Journal articles on the topic 'Contracting'
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1
Hogan, Michael C., Erica Ingham, and S. Sadi Kurdak. "Contraction duration affects metabolic energy cost and fatigue in skeletal muscle." American Journal of Physiology-Endocrinology and Metabolism 274, no. 3 (March 1, 1998): E397—E402. http://dx.doi.org/10.1152/ajpendo.1998.274.3.e397.
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It has been suggested that during a skeletal muscle contraction the metabolic energy cost at the onset may be greater than the energy cost related to holding steady-state force. The purpose of the present study was to investigate the effect of contraction duration on the metabolic energy cost and fatigue process in fully perfused contracting muscle in situ. Canine gastrocnemius muscle ( n = 6) was isolated, and two contractile periods (3 min of isometric, tetanic contractions with 45-min rest between) were conducted by each muscle in a balanced order design. The two contractile periods had stimulation patterns that resulted in a 1:3 contraction-to-rest ratio, with the difference in the two contractile periods being in the duration of each contraction: short duration 0.25-s stimulation/0.75-s rest vs. long duration 1-s stimulation/3-s rest. These stimulation patterns resulted in the same total time of stimulation, number of stimulation pulses, and total time in contraction for each 3-min period. Muscle O2 uptake, the fall in developed force (fatigue), the O2 cost of developed force, and the estimated total energy cost (ATP utilization) of developed force were significantly greater ( P < 0.05) with contractions of short duration. Lactate efflux from the working muscle and muscle lactate concentration were significantly greater with contractions of short duration, such that the calculated energy derived from glycolysis was three times greater in this condition. These results demonstrate that contraction duration can significantly affect both the aerobic and anaerobic metabolic energy cost and fatigue in contracting muscle. In addition, it is likely that the greater rate of fatigue with more rapid contractions was a result of elevated glycolytic production of lactic acid.
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Zuo, Li, Leonardo Nogueira, and Michael C. Hogan. "Reactive oxygen species formation during tetanic contractions in single isolated Xenopus myofibers." Journal of Applied Physiology 111, no. 3 (September 2011): 898–904. http://dx.doi.org/10.1152/japplphysiol.00398.2011.
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Contracting skeletal muscle produces reactive oxygen species (ROS) that have been shown to affect muscle function and adaptation. However, real-time measurement of ROS in contracting myofibers has proven to be difficult. We used amphibian ( Xenopus laevis) muscle to test the hypothesis that ROS are formed during contractile activity in isolated single skeletal muscle fibers and that this contraction-induced ROS formation affects fatigue development. Single myofibers were loaded with 5 μM dihydrofluorescein-DA (Hfluor-DA), a fluorescent probe that reacts with ROS and results in the formation of fluorescein (Fluor) to precisely monitor ROS generation within single myofibers in real time using confocal miscroscopy. Three identical periods of maximal tetanic contractions (1 contraction/3 s for 2 min, separated by 60 min of rest) were conducted by each myofiber ( n = 6) at 20°C. Ebselen (an antioxidant) was present in the perfusate (10 μM) during the second contractile period. Force was reduced by ∼30% during each of the three contraction periods, with no significant difference in fatigue development among the three periods. The Fluor signal, indicative of ROS generation, increased significantly above baseline in both the first (42 ± 14%) and third periods (39 ± 10%), with no significant difference in the increase in fluorescence between the first and third periods. There was no increase of Fluor in the presence of ebselen during the second contractile period. These results demonstrated that, in isolated intact Xenopus myofibers, 1) ROS can be measured in real time during tetanic contractions, 2) contractile activity induced a significant increase above resting levels of ROS production, and 3) ebselen treatment reduced ROS generation to baseline levels but had no effect on myofiber contractility and fatigue development.
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Conley, Kevin E., and Stan L. Lindstedt. "Energy-saving mechanisms in muscle: the minimization strategy." Journal of Experimental Biology 205, no. 15 (August 1, 2002): 2175–81. http://dx.doi.org/10.1242/jeb.205.15.2175.
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SUMMARYMany mechanisms reduce the cost of muscle activity. Here, we describe a set of specializations that reduce the cost of contraction in the high-frequency twitches that are used by a wide variety of animals for either sound production or flight. Minimizing the cost of these contractions means that cellular ATP production can meet ATP demand and sustain the high contractile rate. Two classes of specialization are found that minimize the contractile cost. The first class reduces the muscle work required per contraction. Light appendages such as rattles, insect limbs and membranous wings that require little work for movement are used in high-frequency contractions. The second set of specializations involves processes that minimize energy use. High-frequency muscles tend to have a lower cross-bridge content, fewer attached cross-bridges and shorter length changes per contraction. The result is low muscle-specific forces (stress), small length changes (strain) and rapid contraction times that suggest that these muscles push the lower limit of contractile function. The consequence of function at this lower extreme of contraction is to minimize the contractile cost of high-frequency muscles. Thus, specializations that permit rapid contractions at a low rate of ATP use per twitch are the basis of a minimization strategy for energy saving in muscles contracting at high frequency.
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Qi, M., J. L. Puglisi, K. L. Byron, K. Ojamaa, I. Klein, D. M. Bers, and A. M. Samarel. "Myosin heavy chain gene expression in neonatal rat heart cells: effects of [Ca2+]i and contractile activity." American Journal of Physiology-Cell Physiology 273, no. 2 (August 1, 1997): C394—C403. http://dx.doi.org/10.1152/ajpcell.1997.273.2.c394.
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To determine if mechanical signals or alterations in intracellular Ca2+ concentration ([Ca2+]i) affect myosin heavy chain (MHC) gene expression in spontaneously beating, neonatal rat ventricular myocytes, contractile activity was inhibited with verapamil, KCl, or 2,3-butanedione monoxime (BDM), and their acute and chronic effects on myocyte shortening, [Ca2+]i, and MHC gene expression were examined. Despite their differing effects on [Ca2+]i, verapamil, KCl, and BDM all inhibited contractile activity and markedly downregulated beta-MHC mRNA levels to 24 +/- 5, 21 +/- 7, and 6 +/- 2% of contracting cells, respectively. In contrast, these inhibitors of contraction upregulated alpha-MHC mRNA levels to 163 +/- 19, 156 +/- 7, and 198 +/- 20% of contracting cells, respectively. Transient transfection with a rat beta-MHC promoter-luciferase expression plasmid demonstrated that all inhibitors of contraction significantly decreased beta-MHC promoter activity. Paradoxically, contractile arrest also inhibited alpha-MHC promoter activity, suggesting that increased alpha-MHC mRNA levels resulted from posttranscriptional mechanisms. Actinomycin D mRNA stability assays indicated that alpha-MHC mRNA half-life was prolonged in noncontracting cells (33 h) compared with contracting myocytes (14 h). Contraction-dependent alterations in MHC gene expression were not dependent on release of angiotensin II or other growth factors into the culture medium. Thus intrinsic mechanical signals rather than alterations in [Ca2+]i regulate alpha-MHC and beta-MHC gene expression by both transcriptional and posttranscriptional mechanisms.
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Taylor, Chloe E., Daniel Boulton, Erin J. Howden, Christoph Siebenmann, and Vaughan G. Macefield. "Central command increases muscle sympathetic nerve activity more to contracting than noncontracting muscle during rhythmic isotonic leg exercise." Journal of Neurophysiology 121, no. 5 (May 1, 2019): 1704–10. http://dx.doi.org/10.1152/jn.00075.2019.
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We have previously shown that the increase in muscle sympathetic nerve activity (MSNA) to contracting muscle during sustained isometric exercise is due primarily to central command and that contracting muscle does not express a metaboreceptor-driven increase in MSNA. Here we tested the hypothesis that MSNA increases to the contracting muscle also during rhythmic isotonic exercise, in which muscle metabolites will not accumulate because the contraction is performed without external load. MSNA was recorded from the common peroneal nerve in 10 participants, and negative-going sympathetic spikes were extracted during 50 cycles of sinusoidal (0.15 Hz) isotonic dorsiflexions of the ipsilateral or contralateral ankle. Electromyographic activity (EMG) was recorded from the tibialis anterior muscle on both sides. Cross-correlation analysis between MSNA and EMG revealed a marked cyclic modulation of MSNA to the contracting (ipsilateral) muscle. This modulation, in which MSNA increased during the contraction phase, was three times greater than that to the noncontracting muscle (modulation index = 27.4 ± 3.2% vs. 9.2 ± 1.5%; P < 0.002). There were no differences in either the intensity or the magnitude of modulation of EMG during ipsilateral and contralateral contractions. We conclude that central command increases MSNA to the contracting muscle during rhythmic isotonic exercise. NEW & NOTEWORTHY Muscle sympathetic nerve activity (MSNA) increases to contracting muscle during isometric exercise, but whether this occurs during rhythmic isotonic exercise is unknown. We recorded MSNA to the pretibial flexors during cyclic dorsiflexion of the ipsilateral or contralateral ankle. MSNA showed a cyclic increase during the contraction phase that was significantly higher to the contracting than the noncontracting muscle, supporting central command as the primary mechanism responsible for increasing MSNA.
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Zawieja, D. C., K. L. Davis, R. Schuster, W. M. Hinds, and H. J. Granger. "Distribution, propagation, and coordination of contractile activity in lymphatics." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 4 (April 1, 1993): H1283—H1291. http://dx.doi.org/10.1152/ajpheart.1993.264.4.h1283.
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The propagation and coordination of lymphatic contractions were studied in the mesentery of the rat small intestine using in situ microscopic observation. Indexes of lymphatic diameter were simultaneously measured at two adjacent lymphangions in spontaneously contracting lymphatics (n = 51). Diameter index, contraction frequency, and the percentage of the intersegmental contractions that were propagated and coordinated (PP) were determined at both sites. The conduction velocity of the contractile activity and the percentage of the coordinated contractions that were propagated both antegrade to the direction of lymph flow and retrograde to the flow stream were determined. The results indicate that 1) 80-90% of the lymphatic contractions in the vessels we evaluated were propagated, 2) the wave of contractile activity propagated both centrally and peripherally, and 3) the conduction velocity of the contractile activity was approximately 4-8 mm/s. We tested the hypothesis that gap junctional communication is responsible for the coordination of the contractile event. To accomplish this, we used the gap junction blockers n-heptanol and oleic acid. PP was 90 +/- 4% under normal conditions and fell to a minimum value of 55 +/- 7% during the gap junction blockade. These results indicate that gap junctional communication played an important role in the propagation and coordination of contractions that occurred in spontaneously active lymphatics.
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Rundell, K. W., P. C. Tullson, and R. L. Terjung. "AMP deaminase binding in contracting rat skeletal muscle." American Journal of Physiology-Cell Physiology 263, no. 2 (August 1, 1992): C287—C293. http://dx.doi.org/10.1152/ajpcell.1992.263.2.c287.
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AMP deaminase, which hydrolyses AMP to inosine 5'-monophosphate (IMP) and NH3 at high rates during excessive energy demands in skeletal muscle, is activated when bound to myosin in vitro. We evaluated AMP deaminase binding in vivo during muscle contractions to assess whether binding 1) is inherent to deamination and found only with high rates of IMP production or simply coincident with the contractile process and 2) requires cellular acidosis. AMP deaminase activity (mumol.min-1.g-1) was measured in the supernatant (free) and 10(4)-g pellet (bound) homogenate fractions of muscle of anesthetized rats after in situ contractions to determine the percent bound. In resting muscle, nearly all (approximately 90%) AMP deaminase is free (cytosolic). During contractions when energy balance was well maintained, binding did not significantly differ from resting values. However, during intense contraction conditions that lead to increased IMP concentration, binding increased to approximately 60% (P less than 0.001) in fast-twitch and approximately 50% in slow-twitch muscle. Binding increased in an apparent first-order manner and preceded initiation of IMP formation. Further, binding rapidly declined within 1 min after cessation of intense stimulation, even though the cell remained extremely acidotic. Extensive binding during contractions was also evident without cellular acidosis (iodoacetic acid-treated muscle). Thus the in vivo AMP deaminase-myosin complex association/dissociation is not coupled to changes in cellular acidosis. Interestingly, binding remained elevated after contractions, if energy recovery was limited by ischemia. Our results are consistent with myosin binding having a role in AMP deaminase activation and subsequent IMP formation in contracting muscle.
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McLelland, Grant, David MacManus, and Chris Sheaf. "A semi-empirical model for streamwise vortex intensification." Proceedings of the Institution of Mechanical Engineers, Part G: Journal of Aerospace Engineering 233, no. 12 (April 2019): 4396–409. http://dx.doi.org/10.1177/0954410019838421.
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Vortex intensification plays an important role in a wide range of flows of engineering interest. One scenario of interest is when a streamwise vortex passes through the contracting streamtube of an aircraft intake. There is, however, limited experimental data of flows of this type to reveal the dominant flow physics and to guide the development of vortex models. To this end, the evolution of wing-tip vortices inside a range of streamtube contractions has been measured using stereoscopic particle image velocimetry. A semi-empirical model has been applied to provide new insight on the role of vorticity diffusion during the intensification process. The analysis demonstrates that for mild flow contractions, vorticity diffusion has a negligible influence due to the low rates of diffusion in the vortex flow prior to intensification and the short convective times associated with the streamtube contraction. As the contraction levels increase, there is a substantial increase in the rates of diffusion which is driven by the greater levels of vorticity in the vortex core. A new semi-empirical relationship, as a function of the local streamtube contraction levels and vortex Reynolds number, has been developed. The model comprises a simple correction to vortex filament theory and provides a significant improvement in the estimation of vortex characteristics in contracting flows. For the range of contractions investigated, errors in the estimation of vortex core radius, peak tangential velocity and vorticity are reduced by an order of magnitude. The model can be applied to estimate the change in vortex characteristics for a range of flows with intense axial strain, such as contracting intake streamtubes and swirling flows in turbomachinery.
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Mehta, D., M. F. Wu, and S. J. Gunst. "Role of contractile protein activation in the length-dependent modulation of tracheal smooth muscle force." American Journal of Physiology-Cell Physiology 270, no. 1 (January 1, 1996): C243—C252. http://dx.doi.org/10.1152/ajpcell.1996.270.1.c243.
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The active isometric force developed by a muscle decreases at muscle lengths below an optimal length (Lo). However, when the length of an actively contracting muscle is abruptly decreased, a lower level of isometric force is reached during force redevelopment than when the contraction is initiated at the shorter length. This has been attributed to a deactivation of contractile proteins caused by shortening. In this study, intracellular Ca2+ and myosin light chain (MLC) phosphorylation were measured to assess the mechanisms for the modulation of isometric force caused by changing smooth muscle length before or during isometric contraction. The decline in isometric force between Lo and 0.5Lo was associated with decreases in MLC phosphorylation and intracellular Ca2+ during contractions elicited by acetylcholine or 60 mM KCl. Quick release of the muscle during contraction depressed force redevelopment at the shorter length but not MLC phosphorylation. We conclude that decreases in Ca(2+)-calmodulin-dependent MLC phosphorylation contribute significantly to the decline in isometric force at lengths below Lo, but the depression of contractility associated with the quick release of actively contracted smooth muscle is not caused by a shortening-induced deactivation of contractile proteins.
10
Hespel, P., and E. A. Richter. "Mechanism linking glycogen concentration and glycogenolytic rate in perfused contracting rat skeletal muscle." Biochemical Journal 284, no. 3 (June 15, 1992): 777–80. http://dx.doi.org/10.1042/bj2840777.
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The influence of differences in glycogen concentration on glycogen breakdown and on phosphorylase activity was investigated in perfused contracting rat skeletal muscle. The rats were preconditioned by a combination of swimming exercise and diet (carbohydrate-free or carbohydrate-rich) in order to obtain four sub-groups of rats with varying resting muscle glycogen concentrations (range 10-60 mumol/g wet wt.). Pre-contraction muscle glycogen concentration was closely positively correlated with glycogen breakdown over 15 min of intermittent short tetanic contractions (r = 0.75; P less than 0.001; n = 56) at the same tension development and oxygen uptake. Additional studies in supercompensated and glycogen-depleted hindquarters during electrical stimulation for 20 s or 2 min revealed that the difference in glycogenolytic rate was found at the beginning rather than at the end of the contraction period. Phosphorylase alpha activity was approximately twice as high (P less than 0.001) in supercompensated muscles as in glycogen-depleted muscles after 20 s as well as after 2 min of contractions. It is concluded that glycogen concentration is an important determinant of phosphorylase activity in contracting skeletal muscle, and probably via this mechanism a regulator of glycogenolytic rate during muscle contraction.
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Kato, Tatsuya, Atsushi Sasaki, Hikaru Yokoyama, Matija Milosevic, and Kimitaka Nakazawa. "Effects of neuromuscular electrical stimulation and voluntary commands on the spinal reflex excitability of remote limb muscles." Experimental Brain Research 237, no. 12 (October 10, 2019): 3195–205. http://dx.doi.org/10.1007/s00221-019-05660-6.
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Abstract It is well known that contracting the upper limbs can affect spinal reflexes of the lower limb muscle, via intraneuronal networks within the central nervous system. However, it remains unknown whether neuromuscular electrical stimulation (NMES), which can generate muscle contractions without central commands from the cortex, can also play a role in such inter-limb facilitation. Therefore, the objective of this study was to compare the effects of unilateral upper limb contractions using NMES and voluntary unilateral upper limb contractions on the inter-limb spinal reflex facilitation in the lower limb muscles. Spinal reflex excitability was assessed using transcutaneous spinal cord stimulation (tSCS) to elicit responses bilaterally in multiple lower limb muscles, including ankle and thigh muscles. Five interventions were applied on the right wrist flexors for 70 s: (1) sensory-level NMES; (2) motor-level NMES; (3) voluntary contraction; (4) voluntary contraction and sensory-level NMES; (5) voluntary contraction and motor-level NMES. Results showed that spinal reflex excitability of ankle muscles was facilitated bilaterally during voluntary contraction of the upper limb unilaterally and that voluntary contraction with motor-level NMES had similar effects as just contracting voluntarily. Meanwhile, motor-level NMES facilitated contralateral thigh muscles, and sensory-level NMES had no effect. Overall, our results suggest that inter-limb facilitation effect of spinal reflex excitability in lower limb muscles depends, to a larger extent, on the presence of the central commands from the cortex during voluntary contractions. However, peripheral input generated by muscle contractions using NMES might have effects on the spinal reflex excitability of inter-limb muscles via spinal intraneuronal networks.
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Meisner, Joshua K., Randolph H. Stewart, Glen A. Laine, and Christopher M. Quick. "Lymphatic vessels transition to state of summation above a critical contraction frequency." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 1 (July 2007): R200—R208. http://dx.doi.org/10.1152/ajpregu.00468.2006.
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Although behavior of lymphatic vessels is analogous to that of ventricles, which completely relax between contractions, and blood vessels, which maintain a tonic constriction, the mixture of contractile properties can yield behavior unique to lymphatic vessels. In particular, because of their limited refractory period and slow rate of relaxation, lymphatic vessels lack the contractile properties that minimize summation in ventricles. We, therefore, hypothesized that lymphatic vessels transition to a state of summation when lymphatic vessel contraction frequency exceeds a critical value. We used an isovolumic, controlled-flow preparation to compare the time required for full relaxation with the time available to relax during diastole. We measured transmural pressure and diameter on segments of spontaneously contracting bovine mesenteric lymphatic vessels during 10 isovolumic volume steps. We found that beat-to-beat period (frequency−1) decreased with increases in diameter and that total contraction time was constant or slightly increased with diameter. We further found that the convergence of beat-to-beat period and contraction cycle duration predicted a critical transition value, beyond which the vessel does not have time to fully relax. This incomplete relaxation and resulting mechanical summation significantly increase active tension in diastole. Because this transition occurs within a physiological range, contraction summation may represent a fundamental feature of lymphatic vessel function.
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Gibbings, J. C. "Incompressible flow in contracting ducts." Aeronautical Journal 97, no. 967 (September 1993): 230–46. http://dx.doi.org/10.1017/s0001924000026348.
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This paper describes the incompressible flow through contracting ducts as used in windtunnel circuits. The value of the velocity gradients that are critically adverse to the boundary layer development are specified and the contraction profile is derived for two-dimensional flow. Solutions to the flow through three-dimensional contractions of circular, square, and square to rectangle shape are obtained. These lead to simple rules for scaling the profile of two-dimensional flow to provide three-dimensional shapes having short lengths with the required velocity distributions. The development of both laminar and turbulent boundary layers is calculated to provide criteria for the avoidance of separation.
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Stebbins, C. L., O. A. Carretero, T. Mindroiu, and J. C. Longhurst. "Bradykinin release from contracting skeletal muscle of the cat." Journal of Applied Physiology 69, no. 4 (October 1, 1990): 1225–30. http://dx.doi.org/10.1152/jappl.1990.69.4.1225.
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Results of previous studies from our laboratory suggest that bradykinin has a role in the exercise pressor reflex elicited by static muscle contraction. The purpose of this study was to quantify the release of bradykinin from contracting skeletal muscle. In 18 cats, blood samples were withdrawn directly from the venous effluent of the triceps surae muscles immediately before and after 30 s of static contraction producing peak muscle tensions of 33, 50, and 100% of maximum electrically stimulated contraction. Contractions producing muscle tensions of 50 and 100% of maximum increased muscle venous bradykinin levels by 27 +/- 9 and 19 +/- 10 pg/ml, respectively. Conversely, 33% maximum contraction did not alter muscle venous bradykinin concentrations. However, when captopril was administered to slow the degradation of bradykinin, muscle venous bradykinin increased from 68 +/- 15 pg/ml at rest to 106 +/- 18 after contractions of 33% of maximum. When muscle ischemia was induced by 2 min of arterial occlusion before and during 30 s of 33% of maximum contraction, muscle venous bradykinin increased by 15 +/- 5 pg/ml. In addition, contraction-induced changes in muscle venous pH and lactate strongly correlated with bradykinin concentrations (r = 0.80 and 0.83, respectively). These data demonstrate that static contraction of relatively high intensity evokes the release of bradykinin from skeletal muscle and that ischemia, decreased pH, and increased lactate are strongly correlated with this release.
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Celichowski, Jan, Kazimierz Grottel, and Edyta Bichler. "The area under the record of contractile tension: estimation of work performed by a contracting motor unit." Acta Neurobiologiae Experimentalis 58, no. 2 (June 30, 1998): 165–68. http://dx.doi.org/10.55782/ane-1998-1270.
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The area under twitch tension records was measured for motor units in rat medial gastrocnemius. These measures were compared to measures of tension. The tension varied in significantly larger range than the area. The area of slow motor units was similar to the area of fast resistant units, whereas their tensions differed significantly. The area depended mainly on the amplitude of contraction and to a smaller degree on its time course. The measure of area under the tension record gives a more exact evaluation of the work performed by contracting motor units than the measure of tension alone. The obtained results show that motor units in mammalian muscle are less variable in their ability to perform contractile work and moreover, that slow motor units play a more significant role during contractions than was supposed based on tension measures.
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Waldrop, T. G., and R. W. Stremel. "Muscular contraction stimulates posterior hypothalamic neurons." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 256, no. 2 (February 1, 1989): R348—R356. http://dx.doi.org/10.1152/ajpregu.1989.256.2.r348.
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Recent studies have suggested that the subthalamic locomotor region (STLR) of the posterior hypothalamus is involved in modulating cardiorespiratory responses to feedback from contracting muscles. The purpose of this study was to determine whether neurons in this hypothalamic region alter their discharge frequency during contraction of hindlimb muscles. Stainless steel electrodes were used to record single-unit activity of STLR neurons during static and rhythmic contractions of hindlimb muscles in anesthetized cats. Recordings were also made from neurons in areas outside but surrounding the subthalamic locomotor region. Contraction of the triceps surae muscles was induced by stimulation of the peripheral cut ends of the L7 and S1 ventral roots. Both static and rhythmic contractions of the triceps surae evoked an increase in the discharge rate of the majority of the STLR cells studied. Two types of excitatory responses were observed: 1) abrupt increases in discharge frequency at the onset of muscular contraction and 2) a delayed more gradual increase in firing. Most of the cells that responded to muscular contraction could be activated by mechanical probing of the triceps surae muscles. However, the changes in discharge frequency were unrelated to changes in arterial pressure occurring during muscular contraction. Most of the neurons located outside the STLR were slightly inhibited by or did not respond to muscular contraction. Thus input from contracting muscles exerts predominantly an excitatory effect on neurons in the posterior hypothalamus. These results are consistent with other studies which have concluded that this hypothalamic site is involved in influencing the cardiorespiratory responses to muscular contraction.
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Nedachi, Taku, Hideaki Fujita, and Makoto Kanzaki. "Contractile C2C12 myotube model for studying exercise-inducible responses in skeletal muscle." American Journal of Physiology-Endocrinology and Metabolism 295, no. 5 (November 2008): E1191—E1204. http://dx.doi.org/10.1152/ajpendo.90280.2008.
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Adequate exercise leads to a vast variety of physiological changes in skeletal muscle as well as other tissues/organs and is also responsible for maintaining healthy muscle displaying enhanced insulin-responsive glucose uptake via GLUT4 translocation. We generated highly developed contractile C2C12 myotubes by manipulating intracellular Ca2+ transients with electric pulse stimulation (EPS) that is endowed with properties similar to those of in vivo skeletal muscle in terms of 1) excitation-induced contractile activity as a result of de novo sarcomere formation, 2) activation of both the AMP kinase and stress-activated MAP kinase cascades, and 3) improved insulin responsiveness as assessed by GLUT4 recycling. Tbc1d1, a Rab-GAP implicated in exercise-induced GLUT4 translocation in skeletal muscle, also appeared to be phosphorylated on Ser231 after EPS-induced contraction. In addition, a switch in myosin heavy-chain (MHC) expression from “fast type” to “slow type” was observed in the C2C12 myotubes endowed with EPS-induced repetitive contractility. Taking advantage of these highly developed contractile C2C12 myotubes, we identified myotube-derived factors responsive to EPS-evoked contraction, including the CXC chemokines CXCL1/KC and CXCL5/LIX, as well as IL-6, previously reported to be upregulated in contracting muscles in vivo. Importantly, animal treadmill experiments revealed that exercise significantly increased systemic levels of CXCL1/KC, perhaps derived from contracting muscle. Taken together, these results confirm that we have established a specialized muscle cell culture model allowing contraction-inducible cellular responses to be explored. Utilizing this model, we identified contraction-inducible myokines potentially linked to the metabolic alterations, immune responses, and angiogenesis induced by exercise.
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Hogan, Michael C., L. Bruce Gladden, Bruno Grassi, Creed M. Stary, and Michele Samaja. "Bioenergetics of contracting skeletal muscle after partial reduction of blood flow." Journal of Applied Physiology 84, no. 6 (June 1, 1998): 1882–88. http://dx.doi.org/10.1152/jappl.1998.84.6.1882.
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The purpose of this study was to examine the bioenergetics and regulation of O2 uptake (V˙o 2) and force production in contracting muscle when blood flow was moderately reduced during a steady-state contractile period. Canine gastrocnemius muscle ( n = 5) was isolated, and 3-min stimulation periods of isometric, tetanic contractions were elicited sequentially at rates of 0.25, 0.33, and 0.5 contractions/s (Hz) immediately followed by a reduction of blood flow [ischemic (I) condition] to 46 ± 3% of the value obtained at 0.5 Hz with normal blood flow. TheV˙o 2 of the contracting muscle was significantly ( P < 0.05) reduced during the I condition [6.5 ± 0.8 (SE) ml ⋅ 100 g−1 ⋅ min−1] compared with the same stimulation frequency with normal flow (11.2 ± 1.5 ml ⋅ 100 g−1 ⋅ min−1), as was the tension-time index (79 ± 12 vs. 123 ± 22 N ⋅ g−1 ⋅ min−1, respectively). The ratio ofV˙o 2 to tension-time index remained constant throughout all contraction periods. Muscle phosphocreatine concentration, ATP concentration, and lactate efflux were not significantly different during the I condition compared with the 0.5-Hz condition with normal blood flow. However, at comparable rates of V˙o 2 and tension-time index, muscle phosphocreatine concentration and ATP concentration were significantly less during the I condition compared with normal-flow conditions. These results demonstrate that, in this highly oxidative muscle, the normal balance of O2 supply to force output was maintained during moderate ischemia by downregulation of force production. In addition, 1) the minimal disruption in intracellular homeostasis after the initiation of ischemia was likely a result of steady-state metabolic conditions having already been activated, and 2) the difference in intracellular conditions at comparable rates ofV˙o 2 and tension-time index between the normal flow and I condition may have been due to altered intracellular O2 tension.
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Metzger, J. M., W. I. Lin, and L. C. Samuelson. "Transition in cardiac contractile sensitivity to calcium during the in vitro differentiation of mouse embryonic stem cells." Journal of Cell Biology 126, no. 3 (August 1, 1994): 701–11. http://dx.doi.org/10.1083/jcb.126.3.701.
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Mouse embryonic stem (ES) cells differentiate in vitro into a variety of cell types including spontaneously contracting cardiac myocytes. We have utilized the ES cell differentiation culture system to study the development of the cardiac contractile apparatus in vitro. Difficulties associated with the cellular and developmental heterogeneity of this system have been overcome by establishing attached cultures of differentiating ES cells, and by the micro-dissection of the contracting cardiac myocytes from culture. The time of onset and duration of continuous contractile activity of the individual contracting myocytes was determined by daily visual inspection of the cultures. A functional assay was used to directly measure force production in ES cell-derived cardiac myocyte preparations. The forces produced during spontaneous contractions in the membrane intact preparation, and during activation by Ca2+ subsequent to chemical permeabilization of the surface membranes were determined in the same preparation. Results showed a transition in contractile sensitivity to Ca2+ in ES cell-derived cardiac myocytes during development in vitro. Cardiac preparations isolated from culture following the initiation of spontaneous contractile activity showed marked sensitivity of the contractile apparatus to activation by Ca2+. However, the Ca2+ sensitivity of tension development was significantly decreased in preparations isolated from culture following prolonged continuous contractile activity in vitro. The alteration in Ca2+ sensitivity obtained in vitro paralleled that observed during murine cardiac myocyte development in vivo. This provides functional evidence that ES cell-derived cardiac myocytes recapitulate cardiogenesis in vitro. Alterations in Ca2+ sensitivity could be important in optimizing the cardiac contractile response to variations in the myoplasmic Ca2+ transient during embryogenesis. The potential to stably transfect ES cells with cardiac regulatory genes, together with the availability of a functional assay using control and genetically modified ES cell-derived cardiac myocytes, will permit determination of the functional significance of altered cardiac gene expression during cardiogenesis in vitro.
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Zuo, Li, Amy Shiah, William J. Roberts, Michael T. Chien, Peter D. Wagner, and Michael C. Hogan. "Low Po2 conditions induce reactive oxygen species formation during contractions in single skeletal muscle fibers." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 304, no. 11 (June 1, 2013): R1009—R1016. http://dx.doi.org/10.1152/ajpregu.00563.2012.
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Contractions in whole skeletal muscle during hypoxia are known to generate reactive oxygen species (ROS); however, identification of real-time ROS formation within isolated single skeletal muscle fibers has been challenging. Consequently, there is no convincing evidence showing increased ROS production in intact contracting fibers under low Po2 conditions. Therefore, we hypothesized that intracellular ROS generation in single contracting skeletal myofibers increases during low Po2 compared with a value approximating normal resting Po2. Dihydrofluorescein was loaded into single frog ( Xenopus) fibers, and fluorescence was used to monitor ROS using confocal microscopy. Myofibers were exposed to two maximal tetanic contractile periods (1 contraction/3 s for 2 min, separated by a 60-min rest period), each consisting of one of the following treatments: high Po2 (30 Torr), low Po2 (3–5 Torr), high Po2 with ebselen (antioxidant), or low Po2 with ebselen. Ebselen (10 μM) was administered before the designated contractile period. ROS formation during low Po2 treatment was greater than during high Po2 treatment, and ebselen decreased ROS generation in both low- and high-Po2 conditions ( P < 0.05). ROS accumulated at a faster rate in low vs. high Po2. Force was reduced >30% for each condition except low Po2 with ebselen, which only decreased ∼15%. We concluded that single myofibers under low Po2 conditions develop accelerated and more oxidative stress than at Po2 = 30 Torr (normal human resting Po2). Ebselen decreases ROS formation in both low and high Po2, but only mitigates skeletal muscle fatigue during reduced Po2 conditions.
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Chantler, David. "Contracting in, Contracting out." Criminal Justice Matters 57, no. 1 (September 2004): 22–23. http://dx.doi.org/10.1080/09627250408553643.
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Beaty, O. "Carotid sinus and blood pressure control during hindlimb and forelimb contractions." American Journal of Physiology-Heart and Circulatory Physiology 248, no. 5 (May 1, 1985): H688—H694. http://dx.doi.org/10.1152/ajpheart.1985.248.5.h688.
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Arterial blood pressure (ABP) regulation during exercise involves in part medullary interaction of afferent information from contracting skeletal muscles and the major baroreceptors. This study examined in chloralose-anesthetized dogs the role of the carotid sinus baroreceptors in modulating reflex changes in ABP, nonexercising hindlimb skeletal muscle vascular resistance, and heart rate (HR) evoked by two separately contracting (4, 16, and 48 Hz) groups of skeletal muscle, the right hindlimb and forelimb. When arterial and cardiopulmonary baroreceptor afferent information was interrupted, hindlimb contractions evoked a greater augmentation of ABP (16 and 48 Hz) and no further increase in nonexercising hindlimb perfusion pressure (HLPP). Forelimb contractions, which in the presence of baroreceptors had not affected ABP (4 and 16 Hz), now reduced it profoundly. Nonexercising HLPP, which increased independently of contraction frequency, now was decreased by 4 Hz, not affected by 16 Hz, and increased by 48 Hz. The increase in HR was abolished. Increasing carotid sinus pressure to 220 mmHg in vagotomized dogs abolished the reflex changes evoked by hindlimb skeletal muscle contractions. However, forelimb contractions continued to decrease ABP. Nonexercising HLPP and HR did not change from the precontraction values. These data indicate that the carotid sinus baroreceptor could buffer completely those changes in the selected cardiovascular variables evoked by hindlimb but not forelimb skeletal muscle contractions. Thus the role of the carotid sinus baroreceptors in controlling ABP during exercise depends on the group of skeletal muscle initiating the somatic afferent signal and its influence on the contraction-induced distribution of the efferent signals.
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Kamiński, Marcin, Daniël Paulusma, and Dimitrios M. Thilikos. "Contracting planar graphs to contractions of triangulations." Journal of Discrete Algorithms 9, no. 3 (September 2011): 299–306. http://dx.doi.org/10.1016/j.jda.2011.03.010.
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Lou, F., N. A. Curtin, and R. C. Woledge. "Elastic energy storage and release in white muscle from dogfish scyliorhinus canicula." Journal of Experimental Biology 202, no. 2 (January 15, 1999): 135–42. http://dx.doi.org/10.1242/jeb.202.2.135.
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The production of work by the contractile component (CC) and the storage and release of work in the elastic structures that act in series (the series elastic component, SEC) with the contractile component were measured using white muscle fibres from the dogfish Scyliorhinus canicula. Heat production was also measured because the sum of work and heat is equivalent to the energy cost of the contraction (ATP used). These energy fluxes were evaluated in contractions with constant-velocity shortening either during stimulation or during relaxation. The muscle preparation was tetanized for 0.6 s and shortened by 1 mm (approximately 15 % of L0) at 3.5 or 7.0 mm s-1 (approximately 15 or 30 % of V0), where L0 is the muscle length at which isometric force is greatest and V0 is the maximum velocity of shortening. In separate experiments, the stiffness of the SEC was characterized from measurements of force responses to step changes in the length of contracting muscle. Using the values of SEC stiffness, we evaluated separately the work and heat associated with the CC and with the SEC. The major findings were (1) that work stored in the SEC could be completely recovered as external work when shortening occurred during relaxation (none of the stored work being degraded into heat) and (2) that, when shortening occurred progressively later during the contraction, the total energy cost of the contraction declined towards that of an isometric contraction.
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Balshaw, Thomas G., Garry J. Massey, Thomas M. Maden-Wilkinson, Neale A. Tillin, and Jonathan P. Folland. "Training-specific functional, neural, and hypertrophic adaptations to explosive- vs. sustained-contraction strength training." Journal of Applied Physiology 120, no. 11 (June 1, 2016): 1364–73. http://dx.doi.org/10.1152/japplphysiol.00091.2016.
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Training specificity is considered important for strength training, although the functional and underpinning physiological adaptations to different types of training, including brief explosive contractions, are poorly understood. This study compared the effects of 12 wk of explosive-contraction (ECT, n = 13) vs. sustained-contraction (SCT, n = 16) strength training vs. control ( n = 14) on the functional, neural, hypertrophic, and intrinsic contractile characteristics of healthy young men. Training involved 40 isometric knee extension repetitions (3 times/wk): contracting as fast and hard as possible for ∼1 s (ECT) or gradually increasing to 75% of maximum voluntary torque (MVT) before holding for 3 s (SCT). Torque and electromyography during maximum and explosive contractions, torque during evoked octet contractions, and total quadriceps muscle volume (QUADSVOL) were quantified pre and post training. MVT increased more after SCT than ECT [23 vs. 17%; effect size (ES) = 0.69], with similar increases in neural drive, but greater QUADSVOL changes after SCT (8.1 vs. 2.6%; ES = 0.74). ECT improved explosive torque at all time points (17–34%; 0.54 ≤ ES ≤ 0.76) because of increased neural drive (17–28%), whereas only late-phase explosive torque (150 ms, 12%; ES = 1.48) and corresponding neural drive (18%) increased after SCT. Changes in evoked torque indicated slowing of the contractile properties of the muscle-tendon unit after both training interventions. These results showed training-specific functional changes that appeared to be due to distinct neural and hypertrophic adaptations. ECT produced a wider range of functional adaptations than SCT, and given the lesser demands of ECT, this type of training provides a highly efficient means of increasing function.
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Kirby, Brett S., Rachel R. Markwald, Erica G. Smith, and Frank A. Dinenno. "Mechanical effects of muscle contraction do not blunt sympathetic vasoconstriction in humans." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 4 (October 2005): H1610—H1617. http://dx.doi.org/10.1152/ajpheart.00391.2005.
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Sympathetic vasoconstrictor responses are blunted in the vascular beds of contracting muscle (functional sympatholysis), but the mechanism(s) have been difficult to elucidate. We tested the hypothesis that the mechanical effects of muscle contraction blunt sympathetic vasoconstriction in human muscle. We measured forearm blood flow (Doppler ultrasound) and calculated the reductions in forearm vascular conductance (FVC) in response to reflex increases in sympathetic activity evoked via lower body negative pressure (LBNP). In protocol 1, eight young adults were studied under control resting conditions and during simulated muscle contractions using rhythmic forearm cuff inflations (20 inflations/min) with cuff pressures of 50 and 100 mmHg with the arm below heart level (BH), as well as 100 mmHg with the arm at heart level (HL). Forearm vasoconstrictor responses (%ΔFVC) during LBNP were −26 ± 2% during control conditions and were not blunted by simulated contractions (range = −31 ± 3% to −43 ± 6%). In protocol 2, eight subjects were studied under control conditions and during rhythmic handgrip exercise (20 contractions/min) using workloads of 15% maximum voluntary contraction (MVC) at HL and BH (similar metabolic demand, greater mechanical muscle pump effect for the latter) and 5% MVC BH alone and in combination with superimposed forearm compressions of 100 mmHg (similar metabolic demand, greater mechanical component of contractions for the latter). The forearm vasoconstrictor responses during LBNP were blunted during 15% MVC exercise with the arm at HL (−1 ± 3%) and BH (−2 ± 3%) compared with control (−25 ± 3%; both P < 0.005) but were intact during both 5% MVC alone (−24 ± 4%) and with superimposed compressions (−23 ± 4%). We conclude that mechanical effects of contraction per se do not cause functional sympatholysis in the human forearm and that this phenomenon appears to be coupled with the metabolic demand of contracting skeletal muscle.
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Qi, M., K. Ojamaa, E. G. Eleftheriades, I. Klein, and A. M. Samarel. "Regulation of rat ventricular myosin heavy chain expression by serum and contractile activity." American Journal of Physiology-Cell Physiology 267, no. 2 (August 1, 1994): C520—C528. http://dx.doi.org/10.1152/ajpcell.1994.267.2.c520.
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To quantitatively analyze the effects of serum stimulation and contractile activity and their interaction on cellular growth and cardiac myosin heavy chain (MHC) gene expression, spontaneously contracting neonatal rat ventricular myocytes in primary culture were maintained in serum-free growth medium or growth medium supplemented with fetal bovine serum. Contractile activity in paired cultures was inhibited by addition of the calcium channel blocker verapamil (10 microM) to the culture medium. Both serum stimulation and contractile activity produced myocyte hypertrophy as assessed by increases in total protein, total RNA, protein-to-DNA ratios, and total MHC protein content. MHC isoenzyme analysis indicated that both MHC-alpha and MHC-beta proteins accumulated in response to serum stimulation and/or contractile activity. The increases in MHC-beta protein resulting from serum stimulation and contractile activity occurred in parallel with increases in MHC-beta mRNA. In contrast, MHC-alpha mRNA levels were relatively unaffected by serum stimulation but appeared to decrease in response to contractile activity. The protein kinase inhibitor staurosporine (5 nM) reduced MHC-beta expression in serum-free, contracting cultures and also prevented the serum-induced increase in MHC-beta mRNA observed in both contracting and arrested myocytes. Staurosporine also increased MHC-alpha mRNA levels in serum-free, contracting, and verapamil-arrested myocytes. These data suggest that both humoral and mechanical factors regulate MHC isoenzyme expression and cellular growth in neonatal ventricular myocytes.
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Zult, Tjerk, Stuart Goodall, Kevin Thomas, Tibor Hortobágyi, and Glyn Howatson. "Mirror illusion reduces motor cortical inhibition in the ipsilateral primary motor cortex during forceful unilateral muscle contractions." Journal of Neurophysiology 113, no. 7 (April 2015): 2262–70. http://dx.doi.org/10.1152/jn.00686.2014.
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Forceful, unilateral contractions modulate corticomotor paths targeting the resting, contralateral hand. However, it is unknown whether mirror-viewing of a slowly moving but forcefully contracting hand would additionally affect these paths. Here we examined corticospinal excitability and short-interval intracortical inhibition (SICI) of the right-ipsilateral primary motor cortex (M1) in healthy young adults under no-mirror and mirror conditions at rest and during right wrist flexion at 60% maximal voluntary contraction (MVC). During the no-mirror conditions neither hand was visible, whereas in the mirror conditions participants looked at the right hand's reflection in the mirror. Corticospinal excitability increased during contractions in the left flexor carpi radialis (FCR) (contraction 0.41 mV vs. rest 0.21 mV) and extensor carpi radialis (ECR) (contraction 0.56 mV vs. rest 0.39 mV), but there was no mirror effect (FCR: P = 0.743, ηp2= 0.005; ECR: P = 0.712, ηp2= 0.005). However, mirror-viewing of the contracting and moving wrist attenuated SICI relative to test pulse in the left FCR by ∼9% compared with the other conditions ( P < 0.05, d ≥ 0.62). Electromyographic activity in the resting left hand prior to stimulation was not affected by the mirror (FCR: P = 0.255, ηp2= 0.049; ECR: P = 0.343, ηp2= 0.035) but increased twofold during contractions. Thus viewing the moving hand in the mirror and not just the mirror image of the nonmoving hand seems to affect motor cortical inhibitory networks in the M1 associated with the mirror image. Future studies should determine whether the use of a mirror could increase interlimb transfer produced by cross-education, especially in patient groups with unilateral orthopedic and neurological conditions.
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Koga, S., R. C. I. Wüst, B. Walsh, C. A. Kindig, H. B. Rossiter, and M. C. Hogan. "Increasing temperature speeds intracellular Po2 kinetics during contractions in single Xenopus skeletal muscle fibers." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 304, no. 1 (January 1, 2013): R59—R66. http://dx.doi.org/10.1152/ajpregu.00337.2012.
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Precise determination of the effect of muscle temperature (Tm) on mitochondrial oxygen consumption kinetics has proven difficult in humans, in part due to the complexities in controlling for Tm-related variations in blood flow, fiber recruitment, muscle metabolism, and contractile properties. To address this issue, intracellular Po2 (PiO2) was measured continuously by phosphorescence quenching following the onset of contractions in single Xenopus myofibers ( n = 24) while controlling extracellular temperature. Fibers were subjected to two identical contraction bouts, in random order, at 15°C (cold, C) and 20°C (normal, N; n = 12), or at N and 25°C (hot, H; n = 12). Contractile properties were determined for every contraction. The time delay of the PiO2 response was significantly greater in C (59 ± 35 s) compared with N (35 ± 26 s, P = 0.01) and H (27 ± 14 s, P = 0.01). The time constant for the decline in PiO2 was significantly greater in C (89 ± 34 s) compared with N (52 ± 15 s; P < 0.01) and H (37 ± 10 s; P < 0.01). There was a linear relationship between the rate constant for PiO2 kinetics and Tm ( r = 0.322, P = 0.03). Estimated ATP turnover was significantly greater in H than in C ( P < 0.01), but this increased energy requirement alone with increased Tm could not account for the differences observed in PiO2 kinetics among conditions. These results demonstrate that PiO2 kinetics in single contracting myofibers are dependent on Tm, likely caused by temperature-induced differences in metabolic demand and by temperature-dependent processes underlying mitochondrial activation at the start of muscle contractions.
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MAKISUMI, SHOTARO, GRACE STADNYK, and BENJAMIN STEINHURST. "MODIFIED HANOI TOWERS GROUPS AND LIMIT SPACES." International Journal of Algebra and Computation 21, no. 06 (September 2011): 867–87. http://dx.doi.org/10.1142/s0218196711006443.
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We introduce the k-peg Hanoi automorphisms and Hanoi self-similar groups, a generalization of the Hanoi Towers groups, and give conditions for them to be contracting. We analyze the limit spaces of a particular family of contracting Hanoi groups, [Formula: see text], and show that these are the unique maximal contracting Hanoi groups under a suitable symmetry condition. Finally, we provide partial results on the contraction of Hanoi groups with weaker symmetry.
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Magzoub, Aamir, Mohammed Al-Ayed, Ibrahim Ahmed Shaikh, Mohamed Shafiuddin Habeeb, Khalid Al-Shaibary, and Mohammed Shalayel. "Leptin induces a contracting effect on guinea pig tracheal smooth muscle via the Ob-R receptor mechanism: novel evidence." Canadian Journal of Physiology and Pharmacology 98, no. 11 (November 2020): 810–17. http://dx.doi.org/10.1139/cjpp-2019-0605.
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The purpose of this study was to explore the potential contracting effect of leptin on isolated guinea pig tracheal smooth muscle (TSM), the possible mechanism, and the impact of epithelium denudation or allergen sensitization, respectively. An in vitro experiment investigated the effect of leptin at a concentration of 250–1000 nmol/L on isolated guinea pig TSM with an intact or denuded epithelium. Ovalbumin and IgE were used to test the impact of active and passive sensitization. The isolated TSM strips were incubated in Krebs solution and aerated with carbogen (95% O2 and 5% CO2) via an automated tissue organ bath system (n = 4 for each group). Isometric contractions were recorded digitally using iox2 data acquisition software. The possible mechanism of leptin-induced TSM contraction was examined by preincubation with leptin receptor (Ob-R) antagonist. Leptin had significant concentration-dependent contraction effects on guinea pig TSM (p < 0.05). Epithelium denuding and active or passive sensitization significantly increased the potency of the leptin. Preincubation with a leptin receptor (Ob-R) antagonist significantly reduced the contraction effects, suggesting an Ob-R-mediated mechanism. Leptin had a contracting effect on airway smooth muscles potentiated by either epithelium denuding or sensitization, and the Ob-R mechanism was a possible effect mediator.
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Kovitz, K. L., T. D. Aleskowitch, J. T. Sylvester, and N. A. Flavahan. "Endothelium-derived contracting and relaxing factors contribute to hypoxic responses of pulmonary arteries." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 4 (October 1, 1993): H1139—H1148. http://dx.doi.org/10.1152/ajpheart.1993.265.4.h1139.
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The response of porcine pulmonary arteries to hypoxia depended on their location in the vasculature and the degree and duration of the hypoxic challenge. In rings of pulmonary artery suspended for isometric tension recording (37 degrees C, 16% O2 and 5% CO2), moderate hypoxia (10% and 4% O2) caused endothelium-dependent relaxation in distal arteries but transient endothelium-dependent contraction in proximal arteries. In both proximal and distal arteries, the initial response to anoxia (0% O2) was a transient endothelium-dependent contraction. This was followed by a slowly developing, sustained endothelium-dependent contraction in proximal arteries, or by an endothelium-independent relaxation in distal arteries. The endothelium-dependent relaxation to moderate hypoxia in distal arteries was inhibited only by combined inhibition of endothelium-derived relaxing factor (EDRF)-nitric oxide (NO) synthase [N omega-nitro-L-arginine methyl ester (L-NAME)] and cyclooxygenase (indomethacin), suggesting mediation by EDRF-NO and prostacyclin. Transient endothelium-dependent contractions to moderate hypoxia (proximal arteries) or anoxia (all arteries) were abolished by L-NAME, but the late endothelium-dependent anoxic contraction observed in proximal arteries was not reduced by L-NAME and/or indomethacin. Therefore, hypoxia/anoxia may initiate contraction of pulmonary arteries by decreasing the activity of EDRF-NO, but the contractions appear to be maintained by an increased activity of an endothelium-derived contracting factor.
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Freedman, Stephen M., John L. Wallace, and Eldon A. Shaffer. "Characterization of leukotriene-induced contraction of the guinea-pig gallbladder in vitro." Canadian Journal of Physiology and Pharmacology 71, no. 2 (February 1, 1993): 145–50. http://dx.doi.org/10.1139/y93-020.
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Metabolites of arachidonic acid like prostaglandins have an established role in the pathogenesis of gallstone formation and cholecystitis, but any contribution by leukotrienes is less clear. Leukotrienes might contribute to the disease process by contracting the inflamed and (or) obstructed gallbladder, resulting in further inflammatory damage and biliary pain. To better define the role of leukotrienes, we assessed their effects on gallbladder contracility in vitro. Both leukotriene C4 (LTC4) and D4 (LTD4) had a concentration-dependent excitatory effect on guinea-pig gallbladder smooth muscle. The LTD4-receptor antagonist MK-571 (1 μM) competitively depressed the contractile response, to both LTD4 and LTC4. The source of calcium was defined using ryanodine to deplete intracellular calcium stores and nifedipine to block extracellular entry. Ryanodine (10 μM) antagonized gallbladder contraction at low concentrations of LTD4 (10−10 and 10−9 M). Nifedipine (1 μM) had a greater inhibitory effect on the contractile response at high concentrations of LTD4 (10−8–10−6 M). LTD4-induced contractions were unaffected in tissues pretreated with the neural blocker tetrodotoxin or the muscarinic antagonist atropine. Thus, leukotrienes act directly on the gallbladder smooth muscle, causing contraction at concentrations found in models of cholecystitis, suggesting that these inflammatory mediators contribute to the symptoms and morbidity associated with gallbladder disease.Key words: gallstones, cholecystitis, guinea-pig, gallbladder, leukotriene.
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Hasibuan, Zainuddin. "Contractions Used in “Maleficent” Movie." Journal Polingua : Scientific Journal of Linguistics, Literature and Education 2, no. 2 (October 25, 2016): 15–23. http://dx.doi.org/10.30630/polingua.v6i2.82.
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The tiltle of this research is “Contractions Used in Maleficent Movie”. “Maleficent” movie was directed by Robert Stromberg based on the originally story Disney's Sleeping Beauty La Belle au bois dormant by Charles Perrault. The background of this research, there are many contractions in “Maleficent” movie. This is good to learn and to use them (contractions) in daily life and maybe they are not found in other movies. The contraction spoken by movie players is sometimes very difficult to understand. The researcher choose this movie because this movie is so interest and inspire. The problem of this research is what contractions are used by the author in the movie “Maleficent” and how are contractions used by the author in the movie “Maleficent”. The purpose of this research is to find out contractions used by the author in the movie “Maleficent” and to explain contractions used by the author in the movie “Maleficent”. To achieve that purpose, the researcher conducted the qualitative research by library research. There are many contractions used by the author which can be classified into eight categories. The most dominant contraction is contracted pronoun. The second is verb contractions. The third are contracting not and ambiguous contraction. The fourth are negative contractions and contraction in tag question. The fifth are contracted noun and beware homophones.
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Thomas, G. D., J. Hansen, and R. G. Victor. "Inhibition of alpha 2-adrenergic vasoconstriction during contraction of glycolytic, not oxidative, rat hindlimb muscle." American Journal of Physiology-Heart and Circulatory Physiology 266, no. 3 (March 1, 1994): H920—H929. http://dx.doi.org/10.1152/ajpheart.1994.266.3.h920.
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Previous studies have produced conflicting evidence as to whether sympathetic vasoconstriction is impaired in active skeletal muscle. Because alpha 2-, not alpha 1-, adrenergic vasoconstriction is attenuated by mild acidosis, we hypothesized that alpha 2-mediated sympathetic vasoconstriction would be attenuated in contracting glycolytic muscle, which produces more acidosis than oxidative muscle. We compared effects of lumbar sympathetic nerve stimulation and alpha-adrenergic agonists on arterial pressure, femoral blood flow, and force output during contractions of oxidative or glycolytic muscles in anesthetized rats. We found that 1) sympathetic vasoconstriction was preserved during contractions of oxidative soleus muscle and during low-intensity contractions of glycolytic gastrocnemiusplantaris muscles but was abolished during maximal contractions of these glycolytic muscles; 2) this sympatholytic effect was caused by impaired alpha 2-, not alpha 1-, vasoconstriction; and 3) the increased muscle blood flow resulting from a combination of impaired vasconstriction and increased arterial pressure was paralleled by increased force of gastrocnemius-plantaris muscle contraction. Thus contraction-induced impairment of alpha 2-vasoconstriction can augment muscle blood flow and muscle contraction, but the degree of impairment depends on fiber type and intensity of muscle contraction.
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Muramatsu, M., Y. Iwama, K. Shimizu, H. Asano, Y. Toki, Y. Miyazaki, K. Okumura, H. Hashimoto, and T. Ito. "Hypoxia-elicited contraction of aorta and coronary artery via removal of endothelium-derived nitric oxide." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 5 (November 1, 1992): H1339—H1347. http://dx.doi.org/10.1152/ajpheart.1992.263.5.h1339.
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To characterize endothelium-derived contracting factor 1 (EDCF1) released under hypoxia, vascular rings isolated from spontaneously hypertensive rat (SHR) aorta and canine coronary artery were suspended for isometric tension recording in an organ chamber filled with a Krebs-Henseleit buffer. In SHR aorta precontracted with norepinephrine (10(-7) M), severe hypoxia induced an initial increase in tension by 36.7 +/- 7.5% followed by a 56.9 +/- 5.7% relaxation; moderate hypoxia induced only a sustained increase in tension by 20.6 +/- 2.5%. Inhibition of nitric oxide (NO) production with N omega-nitro-L-arginine methyl ester (L-NAME) (10(-3) M) augmented norepinephrine-induced precontraction by 76.1 +/- 12.3% and totally eliminated the hypoxic contraction. In canine coronary arteries precontracted with KCl (30 mM) in the presence of indomethacin (10(-5) M), severe hypoxia caused a sustained increase in tension by 68.9 +/- 7.3%, which was also abolished with L-NAME. When L-NAME (10(-3) M) was given after the precontraction, both of these vessels developed sustained contractions under normoxia and moderate hypoxia. These results suggest that the vasocontraction currently considered to be induced by EDCF1 is not caused by a contracting factor but rather is a contracting phenomenon derived from continuous inhibition of basal NO synthesis during hypoxia.
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Manoharan, Palanikumar, Tatiana L. Radzyukevich, Hesamedin Hakim Javadi, Cory A. Stiner, Julio A. Landero Figueroa, Jerry B. Lingrel, and Judith A. Heiny. "Phospholemman is not required for the acute stimulation of Na+-K+-ATPase α2-activity during skeletal muscle fatigue." American Journal of Physiology-Cell Physiology 309, no. 12 (December 15, 2015): C813—C822. http://dx.doi.org/10.1152/ajpcell.00205.2015.
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The Na+-K+-ATPase α2-isoform in skeletal muscle is rapidly stimulated during muscle use and plays a critical role in fatigue resistance. The acute mechanisms that stimulate α2-activity are not completely known. This study examines whether phosphorylation of phospholemman (PLM/FXYD1), a regulatory subunit of Na+-K+-ATPase, plays a role in the acute stimulation of α2 in working muscles. Mice lacking PLM (PLM KO) have a normal content of the α2-subunit and show normal exercise capacity, in contrast to the greatly reduced exercise capacity of mice that lack α2 in the skeletal muscles. Nerve-evoked contractions in vivo did not induce a change in total PLM or PLM phosphorylated at Ser63 or Ser68, in either WT or PLM KO. Isolated muscles of PLM KO mice maintain contraction and resist fatigue as well as wild type (WT). Rb+ transport by the α2-Na+-K+-ATPase is stimulated to the same extent in contracting WT and contracting PLM KO muscles. Phosphorylation of sarcolemmal membranes prepared from WT but not PLM KO skeletal muscles stimulates the activity of both α1 and α2 in a PLM-dependent manner. The stimulation occurs by an increase in Na+ affinity without significant change in Vmax and is more effective for α1 than α2. These results demonstrate that phosphorylation of PLM is capable of stimulating the activity of both isozymes in skeletal muscle; however, contractile activity alone is not sufficient to induce PLM phosphorylation. Importantly, acute stimulation of α2, sufficient to support exercise and oppose fatigue, does not require PLM or its phosphorylation.
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Idstrom, J. P., V. H. Subramanian, B. Chance, T. Schersten, and A. C. Bylund-Fellenius. "Oxygen dependence of energy metabolism in contracting and recovering rat skeletal muscle." American Journal of Physiology-Heart and Circulatory Physiology 248, no. 1 (January 1, 1985): H40—H48. http://dx.doi.org/10.1152/ajpheart.1985.248.1.h40.
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The relationship between the oxygen supply and the energy metabolism in perfused rat hindlimb muscles was evaluated both during contractions and during recovery from contractions. The 31P-nuclear magnetic resonance (NMR) technique and conventional biochemical methods were used. Significant correlations were found between the oxygen delivery and the oxygen consumption, lactate release and glucose uptake, respectively. An increased degree of fatigue was observed at the lower oxygen deliveries. In both the soleus and gastrocnemius muscles the oxygen delivery correlated with the intramuscular concentrations of phosphocreatine, lactate, and glycogen. The 31P-NMR experiments showed a correlation between the oxygen delivery and the steady-state level of the phosphocreatine-to-inorganic phosphate (PCr+Pi) ratio during the contraction period. The rate of recovery in PCr/Pi after the contractions was also dependent on the oxygen delivery. The results demonstrate a causal relationship between the oxygen supply and the energy state in contracting as well as recovering skeletal muscles.
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Kruse, Nicholas T., William E. Hughes, Kenichi Ueda, and Darren P. Casey. "Vasoconstrictor responsiveness in contracting human muscle: influence of contraction frequency, contractile work, and metabolic rate." European Journal of Applied Physiology 117, no. 8 (June 17, 2017): 1697–706. http://dx.doi.org/10.1007/s00421-017-3660-7.
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Holt, Gary A., Kay E. Holt, Ashish Chandra, and Richard Hood. "Contracting." Journal of Pharmacy Teaching 7, no. 1 (1999): 85–87. http://dx.doi.org/10.1300/j060v07n01_08.
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Watson, P. A., R. Hannan, L. L. Carl, and K. E. Giger. "Desmin gene expression in cardiac myocytes is responsive to contractile activity and stretch." American Journal of Physiology-Cell Physiology 270, no. 4 (April 1, 1996): C1228—C1235. http://dx.doi.org/10.1152/ajpcell.1996.270.4.c1228.
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Experiments were performed to assess the ability of mechanical stimuli, experienced by ventricular cardiac myocytes during the progression of hypertrophic and dilated pathology, to increase the expression of desmin in cultured neonatal rat cardiac myocytes. Results indicate that both contractile activity and load due to passive stretch increase desmin content in neonatal rat cardiac myocytes through increased desmin gene transcription. Western blot analysis demonstrated that contraction induced a selective increase in desmin protein content in neonatal rat cardiac myocytes above increases observed in the content of total cellular protein. Northern blot analysis indicated that desmin mRNA content increased in response to contraction as well as to alpha-adrenergic stimulation. Desmin mRNA content also increased in cultured neonatal myocytes in response to stretch. Angiotensin II (ANG II) treatment of contracting neonatal cardiac myocytes further increased desmin mRNA content, whereas similar treatment in arrested neonatal cardiac myocytes further increased desmin mRNA content, whereas similar treatment in arrested neonatal cardiac myocytes failed to increase desmin mRNA. This contraction-dependent responsiveness to ANG II is not a function of increases in the density or relative subtype composition of ANG II receptors. Treatment of contracting neonatal rat cardiac myocytes with actinomycin D prevented increases in desmin mRNA content, suggesting regulation of transcription of the desmin gene by contraction. Nuclear run-on experiments indicate that contraction. Nuclear run-on experiments indicate that contraction increases transcription of the desmin gene in cardiac myocytes. These results are consistent with the modulation of desmin gene expression secondarily to changes in the mechanical environment that occur in cardiac tissue undergoing dilation or hypertrophy.
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Jendzjowsky, Nicholas G., and Darren S. DeLorey. "Role of neuronal nitric oxide in the inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle of healthy rats." Journal of Applied Physiology 115, no. 1 (July 1, 2013): 97–106. http://dx.doi.org/10.1152/japplphysiol.00250.2013.
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Isoform-specific nitric oxide (NO) synthase (NOS) contributions to NO-mediated inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle are incompletely understood. The purpose of the present study was to investigate the role of neuronal NOS (nNOS) in the inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle of healthy rats. We hypothesized that acute pharmacological inhibition of nNOS would augment sympathetic vasoconstriction in resting and contracting skeletal muscle, demonstrating that nNOS is primarily responsible for NO-mediated inhibition of sympathetic vasoconstriction. Sprague-Dawley rats ( n = 13) were anesthetized and instrumented with an indwelling brachial artery catheter, femoral artery flow probe, and lumbar sympathetic chain stimulating electrodes. Triceps surae muscles were stimulated to contract rhythmically at 60% of maximal contractile force. In series 1 ( n = 9), the percent change in femoral vascular conductance (%FVC) in response to sympathetic stimulations delivered at 2 and 5 Hz was determined at rest and during muscle contraction before and after selective nNOS blockade with S-methyl-l-thiocitrulline (SMTC, 0.6 mg/kg iv) and subsequent nonselective NOS blockade with Nω-nitro-l-arginine methyl ester (l-NAME, 5 mg/kg iv). In series 2 ( n = 4), l-NAME was injected first, and then SMTC was injected to determine if the effect of l-NAME on constrictor responses was influenced by selective nNOS inhibition. Sympathetic stimulation decreased FVC at rest (−25 ± 7 and −44 ± 8%FVC at 2 and 5 Hz, respectively) and during contraction (−7 ± 3 and −19 ± 5%FVC at 2 and 5 Hz, respectively). The decrease in FVC in response to sympathetic stimulation was greater in the presence of SMTC at rest (−32 ± 6 and −49 ± 8%FVC at 2 and 5 Hz, respectively) and during contraction (−21 ± 4 and −28 ± 4%FVC at 2 and 5 Hz, respectively). l-NAME further increased ( P < 0.05) the sympathetic vasoconstrictor response at rest (−47 ± 4 and −60 ± 6%FVC at 2 and 5 Hz, respectively) and during muscle contraction (−33 ± 3 and −40 ± 6%FVC at 2 and 5 Hz, respectively). The effect of l-NAME was not altered by the order of nNOS inhibition. These data demonstrate that NO derived from nNOS and endothelial NOS contribute to the inhibition of sympathetic vasoconstriction in resting and contracting skeletal muscle.
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Hogan, M. C., S. S. Kurdak, and P. G. Arthur. "Effect of gradual reduction in O2 delivery on intracellular homeostasis in contracting skeletal muscle." Journal of Applied Physiology 80, no. 4 (April 1, 1996): 1313–21. http://dx.doi.org/10.1152/jappl.1996.80.4.1313.
Full textAbstract:
This study was designed to investigate 1) whether a protocol employing a gradual reduction in O2 availability to submaximally contracting muscle results in relatively minor disturbances in intracellular homeostasis and 2) the interaction between tissue oxygenation and the proposed regulators of muscle respiration, metabolism, and force production. O2 delivery to isolated submaximally contracting [isometric contractions at 3 Hz; approximately 50% of peak O2 uptake (VO2)] in situ canine gastrocnemius (n = 6) was manipulated by decreasing arterial PO2 (hypoxemia; H) or muscle blood flow (ischemia; I) during three separate periods in each muscle [control (C), H, or I; each separated by 45 min of rest]. O2 delivery was reduced gradually in small steps every 3 min by H or I during two of the contraction periods (6 steps for a total of 21 min; O2 delivery reduced by 67% by the end of 21 min), whereas C was at normal O2 delivery for a 15-min period. Muscle VO2 was maintained at control levels for the first two O2 delivery reduction steps for the H and I conditions and then fell proportionally with O2 delivery to approximately 35% of the initial value by the end of the 21-min contraction period. Muscle force development generally fell in parallel with VO2. There was no significant changes from the values obtained during C contractions in intracellular concentrations of ATP, phosphocreatine, NH3, calculated free ADP, lactate, and redox state ratios as the O2 delivery was reduced, even with the severe decline in VO2 and developed force. These results demonstrated that when O2 availability was reduced gradually to contracting skeletal muscle, 1) developed force (ATP utilization) was reduced through a tight coupling with aerobic ATP supply, such that there was little additional disruption of intracellular homeostasis, and 2) there was an apparent dissociation of some of the proposed regulators of cell respiration and force development from the control of these processes.
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Miyamoto, Licht, Tatsuro Egawa, Rieko Oshima, Eriko Kurogi, Yosuke Tomida, Koichiro Tsuchiya, and Tatsuya Hayashi. "AICAR stimulation metabolome widely mimics electrical contraction in isolated rat epitrochlearis muscle." American Journal of Physiology-Cell Physiology 305, no. 12 (December 15, 2013): C1214—C1222. http://dx.doi.org/10.1152/ajpcell.00162.2013.
Full textAbstract:
Physical exercise has potent therapeutic and preventive effects against metabolic disorders. A number of studies have suggested that 5′-AMP-activated protein kinase (AMPK) plays a pivotal role in regulating carbohydrate and lipid metabolism in contracting skeletal muscles, while several genetically manipulated animal models revealed the significance of AMPK-independent pathways. To elucidate significance of AMPK and AMPK-independent signals in contracting skeletal muscles, we conducted a metabolomic analysis that compared the metabolic effects of 5-aminoimidazole-4-carboxamide-1-β-d-ribonucleoside (AICAR) stimulation with the electrical contraction ex vivo in isolated rat epitrochlearis muscles, in which both α1- and α2-isoforms of AMPK and glucose uptake were equally activated. The metabolomic analysis using capillary electrophoresis time-of-flight mass spectrometry detected 184 peaks and successfully annotated 132 small molecules. AICAR stimulation exhibited high similarity to the electrical contraction in overall metabolites. Principal component analysis (PCA) demonstrated that the major principal component characterized common effects whereas the minor principal component distinguished the difference. PCA and a factor analysis suggested a substantial change in redox status as a result of AMPK activation. We also found a decrease in reduced glutathione levels in both AICAR-stimulated and contracting muscles. The muscle contraction-evoked influences related to the metabolism of amino acids, in particular, aspartate, alanine, or lysine, are supposed to be independent of AMPK activation. Our results substantiate the significance of AMPK activation in contracting skeletal muscles and provide novel evidence that AICAR stimulation closely mimics the metabolomic changes in the contracting skeletal muscles.
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Toda, N. "Mechanisms of contracting action of oxyhemoglobin in isolated monkey and dog cerebral arteries." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 1 (January 1, 1990): H57—H63. http://dx.doi.org/10.1152/ajpheart.1990.258.1.h57.
Full textAbstract:
Oxyhemoglobin (HbO2) produced a concentration-dependent contraction of monkey and dog cerebral artery strips, which was significantly attenuated by endothelium denudation. The contractile response was suppressed by treatment with indomethacin, aspirin, and diphloretin phosphate, a prostaglandin (PG) receptor antagonist. OKY 046, a thromboxane synthase inhibitor, attenuated both the contractions caused by HbO2 and PGF2 alpha. Contractions by arachidonic acid (AA) of the monkey arteries were markedly inhibited by indomethacin and moderately attenuated by endothelium denudation. Treatment with superoxide dismutase and catalase failed to reduce the response to HbO2 and AA. The median effective concentration of HbO2 in producing dog cerebral artery contraction was approximately 1,000 times as high as the median inhibitory concentration in inhibiting the effect of endothelium-derived relaxing factor (EDRF) released from dog femoral arteries in response to acetylcholine. It is concluded that contractions caused by HbO2 are not associated with suppression of EDRF released spontaneously from monkey and dog cerebral arteries, but with vasoconstrictor PGs released mainly from endothelium. Thromboxane A2, superoxide anions, and hydrogen peroxide do not appear to be involved.
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Pandolfino, John E., Zhiyue Lin, Sabine Roman, and Peter J. Kahrilas. "The time course and persistence of “concurrent contraction” during normal peristalsis." American Journal of Physiology-Gastrointestinal and Liver Physiology 301, no. 4 (October 2011): G679—G683. http://dx.doi.org/10.1152/ajpgi.00214.2011.
Full textAbstract:
Whereas conventional manometry depicts peristalsis as pressure variation over time, high-resolution manometry makes it equally feasible to depict pressure variation along the lumen (spatial pressure variation plots). This study analyzed the characteristics of spatial pressure variation plots during normal peristalsis. High-resolution manometry studies of 72 normal subjects were analyzed with custom MATLAB programs. A coordinate-based strategy was used to normalize both timing of peristalsis and esophageal length. A spatial pressure variation function was devised to localize the proximal (P) and the distal troughs (D) on each subject's composite pressure topography and track the length within the P-D segment contracting concurrently in the course of peristalsis. The timing at which this function peaked was compared with that of the contractile deceleration point (CDP). The length of concurrent contraction during normal peristalsis had an average span of 9.3 cm, encompassing 61% of the distal P-D length of the esophagus. The timing of the CDP position closely matched that of maximal length within the P-D segment contracting concurrently ( r = 0.90, P < 0.001). The pressure morphology of the maximal concurrent contraction was that of a smooth curve, and it was extremely rare to see multiple peaks along the vertical axis (seen in 4 of 72 subjects). Concurrent contraction involving ∼60% of the P-D span occurred with normal peristalsis. The segment of concurrent contraction progressively increased as peristalsis progressed, peaked at the CDP, and then progressively decreased. How abnormalities of the extent or timing of concurrent contraction relate to clinical syndromes requires further investigation.
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Wu, David M., Hajime Kawamura, Kenji Sakagami, Masato Kobayashi, and Donald G. Puro. "Cholinergic regulation of pericyte-containing retinal microvessels." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 6 (June 1, 2003): H2083—H2090. http://dx.doi.org/10.1152/ajpheart.01007.2002.
Full textAbstract:
The aim of this study was to test the hypothesis that the neurotransmitter acetylcholine regulates the function of pericyte-containing retinal microvessels. A vasoactive role for acetylcholine is suggested by the presence of muscarinic receptors on pericytes, which are abluminally positioned contractile cells that may regulate capillary perfusion. However, little is known about the response of retinal microvessels to this neurotransmitter. Here we assessed the effects of cholinergic agonists on microvessels freshly isolated from the adult rat retina. Ionic currents were monitored via perforated patch pipettes; intracellular Ca2+ levels were quantified with the use of fura 2, and microvascular contractions were visualized with the aid of time-lapse photography. We found that activation of muscarinic receptors elevated pericyte calcium levels, increased depolarizing Ca2+-activated chloride currents and caused pericytes to contract in a Ca2+-dependent manner. Most contracting pericytes were near capillary bifurcations. Contraction of a pericyte caused the adjacent capillary lumen to constrict. Thus acetylcholine may serve as a vasoactive signal by regulating pericyte contractility and thereby capillary perfusion in the retina.
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Armon, Shahaf, Matthew Storm Bull, Andres Aranda-Diaz, and Manu Prakash. "Ultrafast epithelial contractions provide insights into contraction speed limits and tissue integrity." Proceedings of the National Academy of Sciences 115, no. 44 (October 11, 2018): E10333—E10341. http://dx.doi.org/10.1073/pnas.1802934115.
Full textAbstract:
By definition of multicellularity, all animals need to keep their cells attached and intact, despite internal and external forces. Cohesion between epithelial cells provides this key feature. To better understand fundamental limits of this cohesion, we study the epithelium mechanics of an ultrathin (∼25 μm) primitive marine animal Trichoplax adhaerens, composed essentially of two flat epithelial layers. With no known extracellular matrix and no nerves or muscles, T. adhaerens has been claimed to be the “simplest known living animal,” yet is still capable of coordinated locomotion and behavior. Here we report the discovery of the fastest epithelial cellular contractions known in any metazoan, to be found in T. adhaerens dorsal epithelium (50% shrinkage of apical cell area within one second, at least an order of magnitude faster than other known examples). Live imaging reveals emergent contractile patterns that are mostly sporadic single-cell events, but also include propagating contraction waves across the tissue. We show that cell contraction speed can be explained by current models of nonmuscle actin–myosin bundles without load, while the tissue architecture and unique mechanical properties are softening the tissue, minimizing the load on a contracting cell. We propose a hypothesis, in which the physiological role of the contraction dynamics is to resist external stresses while avoiding tissue rupture (“active cohesion”), a concept that can be further applied to engineering of active materials.
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Kelley, C., P. D'Amore, H. B. Hechtman, and D. Shepro. "Microvascular pericyte contractility in vitro: comparison with other cells of the vascular wall." Journal of Cell Biology 104, no. 3 (March 1, 1987): 483–90. http://dx.doi.org/10.1083/jcb.104.3.483.
Full textAbstract:
Collagen lattices containing bovine retinal pericytes (RPs), vascular smooth muscle cells (VSMCs), pulmonary microvessel endothelial cells (PMECs), or aortic endothelial cells (AECs) were prepared and contraction was quantitated by measuring the resulting change in lattice area. VSMCs were the most efficient at lattice contraction followed by RPs and then PMECs. AECs did not contract the lattices. To document further that these observations represent contraction, cells were grown on inert silicone rubber sheets. Substratum wrinkling was indicative of tension development and quantitated as percent of cells contracted. RPs were more contractile than PMECs, and AECs were incapable of developing tension. VSMCs were less contractile than RPs, unlike the comparative contractility observed with the lattice system. Alteration of actin-containing filaments by cytochalasin B significantly reduced RP contraction of silicone rubber and inhibited their contraction of collagen lattices in a dose-dependent manner. Rhodamine-phalloidin staining of contracting RPs revealed microfilament bundle orientations that suggested their association in the force applied for contraction. RP, VSMC and PMEC contraction of collagen lattices was directly proportional to the concentration of fetal calf serum. Also, RP contraction was greater in calf serum than calf plasma-derived serum, an indication that RPs respond to substances that appear continuously and episodically in blood. These in vitro findings support the theory that pericytes in vivo are contractile but that endothelial cells may also contribute to microvascular tonus.
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Heise, Elizabeth. "Contracting Around Gender Constructs: Transgender Men at Women's Colleges." Michigan Journal of Gender & Law, no. 26.1 (2019): 175. http://dx.doi.org/10.36641/mjgl.26.1.contracting.
Full textAbstract:
As the transgender community gains increasing visibility in society, women’s colleges have begun to address new questions about who is eligible to attend. One such question is whether students who come out as transgender men after matriculation are eligible to remain enrolled and graduate from these institutions. The main claims relevant to this discussion are (1) colleges’ right to retain their identity as all-women’s institutions; (2) the parallel rights of cisgender female students who explicitly choose to attend an all-women’s institution, and (3) transgender students’ competing right to avoid arbitrary or capricious dismissal based on gender identity. This Note posits that contract law provides a useful framework for colleges to evaluate this question since both express and implied contracts form the basis of the student- college relationship. Ultimately, this Note argues that, although solutions that satisfy all parties are impossible, harms can be minimized if transgender students are permitted to graduate and given appropriate support throughout the transition process, and other policies are adapted to address the concerns of cisgender female students.