fibers compliant in the rigor state?

To see whether the SII portion of the cross-bridge in rigor fibers is longitudinally compliant, we chemically cross-linked with dimethyl suberimidate the entire rod portion (including the SII portion) of myosin onto the surface of thick filaments in glycerinated rabbit psoas fibers, and studied the effect of the SII fixation on the stiffness of the rigor fibers. The cross-linking of fiber segments with full filament overlap increased the rigor stiffness by approximately 25%. Almost the same absolute amount of the stiffness increase was also observed in rigor fibers with half- or no filament overlap after the cross-linking, and a similar but somewhat larger increment of stiffness was observed in fiber segments cross-linked in relaxing solution. These results indicate that the stiffness increase is not produced by the fixation of the SII portion onto the thick filament surface, but is caused instead by the cross-linking of some parallel elastic elements in muscle, and therefore indicate that the SII portion of the cross-bridge is hardly longitudinally compliant in rigor fibers.

Lateral Stiffness of Core and Outrigger Systems

It is common to increase the lateral stiffness of braced cores by placing horizontal trusses or outriggers from the core to the exterior columns. Outriggers, in effect, apply moments which reduce the rotation of the core at outrigger locations. The smaller rotations at those points in turn reduce the overall sway of the structure. How effective are such outriggers? What are the primary parameters which control their effectiveness? Where along the height are they most effective? For such systems, where should an increment of material be added to affect the largest increment in lateral stiffness? Structural engineers need quantitative answers to such questions to make design decisions. Taranath, McNabb and Muvdi and others have analyzed such systems and have provided insights useful for design. McNabb and Muvdi3 analyzed the case of multiple outriggers and concluded that the gain in stiffness decreases as more outriggers are added. Herein the case of outriggers at only one location is analyzed. The work presented generalizes the results of the references cited by explicitly considering flexible outriggers, nonprismatic elements and a triangularly distributed lateral load. The system model analyzed is shown in Tables 1 and 2. The outriggers are prismatic with a moment of inertia, IG; they can be located at any height, bH, from the base. The exterior columns are pin ended; their area increases linearly from the outrigger location to the base. The vertical core is nonprismatic, with a moment of inertia which increases linearly from the top to the base. Two load models are used; one is a uniform load, the other is a triangular load. The model is statically indeterminate to the second degree, however it is antisymmetric, therefore only one redundant needs to be determined.

The mechanical behavior of the human forearm in response to transient perturbations.

Static and dynamic components of mechanical impedance of human forearm were evaluated by applying two kinds of perturbations: 1) large viscoelastic loads, and 2) small pseudo-random perturbations. When the task involved the active resistance of the perturbations, both stiffness and viscosity increased relatively to their values in the passive task, the increment in stiffness being larger than that in viscosity. The time course of such changes was investigated during the transition between the two operating points defined by the instructions "do not resist" and "resist" the applied perturbations. The changes in stiffness and viscosity were relatively slow, those in the latter lagging behind those in the former.

Examination of elastic non-uniformity in the arterial system using a hydraulic model.

Pressure wave propagation has been examined in a model artery with spatially varying compliance. Although results were affected by viscous losses, appropriate allowance for such losses produced agreement between experimental findings and predictions of linear wave transmission theory. Particularly, the ability of non-uniformity of the tube wall to generate amplification of the pressure wave was confirmed. However, extrapolation to the physiological situation suggests that reflections from discrete sites in peripheral beds have a greater effect on pressure wave propagation than does elastic non-uniformity of major vessels. A theoretical analysis has demonstrated that the effects of elastic non-uniformity can be interpreted as the integrated effects of infinitesimal reflections from each progressive increment in wall stiffness.