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1
Kulik, T. J., J. N. Evans, and W. J. Gamble. "Stretch-induced contraction in pulmonary arteries." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 6 (1988): H1391—H1398. http://dx.doi.org/10.1152/ajpheart.1988.255.6.h1391.
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Stretch stimulates contraction of systemic blood vessels, but the response has not been described in pulmonary vessels. To determine whether pulmonary arteries contract when stretched, isolated cylindrical segments of pulmonary arteries were suspended between two parallel wires, stretched, and the active force was generated in response to stretch measured. Eighty-nine percent of segments from small (in situ diameter less than 1,000 microns) feline pulmonary arteries contracted when stretched, and in 65% of these the magnitude of stretch was related to the magnitude of contraction. Large (in situ diameter greater than or equal to 1,000 microns) feline pulmonary arteries did not contract with stretch. Multiple, rapidly repeated stretches resulted in a diminution of active force development. Stretch-induced contraction required external Ca2+ and was abolished by diltiazem (10 microns), but it was not affected by phenoxybenzamine, phentolamine, diethylcarbamazine, or mechanical removal of endothelium. Indomethacin blunted but did not abolish stretch-induced contraction, an effect that may have been nonspecific. This study suggests that stretch can act, probably directly, on smooth muscle in small feline pulmonary arteries to elicit contraction and that it may be a determinant of pulmonary vascular tone. In addition, feline pulmonary arteries are suitable for the in vitro study of stretch-induced contraction.
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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 (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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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 (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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Tangney, Jared R., Stuart G. Campbell, Andrew D. McCulloch, and Jeffrey H. Omens. "Timing and magnitude of systolic stretch affect myofilament activation and mechanical work." American Journal of Physiology-Heart and Circulatory Physiology 307, no. 3 (2014): H353—H360. http://dx.doi.org/10.1152/ajpheart.00233.2014.
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Dyssynchronous activation of the heart leads to abnormal regional systolic stretch. In vivo studies have suggested that the timing of systolic stretch can affect regional tension and external work development. In the present study, we measured the direct effects of systolic stretch timing on the magnitude of tension and external work development in isolated murine right ventricular papillary muscles. A servomotor was used to impose precisely timed stretches relative to electrical activation while a force transducer measured force output and strain was monitored using a charge-couple device camera and topical markers. Stretches taking place during peak intracellular Ca2+ statistically increased peak tension up to 270%, whereas external work due to stretches in this interval reached values of 500 J/m. An experimental analysis showed that time-varying elastance overestimated peak tension by 100% for stretches occurring after peak isometric tension. The addition of the force-velocity relation explained some effects of stretches occurring before the peak of the Ca2+ transient but had no effect in later stretches. An estimate of transient deactivation was measured by performing quick stretches to dissociate cross-bridges. The timing of transient deactivation explained the remaining differences between the model and experiment. These results suggest that stretch near the start of cardiac tension development substantially increases twitch tension and mechanical work production, whereas late stretches decrease external work. While the increased work can mostly be explained by the time-varying elastance of cardiac muscle, the decreased work in muscles stretched after the peak of the Ca2+ transient is largely due to myofilament deactivation.
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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 (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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Gardner, D. G., H. Wirtz, and L. G. Dobbs. "Stretch-dependent regulation of atrial peptide synthesis and secretion in cultured atrial cardiocytes." American Journal of Physiology-Endocrinology and Metabolism 263, no. 2 (1992): E239—E244. http://dx.doi.org/10.1152/ajpendo.1992.263.2.e239.
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We have developed a novel system to study stretch-dependent secretion of atrial natriuretic peptide (ANP) using cultured neonatal rat atriocytes in vitro. Application of tension (i.e., 2 sequential stretches) to cells grown on a flexible culture surface effected a dose-dependent increase in immunoreactive (ir) ANP release into the medium. Analysis of atriocyte cytoplasmic RNA 24 h poststretch revealed an increase in ANP mRNA levels of about ninefold relative to the unstretched controls. Medium ATP levels, measured as an index of cellular damage, were similar in control and stretched cells. Furthermore, cooling the cultures to 0 degrees C suppressed both basal as well as stretch-stimulated release. These findings argue against cellular damage and nonspecific release of irANP as an explanation for the increase in medium immunoreactivity. Stretch was incapable of amplifying the secretory response to prostaglandin F2 alpha, suggesting possible overlap in the pathways whereby these stimuli effect release of the peptide. The calcium channel blocker verapamil had no effect on stretch-dependent irANP release, whereas calmidzolium, a calmodulin inhibitor, suppressed basal as well as stretch-dependent secretion, implying a potentially important relationship between intracellular calcium metabolism and irANP release.
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Kubo, Yusuke, Bernd Hoffmann, Katja Goltz, et al. "Different Frequency of Cyclic Tensile Strain Relates to Anabolic/Catabolic Conditions Consistent with Immunohistochemical Staining Intensity in Tenocytes." International Journal of Molecular Sciences 21, no. 3 (2020): 1082. http://dx.doi.org/10.3390/ijms21031082.
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Tenocytes are mechanosensitive cells intimately adapting their expression profile and hence, their phenotype to their respective mechanomilieu. The immunolocalization and expression intensity of tenogenic, anabolic and catabolic markers in tenocytes in response to in vitro mechanical loading have not been monitored by immunohistochemical staining (IHC). Thus, we investigated the association between IHC intensities, different stimulation frequencies, and tenogenic metabolism using a versatile mechanical stretcher. Primary tenocytes obtained from murine Achilles tendons were transferred to poly(dimethylsiloxane) (PDMS) elastomeric chamber. Chambers were cyclically stretched by 5% in uniaxial direction at a variation of tensile frequency (1 or 2 Hz) for 3 h. After stretching, cell physiology, IHC intensities of tendon-related markers, and protein level of the angiogenesis marker vascular endothelial growth factor (VEGF) were evaluated. Cell proliferation in tenocytes stimulated with 1 Hz stretch was significantly higher than with 2 Hz or without stretch, while 2 Hz stretch induced significantly reduced cell viability and proliferation with microscopically detectable apoptotic cell changes. The amount of scleraxis translocated into the nuclei and tenomodulin immunoreactivity of tenocytes treated with stretch were significantly higher than of non-stretched cells. The collagen type-1 expression level in tenocytes stretched at 1 Hz was significantly higher than in those cultivated with 2 Hz or without stretching, whereas the matrix metalloproteinase (MMP)-1 and MMP-13 immunoreactivities of cells stretched at 2 Hz were significantly higher than in those stimulated with 1 Hz or without stretching. The secreted VEGF-protein level of tenocytes stretched at 2 Hz was significantly higher than without stretching. Our IHC findings consistent with cell physiology suggest that appropriate stretching can reproduce in vitro short-term tenogenic anabolic/catabolic conditions and allow us to identify an anabolic stretching profile.
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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 (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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Fasciano, Robert W., and Leslie Tung. "Factors governing mechanical stimulation in frog hearts." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 6 (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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JU, YIGUANG, HONGSHENG GUO, KAORU MARUTA, and FENGSHAN LIU. "On the extinction limit and flammability limit of non-adiabatic stretched methane–air premixed flames." Journal of Fluid Mechanics 342 (July 10, 1997): 315–34. http://dx.doi.org/10.1017/s0022112097005636.
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Extinction limits and the lean flammability limit of non-adiabatic stretched premixed methane–air flames are investigated numerically with detailed chemistry and two different Planck mean absorption coefficient models. Attention is paid to the combined effect of radiative heat loss and stretch at low stretch rate. It is found that for a mixture at an equivalence ratio lower than the standard lean flammability limit, a moderate stretch can strengthen the combustion and allow burning. The flame is extinguished at a high stretch rate due to stretch and is quenched at a low stretch rate due to radiation loss. A O-shaped curve of flame temperature versus stretch rate with two distinct extinction limits, a radiation extinction limit and a stretch extinction limit respectively on the left- and right-hand sides, is obtained. A C-shaped curve showing the flammability limit of the stretched methane–air flame is obtained by plotting these two extinction limits in the mixture strength coordinate. A good agreement is shown on comparing the predicted results with the experimental data. For equivalence ratio larger than a critical value, it is found that the O-shaped temperature curve opens up in the middle of the stable branch, so that the stable branch divides into two stable flame branches; a weak flame branch and a normal flame branch. The weak flame can survive between the radiation extinction limit and the opening point (jump limit) while the normal flame branch can survive from its stretch extinction limit to zero stretch rate. Finally, a G-shaped curve showing both extinction limits and jump limits of stretched methane–air flames is presented. It is found that the critical equivalence ratio for opening up corresponds to the standard flammability limit measured in microgravity. Furthermore, the results show that the flammability limit (inferior limit) of the stretched methane–air flame is lower than the standard flammability limit because flames are strengthened by a moderate stretch at Lewis number less than unity.
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Nicol, Caroline, and Paavo V. Komi. "Quantification of Achilles Tendon Force Enhancement by Passively Induced Dorsiflexion Stretches." Journal of Applied Biomechanics 15, no. 3 (1999): 221–32. http://dx.doi.org/10.1123/jab.15.3.221.
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Magnitude of the reflex contribution to force enhancement was investigated in vivo during passive stretches of the Achilles tendon (AT) of one female subject. Thirty passive (5 × 6) dorsiflexions were induced by a motorized ankle ergometer. Achilles tendon force (ATF) was sensed by a buckle transducer applied surgically around the right AT. Single passive stretches resulted in a low but rather linear ATF increase in the absence of EMG (surface electrodes) activity. In the presence of reflexes, a clear ATF enhancement occurred 13–15 ms after the beginning of the EMG reflex responses. In double dorsiflexions at either 1.2 or 1.9 rad · s-1, which were separated by a maintained stretched position of either 40 or 90 ms, the first stretch resulted in initial linear ATF increase, followed by an additional force enhancement during the plateau phase. This reflexly induced increase represented 94 ± 4 N and 184 ± 1 N, respectively, for the 40 and the 90 ms plateaus, corresponding to 210 ± 85% and 486 ± 177% enhancements as compared to the first passive stretch effect. The results suggest further that timing of the stretch during the twitch response influences the magnitude and rate of force potentiation.
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Wang, Bao-Wei, Huei-Fong Hung, Hang Chang, Peiliang Kuan та Kou-Gi Shyu. "Mechanical stretch enhances the expression of resistin gene in cultured cardiomyocytes via tumor necrosis factor-α". American Journal of Physiology-Heart and Circulatory Physiology 293, № 4 (2007): H2305—H2312. http://dx.doi.org/10.1152/ajpheart.00361.2007.
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The heart is a resistin target tissue and can function as an autocrine organ. We sought to investigate whether cyclic mechanical stretch could induce resistin expression in cardiomyocytes and to test whether there is a link between the stretch-induced TNF-α and resistin. Neonatal Wistar rat cardiomyocytes grown on a flexible membrane base were stretched by vacuum to 20% of maximum elongation at 60 cycles/min. Cyclic stretch significantly increased resistin protein and mRNA expression after 2–18 h of stretch. Addition of PD-98059, TNF-α antibody, TNF-α receptor antibody, and ERK MAP kinase small interfering RNA 30 min before stretch inhibited the induction of resistin protein. Cyclic stretch increased, whereas PD-98059 abolished, the phosphorylated ERK protein. Gel-shift assay showed a significant increase in DNA-protein binding activity of NF-κB after stretch, and PD-98059 abolished the DNA-protein binding activity induced by cyclic stretch. DNA binding complexes induced by cyclic stretch could be supershifted by p65 monoclonal antibody. Cyclic stretch increased resistin promoter activity, whereas PD-98059 and p65 antibody decreased resistin promoter activity. Cyclic stretch significantly increased TNF-α secretion from myocytes. Recombinant resistin protein and conditioned medium from stretched cardiomyocytes reduced glucose uptake in cardiomyocytes, and recombinant small interfering RNA of resistin or TNF-α antibody reversed glucose uptake. In conclusion, cyclic mechanical stretch enhances resistin expression in cultured rat neonatal cardiomyocytes. The stretch-induced resistin is mediated by TNF-α, at least in part, through ERK MAP kinase and NF-κB pathways. Glucose uptake in cardiomyocytes was reduced by resistin upregulation.
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Patil, Amit, Arne Nordmark, and Anders Eriksson. "Free and constrained inflation of a pre-stretched cylindrical membrane." Proceedings of the Royal Society A: Mathematical, Physical and Engineering Sciences 470, no. 2169 (2014): 20140282. http://dx.doi.org/10.1098/rspa.2014.0282.
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This paper presents the free and constrained inflation of a pre-stretched hyperelastic cylindrical membrane and a subsequent constrained deflation. The membrane material is assumed as a homogeneous and isotropic Mooney–Rivlin solid. The constraining soft cylindrical substrate is assumed to be a distributed linear stiffness normal to the undeformed surface. Both frictionless and adhesive contact are modelled during the inflation as an interaction between the dry surfaces of the membrane and the substrate. An adhesive contact is modelled during deflation. The free and constrained inflation yields governing equations and boundary conditions, which are solved by a finite difference method in combination with a fictitious time integration method. Continuity in the principal stretches and stresses at the contact boundary is dependent on the contact conditions and inflation–deflation phase. The pre-stretch has a counterintuitive softening effect on free and constrained inflation. The variation of limit point pressures with pre-stretch and the occurrence of a cusp point is shown. Interesting trends are observed in the stretch and stress distributions after the interaction of the membrane with soft substrate, which underlines the effect of material parameters, pre-stretch and constraining properties.
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Mitchell, Ulrike H., J. William Myrer, J. Ty Hopkins, Iain Hunter, J. Brent Feland, and Sterling C. Hilton. "Acute Stretch Perception Alteration Contributes to the Success of the PNF “Contract-Relax” Stretch." Journal of Sport Rehabilitation 16, no. 2 (2007): 85–92. http://dx.doi.org/10.1123/jsr.16.2.85.
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Context:Some researchers have suggested that an alteration of stretch perception could be responsible for the success of the contract-relax (CR) stretch, a stretch technique derived from proprioceptive neuromuscular facilitation (PNF).Objective:This study was conducted to determine if the alteration of the stretch perception is a possible explanation for the range of motion (ROM) gains of the CR stretch.Participants:Eighteen subjects performed two stretches in randomized order: the slow stretch and the CR stretch.Main Outcome Measure:The stretch intensity was controlled. The stretch force was measured and compared between the slow stretch and CR stretch.Results:There was a significant difference between the stretch force that could be applied in the PNF stretch (126.0 N) and the slow stretch (108.4 N); P = 0.00086. The average stretch tolerance progressively increased with successive trials from 120.6 N in the first trial to 132.4 N in the fourth trial.Conclusion:The alteration of stretch perception plays a role in the success of the CR form of PNF stretching. At least four repetitions of the CR stretch are recommended to get the greatest ROM gain.
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Law, Roberta Y. W., Lisa A. Harvey, Michael K. Nicholas, Lois Tonkin, Maria De Sousa, and Damien G. Finniss. "Stretch Exercises Increase Tolerance to Stretch in Patients With Chronic Musculoskeletal Pain: A Randomized Controlled Trial." Physical Therapy 89, no. 10 (2009): 1016–26. http://dx.doi.org/10.2522/ptj.20090056.
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Background: Stretch is commonly prescribed as part of physical rehabilitation in pain management programs, yet little is known about its effectiveness.Objective: A randomized controlled trial was conducted to investigate the effects of a 3-week stretch program on muscle extensibility and stretch tolerance in patients with chronic musculoskeletal pain.Design: A within-subject design was used, with one leg of each participant randomly allocated to an experimental (stretch) condition and the other leg randomly allocated to a control (no-stretch) condition.Patients and Setting: Thirty adults with pain of musculoskeletal origin persisting for at least 3 months were recruited from patients enrolled in a multidisciplinary pain management program at a hospital in Sydney, Australia.Intervention: The hamstring muscles of the experimental leg were stretched daily for 1 minute over 3 weeks; the control leg was not stretched. This intervention was embedded within a pain management program and supervised by physical therapists.Measurements: Primary outcomes were muscle extensibility and stretch tolerance, which were reflected by passive hip flexion angles measured with standardized and nonstandardized torques, respectively. Initial measurements were taken before the first stretch on day 1, and final measurements were taken 1 to 2 days after the last stretch. A blinded assessor was used for testing.Results: Stretch did not increase muscle extensibility (mean between-group difference in hip flexion was 1°, 95% confidence interval=−2° to 4°), but it did improve stretch tolerance (mean between-group difference in hip flexion was 8°, 95% confidence interval=5° to 10°).Conclusion: Three weeks of stretch increases tolerance to the discomfort associated with stretch but does not change muscle extensibility in patients with chronic musculoskeletal pain.
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Carson, J. A., R. J. Schwartz, and F. W. Booth. "SRF and TEF-1 control of chicken skeletal alpha-actin gene during slow-muscle hypertrophy." American Journal of Physiology-Cell Physiology 270, no. 6 (1996): C1624—C1633. http://dx.doi.org/10.1152/ajpcell.1996.270.6.c1624.
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The purpose of this study was to delineate the alpha-actin regulatory elements and transcription factors that are responsible for conferring stretch-overload responsiveness during hypertrophy of the anterior latissimus dorsi (ALD) muscle of young chickens by weighting one wing. Minimal promoter constructs were evaluated by direct injection into the ALD, which demonstrated that both serum response element 1 (SRE1) and the transcriptional enhancer factor 1 (TEF-1) elements were sufficient for increased expression during stretch overload. A mutated SRE1 prevented expression in both basal and stretched ALD muscles, whereas a mutated TEF-1 element reduced actin promoter function in both control and stretched muscles. The serum response factor (SRF)-SRE1 binding complex demonstrated faster migration in mobility shift assays from day 3-and day 6-stretched ALD nuclear extracts relative to their control. TEF-1 binding was qualitatively increased in stretched extracts at day 3 but not day 6 of stretch overload. Skeletal alpha-actin mRNA accumulated from day 3 to day 6 of stretch overload. These data demonstrate that SRE1 is necessary and sufficient for stretch-overload responsiveness from the skeletal alpha-actin promoter and that the SRF-SRE1 binding complex migrates faster in stretched nuclear extracts of hypertrophied relative to control extracts from intact ALD muscles of chickens.
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DiPaolo, Brian C., Nurit Davidovich, Marcelo G. Kazanietz, and Susan S. Margulies. "Rac1 pathway mediates stretch response in pulmonary alveolar epithelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 305, no. 2 (2013): L141—L153. http://dx.doi.org/10.1152/ajplung.00298.2012.
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Alveolar epithelial cells (AECs) maintain the pulmonary blood-gas barrier integrity with gasketlike intercellular tight junctions (TJ) that are anchored internally to the actin cytoskeleton. We have previously shown that AEC monolayers stretched cyclically and equibiaxially undergo rapid magnitude- and frequency-dependent actin cytoskeletal remodeling to form perijunctional actin rings (PJARs). In this work, we show that even 10 min of stretch induced increases in the phosphorylation of Akt and LIM kinase (LIMK) and decreases in cofilin phosphorylation, suggesting that the Rac1/Akt pathway is involved in these stretch-mediated changes. We confirmed that Rac1 inhibitors wortmannin or EHT-1864 decrease stretch-stimulated Akt and LIMK phosphorylation and that Rac1 agonists PIP3 or PDGF increase phosphorylation of these proteins in unstretched cells. We also confirmed that Rac1 pathway inhibition during stretch modulated stretch-induced changes in occludin content and monolayer permeability, actin remodeling and PJAR formation, and cell death. As further validation, overexpression of Rac GTPase-activating protein β2-chimerin also preserved monolayer barrier properties in stretched monolayers. In summary, our data suggest that constitutive activity of Rac1, which is necessary for stretch-induced activation of the Rac1 downstream proteins, mediates stretch-induced increases in permeability and PJAR formation.
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De-Doncker, Laurent, Florence Picquet, Julien Petit, and Maurice Falempin. "Effects of Hypodynamia-Hypokinesia on the Muscle Spindle Discharges of Rat Soleus Muscle." Journal of Neurophysiology 89, no. 6 (2003): 3000–3007. http://dx.doi.org/10.1152/jn.00875.2002.
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The aim of this study was to determine whether Ia and II fiber discharges of soleus muscle spindles were modified after a 14-day period of hypodynamia (absence of weight bearing) and hypokinesia (reduction of motor activity). Fifty-one and 38 afferent fibers were studied, respectively, in control and hypodynamia-hypokinesia (HH) groups. Under deep anesthesia (pentobarbital, 30 mg/kg), a L3–L6 laminectomy was performed. Unitary potentials from the L5 dorsal root were recorded in response to ramp-and-hold stretches applied at two stretch amplitudes (3 and 4 mm) and four stretch velocities (6, 10, 15, and 30 mm/s) and to sinusoidal stretches applied at four stretch amplitudes (0.12, 0.25, 0.5, and 1 mm) and six stretch frequencies (0.5, 1, 2, 3, 6, and 10 Hz). In both animal groups, the Ia fibers showed higher dynamic index values, smaller linear range, and higher vibration sensitivity than the II fibers. They also exhibited a pause in their discharges during the stretch release contrary to II fibers, which displayed no pause in their responses. After HH, our results showed that for both fiber types all parameters measured under ramp-and-hold stretches (except the static sensitivity) were significantly increased and under sinusoidal stretches, the vibration sensitivity increased, and the response amplitude only increased at 0.12-mm stretch amplitude. The linear range of Ia afferents was limited to 0.12 mm, whereas it was unchanged for the II fibers. After HH, the stretches could be better transmitted to the muscle spindles, probably resulting from changes in passive mechanical properties of the soleus.
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ElMeligy, Maha, and Taher El-Bitar. "Strain Hardening and Stretch Formability Behavior of Triple Phase (TP) Steel Strips." Acta Metallurgica Slovaca 27, no. 3 (2021): 152–56. http://dx.doi.org/10.36547/ams.27.3.1048.
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The current work explores the strain hardening and stretches formability behaviour of the developed Triple Phase (TP) steel. Double quenched TP steel strips posse three distinguished stages of strain hardening on tensile forming. 1st stage represents the highest n-value reflecting resistance to homogeneous deformation, where steel can be safely stretched. 2nd and 3rd stage reveals lower n-values, where localized thinning exist. On Erichsen testing, the relationship between punch forming force and punch stroke exhibits two forming regions. The 1st region is delineated by a straight line showing an ultra-high strain-hardening rate, which represents a reversible elastic stretch forming. The 2nd forming region continues to a higher Erichsen punch stroke than that of the 1st region and presents the permanent plastic stretch forming behaviour. It is found that bainite and martensite clusters created, by double quenching, in TP-steel exaggerated the elastic stretch forming limit 10 times higher than the as-hot rolled condition. 7 min. holding time of strips in the salt bath is considered the most effective for the creation of a useful volume fraction of the bainite phase. However, 21 min. holding time in salt bath grows martensite laths through the bainite aggregates, affecting negatively on stretch formability.
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Gao, Song, and James A. Carson. "Lewis lung carcinoma regulation of mechanical stretch-induced protein synthesis in cultured myotubes." American Journal of Physiology-Cell Physiology 310, no. 1 (2016): C66—C79. http://dx.doi.org/10.1152/ajpcell.00052.2015.
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Mechanical stretch can activate muscle and myotube protein synthesis through mammalian target of rapamycin complex 1 (mTORC1) signaling. While it has been established that tumor-derived cachectic factors can induce myotube wasting, the effect of this catabolic environment on myotube mechanical signaling has not been determined. We investigated whether media containing cachectic factors derived from Lewis lung carcinoma (LLC) can regulate the stretch induction of myotube protein synthesis. C2C12 myotubes preincubated in control or LLC-derived media were chronically stretched. Protein synthesis regulation by anabolic and catabolic signaling was then examined. In the control condition, stretch increased mTORC1 activity and protein synthesis. The LLC treatment decreased basal mTORC1 activity and protein synthesis and attenuated the stretch induction of protein synthesis. LLC media increased STAT3 and AMP-activated protein kinase phosphorylation in myotubes, independent of stretch. Both stretch and LLC independently increased ERK1/2, p38, and NF-κB phosphorylation. In LLC-treated myotubes, the inhibition of ERK1/2 and p38 rescued the stretch induction of protein synthesis. Interestingly, either leukemia inhibitory factor or glycoprotein 130 antibody administration caused further inhibition of mTORC1 signaling and protein synthesis in stretched myotubes. AMP-activated protein kinase inhibition increased basal mTORC1 signaling activity and protein synthesis in LLC-treated myotubes, but did not restore the stretch induction of protein synthesis. These results demonstrate that LLC-derived cachectic factors can dissociate stretch-induced signaling from protein synthesis through ERK1/2 and p38 signaling, and that glycoprotein 130 signaling is associated with the basal stretch response in myotubes.
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Menary, Gary H., C. W. Tan, and C. G. Armstrong. "The Effect of Temperature, Strain Rate and Strain on the Induced Mechanical Properties of Biaxially Stretched PET." Key Engineering Materials 504-506 (February 2012): 1117–22. http://dx.doi.org/10.4028/www.scientific.net/kem.504-506.1117.
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The study is focused on the effect of strain rate, temperature and stretch ratio on the room temperature mechanical properties of PET (Polyethylene terephthalate) following biaxial deformation. Specimens were biaxially stretched within a temperature range 80-110°C, a strain rate in the range 1-16/s and stretch ratio in the range 1-2.8. The tensile moduli of the stretched specimens were obtained using tensile testing. Results show that post-stretching room temperature modulus increases with decreasing temperature, increasing strain rate, and stretch ratio.
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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 (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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Rassier, Dilson E., Eun-Jeong Lee, and Walter Herzog. "Modulation of passive force in single skeletal muscle fibres." Biology Letters 1, no. 3 (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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Lin, D. C., and W. Z. Rymer. "Mechanical properties of cat soleus muscle elicited by sequential ramp stretches: implications for control of muscle." Journal of Neurophysiology 70, no. 3 (1993): 997–1008. http://dx.doi.org/10.1152/jn.1993.70.3.997.
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1. Force changes in areflexive cat soleus muscle in decerebrate cats were recorded in response to two sequential constant velocity (ramp) stretches, separated by a variable time interval during which the length was held constant. Initial (i.e., prestretch) background force was generated by activating the crossed-extension reflex, and stretch reflexes were eliminated by section of ipsilateral dorsal roots. 2. For the initial 400-900 microns of the first stretch, the muscle exhibited high stiffness, classically termed "short-range stiffness." This high stiffness region was followed by an abrupt reduction in stiffness, called muscle "yield," after which force remained at a relatively constant level, achieving a plateau in force. This plateau force level depended largely on stretch velocity, but this dependence was much less than proportional to the increase in stretch velocity, in that a 10-fold increase in velocity produced < 2-fold increase in plateau force. 3. In experiments where the velocities of the two sequential ramp stretches were identical, the force plateau level was the same for each stretch, regardless of the time elapsed before the second stretch (varied from 0 to 500 ms). In contrast, measures of stiffness during the initial portion of the second stretch showed time-dependent magnitude reductions. However, stiffness recovered quickly after the first stretch was completed, returning to control values within 30-40 ms. 4. In one preparation, in which the velocities of the two sequential ramp stretches were different, the force plateau elicited during the second stretch exhibited velocity dependence comparable with that recorded in the earlier single velocity studies. Furthermore, muscle yield was still evident in the case where the force change was due solely to the change in velocity and where short-range stiffness had not yet recovered fully from the initial stretch. On the basis of these findings, we argue that the classical descriptions of short-range stiffness and yield are inadequate and that the change in force that has typically been called the muscle yield reflects a transition between short-range, transient elastic behavior to steady-state, essentially viscous behavior. 5. To examine changes in the muscle's mechanical stiffness during single ramp stretches, a single pulse perturbation was superimposed at various times before, during, and subsequent to the constant velocity stretch. The force increment elicited in response to each pulse decreased relative to the initial isometric value, remained essentially constant until the end of the ramp, and then returned to its prestretch magnitude shortly (30-40 ms) after stretch termination.(ABSTRACT TRUNCATED AT 400 WORDS)
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Carson, James A., and Frank W. Booth. "Serum response factor mRNA induction in the hypertrophying chicken patagialis muscle." Journal of Applied Physiology 86, no. 1 (1999): 377–82. http://dx.doi.org/10.1152/jappl.1999.86.1.377.
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Gene expression in the stretched chicken patagialis (Pat) muscle has not been extensively examined. This study’s purpose was to determine the Pat muscle’s expression pattern of serum response factor (SRF), skeletal α-actin, and MyoD mRNAs after 3 days (onset of stretch), 6 days (end of first week of rapid growth), and 14 days (slowed rate of stretch-induced growth) of stretch. SRF mRNA demonstrated two species (B1 and B2), with B2 being more prevalent in the predominantly fast-twitch Pat muscle, compared with the slow-tonic muscle. Stretch overload increased B1 and B2 SRF mRNA concentrations, and the increase in B1 SRF mRNA concentration was greater at day 6compared with days 3 or 14. MyoD mRNA concentration was greater in 3-day-stretched Pat muscles, compared with days 6 or 14 . Skeletal α-actin mRNA concentration was not changed during the study. Gel mobility shift assays demonstrated that SRF binding with serum response element 1 of the skeletal α-actin promoter had no altered binding patterns from 6-day-stretched Pat nuclear extracts. It appears that SRF and MyoD mRNAs are induced in the stretch-overloaded Pat muscle but at different time points.
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Hayashi, Naoyuki, Shawn G. Hayes, and Marc P. Kaufman. "Comparison of the exercise pressor reflex between forelimb and hindlimb muscles in cats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 281, no. 4 (2001): R1127—R1133. http://dx.doi.org/10.1152/ajpregu.2001.281.4.r1127.
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In thirteen cats anesthetized with α-chloralose, we compared the cardiovascular and ventilatory responses to both static contraction and tendon stretch of a hindlimb muscle group, the triceps surae, with those to contraction and stretch of a forelimb muscle group, the triceps brachii. Static contraction and stretch of both muscle groups increased mean arterial pressure and heart rate, and the responses were directly proportional to the developed tension. The cardiovascular increases, however, were significantly greater ( P < 0.05) when the triceps brachii muscles were contracted or stretched than when the triceps surae muscles were contracted or stretched, even when the tension developed by either maneuver was corrected for muscle weight. Likewise, the ventilatory increases were greater when the triceps brachii muscles were stretched than when the triceps surae muscles were stretched. Contraction of either muscle group did not increase ventilation. Our results suggest that in the anesthetized cat the cardiovascular responses to both static contraction and tendon stretch are greater when arising from forelimb muscles than from hindlimb muscles.
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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 (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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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 (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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Sevieux, Nancy, Jawed Alam та 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, № 6 (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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Miller, Joshua, and Matthew J. Comeau. "Stretch or No Stretch?" Strength and Conditioning Journal 24, no. 1 (2002): 20. http://dx.doi.org/10.1519/00126548-200202000-00005.
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Miller, Joshua, and Matthew J. Comeau. "Stretch or No Stretch?" Strength and Conditioning Journal 24, no. 1 (2002): 21. http://dx.doi.org/10.1519/00126548-200202000-00006.
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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 (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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Matusiak, Malgorzata, and Otgonsuren Sukhbat. "Liquid Moisture Transport in Knitted Fabrics in Relaxed and Stretched State." Communications in Development and Assembling of Textile Products 3, no. 2 (2022): 127–36. http://dx.doi.org/10.25367/cdatp.2022.3.p127-136.
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The aim of this work was to analyze the influence of stretch on liquid moisture transport through the knitted fabrics for T-shirts. Five variants of cotton and cotton blended fabrics were measured by means of the Moisture Management Tester. Measurements have been performed for samples in the unstretched state and samples stretched by 15%. To precisely stretch the fabrics, the MMT Stretch Fabric Fixture has been applied. The results have been analyzed statistically in order to assess the influence of stretch on the parameters characterizing the moisture transport through the fabrics.
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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 (2007): 18–25. http://dx.doi.org/10.1152/japplphysiol.00565.2006.
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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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Saygili, Erol, Obaida R. Rana, Esra Saygili, et al. "Losartan prevents stretch-induced electrical remodeling in cultured atrial neonatal myocytes." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 6 (2007): H2898—H2905. http://dx.doi.org/10.1152/ajpheart.00546.2006.
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Atrial fibrillation (AF) is the most frequent arrhythmia found in clinical practice. In recent studies, a decrease in the development or recurrence of AF was found in hypertensive patients treated with angiotensin-converting enzyme inhibitors or angiotensin receptor-blocking agents. Hypertension is related to an increased wall tension in the atria, resulting in increased stretch of the individual myocyte, which is one of the major stimuli for the remodeling process. In the present study, we used a model of cultured atrial neonatal rat cardiomyocytes under conditions of stretch to provide insight into the mechanisms of the preventive effect of the angiotensin receptor-blocking agent losartan against AF on a molecular level. Stretch significantly increased protein-to-DNA ratio and atrial natriuretic factor mRNA expression, indicating hypertrophy. Expression of genes encoding for the inward rectifier K+current ( IK1), Kir2.1, and Kir2.3, as well as the gene encoding for the ultrarapid delayed rectifier K+current ( IKur), Kv1.5, was significantly increased. In contrast, mRNA expression of Kv4.2 was significantly reduced in stretched myocytes. Alterations of gene expression correlated with the corresponding current densities: IK1and IKurdensities were significantly increased in stretched myocytes, whereas transient outward K+current ( Ito) density was reduced. These alterations resulted in a significant abbreviation of the action potential duration. Losartan (1 μM) prevented stretch-induced increases in the protein-to-DNA ratio and atrial natriuretic peptide mRNA expression in stretched myocytes. Concomitantly, losartan attenuated stretch-induced alterations in IK1, IKur, and Itodensity and gene expression. This prevented the stretch-induced abbreviation of action potential duration. Prevention of stretch-induced electrical remodeling might contribute to the clinical effects of losartan against AF.
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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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Cleland, C. L., and W. Z. Rymer. "Neural mechanisms underlying the clasp-knife reflex in the cat. I. Characteristics of the reflex." Journal of Neurophysiology 64, no. 4 (1990): 1303–18. http://dx.doi.org/10.1152/jn.1990.64.4.1303.
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1. The goal of this study was to characterize the clasp-knife reflex by the use of stretch and isometric contraction of ankle extensor and flexor muscles in decerebrated cats with bilateral dorsal hemisections of their spinal cords at segment T12. 2. Stretch of an extensor muscle evoked inhibition in both homonymous and synergistic extensor muscles. The similarities between homonymous and synergistic inhibition suggest that similar neural mechanisms were responsible. 3. Homonymous and synergistic clasp-knife inhibition showed several characteristic features: 1) inhibition was evoked only by large stretches that produced significant muscle force. Short stretches that did not produce large forces evoked only excitation; 2) the magnitude of clasp-knife inhibition increased with increasing initial motor output, as reflected in the level of rectified EMG; 3) the time course of reflex inhibition evoked by ramp-and-hold stretch was characterized by segmentation of EMG during ramp stretch, dynamic overshoot of inhibition at the end-of-ramp stretch, and slow but usually complete decay of inhibition during maintained stretch; 4) inhibition persisted beyond the termination of stretch, and 5) inhibition showed adaptation to repeated stretch. 4. Isometric contraction of the soleus or medial gastrocnemius, produced by electrical stimulation of the muscle nerve, also evoked powerful synergistic-reflex inhibition via similar mechanisms as stretch-evoked, clasp-knife inhibition. Stretch evoked a greater degree of inhibition than did contraction, indicating that receptors responsive to both stretch and contraction contribute to clasp-knife inhibition. 5. The reflex effects produced by stretching the soleus or medial gastrocnemius were not confined to the homonymous and close synergistic muscles. Extensor muscles were inhibited and flexor muscles were excited throughout the hindlimb, which paralleled the pattern of a flexion-withdrawal reflex evoked by cutaneous stimulation. 6. Stretch of a flexor muscle, the tibialis anterior, evoked the same spatial pattern and time course of reflex action as stretch of an extensor muscle--inhibition of extensor muscles and excitation of flexor muscles throughout the hindlimb, including homonymous excitation of the tibialis anterior. 7. We conclude that neither Golgi tendon organs nor secondary spindle afferents are likely to contribute significantly to clasp-knife inhibition because their responses to stretch and isometric contraction differ from the reflex actions evoked by stretch and contraction.(ABSTRACT TRUNCATED AT 400 WORDS)
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Fisher, Jacob L., and Susan S. Margulies. "Na+-K+-ATPase activity in alveolar epithelial cells increases with cyclic stretch." American Journal of Physiology-Lung Cellular and Molecular Physiology 283, no. 4 (2002): L737—L746. http://dx.doi.org/10.1152/ajplung.00030.2001.
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Na+-K+-ATPase pumps (Na+ pumps) in the alveolar epithelium create a transepithelial Na+ gradient crucial to keeping fluid from the pulmonary air space. We hypothesized that alveolar epithelial stretch stimulates Na+ pump trafficking to the basolateral membrane (BLM) and, thereby, increases overall Na+ pump activity. Alveolar type II cells were isolated from Sprague-Dawley rats and seeded onto elastic membranes coated with fibronectin or 5-day-conditioned extracellular matrix. After 2 days in culture, cells were uniformly stretched for 1 h in a custom-made device. Na+ pump activity was subsequently assessed by ouabain-inhibitable uptake of 86Rb+, a K+ tracer, and BLM Na+ pump abundance was measured. In support of our hypothesis, cells increased Na+pump activity in a “dose-dependent” manner when stretched to 12, 25, or 37% change in surface area (ΔSA), and cells stretched to 25% ΔSA more than doubled Na+ pump abundance in the BLM. Cells on 5-day matrix tolerated higher strain than cells on fibronectin before the onset of Na+ pump upregulation. Treatment with Gd3+, a stretch-activated channel blocker, amiloride, a Na+ channel blocker, or both reduced but did not abolish stretch-induced effects. Sustained tonic stretch, unlike cyclic stretch, elicited no significant Na+ pump response.
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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 (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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Liu, Xiang, Lin J. Hymel та Emel Songu-Mize. "Role of Na+ and Ca2+ in stretch-induced Na+-K+-ATPase α-subunit regulation in aortic smooth muscle cells". American Journal of Physiology-Heart and Circulatory Physiology 274, № 1 (1998): H83—H89. http://dx.doi.org/10.1152/ajpheart.1998.274.1.h83.
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This study was designed to test the role of Na+ and Ca2+ entry in the stretch-induced Na+-K+-ATPase α1- and α2-isoform upregulation observed in our previous studies. We measured intracellular Na+ in cyclically stretched rat aortic smooth muscle cells, with or without gadolinium treatment, for various durations and performed Western blotting to analyze the effects of stretch and the calcium channel blocker isradipine on the expression of α-isoforms. Intracellular Na+was elevated significantly after 1- and 2-h stretch, but returned to baseline after 1-, 2-, and 4-day stretch. This increase in intracellular Na+ was blocked by gadolinium. Both α1- and α2-isoforms were upregulated after either 2 or 4 days of cyclical stretch. Isradipine had no apparent effect on stretch-induced upregulation on either α-isoform, thus suggesting that Ca2+ entry through L-type channels is not involved in the stretch-induced upregulation. We therefore conclude that a transient intracellular Na+ elevation during stretch may serve as a signal to mediate the α1- and α2-isoform upregulation.
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Park, John M., Joseph G. Borer, Michael R. Freeman, and Craig A. Peters. "Stretch activates heparin-binding EGF-like growth factor expression in bladder smooth muscle cells." American Journal of Physiology-Cell Physiology 275, no. 5 (1998): C1247—C1254. http://dx.doi.org/10.1152/ajpcell.1998.275.5.c1247.
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Cultured rat bladder smooth muscle cells (SMC) were grown on collagen-coated silicone membranes and subjected to continuous cycles of stretch-relaxation. Semiquantitative RT-PCR analysis revealed a time-dependent increase in heparin-binding epidermal growth factor (EGF)-like growth factor (HB-EGF) mRNA levels after stretch, with maximal levels appearing after 4 h. Immunostaining for proHB-EGF revealed higher levels of HB-EGF protein in the stretched than in the nonstretched SMC. The ANG II receptor type 1 antagonist losartan markedly suppressed stretch-activated HB-EGF expression. ANG II levels were 3.3-fold higher in the stretch- than in the non-stretch-conditioned media. Stretch stimulation of bladder SMC that had been transiently transfected with an HB-EGF promoter-luciferase expression construct resulted in an 11-fold increase in reporter activity. Mechanical stretch induced a 4.7-fold increase in tritiated thymidine incorporation rate, and this was reduced by 25% in the presence of losartan. We conclude that mechanical stretch activates HB-EGF gene expression in bladder SMC and that this is mediated in part by autocrine ANG II secretion.
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Krishnan, Ramaswamy, Elizabeth Peruski Canović, Andreea L. Iordan, et al. "Fluidization, resolidification, and reorientation of the endothelial cell in response to slow tidal stretches." American Journal of Physiology-Cell Physiology 303, no. 4 (2012): C368—C375. http://dx.doi.org/10.1152/ajpcell.00074.2012.
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Mechanical stretch plays an important role in regulating shape and orientation of the vascular endothelial cell. This morphological response to stretch is basic to angiogenesis, neovascularization, and vascular homeostasis, but mechanism remains unclear. To elucidate mechanisms, we used cell mapping rheometry to measure traction forces in primary human umbilical vein endothelial cells subjected to periodic uniaxial stretches. Onset of periodic stretch of 10% strain amplitude caused a fluidization response typified by attenuation of traction forces almost to zero. As periodic stretch continued, the prompt fluidization response was followed by a slow resolidification response typified by recovery of the traction forces, but now aligned along the axis perpendicular to the imposed stretch. Reorientation of the cell body lagged reorientation of the traction forces, however. Together, these observations demonstrate that cellular reorientation in response to periodic stretch is preceded by traction attenuation by means of cytoskeletal fluidization and subsequent traction recovery transverse to the stretch direction by means of cytoskeletal resolidification.
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Zheng, Wei, Elisabeth A. Seftor, Cynthia J. Meininger, Mary J. C. Hendrix та Robert J. Tomanek. "Mechanisms of coronary angiogenesis in response to stretch: role of VEGF and TGF-β". American Journal of Physiology-Heart and Circulatory Physiology 280, № 2 (2001): H909—H917. http://dx.doi.org/10.1152/ajpheart.2001.280.2.h909.
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To test the hypotheses that cyclic stretch of 1) cardiac myocytes produces factors that trigger angiogenic events in coronary microvascular endothelial cells (CMEC) and 2) CMEC enhances the expression of growth factors, cardiac myocytes and CMEC were subjected to cyclic stretch in a Flexercell Strain Unit. Vascular endothelial growth factor (VEGF) but not basic fibroblast growth factor mRNA and protein levels increased approximately twofold in myocytes after 1 h of stretch. CMEC DNA synthesis increased approximately twofold when conditioned medium from stretched myocytes or VEGF protein was added, and addition of VEGF neutralizing antibody blocked the increase. CMEC migration and tube formation increased with the addition of conditioned media but were markedly attenuated by VEGF neutralizing antibody. Myocyte tumor growth factor-β (TGF-β) increased 2.5-fold after 1 h of stretch, and the addition of TGF-β neutralizing antibodies inhibited the stretch-induced upregulation of VEGF. Stretch of CMEC increased VEGF mRNA in these cells (determined by Northern blot and RT-PCR) and increased the levels of VEGF protein (determined by ELISA analysis) in the conditioned media. Therefore, cyclic stretch of cardiac myocytes and CMEC appears to be an important primary stimulus for coronary angiogenesis through both paracrine and autocrine VEGF pathways. These data indicate that 1) CMEC DNA synthesis, migration, and tube formation are increased in response to VEGF secreted from stretched cardiac myocytes; 2) VEGF in CMEC subjected to stretch is upregulated and secreted; and 3) TGF-β signaling may regulate VEGF expression in cardiac myocytes.
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GRUDEN, GABRIELLA, STEPHEN THOMAS, DAVINA BURT, et al. "Interaction of Angiotensin II and Mechanical Stretch on Vascular Endothelial Growth Factor Production by Human Mesangial Cells." Journal of the American Society of Nephrology 10, no. 4 (1999): 730–37. http://dx.doi.org/10.1681/asn.v104730.
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Abstract. The antiproteinuric effect of angiotensin-converting enzyme inhibitors underscores the importance of a hemodynamic injury and the renin-angiotensin system in the proteinuria of various glomerular diseases. Vascular endothelial growth factor (VEGF), a potent promoter of vascular permeability, is induced in mesangial cells by both mechanical stretch and TGF-β1. This study investigates the effect of TGF-β blockade, angiotensin II (AngII), and the interaction between AngII and stretch on human mesangial cell VEGF production. Exposure to AngII (1 μM) induced a significant increase in VEGF mRNA and protein levels (1.5 ± 0.1 and 1.7 ± 0.3, respectively, fold increase over control, P < 0.05). The AngII receptor (AT1) antagonist Losartan (10 μM) prevented AngII-induced, but not stretch-induced, VEGF protein secretion (AngII 1.7 ± 0.3, AngII + Losartan 1.0 ± 0.1, P < 0.05; stretch 2.4 ± 0.4, stretch + Losartan 2.6 ± 0.5). Stretch-induced VEGF production was also unaffected by the addition of an anti-TGF-β neutralizing antibody (stretch 2.85 ± 0.82 versus stretch + anti-TGF-β 2.84 ± 0.01, fold increase over control). Simultaneous exposure to both AngII and stretch for 12 h had an additive effect on VEGF production (AngII 1.6 ± 0.1, stretch 2.6 ± 0.27, AngII + stretch 3.1 ± 0.35). Conversely, preexposure to stretch magnified AngII-induced VEGF protein secretion (unstretched + AngII 1.3 ± 0.0, stretched + AngII 1.9 ± 0.1, P < 0.01) with a parallel 1.5-fold increase in AT1 receptor levels. AngII and stretch can both independently induce VEGF production; in addition, mechanical stretch upregulates the AT1 receptor, enhancing the cellular response to AngII.
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Tatsumi, Ryuichi, Akihito Hattori, Yoshihide Ikeuchi, Judy E. Anderson, and Ronald E. Allen. "Release of Hepatocyte Growth Factor from Mechanically Stretched Skeletal Muscle Satellite Cells and Role of pH and Nitric Oxide." Molecular Biology of the Cell 13, no. 8 (2002): 2909–18. http://dx.doi.org/10.1091/mbc.e02-01-0062.
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Application of mechanical stretch to cultured adult rat muscle satellite cells results in release of hepatocyte growth factor (HGF) and accelerated entry into the cell cycle. Stretch activation of cultured rat muscle satellite cells was observed only when medium pH was between 7.1 and 7.5, even though activation of satellite cells was accelerated by exogenous HGF over a pH range from 6.9 to 7.8. Furthermore, HGF was only released in stretched cultures when the pH of the medium was between 7.1 and 7.4. Conditioned medium from stretched satellite cell cultures stimulated activation of unstretched satellite cells, and the addition of anti-HGF neutralizing antibodies to stretch-conditioned medium inhibited the stretch activation response. Conditioned medium from satellite cells that were stretched in the presence of nitric-oxide synthase (NOS) inhibitorN ω-nitro-l-arginine methyl ester hydrochloride did not accelerate activation of unstretched control satellite cells, and HGF was not released into the medium. Conditioned medium from unstretched cells that were treated with a nitric oxide donor, sodium nitroprusside dihydrate, was able to accelerate the activation of satellite cells in vitro, and HGF was found in the conditioned medium. Immunoblot analysis indicated that both neuronal and endothelial NOS isoforms were present in satellite cell cultures. Furthermore, assays of NOS activity in stretched satellite cell cultures demonstrated that NOS is stimulated when satellite cells are stretched in vitro. These experiments indicate that stretch triggers an intracellular cascade of events, including nitric oxide synthesis, which results in HGF release and satellite cell activation.
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Grigg, Peter, and Daniel R. Robichaud. "Rat Cutaneous RA Afferents Activated by Two-Dimensional Skin Stretch." Journal of Neurophysiology 92, no. 1 (2004): 484–91. http://dx.doi.org/10.1152/jn.01011.2003.
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Skin develops biaxial stresses and strains when stretched. Rapidly adapting cutaneous mechanoreceptor neurons are known to be stretch sensitive, yet in the past, they have been studied using stretch stimuli applied along only a single direction. In this study, cutaneous rapidly adapting mechanoreceptors were studied in preparations of isolated skin in which the skin was stretched dynamically using biaxial stretch stimuli and in which loads and displacements were measured along two directions. Stretch stimuli followed a pseudo-Gaussian waveform and were applied along either one or two directions simultaneously. Associations between spikes and mechanical variables were determined using multiple logistic regression. When the skin was actuated along a single direction, holding the orthogonal axis fixed, spike responses were strongly associated with mechanical variables along the actuated direction. The variables were stress and its rate of change, the rate of change of strain, and the product of stress and its rate of change, which is proportional to strain energy density. When the skin was stretched along a single direction, spikes were very poorly associated with stress variables measured along the direction orthogonal to the stretch. Afferents showed weak directional selectivity: they were slightly more responsive to the variable stress along the circumferential direction of the hindlimb. When the skin was stretched biaxially (i.e., along both directions simultaneously) with identical pseudo-Gaussian noise stimuli, neuronal responses were associated with the same variables as above, but the associations were weaker.
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Birmingham, J. T., Z. B. Szuts, L. F. Abbott, and Eve Marder. "Encoding of Muscle Movement on Two Time Scales by a Sensory Neuron That Switches Between Spiking and Bursting Modes." Journal of Neurophysiology 82, no. 5 (1999): 2786–97. http://dx.doi.org/10.1152/jn.1999.82.5.2786.
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The gastropyloric receptor (GPR) neurons of the stomatogastric nervous system of the crab Cancer borealis are muscle stretch receptors that can fire in either a spiking or a bursting mode of operation. Our goal is to understand what features of muscle stretch are encoded by these two modes of activity. To this end, we characterized the responses of the GPR neurons in both states to sustained and rapidly varying imposed stretches. The firing rates of spiking GPR neurons in response to rapidly varying stretches were directly related to stretch amplitude. For persistent stretches, spiking-mode firing rates showed marked adaptation indicating a more complex relationship. Interspike intervals of action potentials fired by GPR neurons in the spiking mode were used to construct an accurate estimate of the time-dependent amplitude of stretches in the frequency range of the gastric mill rhythm (0.05–0.2 Hz). Spike trains arising from faster stretches (similar to those of the pyloric rhythm) were decoded using a linear filter to construct an estimate of stretch amplitude. GPR neurons firing in the bursting mode were relatively unaffected by rapidly varying stretches. However, the burst rate was related to the amplitude of long, sustained stretches, and very slowly varying stretches could be reconstructed from burst intervals. In conclusion, the existence of spiking and bursting modes allows a single neuron to encode both rapidly and slowly varying stimuli and thus to report cycle-by-cycle muscle movements as well as average levels of muscle tension.
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Mariano, José Roberto, Maristela Cavicchioli Makrakis, Elaine Antoniassi Luiz Kashiwaqui, Elaine Fernandes Celestino, and Sergio Makrakis. "Longitudinal habitat disruption in Neotropical streams: fish assemblages under the influence of culverts." Neotropical Ichthyology 10, no. 4 (2012): 771–84. http://dx.doi.org/10.1590/s1679-62252012000400010.
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This study assessed differences in fish assemblages existing upstream and downstream two types of culverts, one on each of two different Neotropical streams. We analyzed the composition and structure of the ichthyofauna and tested for spatial patterns. Fish sampling was carried out monthly between November 2009 and October 2010 using different fishing gears. We collected 2,220 fish of 33 species; 901 in stretches of the Lopeí stream - circular culvert and 1,310 in stretches of the Pindorama stream - box culvert. Fish abundance was similar in upstream and downstream stretches of the circular culvert, whereas it was slightly higher in the upstream than downstream stretch for the box culvert. Characiformes predominated in the upstream stretch of both culverts. On the other hand, Siluriformes was abundant in the downstream stretch of the circular culvert, with similar abundance in the stretches of the box culvert. Species richness and diversity (Shannon-Weiner Index) were higher in the downstream stretch of the circular culvert, but they were similar in both stretches of the box culvert. The most abundant species were Astyanax altiparanae, A. paranae, A. fasciatus, Ancistrus sp., and Hypostomus sp. The last two species were more abundant in the downstream stretch of the circular culvert, and similar in stretches of the box culvert. Our study indicated variations in the species abundance, richness, and diversity between upstream and downstream stretches in particular of the circular culvert in the Lopeí stream, suggesting that fish movements are restrained more intensively in this culvert, especially for Siluriformes. The drop in the circular culvert outlet probably created passage barriers especially for those fish that has no ability to jump, where downstream erosion could lead to culvert perching. Studies on appropriate road crossing design or installation are fundamental whereas improvements in these structures can restore the connectivity of fish populations and communities in streams.
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Lockhart, Nicole C., and Susan V. Brooks. "Neutrophil accumulation following passive stretches contributes to adaptations that reduce contraction-induced skeletal muscle injury in mice." Journal of Applied Physiology 104, no. 4 (2008): 1109–15. http://dx.doi.org/10.1152/japplphysiol.00850.2007.
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Skeletal muscles can be injured by their own contractions, especially when the muscle is stretched during a lengthening contraction. Exposing a muscle to a conditioning protocol of stretches without activation (passive stretches) before lengthening contractions reduces contraction-induced injury. Although passive stretching does not damage muscle fibers, neutrophils are elevated in the muscle after passive stretches. Our purpose was to investigate the relationship between neutrophil accumulation following passive stretches and the protection from subsequent contraction-induced injury provided by the passive stretches. Our hypothesis was that passive stretch conditioning would not provide protection from subsequent lengthening contraction-induced injury under circumstances when the increase in muscle neutrophils in response to the conditioning was prevented. Extensor digitorum longus muscles of mice were conditioned with passive stretches 14 days before exposure to a protocol of damaging lengthening contractions. Mice were either untreated or treated with an antibody (RB6-8C5) that reduced the level of circulating neutrophils by over 95% before administration of passive stretches. Neutrophil levels recovered in treated mice by the time lengthening contractions were performed. Lengthening contractions were also administered to muscles with no prior exposure to passive stretches. Maximum isometric force, number of damaged fibers, and muscle neutrophil concentration were measured 3 days after lengthening contractions. Compared with nonconditioned control muscles, the severity of contraction-induced injury was not reduced by prior passive stretch conditioning when mice were treated with RB6-8C5 before conditioning. We conclude that neutrophils contribute to adaptations that protect muscles from injury.
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Page, E., J. Upshaw-Earley, G. E. Goings, and D. A. Hanck. "Inhibition of atrial peptide secretion at different stages of the secretory process: Ca2+ dependence." American Journal of Physiology-Cell Physiology 261, no. 6 (1991): C1162—C1172. http://dx.doi.org/10.1152/ajpcell.1991.261.6.c1162.
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We have used a noncontracting in vitro preparation of stretched and unstretched rat atria to estimate contributions of constitutive and regulated pathways to the rates of stretch-augmented and basal secretion of immunoreactive atrial natriuretic peptide (ANP) and to examine effects of inhibition of the secretory sequence by 1) protein synthesis inhibitors, 2) disruption of forward vesicular traffic between endoplasmic reticulum and Golgi with brefeldin A (BFA, and 3) cellular ATP depletion. Protein synthesis inhibition with cycloheximide for 44 min slowed neither basal nor stretch-augmented ANP secretion but instead accelerated stretch-augmented secretion at low (but not at physiological) external Ca2+ concentration, suggesting that the constitutive component does not contribute substantially to either basal or stretch-augmented secretion. BFA, which disassembled Golgi cisternae, increased the stretch-augmented secretory rate via the regulated pathway and prevented Ca(2+)-dependent inactivation with time. Cellular ATP depletion rapidly and completely inhibited stretch-augmented secretion. We conclude that both basal and stretch-augmented utilize the energy-dependent regulated pathway, drawing on a large reservoir of concentrated prohormone stored in granules that is not detectably depleted during 44 min of stretch-augmented secretion at 37 degrees C.