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Journal articles on the topic 'Length of stretch'
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1
Adekoya, A. O., M. B. Fetuga, T. A. Ogunlesi, A. O. Adekoya, O. O. Oba-Daini, and E. D. Ajibola. "Flaccid penile length and stretch factor in the newborn." Research Journal of Health Sciences 9, no. 1 (April 7, 2021): 23–29. http://dx.doi.org/10.4314/rejhs.v9i1.3.
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Objective: Little is known about the flaccid penile length in the newborn and the degree of stretch of the penis among investigators while measuring the stretched penile length. This study aimed to document the flaccid penile length and the stretch factor in the newborn.Methods: This cross-sectional study was carried out on 200 term male infants within the first 72 hours of life. The flaccid penile length and the stretched penile length were measured with a wooden spatula and the stretch factor was calculated.Results: The mean (±SD) flaccid and stretched penile length were 30.9 ± 3.8 mm and 38.9 ± 4.0 mm respectively. The mean stretch factor was 26.4 %. Both testes had the same mean volume of 1.6 ± 0.5 ml. There was a significant correlation between flaccid and stretched penile lengths (r = 0.775, p = 0.000). The flaccid penile length was a significant predictor of the stretched penile length.Conclusion: This study has been able to determine the stretch factor while measuring the flaccid and stretch penile lengths in Nigerian newborn infants. It is recommended that the flaccid penile length be measured along with the stretched penile length and determine the stretch factor in order to compare how much investigators stretch the penis during measurement. This will allow for detailed comparison of penile anthropometry across different ethnic groups and races.
Keywords: flaccid penile length, newborn, stretch factor, stretched penile length.
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Rassier, Dilson E., Eun-Jeong Lee, and Walter Herzog. "Modulation of passive force in single skeletal muscle fibres." Biology Letters 1, no. 3 (June 28, 2005): 342–45. http://dx.doi.org/10.1098/rsbl.2005.0337.
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In this study, we investigated the effects of activation and stretch on the passive force–sarcomere length relationship in skeletal muscle. Single fibres from the lumbrical muscle of frogs were placed at varying sarcomere lengths on the descending limb of the force–sarcomere length relationship, and tetanic contractions, active stretches and passive stretches (amplitudes of ca 10% of fibre length at a speed of 40% fibre length/s) were performed. The passive forces following stretch of an activated fibre were higher than the forces measured after isometric contractions or after stretches of a passive fibre at the corresponding sarcomere length. This effect was more pronounced at increased sarcomere lengths, and the passive force–sarcomere length relationship following active stretch was shifted upwards on the force axis compared with the corresponding relationship obtained following isometric contractions or passive stretches. These results provide strong evidence for an increase in passive force that is mediated by a length-dependent combination of stretch and activation, while activation or stretch alone does not produce this effect. Based on these results and recently published findings of the effects of Ca 2+ on titin stiffness, we propose that the observed increase in passive force is caused by the molecular spring titin.
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Minozzo, Fabio C., and Dilson E. Rassier. "Effects of blebbistatin and Ca2+ concentration on force produced during stretch of skeletal muscle fibers." American Journal of Physiology-Cell Physiology 299, no. 5 (November 2010): C1127—C1135. http://dx.doi.org/10.1152/ajpcell.00073.2010.
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When activated muscle fibers are stretched at low speeds [≤2 optimal length ( Lo)/s], force increases in two phases, marked by a change in slope [critical force (Pc)] that happens at a critical sarcomere length extension ( Lc). Some studies attribute Pc to the number of attached cross bridges before stretch, while others attribute it to cross bridges in a pre-power-stroke state. In this study, we reinvestigated the mechanisms of forces produced during stretch by altering either the number of cross bridges attached to actin or the cross-bridge state before stretch. Two sets of experiments were performed: 1) activated fibers were stretched by 3% Lo at speeds of 1.0, 2.0, and 3.0 Lo/s in different pCa2+ (4.5, 5.0, 5.5, 6.0), or 2) activated fibers were stretched by 3% Lo at 2 Lo/s in pCa2+ 4.5 containing either 5 μM blebbistatin(+/−) or its inactive isomer (+/+). All stretches started at a sarcomere length (SL) of 2.5 μm. When fibers were activated at a pCa2+ of 4.5, Pc was 2.47 ± 0.11 maximal force developed before stretch (Po) and decreased with lower concentrations of Ca2+. Lc was not Ca2+ dependent; the pooled experiments provided a Lc of 14.34 ± 0.34 nm/half-sarcomere (HS). Pc and Lc did not change with velocities of stretch. Fibers activated in blebbistatin(+/−) showed a higher Pc (2.94 ± 0.17 Po) and Lc (16.30 ± 0.38 nm/HS) than control fibers (Pc 2.31 ± 0.08 Po; Lc 14.05 ± 0.63 nm/HS). The results suggest that forces produced during stretch are caused by both the number of cross bridges attached to actin and the cross bridges in a pre-power-stroke state. Such cross bridges are stretched by large amplitudes before detaching from actin and contribute significantly to the force developed during stretch.
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Joumaa, V., F. Bertrand, S. Liu, S. Poscente, and W. Herzog. "Does partial titin degradation affect sarcomere length nonuniformities and force in active and passive myofibrils?" American Journal of Physiology-Cell Physiology 315, no. 3 (September 1, 2018): C310—C318. http://dx.doi.org/10.1152/ajpcell.00183.2017.
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The aim of this study was to determine the role of titin in preventing the development of sarcomere length nonuniformities following activation and after active and passive stretch by determining the effect of partial titin degradation on sarcomere length nonuniformities and force in passive and active myofibrils. Selective partial titin degradation was performed using a low dose of trypsin. Myofibrils were set at a sarcomere length of 2.4 µm and then passively stretched to sarcomere lengths of 3.4 and 4.4 µm. In the active condition, myofibrils were set at a sarcomere length of 2.8 µm, activated, and actively stretched by 1 µm/sarcomere. The extent of sarcomere length nonuniformities was calculated for each sarcomere as the absolute difference between sarcomere length and the mean sarcomere length of the myofibril. Our main finding is that partial titin degradation does not increase sarcomere length nonuniformities after passive stretch and activation compared with when titin is intact but increases the extent of sarcomere length nonuniformities after active stretch. Furthermore, when titin was partially degraded, active and passive stresses were substantially reduced. These results suggest that titin plays a crucial role in actively stretched myofibrils and is likely involved in active and passive force production.
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Chapple, W. D. "Mechanics of stretch in activated crustacean slow muscle. I. Factors affecting peak force." Journal of Neurophysiology 62, no. 5 (November 1, 1989): 997–1005. http://dx.doi.org/10.1152/jn.1989.62.5.997.
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1. The active stiffness of ventral superficial abdominal muscle (VSM) of the hermit crab, Pagurus pollicarus, was measured with ramp stretches of different amplitudes and velocities. Active stiffness was calculated by subtracting the peak force produced by passive stretch and the isometric force just before stretch from the peak force produced by stretching active muscle. The result was then divided by stretch length to give stiffness. 2. The relationship between force just before stretch (the level of activation) and active stiffness was curvilinear and was found to apply under a variety of experiment conditions. For pooled data from eight experiments, active stiffness (GN.m-2.m-1) = 3.2*stress (MN/m2)-7.6*stress2. Decreasing the number of motor units or activating the inhibitor did not alter this relationship nor did the addition of proctolin, octopamine, or 5-HT to the bath. The relationship also applied during the rising phase of isometric tension. However, stiffness declined more rapidly than predicted by this relationship after the end of tetanus. 3. Active stiffness varied inversely with stretch amplitude for fast stretches, and the slope of this relationship increased with increasing muscle activation. At lower stretch velocities, the slope was much less than at rapid stretch velocities, so at low levels of activation and stretch velocity, active stiffness was essentially independent of stretch length. 4. Active stiffness covaried with muscle force as both were sampled at shorter and shorter lengths on the ascending limb of the length-tension curve.(ABSTRACT TRUNCATED AT 250 WORDS)
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Azizi, Emanuel, and Emily M. Abbott. "Anticipatory motor patterns limit muscle stretch during landing in toads." Biology Letters 9, no. 1 (February 23, 2013): 20121045. http://dx.doi.org/10.1098/rsbl.2012.1045.
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To safely land after a jump or hop, muscles must be actively stretched to dissipate mechanical energy. Muscles that dissipate energy can be damaged if stretched to long lengths. The likelihood of damage may be mitigated by the nervous system, if anticipatory activation of muscles prior to impact alters the muscle's operating length. Anticipatory motor recruitment is well established in landing studies and motor patterns have been shown to be modulated based on the perceived magnitude of the impact. In this study, we examine whether motor recruitment in anticipation of landing can serve a protective function by limiting maximum muscle length during a landing event. We use the anconeus muscle of toads, a landing muscle whose recruitment is modulated in anticipation of landing. We combine in vivo measurements of muscle length during landing with in vitro characterization of the force–length curve to determine the muscle's operating length. We show that muscle shortening prior to impact increases with increasing hop distance. This initial increase in muscle shortening functions to accommodate the larger stretches required when landing after long hops. These predictive motor strategies may function to reduce stretch-induced muscle damage by constraining maximum muscle length, despite variation in the magnitude of impact.
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Willems, Mark E. T., and William T. Stauber. "Effect of Contraction History on Torque Deficits by Stretches of Active Rat Skeletal Muscles." Canadian Journal of Applied Physiology 27, no. 4 (August 1, 2002): 323–35. http://dx.doi.org/10.1139/h02-018.
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Effects of contraction history on torque deficits by stretches of active skeletal muscles were examined. After three contractions using maximal and submaximal activation (80 and 20 Hz) at an ankle position of 40° (i.e., long muscle length) and with maximal activation at 120° (i.e., short muscle length), the isometric and stretch torques (15 stretches) of rat plantar flexor muscles (bout 1) were measured. Controls were unconditioned. Stretches (i.e., ankle rotation from 90° to 40°, velocity: 50°•s−1) were imposed on maximal isometric contractions at 90° (i.e. preloaded stretches). All groups performed a second bout following 2 hours of rest after bout 1. After maximal contractions at long muscle length, preload torque at 90° and stretch torque at 40° for stretch 1 of bout 1 were 25% and 18% lower than the other groups. However, for all groups, bout 1 ended and bout 2 began and ended with similar isometric and stretch torques. Stretches early in bout 2, with preloads similar to stretches in bout 1, had greater stretch torques resulting in larger torque deficits. Torque deficits, possibly caused by damage to muscle structures and excitation-contraction uncoupling, were not prevented by a history of isometric contractions. Different contraction histories can result in similar isometric torques but different stretch torques. Key words: injury, warm-up, isometric contractions, prevention, eccentric contractions
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Rassier, Dilson E., and Ivan Pavlov. "Force produced by isolated sarcomeres and half-sarcomeres after an imposed stretch." American Journal of Physiology-Cell Physiology 302, no. 1 (January 2012): C240—C248. http://dx.doi.org/10.1152/ajpcell.00208.2011.
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When a stretch is imposed to activated muscles, there is a residual force enhancement that persists after the stretch; the force is higher than that produced during an isometric contraction in the corresponding length. The mechanisms behind the force enhancement remain elusive, and there is disagreement if it represents a sarcomeric property, or if it is associated with length nonuniformities among sarcomeres and half-sarcomeres. The purpose of this study was to investigate the effects of stretch on single sarcomeres and myofibrils with predetermined numbers of sarcomeres ( n = 2, 3. . . , 8) isolated from the rabbit psoas muscle. Sarcomeres were attached between two precalibrated microneedles for force measurements, and images of the preparations were projected onto a linear photodiode array for measurements of half-sarcomere length (SL). Fully activated sarcomeres were subjected to a stretch (5–10% of initial SL, at a speed of 0.3 μm·s−1·SL−1) after which they were maintained isometric for at least 5 s before deactivation. Single sarcomeres showed two patterns: 31 sarcomeres showed a small level of force enhancement after stretch (10.46 ± 0.78%), and 28 sarcomeres did not show force enhancement (−0.54 ± 0.17%). In these preparations, there was not a strong correlation between the force enhancement and half-sarcomere length nonuniformities. When three or more sarcomeres arranged in series were stretched, force enhancement was always observed, and it increased linearly with the degree of half-sarcomere length nonuniformities. The results show that the residual force enhancement has two mechanisms: 1) stretch-induced changes in sarcomeric structure(s); we suggest that titin is responsible for this component, and 2) stretch-induced nonuniformities of half-sarcomere lengths, which significantly increases the level of force enhancement.
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Fasciano, Robert W., and Leslie Tung. "Factors governing mechanical stimulation in frog hearts." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 6 (December 1, 1999): H2311—H2320. http://dx.doi.org/10.1152/ajpheart.1999.277.6.h2311.
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Because stretch-induced activation may be important in generating clinically relevant arrhythmias in the heart, we delineated the ability of different types of stretches to activate ventricular tissue. Geometrically simple sheets of frog ( Rana catesbeiana) ventricular tissue were mounted to allow stretches to be applied perpendicular to one edge. Every heart could be activated by a stretch pulse ( n = 25), and several parameters were varied to determine their effects on mechanical activation threshold. At shorter coupling intervals, a larger stretch was needed to excite the tissue, and activation-recovery intervals were shorter, similar to previously published electrically probed strength-interval and restitution relations. Additionally, the tissue became easier to activate as the speed of the stretch increased from 0.09 to 2.6% length/ms. The increment in stretch needed for activation decreased as the baseline stretch increased from 0 to 6% length. Thus we show that mechanical activation is similar to electrical activation and that increasing uniquely mechanical parameters such as the speed of the applied stretch or baseline level of stretch can decrease the mechanical activation threshold.
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Matsumoto, H., C. B. Baron, and R. F. Coburn. "Smooth muscle stretch-activated phospholipase C activity." American Journal of Physiology-Cell Physiology 268, no. 2 (February 1, 1995): C458—C465. http://dx.doi.org/10.1152/ajpcell.1995.268.2.c458.
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Rabbit aortic muscles were stretched from a holding length of 0.6 maximum length (Lmax) to lengths as great as 1.0 Lmax and the new length maintained. When muscles were stretched to 1.0 Lmax, inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] and inositol 1,4-bisphosphate [Ins(1,4)P2] contents were increased at 375 ms (uncorrected for freezing time) poststretch to 209 +/- 27 and 139.8 +/- 12% (SE), respectively, of control values. Increases in Ins(1,4,5)P3 and Ins(1,4)P2 contents reached an apparent maximum at approximately 500 ms, i.e., to 243.7 +/- 15.8 and 180.9 +/- 16.2% of control, and were decreased to near control levels at 1,700 ms poststretch. The stretch threshold for phospholipase C (PLC) activation was 0.85 Lmax. The latency to onset of PLC activation, correcting for the time for freezing, was 275 to 375 ms. Maximal PLC activity was 91 pmol.s-1.100 nmol total lipid P(i)-1, which corresponded to 10% of total phosphatidylinositol bisphosphate being hydrolyzed per second. The mechanism of stretch-activated PLC activity involved influx of Ca2+ via gadolinium-sensitive ion channels, but not via nifedipine-sensitive ion channels.
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Stelzer, Julian E., and Richard L. Moss. "Contributions of Stretch Activation to Length-dependent Contraction in Murine Myocardium." Journal of General Physiology 128, no. 4 (September 25, 2006): 461–71. http://dx.doi.org/10.1085/jgp.200609634.
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The steep relationship between systolic force production and end diastolic volume (Frank-Starling relationship) in myocardium is a potentially important mechanism by which the work capacity of the heart varies on a beat-to-beat basis, but the molecular basis for the effects of myocardial fiber length on cardiac work are still not well understood. Recent studies have suggested that an intrinsic property of myocardium, stretch activation, contributes to force generation during systolic ejection in myocardium. To examine the role of stretch activation in length dependence of activation we recorded the force responses of murine skinned myocardium to sudden stretches of 1% of muscle length at both short (1.90 μm) and long (2.25 μm) sarcomere lengths (SL). Maximal Ca2+-activated force and Ca2+ sensitivity of force were greater at longer SL, such that more force was produced at a given Ca2+ concentration. Sudden stretch of myocardium during an otherwise isometric contraction resulted in a concomitant increase in force that quickly decayed to a minimum and was followed by a delayed development of force, i.e., stretch activation, to levels greater than prestretch force. At both maximal and submaximal activations, increased SL significantly reduced the initial rate of force decay following stretch; at submaximal activations (but not at maximal) the rate of delayed force development was accelerated. This combination of mechanical effects of increased SL would be expected to increase force generation during systolic ejection in vivo and prolong the period of ejection. These results suggest that sarcomere length dependence of stretch activation contributes to the steepness of the Frank-Starling relationship in living myocardium.
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Murata, Jun, and Kanji Matsukawa. "Cardiac vagal and sympathetic efferent discharges are differentially modified by stretch of skeletal muscle." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 1 (January 1, 2001): H237—H245. http://dx.doi.org/10.1152/ajpheart.2001.280.1.h237.
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We directly measured cardiac vagal efferent nerve activity (CVNA) and cardiac sympathetic efferent nerve activity (CSNA) in cats decerebrated at the level of the precollicular-premammillary body while the hindlimb or the triceps surae muscle was passively stretched. CVNA gradually decreased during passive stretch of the hindlimb, and this decrease was sustained throughout the stretch. CSNA increased at the onset of passive stretch, but this increase was not sustained. CVNA and CSNA responded differentially to graded passive stretches of the triceps surae muscle as well as the hindlimb. The sustained decrease in CVNA but not the initial increase in CSNA became greater depending on muscle length and developed tension. The time course and direction of the cardiac autonomic responses to muscle stretch were not affected by partial sinoaortic denervation, although the magnitude of the CSNA response was augmented. We conclude that the muscle mechanoreflex contributes to differential regulation of cardiac parasympathetic and sympathetic efferent discharges during passive stretch of skeletal muscle irrespective of arterial baroreceptor input.
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Rassier, Dilson E., and Walter Herzog. "Active force inhibition and stretch-induced force enhancement in frog muscle treated with BDM." Journal of Applied Physiology 97, no. 4 (October 2004): 1395–400. http://dx.doi.org/10.1152/japplphysiol.00377.2004.
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There is evidence that the stretch-induced residual force enhancement observed in skeletal muscles is associated with 1) cross-bridge dynamics and 2) an increase in passive force. The purpose of this study was to characterize the total and passive force enhancement and to evaluate whether these phenomena may be associated with a slow detachment of cross bridges. Single fibers from frog lumbrical muscles were placed at a length 20% longer than the plateau of the force-length relationship, and active and passive stretches (amplitudes of 5 and 10% of fiber length and at a speed of 40% fiber length/s) were performed. Experiments were conducted in Ringer solution and with the addition of 2, 5, and 10 mM of 2,3-butanedione monoxime (BDM), a cross-bridge inhibitor. The steady-state active and passive isometric forces after stretch of an activated fiber were higher than the corresponding forces measured after isometric contractions or passive stretches. BDM decreased the absolute isometric force and increased the total force enhancement in all conditions investigated. These results suggest that total force enhancement is directly associated with cross-bridge kinetics. Addition of 2 mM BDM did not change the passive force enhancement after 5 and 10% stretches. Addition of 5 and 10 mM did not change (5% stretches) or increased (10% stretches) the passive force enhancement. Increasing stretch amplitudes and increasing concentrations of BDM caused relaxation after stretch to be slower, and because passive force enhancement is increased at the greatest stretch amplitudes and the highest BDM concentrations, it appears that passive force enhancement may be related to slow-detaching cross bridges.
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Bakenecker, Patrick, Brent J. Raiteri, and Daniel Hahn. "Force enhancement in the human vastus lateralis is muscle-length-dependent following stretch but not during stretch." European Journal of Applied Physiology 120, no. 12 (September 5, 2020): 2597–610. http://dx.doi.org/10.1007/s00421-020-04488-1.
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Abstract Purpose Force enhancement is the phenomenon of increased forces during (transient force enhancement; tFE) and after (residual force enhancement; rFE) eccentric muscle actions compared with fixed-end contractions. Although tFE and rFE have been observed at short and long muscle lengths, whether both are length-dependent remains unclear in vivo. Methods We determined maximal-effort vastus lateralis (VL) force-angle relationships of eleven healthy males and selected one knee joint angle at a short and long muscle lengths where VL produced approximately the same force (85% of maximum). We then examined tFE and rFE at these two lengths during and following the same amount of knee joint rotation. Results We found tFE at both short (11.7%, P = 0.017) and long (15.2%, P = 0.001) muscle lengths. rFE was only observed at the long (10.6%, P < 0.001; short: 1.3%, P = 0.439) muscle length. Ultrasound imaging revealed that VL muscle fascicle stretch magnitude was greater at long compared with short muscle lengths (mean difference: (tFE) 1.7 mm, (rFE) 1.9 mm, P ≤ 0.046), despite similar isometric VL forces across lengths (P ≥ 0.923). Greater fascicle stretch magnitude was likely to be due to greater preload forces at the long compared with short muscle length (P ≤ 0.001). Conclusion At a similar isometric VL force capacity, tFE was not muscle-length-dependent at the lengths we tested, whereas rFE was greater at longer muscle length. We speculate that the in vivo mechanical factors affecting tFE and rFE are different and that greater stretch of a passive component is likely contributing more to rFE at longer muscle lengths.
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Wood, S. A., D. L. Morgan, and U. Proske. "Effects of repeated eccentric contractions on structure and mechanical properties of toad sartorius muscle." American Journal of Physiology-Cell Physiology 265, no. 3 (September 1, 1993): C792—C800. http://dx.doi.org/10.1152/ajpcell.1993.265.3.c792.
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It has been proposed that lengthening of active muscle at long lengths is nonuniformly distributed between sarcomeres, with a few being stretched beyond overlap and most hardly being stretched at all. A small fraction of the overstretched sarcomeres may fail to reinterdigitate on subsequent relaxation, leading to progressive changes in the muscle's mechanical properties. Sartorius muscles of the toad Bufo marinus were subjected to repeated lengthening (eccentric) contractions at long lengths, while controls were passively stretched and then contracted isometrically or stretched at short lengths. The muscles undergoing eccentric contractions showed a progressive shift to the right of the length-tension curve, a fall in the yield point during stretch, an increase in slope of the tension response during stretch, and a fall in isometric tension. In control muscles, changes, if any, were significantly less. In electron micrographs, muscle fibers that had been subjected to a series of eccentric contractions showed sarcomeres with A bands displaced toward one half-sarcomere, leaving no overlap in the other half. Adjacent regions often looked normal. These results are all in agreement with the predictions of the nonuniform stretch of sarcomeres hypothesis.
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Guan, Saipeng, Hai Zhong, Jianping Yang, and Chongwen Yu. "Study on the processing of stretch-broken ramie yarns in a cotton spinning system." Textile Research Journal 87, no. 16 (August 11, 2016): 2018–27. http://dx.doi.org/10.1177/0040517516663153.
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In this study, conventional long ramie fiber was stretch-broken into short fibers with lengths of 30 mm, 35 mm, 40 mm, 45 mm, and 50 mm. Then, these stretch-broken fibers were processed in a cotton spinning system. The results show that, compared to long ramie fibers processed in a conventional ramie spinning system, the stretch-broken fibers, with reasonable fiber length and high length uniformity, can be processed in a cotton spinning system with high efficiency and generally have better resultant yarn quality. For all of the stretch-broken yarns, the yarn processed from fiber with 40 mm length shows the best comprehensive performance.
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MALAMUD, JEAN G. "The Tension in a Locust Flight Muscle at Varied Muscle Lengths." Journal of Experimental Biology 144, no. 1 (July 1, 1989): 479–94. http://dx.doi.org/10.1242/jeb.144.1.479.
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1. Tension in a resting muscle increases when the muscle is stretched. If the stretch is maintained, the tension decays (stress relaxation). The time course of stress relaxation in the metathoracic second tergocoxal muscle (Tcx2) of the locust Schistocerca americana was found to be adequately described by a multiexponential function with four or more time constants. These constants were independent of strain, and the slowest had a value of more than 60min. Tension continued to diminish even when stretch was maintained for 2–4h. 2. Tension in a stretched, unstimulated muscle increased with increased length of stretch. Resting tension in the locust Tcx2 at the in vivo length was estimated to be 1 Ncm−2 or less. At 10% strain, resting tension was about 2 Ncm−2. The stiffness of the unstimulated locust muscle was similar to that of unstimulated frog muscles. 3. The active tetanic tension was maximal (average = 32.4 N cm−2) at slightly less than the in vivo muscle length. Tetanic tension was 50% or more of its maximum value over a range of 80–130% of the in vivo muscle length. 4. The active twitch tension was maximal at slightly greater than the in vivo muscle length. The ratio twitch/tetanic force increased with muscle length. 5. Twitch relaxation time increased with muscle length, but the time to peak for twitch force was nearly independent of muscle length in a stretched muscle.
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Coburn, R. F. "Stretch-induced membrane depolarization in ferret trachealis smooth muscle cells." Journal of Applied Physiology 62, no. 6 (June 1, 1987): 2320–25. http://dx.doi.org/10.1152/jappl.1987.62.6.2320.
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We determined the effects of increasing the length of the ferret trachealis muscle on smooth muscle membrane potentials recorded on successive impalements by microelectrodes. The preparation included the paratracheal ganglion nerve plexus as well as trachealis muscle. With sustained increases in muscle length over the range 0.5–0.8 to 1.2 maximal length (Lmax), depolarization occurred, which was related to the amplitude of the length increase. Membrane depolarizations were also evoked after stretching to lengths approximately 1.1 Lmax and returning to the control length. Stretch-induced membrane depolarizations developed after the stretch maneuver was complete; were slowly reversible; were not influenced by tetrodotoxin or atropine; were related to stretch rather than to maintained increase in muscle length; were not transmitted to adjacent nonstretched segments of the trachea; and were often associated with slow waves which appear to be secondary to membrane depolarization rather than stretch per se.
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Kumar, V., C. Prakash, G. Manigandan, and V. R. Sampath. "Investigation of the Influence of Stretch on the Air Permeability of Knitted Fabric: Effect of Loop Length." Fibres and Textiles in Eastern Europe 29, no. 1(145) (February 28, 2021): 53–56. http://dx.doi.org/10.5604/01.3001.0014.5045.
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Most of the time, a certain degree of stretch prominently and incrementally occurs in intimate wear, leisure wear, sportswear, medical textiles etc., during their action. Variations in the stretch gradient would definitely cause changes in the air permeability of knitted fabrics. The influence of variables such as loop length, the presence of an elastomeric component and fabric structure on the air permeability of cotton single jersey and pique knitted fabrics in a stretched state was critically analysed. In this work, changes in the air permeability of cotton jersey samples with and without elastomer were investigated and reported by keeping the samples in static up to an incremental stretch of 40% at a rate of 10% of the stretch gradient, in a dry relaxed state, wet relaxed state and fully relaxed state.
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Gordon, A. M., and E. B. Ridgway. "Stretch of active muscle during the declining phase of the calcium transient produces biphasic changes in calcium binding to the activating sites." Journal of General Physiology 96, no. 5 (November 1, 1990): 1013–35. http://dx.doi.org/10.1085/jgp.96.5.1013.
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In voltage-clamped barnacle single muscle fibers, muscle shortening during the declining phase of the calcium transient increases myoplasmic calcium. This extra calcium is probably released from the activating sites by a change in affinity when cross-bridges break (Gordon, A. M., and E. B. Ridgway, 1987. J. Gen. Physiol. 90:321-340). Stretching the muscle at similar times causes a more complex response, a rapid increase in intracellular calcium followed by a transient decrease. The amplitudes of both phases increase with the rate and amplitude of stretch. The rapid increase, however, appears only when the muscle is stretched more than approximately 0.4%. This is above the length change that produces the breakpoint in the force record during a ramp stretch. This positive phase in response to large stretches is similar to that seen on equivalent shortening at the same point in the contraction. For stretches at different times during the calcium transient, the peak amplitude of the positive phase has a time course that is delayed relative to the calcium transient, while the peak decrease during the negative phase has an earlier time course that is more similar to the calcium transient. The amplitudes of both phases increase with increasing strength of stimulation and consequent force. When the initial muscle the active force. A large decrease in length (which drops the active force to zero) decreases the extra calcium seen on a subsequent restretch. After such a shortening step, the extra calcium on stretch recovers (50 ms half time) toward the control level with the same time course as the redeveloped force. Conversely, stretching an active fiber decreases the extra calcium on a subsequent shortening step that is imposed shortly afterward. Enhanced calcium binding due to increased length alone cannot explain our data. We hypothesize that the calcium affinity of the activating sites increases with cross-bridge attachment and further with cross-bridge strain. This accounts for the biphasic response to stretch as follows: cross-bridges detached by stretch first decrease calcium affinity, then upon reattachment increase calcium affinity due to the strained configuration brought on by the stretch. The experiments suggest that cross-bridge attachment and strain can modify calcium binding to the activating sites in intact muscle.
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Antonio, J., and W. J. Gonyea. "Role of muscle fiber hypertrophy and hyperplasia in intermittently stretched avian muscle." Journal of Applied Physiology 74, no. 4 (April 1, 1993): 1893–98. http://dx.doi.org/10.1152/jappl.1993.74.4.1893.
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In the chronic stretch model, muscle fiber hyperplasia precedes fiber hypertrophy [Alway et al. Am. J. Physiol. 259 (Cell Physiol. 28): C92-C102, 1990]. This study was undertaken to determine if an intermittent stretch protocol would induce fiber hypertrophy without fiber hyperplasia. A weight equalt to 10% of the bird's mass was attached to the right wing of seven adult quail while the left wing served as the intra-animal control. The weight was attached to the wing for 24-h periods interspersed with a 48- to 72-hr rest interval. The actual stretch time was 5 days while the length of the treatment period was 15 days. Muscle mass and length increased significantly 53.1 +/- 9.0 and 26.1 +/- 7.3% in the stretched anterior latissimus dorsi. Fiber number, which was determined from a histological section in the midregion of the muscle, did not change (control 1,651.6 +/- 94.8; stretch 1,626.0 +/- 70.9). The slow tonic fiber areas increased significantly an average of 28.6 +/- 5.7%, whereas the fast fibers increased 18.5 +/- 8.4% when compared with control values. Mean fiber area (average of slow and fast fibers) increased significantly by 27.8 +/- 6.0% in the stretched anterior latissimus dorsi. There were no differences in the percentage of slow fibers or volume density of noncontractile tissue. These data indicate that muscle adapts differently to intermittent stretch than it does to chronic stretch despite an equivalent load and stretch duration. In contrast to chronic stretch, 5 days of intermittent stretch produces muscle fiber hypertrophy without fiber hyperplasia.
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GRIFFITHS, R. I. "The Mechanics of the Medial Gastrocnemius Muscle in the Freely Hopping Wallaby (Thylogale Billardierii)." Journal of Experimental Biology 147, no. 1 (November 1, 1989): 439–56. http://dx.doi.org/10.1242/jeb.147.1.439.
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Muscle force, electromyogram and length were monitored in the medial head of the gastrocnemius (MG) muscle in freely hopping wallabies (Thylogale billardierii Desmarest). During take-off hops from rest, MG muscle developed force with an isometric contraction. For constant-speed hops, force was produced in MG muscle during rapid stretch. The muscle resisted this stretch with a constant impedance that was independent of hopping speed. The rate of stretch of the muscle during high-speed hopping was as high as 1 ms−1 (5–6 muscle lengths per second) at the onset of stretch and slowed to no stretch at the peak of force. Since the mechanical impedance was constant while the stretch velocity changed, there was no significant viscosity present in the muscle. The tendon stretched by 3.2% at 7kmh−1 hopping and by 4.4% at 18kmh−1 hopping. Elastic energy storage in the tendons increased with hopping speed but the percentage of total work done by elastic recoil of the whole muscle did not increase at higher hopping speeds. The significance of the muscle stretch is in producing high forces rapidly and, in addition, there is considerable energy storage in the tend
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Hao, Hailing, and David I. Shreiber. "Axon Kinematics Change During Growth and Development." Journal of Biomechanical Engineering 129, no. 4 (February 14, 2007): 511–22. http://dx.doi.org/10.1115/1.2746372.
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The microkinematic response of axons to mechanical stretch was examined in the developing chick embryo spinal cord during a period of rapid growth and myelination. Spinal cords were isolated at different days of embryonic (E) development post-fertilization (E12, E14, E16, and E18) and stretched 0%, 5%, 10%, 15%, and 20%, respectively. During this period, the spinal cord grew ∼55% in length, and white matter tracts were myelinated significantly. The spinal cords were fixed with paraformaldehyde at the stretched length, sectioned, stained immunohistochemically for neurofilament proteins, and imaged with epifluorescence microscopy. Axons in unstretched spinal cords were undulated, or tortuous, to varying degrees, and appeared to straighten with stretch. The degree of tortuosity (ratio of the segment’s pathlength to its end-to-end length) was quantified in each spinal cord by tracing several hundred randomly selected axons. The change in tortuosity distributions with stretch indicated that axons switched from non-affine, uncoupled behavior at low stretch levels to affine, coupled behavior at high stretch levels, which was consistent with previous reports of axon behavior in the adult guinea pig optic nerve (Bain, Shreiber, and Meaney, J. Biomech. Eng., 125(6), pp. 798–804). A mathematical model previously proposed by Bain et al. was applied to quantify the transition in kinematic behavior. The results indicated that significant percentages of axons demonstrated purely non-affine behavior at each stage, but that this percentage decreased from 64% at E12 to 30% at E18. The decrease correlated negatively to increases in both length and myelination with development, but the change in axon kinematics could not be explained by stretch applied during physical growth of the spinal cord. The relationship between tissue-level and axonal-level deformation changes with development, which can have important implications in the response to physiological forces experienced during growth and trauma.
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Rassier, Dilson E., and Walter Herzog. "Relationship between force and stiffness in muscle fibers after stretch." Journal of Applied Physiology 99, no. 5 (November 2005): 1769–75. http://dx.doi.org/10.1152/japplphysiol.00010.2005.
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The purpose of this study was to evaluate the relationship between force and stiffness after stretch of activated fibers, while simultaneously changing contractility by interfering with the cross-bridge kinetics and muscle activation. Single fibers dissected from lumbrical muscles of frogs were placed at a length 20% longer than the plateau of the force-length relationship, activated, and stretched by 5 and 10% of fiber length (speed: 40% fiber length/s). Experiments were conducted with maximal and submaximal stimulation in Ringer solution and with the addition of 2 and 5 mM of the myosin inhibitor 2,3-butanedione monoxime (BDM) to the solution. The steady-state force after stretch of an activated fiber was higher than the isometric force produced at the corresponding length in all conditions investigated. Lowering the frequency of stimulation decreased the force and stiffness during isometric contractions, but it did not change force enhancement and stiffness enhancement after stretch. Administration of BDM decreased the force and stiffness during isometric contractions, but it increased the force enhancement and stiffness enhancement after stretch. The relationship between force enhancement and stiffness suggests that the increase in force after stretch may be caused by an increase in the proportion of cross bridges attached to actin. Because BDM places cross bridges in a weakly bound, pre-powerstroke state, our results further suggest that force enhancement is partially associated with a recruitment of weakly bound cross bridges into a strongly bound state.
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Standley, Paul R., Tamar J. Obards, and Cherie L. Martina. "Cyclic stretch regulates autocrine IGF-I in vascular smooth muscle cells: implications in vascular hyperplasia." American Journal of Physiology-Endocrinology and Metabolism 276, no. 4 (April 1, 1999): E697—E705. http://dx.doi.org/10.1152/ajpendo.1999.276.4.e697.
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Vascular smooth muscle cells (VSMC) subjected to acute or chronic stretch display enhanced growth rates in vitro and in vivo. Clinical examples of vascular hyperplasia (e.g., systolic hypertension and postinjury restenosis) suggest that local insulin-like growth factor I (IGF-I) expression is enhanced. Therefore, we investigated the role of in vitro cyclic stretch on rat VSMC IGF-I secretion and cellular growth. In serum-free medium, cyclic stretch (1 Hz at 120% resting length for 48 h) stimulated thymidine incorporation ∼40% above that seen in nonstretched cells. Graded stretch magnitude (100–125% resting length) yielded graded increases in VSMC growth. Exogenous IGF-I increased growth of serum-starved, nonstretched VSMC in a dose-dependent manner, with maximal growth seen with 10−7 M. IGF-I secretion from stretched cells was 20- to 30-fold greater than from those cells cultured in a static environment. Stretch-induced increases in growth were completely blocked on addition of anti-IGF-I and partially blocked with platelet-derived growth factor (PDGF) antibodies and with a tyrosine kinase inhibitor (tyrphostin-1). Finally, blockade of stretch-activated cation channels with GdCl3 profoundly inhibited stretch-induced growth. We conclude that stretch increases VSMC IGF-I secretion and that such autocrine IGF-I is required for stretch-induced growth. PDGF and stretch-sensitive cation channels are likely additional components of a complex pathway that regulates stretch-induced VSMC seen in systolic hypertension and postinjury restenosis.
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Li, Yan Ru, Wan Shan Chen, Zhen Hai Wang, and Hai Bo Jiang. "Calculation of Stretch Stress of Double-Layer Plate Composites." Key Engineering Materials 861 (September 2020): 529–33. http://dx.doi.org/10.4028/www.scientific.net/kem.861.529.
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The stretch stress of each layer of laminate composite undergoes complex changes after being stretched, which significantly affects the stretch strength. In order to determine the magnitude of the change, the paper directly solved the stretch stress using the analytical method through simple assumptions, and obtained the analytical calculation formula. Studies on double-layer plates show that the magnitude of stretch stress is closely related to the elastic modulus, length and thickness dimensions of the plate layer, the shear modulus of the adhesive, the thickness of the adhesive layer, and the external stress, and the maximum stress occurs at the middle section. The calculation of the formula provides a convenient way to check the stretch strength.
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Héroux, Martin Eric, Ida Anderman, Sofia Nykvist Vouis, Joanna Diong, Peter William Stubbs, and Robert D. Herbert. "History-dependence of muscle slack length in humans: effects of contraction intensity, stretch amplitude, and time." Journal of Applied Physiology 129, no. 4 (October 1, 2020): 957–66. http://dx.doi.org/10.1152/japplphysiol.00106.2020.
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The slack length of a relaxed human skeletal muscle is not fixed; it can be modified by contraction and stretch. Contraction of the human vastus lateralis muscle at short lengths reduces the muscle’s slack length. Even very weak contractions are sufficient to induce this effect. The effect persists for at least 5 min but can be reduced or abolished with a large-amplitude passive stretch.
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Gunst, Susan J., and Ming-Fang Wu. "Selected Contribution: Plasticity of airway smooth muscle stiffness and extensibility: role of length-adaptive mechanisms." Journal of Applied Physiology 90, no. 2 (February 1, 2001): 741–49. http://dx.doi.org/10.1152/jappl.2001.90.2.741.
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Airway smooth muscle exhibits the property of length adaptation, which enables it to optimize its contractility to the mechanical conditions under which it is activated. Length adaptation has been proposed to result from a dynamic modulation of contractile and cytoskeletal filament organization, in which the cell structure adapts to changes in cell shape at different muscle lengths. Changes in filament organization would be predicted to alter muscle stiffness and extensibility. We analyzed the effects of tracheal muscle length at the time of contractile activation on the stiffness and extensibility of the muscle during subsequent stretch over a constant range of muscle lengths. Muscle strips were significantly stiffer and less extensible after contractile activation at a short length than after activation at a long length, consistent with the prediction of a shorter, thicker array of the cytoskeletal filaments at a short muscle length. Stretch beyond the length of contractile activation resulted in a persistent reduction in stiffness, suggesting a stretch-induced structural rearrangement. Our results support a model in which the filament organization of airway smooth muscle cells is plastic and can be acutely remodeled to adapt to the changes in the external physical environment.
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Gajdosik, Richard L., Darl W. Vander Linden, and Ann K. Williams. "Influence of Age on Length and Passive Elastic Stiffness Characteristics of the Calf Muscle-Tendon Unit of Women." Physical Therapy 79, no. 9 (September 1, 1999): 827–38. http://dx.doi.org/10.1093/ptj/79.9.827.
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Abstract Background and Purpose. Therapeutic stretching of the calf muscle-tendon unit is used to increase its length and to ameliorate decreased dorsiflexion range of motion (ROM), but the influence of age on the passive properties of the calf muscle-tendon unit has not been studied adequately. The purpose of this study was to examine the influence of age on length and passive elastic stiffness (PES) characteristics of the calf muscle-tendon unit when stretched through the full, available dorsiflexion ROM. Subjects. Twenty-four younger women (aged 20–39 years), 24 middle-aged women (aged 40–59 years), and 33 older women (aged 60–84 years) participated. Methods. An isokinetic dynamometer was used to passively stretch the right calf muscle-tendon unit from relaxed plantar flexion to the maximal angle of available dorsiflexion at 5°·s−1. The maximal passive resistive torque was measured, and passive angle-torque curves were constructed for a full ROM from an initial angle of passive resistive torque to the maximal dorsiflexion angle. The full ROM represented length extensibility. The average PES was calculated for this full stretch ROM and for the first half and the last half of this stretch ROM. The maximal passive dorsiflexion angle, maximal passive resistive torque, angular change for the full stretch ROM, and average PES for the full stretch ROM and the first half and the last half of the full stretch ROM were examined for group differences and their relationships with age. Results. The maximal passive dorsiflexion angle, maximal passive resistive torque, angular change for the full stretch ROM, and average PES within the last half of the full stretch ROM were less for the older women than for the younger women. Age was negatively associated with these variables. Conclusion and Discussion. Decreased maximal passive dorsiflexion ROM in older women was associated with decreased maximal passive resistive torque, decreased calf muscle-tendon unit length extensibility, and decreased average PES within the last half of their available passive dorsiflexion ROM.
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Cavagna, G. A., M. Mazzanti, N. C. Heglund, and G. Citterio. "Mechanical transients initiated by ramp stretch and release to Po in frog muscle fibers." American Journal of Physiology-Cell Physiology 251, no. 4 (October 1, 1986): C571—C579. http://dx.doi.org/10.1152/ajpcell.1986.251.4.c571.
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Single fibers from the tibialis muscle of Rana temporaria were subjected to ramp stretches during tetanic stimulation at a sarcomere length of approximately 2 microns. Immediately after the stretch, or after different time delays, the active fiber was released against a constant force equal to the isometric force (Po) exerted immediately before the stretch. Four phases were detected after release: an elastic recoil of the fiber's undamped elements, a transient rapid shortening, a marked reduction in the velocity of shortening (often to 0), and an apparently steady shortening (sometimes absent). Increasing the amplitude of the stretch from approximately 2 to 10% of the fiber rest length led to an increase in phase 2 shortening from approximately 5 to 10 nm per half-sarcomere. Phase 2 shortening increased further (up to 14 nm per half-sarcomere) if a time interval of 5-10 ms was left between the end of large ramp stretches and release to Po. After 50- to 100-ms time intervals, shortening occurred in two steps of approximately 5 nm per half-sarcomere each. These findings suggest that phase 2 is due to charging, during and after the stretch, of a damped element, which can then shorten against Po in at least two steps of approximately 5 nm/half sarcomere each.
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Marozaitė, Laima, and Valentinas Šaulys. "STREAM SELF-PURIFICATION EFFICIENCY / REGULIUOTO UPELIO SAVAIMINIO APSIVALYMO EFEKTYVUMO VERTINIMAS." Mokslas – Lietuvos ateitis 7, no. 4 (September 29, 2015): 430–35. http://dx.doi.org/10.3846/mla.2015.804.
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The article identifies factors that have influence on the processes of river self-purification from biogenic substances when the stretches of the river are regulated and unregulated. In order to assess and compare the processes of self-purification, regulated and unregulated stretches of the river of the same length were chosen. It can be showed conclusively that the river in the unregulated stretch purifies from biogenic substances better. Rate a of nitrates self-purification in an unregulated stretch was 0.42 and in regulated stretch it was 0.106. Rate a of phosphates self-purification in an unregulated stretch was 0.286 and in regulated stretch it was 0.22. Straipsnyje nagrinėjami veiksniai, darantys įtaką upių savaiminio apsivalymo procesams nuo biogeninių medžiagų, kai upės ruožai yra reguliuoti ir nereguliuoti. Savaiminio apsivalymo procesams vertinti ir lyginti buvo pasirinkti vienodo ilgio reguliuotas ir nereguliuotas upės ruožai. Beveik užtikrintai galime teigti, kad nereguliuotame ruože upelis nuo biogeninių medžiagų apsivalo geriau. Nitratų savaiminio apsivalymo koeficientas a nereguliuotame ruože lygus 0,42, o reguliuotame – 0,106. Fosfatų savaiminio apsivalymo koeficientas a nereguliuotame ruože lygus 0,286, o reguliuotame – 0,22.
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Sevieux, Nancy, Jawed Alam, and Emel Songu-Mize. "Effect of cyclic stretch on α-subunit mRNA expression of Na+-K+-ATPase in aortic smooth muscle cells." American Journal of Physiology-Cell Physiology 280, no. 6 (June 1, 2001): C1555—C1560. http://dx.doi.org/10.1152/ajpcell.2001.280.6.c1555.
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We previously demonstrated that protein expression of both α1- and α2-catalytic subunits of the Na+-K+-ATPase is elevated after a 2- to 4-day chronic cyclic stretch regimen in cultured aortic smooth muscle cells (ASMC). In the present study, we investigated whether cyclic stretch affects mRNA expression of the α-isoforms of the Na+-K+-ATPase. Using a stretch apparatus, rat ASMC were cyclically stretched 10 or 20% of their length for 1, 3, or 6 h. α-Isoform mRNA levels were measured using Northern analysis. A 3-h 10% stretch had no significant affect on mRNA expression for either isoform, but a 20% stretch increased mRNA of both isoforms approximately twofold. Whereas a 6-h 20% stretch increased α1 mRNA by 3.3-fold, α2 was not affected any further. Actinomycin D blocked the stretch-induced stimulation of mRNA expression of both α-subunits. In conclusion, cyclic stretch stimulates the mRNA expression of both α1- and α2-subunits of Na+-K+-ATPase. The sensitivity of the two genes to the degree and duration of stretch is different. The stretch-induced increase of mRNA may be a result of increased transcription.
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De-Doncker, Laurent, Florence Picquet, Julien Petit, and Maurice Falempin. "Characterization of Spindle Afferents in Rat Soleus Muscle Using Ramp-and-Hold and Sinusoidal Stretches." Journal of Neurophysiology 89, no. 1 (January 1, 2003): 442–49. http://dx.doi.org/10.1152/jn.00153.2002.
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The discharge properties of 51 afferents were studied in the rat soleus muscle spindles. Under deep anesthesia using a pentobarbital sodium solution (30 mg/kg), a laminectomy was performed and the right L4 and L5 dorsal and ventral roots were transected near their entry into the spinal cord. In situ, the minimal ( L min) muscle length [3 ± 0.08 (SE) cm] of the soleus was measured at full ankle extension. Unitary potentials from the L5dorsal root were recorded in response to ramp-and-hold stretches applied at 3 mm (S3) and 4 mm (S4) amplitudes and four stretch velocities (6, 10, 15, and 30 mm/s), sinusoidal stretches performed at four amplitudes (0.12, 0.25, 0.5, and 1 mm) and six stretch frequencies (0.5, 1, 2, 3, 6, and 10 Hz), and vibrations applied at 50-, 100-, and 150-Hz frequencies. These two kinds of stretches were performed at three different muscle lengths ( L min+10%, L min+15%, and L min+20%), whereas vibrations were applied at L min+20% muscle length. Conduction velocity of the fibers was calculated but did not allow to discriminate different fiber types. However, the mean conduction velocity of the first fiber group (43.3 ± 0.8 m/s) was significantly higher than that of the second fiber group (33.9 ± 0.9 m/s). Three parameters allowed to differentiate the responses of primary and secondary endings: the dynamic index (DI), the discharge during the stretch release from the ramp-and-hold stretches, and the linear range and the vibration sensitivity from sinusoidal stretches. The slope histogram of the linear regression based on the DI and the stretch velocity was clearly bimodal. Therefore the responses were separated into two groups. During the stretch release at a velocity of 3 mm/s, the first response group ( n = 26) exhibited a pause, whereas the second ( n = 25) did not. The linear range of the second ending group (0.12–1 mm) was broader than that of the first (0.12–0.25 mm). The first ending group showed a higher sensitivity to high-vibration frequencies of small amplitude than the second. In comparison with the literature, we can assert that the first and the second ending groups corresponded to the primary and secondary endings, respectively. In conclusion, our study showed that in rat soleus muscle spindles, it was possible to immediately classify the discharge of Ia and II fibers by using some parameters measured under ramp-and-hold and sinusoidal stretches.
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Meiss, R. A. "Stiffness of active smooth muscle during forced elongation." American Journal of Physiology-Cell Physiology 253, no. 3 (September 1, 1987): C484—C493. http://dx.doi.org/10.1152/ajpcell.1987.253.3.c484.
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The stiffness of isometrically contracting mesotubarium superius and ovarian ligament smooth muscle from estrous female rabbits was measured continuously by using sinusoidal length perturbations (at 80 Hz, less than 15 microns peak to peak). Muscles were stimulated with alternating current fields, and all records were digitized using a microcomputer system. Phase-angle data were used to resolve computed stiffness into elastic and viscous components. Stiffness measurements were continued during long ramp-type stretches (up to 25% of muscle length) delivered as soon as force was maximal. To use the period of isometric tension development as a standard for comparison, the expected stiffness was computed during the long stretch. Stiffness was reduced in approximate proportion to the ramp stretch rate, and the reduction was confined largely to the elastic component. Cooling the muscle increased the stiffness deviation at a given stretch rate. It is proposed that the long stretch detaches cross bridges that can reattach to new sites as myofilaments shear past one another. At higher shearing speeds, less time is available for reattachment and stiffness is further reduced.
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Rodriguez, Casey. "On stretch-limited elastic strings." Proceedings of the Royal Society A: Mathematical, Physical and Engineering Sciences 477, no. 2249 (May 2021): 20210181. http://dx.doi.org/10.1098/rspa.2021.0181.
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Motivated by the increased interest in modelling non-dissipative materials by constitutive relations more general than those from Cauchy elasticity, we initiate the study of a class of stretch-limited elastic strings : the string cannot be compressed smaller than a certain length less than its natural length nor elongated larger than a certain length greater than its natural length. In particular, we consider equilibrium states for a string suspended between two points under the force of gravity (catenaries). We study the locations of the supports resulting in tensile states containing both extensible and inextensible segments in two situations: the degenerate case when the string is vertical and the non-degenerate case when the supports are at the same height. We then study the existence and multiplicity of equilibrium states in general with multiplicity differing markedly from strings satisfying classical constitutive relations.
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Syme, Douglas A., and Michael J. Grattan. "Effects of stretch on work from fast and slow muscles of mice: damped and undamped energy release." Canadian Journal of Physiology and Pharmacology 80, no. 9 (September 1, 2002): 887–900. http://dx.doi.org/10.1139/y02-110.
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Stretching active muscle increases the work performed during subsequent shortening. The effects of a preceding stretch on work done by the undamped or lightly damped series compliance (SC) and by the contractile component (CC), which includes cross bridges and damped elements, were assessed using mouse soleus (slow) and extensor digitorum longus (fast) muscles with limited tendon. Increasing stretch amplitude (010% fibre length) increased work done by the SC up to a limit, but did not effect work done by the CC. Increasing stretch velocity (10100% Vmax) had almost no effect on work done by either component. Increasing the delay between the end of stretch and onset of shortening (060 ms) caused a decrease in SC work, with no effect on CC work. Recoil of the SC was responsible for 5070% of the total work done during shortening after stretch. Usually only 1040% of the energy imparted during the stretch was recovered as work during subsequent shortening; large stretches and long delays between stretch and shortening further reduced this recovery by one third to one fifth. Results are interpreted in the context of a loss of energy stored in the SC owing to forcible detachment of cross bridges with large stretches and cyclic detachment with long delays.Key words: compliance, stretch, work, muscle, undamped.
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Butterfield, Timothy A., and Walter Herzog. "Effect of altering starting length and activation timing of muscle on fiber strain and muscle damage." Journal of Applied Physiology 100, no. 5 (May 2006): 1489–98. http://dx.doi.org/10.1152/japplphysiol.00524.2005.
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Muscle strain injuries are some of the most frequent injuries in sports and command a great deal of attention in an effort to understand their etiology. These injuries may be the culmination of a series of subcellular events accumulated through repetitive lengthening (eccentric) contractions during exercise, and they may be influenced by a variety of variables including fiber strain magnitude, peak joint torque, and starting muscle length. To assess the influence of these variables on muscle injury magnitude in vivo, we measured fiber dynamics and joint torque production during repeated stretch-shortening cycles in the rabbit tibialis anterior muscle, at short and long muscle lengths, while varying the timing of activation before muscle stretch. We found that a muscle subjected to repeated stretch-shortening cycles of constant muscle-tendon unit excursion exhibits significantly different joint torque and fiber strains when the timing of activation or starting muscle length is changed. In particular, measures of fiber strain and muscle injury were significantly increased by altering activation timing and increasing the starting length of the muscle. However, we observed differential effects on peak joint torque during the cyclic stretch-shortening exercise, as increasing the starting length of the muscle did not increase torque production. We conclude that altering activation timing and muscle length before stretch may influence muscle injury by significantly increasing fiber strain magnitude and that fiber dynamics is a more important variable than muscle-tendon unit dynamics and torque production in influencing the magnitude of muscle injury.
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Miller, Steven M., and J. H. Szurszewski. "Circumferential, not longitudinal, colonic stretch increases synaptic input to mouse prevertebral ganglion neurons." American Journal of Physiology-Gastrointestinal and Liver Physiology 285, no. 6 (December 2003): G1129—G1138. http://dx.doi.org/10.1152/ajpgi.00292.2003.
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The relationship between longitudinal and circular muscle tension in the mouse colon and mechanosensory excitatory synaptic input to neurons in the superior mesenteric ganglion (SMG) was investigated in vitro. Electrical activity was recorded intracellularly from SMG neurons, and muscle tension was simultaneously monitored in the longitudinal, circumferential, or both axes. Colonic intraluminal pressure and volume changes were also monitored simultaneously with muscle tension changes. The results showed that the frequency of fast excitatory postsynaptic potentials (fEPSPs) in SMG neurons increased when colonic muscle tension decreased, when the colon relaxed and refilled with fluid after contraction, and during receptive relaxation preceding spontaneous colonic contractions. In contrast, fEPSP frequency decreased when colonic muscle tension increased during spontaneous colonic contraction and emptying. Manual stretch of the colon wall to 10-15% beyond resting length in the circumferential axis of flat sheet preparations increased fEPSP frequency in SMG neurons, but stretch in the longitudinal axis to 15% beyond resting length in the same preparations did not. There was no increase in synaptic input when tubular colon segments were stretched in their long axes up to 20% beyond their resting length. The circumferential stretch-sensitive increase in the frequency of synaptic input to SMG neurons persisted when the colonic muscles were relaxed pharmacologically by nifedipine (2 μM) or nicardipine (3 μM). These results suggest that colonic mechanosensory afferent nerves projecting to the SMG function as length or stretch detectors in parallel to the circular muscle layer.
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Gregory, J. E., D. L. Morgan, and U. Proske. "Changes in size of the stretch reflex of cat and man attributed to aftereffects in muscle spindles." Journal of Neurophysiology 58, no. 3 (September 1, 1987): 628–40. http://dx.doi.org/10.1152/jn.1987.58.3.628.
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1. This is a report of experiments carried out on the cat and on man, which demonstrate that conditioning of a muscle by contraction and movement can lead to changes in amplitude of stretch reflexes elicited in that muscle. 2. In triceps surae of the cat, the reflex response to a brief stretch was recorded after conditioning with a whole-muscle contraction followed by a pause at a length either 5 mm longer or shorter than the length at which the reflex was elicited. Following conditioning at the long length the reflex response was less than half as large as that following conditioning at the short length. 3. The changes in reflex amplitude could be correlated with an altered stretch responsiveness of muscle spindles in the soleus muscle. When the muscle had been held long during conditioning, a subsequent brief stretch applied at an intermediate length elicited fewer impulses in primary endings of spindles than after conditioning at a short length. 4. The same kind of experiment was then carried out on adult human subjects. When a tendon tap was applied to the Achilles tendon after a voluntary contraction and relaxation of triceps surae with the muscle at a long length, (foot dorsiflexed) the reflex was frequently less than half the size it had been after a contraction at a short length (foot plantarflexed). It was concluded that the same kind of spindle aftereffects as observed for cat soleus spindles were responsible for the changes in reflex amplitude. 5. It was found both in the cat and in human subjects that the changes in reflex amplitude after conditioning became progressively less as the test length was made longer. 6. The explanation put forward to account for these observations is that stable cross-bridges form between actin and myosin filaments of passive intrafusal (and extrafusal) fibers. When the muscle is shortened several seconds after a contraction at a long length, the intrafusal fibers, stiffened by the presence of cross-bridges, fall slack. Slack does not develop after a contraction at a short muscle length, as the fiber is stretched to the test length. Since any slack must first be taken up by the test stretch, there is a smaller afferent response and consequently a smaller reflex contraction in response to a tendon tap after conditioning at a long length.(ABSTRACT TRUNCATED AT 400 WORDS)
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Kim, Yoori, Ki Seok Kim, Kristy L. Kounovsky, Rakwoo Chang, Gun Young Jung, Juan J. dePablo, Kyubong Jo, and David C. Schwartz. "Nanochannel confinement: DNA stretch approaching full contour length." Lab on a Chip 11, no. 10 (2011): 1721. http://dx.doi.org/10.1039/c0lc00680g.
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Lynch, Gordon S., and John A. Faulkner. "Contraction-induced injury to single muscle fibers: velocity of stretch does not influence the force deficit." American Journal of Physiology-Cell Physiology 275, no. 6 (December 1, 1998): C1548—C1554. http://dx.doi.org/10.1152/ajpcell.1998.275.6.c1548.
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We tested the null hypothesis that the severity of injury to single muscle fibers following a single pliometric (lengthening) contraction is not dependent on the velocity of stretch. Each single permeabilized fiber obtained from extensor digitorum longus muscles of rats was maximally activated and then exposed to a single stretch of either 5, 10, or 20% strain [% of fiber length ( L f)] at a velocity of 0.5, 1.0, or 2.0 L f /s. The force deficit, the difference between maximum tetanic isometric force (Po) before and after the stretch expressed as a percentage of the control value for Po before the stretch, provided an estimate of the magnitude of muscle injury. Despite a fourfold range from the lowest to the highest velocities, force deficits were not different among stretches of the same strain. At stretches of 20% strain, even an eightfold range of velocities produced no difference in the force deficit, although 40% of the fibers were torn apart at a velocity of 4 L f /s. We conclude that, within the range of velocities tolerated by single permeabilized fibers, the severity of contraction-induced injury is not related to the velocity of stretch.
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Rassier, Dilson E., and Walter Herzog. "Considerations on the history dependence of muscle contraction." Journal of Applied Physiology 96, no. 2 (February 2004): 419–27. http://dx.doi.org/10.1152/japplphysiol.00653.2003.
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When a skeletal muscle that is actively producing force is shortened or stretched, the resulting steady-state isometric force after the dynamic phase is smaller or greater, respectively, than the purely isometric force obtained at the corresponding final length. The cross-bridge model of muscle contraction does not readily explain this history dependence of force production. The most accepted proposal to explain both, force depression after shortening and force enhancement after stretch, is a nonuniform behavior of sarcomeres that develops during and after length changes. This hypothesis is based on the idea of instability of sarcomere lengths on the descending limb of the force-length relationship. However, recent evidence suggests that skeletal muscles may be stable over the entire range of active force production, including the descending limb of the force-length relationship. The purpose of this review was to critically evaluate hypotheses aimed at explaining the history dependence of force production and to provide some novel insight into the possible mechanisms underlying these phenomena. It is concluded that the sarcomere nonuniformity hypothesis cannot always explain the total force enhancement observed after stretch and likely does not cause all of the force depression after shortening. There is evidence that force depression after shortening is associated with a reduction in the proportion of attached cross bridges, which, in turn, might be related to a stress-induced inhibition of cross-bridge attachment in the myofilament overlap zone. Furthermore, we suggest that force enhancement is not associated with instability of sarcomeres on the descending limb of the force-length relationship and that force enhancement has an active and a passive component. Force depression after shortening and force enhancement after stretch are likely to have different origins.
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Pinniger, Gavin J., and Andrew G. Cresswell. "Residual force enhancement after lengthening is present during submaximal plantar flexion and dorsiflexion actions in humans." Journal of Applied Physiology 102, no. 1 (January 2007): 18–25. http://dx.doi.org/10.1152/japplphysiol.00565.2006.
Full textAbstract:
Stretch of an activated muscle causes a transient increase in force during the stretch and a sustained, residual force enhancement (RFE) after the stretch. The purpose of this study was to determine whether RFE is present in human muscles under physiologically relevant conditions (i.e., when stretches were applied within the working range of large postural leg muscles and under submaximal voluntary activation). Submaximal voluntary plantar flexion (PFv) and dorsiflexion (DFv) activation was maintained by providing direct visual feedback of the EMG from soleus or tibialis anterior, respectively. RFE was also examined during electrical stimulation of the plantar flexion muscles (PFs). Constant-velocity stretches (15°/s) were applied through a range of motion of 15° using a custom-built ankle torque motor. The muscles remained active throughout the stretch and for at least 10 s after the stretch. In all three activation conditions, the stable joint torque measured 9–10 s after the stretch was greater than the isometric joint torque at the final joint angle. When expressed as a percentage of the isometric torque, RFE values were 7, 13, and 12% for PFv, PFs, DFv, respectively. These findings indicate that RFE is a characteristic of human skeletal muscle and can be observed during submaximal (25%) voluntary activation when stretches are applied on the ascending limb of the force-length curve. Although the underlying mechanisms are unclear, it appears that sarcomere popping and passive force enhancement are insufficient to explain the presence of RFE in these experiments.
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Cheatham, Scott W., and Russell Baker. "Quantification of the Rockfloss® Floss Band Stretch Force at Different Elongation Lengths." Journal of Sport Rehabilitation 29, no. 3 (March 1, 2020): 377–80. http://dx.doi.org/10.1123/jsr.2019-0034.
Full textAbstract:
Context: Floss bands are a popular intervention used by sports medicine professionals to enhance myofascial function and mobility. The bands are often wrapped around a region of the body in an overlapping fashion (eg, 50%) and then tensioned by stretching the band to a desired length (eg, 50%). To date, no research has investigated the stretch force of the bands at different elongation lengths. Objective: The purpose of this clinical study was to quantify the Rockfloss® band stretch force at 6 different elongation lengths (ie, 25%–150%) for the 5.08- and 10.16-cm width bands. Design: Controlled laboratory study. Setting: University kinesiology laboratory. Participants: One trained researcher conducted all measurements. Procedures: The stretch force of a floss band was measured at 6 different elongation lengths with a force gauge. Main Outcome Measures: Band tension force at different band elongation lengths. Results: The stretch force values for the 5.08-cm width (2 in) were as follows: 25% = 13.53 (0.25) N, 50% = 24.57 (0.28) N, 75% = 36.18 (0.39) N, 100% = 45.89 (0.62) N, 125% = 54.68 (0.26) N, and 150% = 62.54 (0.40) N. The stretch force values for the 10.16-cm width (4 in) were as follows: 25% = 16.70 (0.35) N, 50% = 31.90 (0.52) N, 75% = 47.45 (0.44) N, 100% = 57.75 (0.24) N, 125% = 69.02 (0.28) N, and 150% = 81.10 (0.67) N. Both bandwidths demonstrated a linear increase in stretch force as the bands became longer. Conclusion: These values may help professionals to understand and document the tension force being applied at different lengths to produce a more beneficial application during treatment. Future research should determine how the different length/tensions effect the local myofascia, arterial, and vascular systems.
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Choi, Hwan, Tishya Anne Leong Wren, and Katherine Muterspaugh Steele. "Gastrocnemius operating length with ankle foot orthoses in cerebral palsy." Prosthetics and Orthotics International 41, no. 3 (September 9, 2016): 274–85. http://dx.doi.org/10.1177/0309364616665731.
Full textAbstract:
Background:Many individuals with cerebral palsy wear ankle foot orthoses during daily life. Orthoses influence joint motion, but how they impact muscle remains unclear. In particular, the gastrocnemius is commonly stiff in cerebral palsy. Understanding whether orthoses stretch or shorten this muscle during daily life may inform orthosis design and rehabilitation.Objectives:This study investigated the impact of different ankle foot orthoses on gastrocnemius operating length during walking in children with cerebral palsy.Study design:Case series, within subject comparison of gastrocnemius operating length while walking barefoot and with two types of ankle foot orthoses.Methods:We performed gait analyses for 11 children with cerebral palsy. Each child was fit with two types of orthoses: a dynamic ankle foot orthosis (Cascade dynamic ankle foot orthosis) and an adjustable dynamic response ankle foot orthosis (Ultraflex ankle foot orthosis). Musculoskeletal modeling was used to quantify gastrocnemius musculotendon operating length and velocity with each orthosis.Results:Walking with ankle foot orthoses could stretch the gastrocnemius more than barefoot walking for some individuals; however, there was significant variability between participants and orthoses. At least one type of orthosis stretched the gastrocnemius during walking for 4/6 and 3/5 of the Gross Motor Functional Classification System Level I and III participants, respectively. AFOs also reduced peak gastrocnemius lengthening velocity compared to barefoot walking for some participants, with greater reductions among the Gross Motor Functional Classification System Level III participants. Changes in gastrocnemius operating length and lengthening velocity were related to changes in ankle and knee kinematics during gait.Conclusion:Ankle foot orthoses impact gastrocnemius operating length during walking and, with proper design, may assist with stretching tight muscles in daily life.Clinical relevanceDetermining whether ankle foot orthoses stretch tight muscles can inform future orthotic design and potentially provide a platform for integrating therapy into daily life. However, stretching tight muscles must be balanced with other goals of orthoses such as improving gait and preventing bone deformities.
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Leonard, T. R., M. DuVall, and W. Herzog. "Force enhancement following stretch in a single sarcomere." American Journal of Physiology-Cell Physiology 299, no. 6 (December 2010): C1398—C1401. http://dx.doi.org/10.1152/ajpcell.00222.2010.
Full textAbstract:
It has been accepted for half a century that, for a given level of activation, the steady-state isometric force of a muscle sarcomere depends exclusively on the amount of overlap between the contractile filaments actin and myosin, or equivalently sarcomere length (Gordon AM et al., J Physiol 184: 170–192, 1966). Moreover, according to the generally accepted paradigm of muscle contraction, the cross-bridge theory (Huxley AF, Prog Biophys Biophys Chem 7: 255–318, 1957), this steady-state isometric sarcomere force is independent of the muscle's contractile history (Huxley AF, Prog Biophys Biophys Chem 7: 255–318, 1957; Walcott S and Herzog W, Math Biosci 216: 172–186, 2008); i.e., it is independent of whether a muscle is held at a constant length before and during the contraction or whether the muscle is shortened or lengthened to the same constant length. This, however, is not the case, as muscles and single fibers that are stretched show greatly increased steady-state isometric forces compared with preparations that are held at a constant length (Abbott BC and Aubert XM, J Physiol 117: 77–86, 1952; De Ruiter CJ et al., J Physiol 526.3: 671–681, 2000; Edman KAP et al., J Physiol 281: 139–155, 1978; Edman KAP et al., J Gen Physiol 80: 769–784, 1982; Edman KAP and Tsuchiya T, J Physiol 490.1: 191–205, 1996). This so-called “residual force enhancement” (Edman KAP et al., J Gen Physiol 80: 769–784, 1982) offers a perplexing puzzle for muscle physiologists. Many theories have been advanced to address the discrepancy between prediction and observation with the most popular and accepted being the sarcomere length nonuniformity theory (Morgan DL, Biophys J 57: 209–221, 1990), which explains the residual force enhancement with the development of large nonuniformities in sarcomere lengths during muscle stretching. Here, we performed experiments in mechanically isolated sarcomeres and observed that the residual force enhancement following active stretching is preserved. Since our preparation utilizes a single sarcomere, a redistribution of the length of neighboring sarcomeres to produce the higher force following stretch is, by design, precluded. Furthermore, the enhanced forces in the single sarcomeres always exceed the isometric forces on the plateau of the force-length relationship, thereby eliminating the possibility that our result might have been obtained because of a redistribution of half-sarcomere lengths. Since force enhancement in single myofibrils has been associated with actin-titin interactions (Kulke M et al., Circ Res 89: 874–881, 2001; Li Q et al., Biophys J 69: 1508–1518, 1995) and calcium binding to titin (Joumaa V et al., Am J Physiol Cell Physiol 294: C74–C78, 2008; Labeit D et al., Proc Natl Acad Sci USA 100: 13716–13721, 2003), titin may regulate the sarcomeric force enhancement observed here.
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Ettema, G. J., A. J. van Soest, and P. A. Huijing. "The role of series elastic structures in prestretch-induced work enhancement during isotonic and isokinetic contractions." Journal of Experimental Biology 154, no. 1 (November 1, 1990): 121–36. http://dx.doi.org/10.1242/jeb.154.1.121.
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The influence of series elastic structures on the dynamics of the contractile machinery was examined in the gastrocnemius medialis (GM) of five male Wistar rats, with respect to enhancement of work of a muscle-tendon complex after active stretch. Imposed isotonic and isokinetic contractions were preceded by either an isometric phase (PI) or an active stretch (PS). The effects of fibre length differences at the onset of shortening, due to differences of extension of tendinous structures, were studied. For the isotonic experiments fibre length and shortening velocity were estimated 30 ms after release and compared with the PI length-velocity curve determined at the same force level. For shortening above the optimum length, about half of the enhanced shortening found after prestretch could be explained by PS-PI fibre length differences. Below the optimum length, PS shortening velocity was somewhat lower than expected on the basis of length-velocity characteristics. Enhancement of work output due to stretch was different for isokinetic and isotonic shortening. In isokinetic shortening, following prestretch, fibre work was limited because of enhanced shortening of the tendinous structures. In stretch-shortening cycles imposed on a muscle-tendon complex, the length of the complex affected all prestretch effects, i.e. potentiation of the contractile element, contractile element interaction with the tendinous structures, and elastic energy release. It is concluded that, besides potentiation effects and enhanced elastic energy release, the influence of series elastic structures on fibre dynamics determines active stretch-induced work enhancement. The contribution by these mechanisms to this work enhancement depends largely on the type of stretch-shortening cycle.
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Cavagna, G. A., M. Mazzanti, N. C. Heglund, and G. Citterio. "Storage and release of mechanical energy by active muscle: a non-elastic mechanism?" Journal of Experimental Biology 115, no. 1 (March 1, 1985): 79–87. http://dx.doi.org/10.1242/jeb.115.1.79.
Full textAbstract:
In frog muscle fibres, tetanically stimulated at a sarcomere length of about 2 micron, stretched at a velocity of 1 lengths-1 and released against a force equal to the maximum isometric, P0, a phase of rapid isotonic shortening takes place after release. As the amplitude of the stretch is increased from 1.5 to 9% of the initial length: (1) the amount of rapid isotonic shortening increases up to 9–10 nm per half sarcomere and (2) the stiffness of the fibre (an indication of the number of bridges attached) decreases to a value about equal to that measured during an isometric contraction. If a 5–10 ms delay is left between the end of stretch and release, the amount of rapid isotonic shortening increases to about 12 nm hs-1. A 300–500 ms delay, however, results in a decrease in rapid isotonic shortening to about 5 nm hs-1 and also results in a velocity transients against P0 that are similar to those described during release from a state of isometric contraction. It is concluded that the force attained after large, fast stretches is due to a greater force developed by each bridge and not to a greater number of bridges. After the elastic recoil (when the force is suddenly reduced to P0), these strained bridges are able to shorten by about 12 nm hs-1, suggesting that, during and immediately after stretching, they are charged to levels of potential energy greater than those attained in an isometric contraction.
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Saripalli, Anjali L., Kristoffer B. Sugg, Christopher L. Mendias, Susan V. Brooks, and Dennis R. Claflin. "Active shortening protects against stretch-induced force deficits in human skeletal muscle." Journal of Applied Physiology 122, no. 5 (May 1, 2017): 1218–26. http://dx.doi.org/10.1152/japplphysiol.01054.2016.
Full textAbstract:
Skeletal muscle contraction results from molecular interactions of myosin “crossbridges” with adjacent actin filament binding sites. The binding of myosin to actin can be “weak” or “strong,” and only strong binding states contribute to force production. During active shortening, the number of strongly bound crossbridges declines with increasing shortening velocity. Forcibly stretching a muscle that is actively shortening at high velocity results in no apparent negative consequences, whereas stretch of an isometrically (fixed-length) contracting muscle causes ultrastructural damage and a decline in force-generating capability. Our working hypothesis is that stretch-induced damage is uniquely attributable to the population of crossbridges that are strongly bound. We tested the hypothesis that stretch-induced force deficits decline as the prevailing shortening velocity is increased. Experiments were performed on permeabilized segments of individual skeletal muscle fibers obtained from human subjects. Fibers were maximally activated and allowed either to generate maximum isometric force (Fo), or to shorten at velocities that resulted in force maintenance of ≈50% Fo or ≈2% Fo. For each test condition, a rapid stretch equivalent to 0.1 × optimal fiber length was applied. Relative to prestretch Fo, force deficits resulting from stretches applied during force maintenance of 100, ≈50, and ≈2% Fo were 23.2 ± 8.6, 7.8 ± 4.2, and 0.3 ± 3.3%, respectively (means ± SD, n = 20). We conclude that stretch-induced damage declines with increasing shortening velocity, consistent with the working hypothesis that the fraction of strongly bound crossbridges is a causative factor in the susceptibility of skeletal muscle to stretch-induced damage. NEW & NOTEWORTHY Force deficits caused by stretch of contracting muscle are most severe when the stretch is applied during an isometric contraction, but prevented if the muscle is shortening at high velocity when the stretch occurs. This study indicates that velocity-controlled modulation of the number of strongly bound crossbridges is the basis for the observed relationship between stretch-induced muscle damage and prevailing shortening velocity.
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Blazevich, A. J., D. Cannavan, C. M. Waugh, F. Fath, S. C. Miller, and A. D. Kay. "Neuromuscular factors influencing the maximum stretch limit of the human plantar flexors." Journal of Applied Physiology 113, no. 9 (November 1, 2012): 1446–55. http://dx.doi.org/10.1152/japplphysiol.00882.2012.
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Maximum joint range of motion is an important parameter influencing functional performance and musculoskeletal injury risk. Nonetheless, a complete description of the muscle architectural and tendon changes that occur during stretch and the factors influencing maximum range of motion is lacking. We measured muscle-tendon elongation and fascicle lengthening and rotation sonographically during maximal plantar flexor stretches in 21 healthy men. Electromyogram (EMG) recordings were obtained synchronously with ultrasound and joint moment data, and H-reflex measurements were made with the ankle at neutral (0°) and dorsiflexed (50% maximal passive joint moment) positions; the maximum H amplitude (normalized to maximum M-wave amplitude; Mmax) and H-amplitude elicited at a stimulation intensity that evoked 10% Mmaxwere obtained. Maximal stretch was accomplished through significant muscle (14.9%; 30 mm) and tendon lengthening (8.4%; 22 mm). There were similar relative changes in fascicle length and angle, but planimetric modeling indicated that the contribution of fascicle rotation to muscle lengthening was small (<4 mm). Subjects with a greater range of motion showed less resistance to stretch and a greater passive joint moment at stretch termination than less flexible subjects (i.e., greater stretch tolerance). Also, greater fascicle rotation accompanied muscle elongation (9.7 vs. 5.9%) and there was a greater tendon length at stretch termination in more flexible subjects. Finally, a moderate correlation between the angle of EMG onset and maximum range of motion was obtained ( r = 0.60, P < 0.05), despite there being no difference in H-reflex magnitudes between the groups. Thus clear differences in the neuromuscular responses to stretch were observed between “flexible” and “inflexible” subjects.