Sarcomere length in experimental myocardial infarction: evidence for sarcomere overstretch in dyskinetic ventricular regions.
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Differences in maximal activation properties of skinned short- and long-sarcomere muscle fibres from the claw of the freshwater crustacean Cherax destructor.
Single fibres of different sarcomere length at rest have been isolated from the claw muscle of the yabby (Cherax destructor), a decapod crustacean. Fibres of either long (SL > 6 microns) or short (SL < 4 microns) sarcomere length have been mechanically skinned and were maximally activated by Ca2+ and Sr2+ under various experimental conditions (ionic strength, in the presence of 2,3 butanedione monoxime (BDM)) to determine differences in their contractile properties. Isometric force was measured simultaneously with either myofibrillar MgATPase or fibre stiffness in both fibre types. The ultrastructure of individual long- and short-sarcomere fibres was also determined by electron microscopy. The long-sarcomere fibres developed greater tension (30.48 +/- 1.72 N cm-2) when maximally activated by Ca2+ compared with the short-sarcomere fibres (18.60 +/- 0.80 N cm-2). The difference in the maximum Ca(2+)-activated force can be explained by the difference in the amount of filament overlap between the two fibre types. The maximum Ca(2+)-activated myofibrillar MgATPase rate in the short-sarcomere fibres (1.60 +/- 0.27 mmol ATP l-1s-1) was higher, but not significantly different from the ATPase rate in fibres with long-sarcomeres (1.09 +/- 0.14 mmol ATP l-1s-1). As the concentration of myosin is estimated to be higher only by a factor of 1.22 in the short-sarcomere preparations there is no evidence to suggest that the myofibrillar MgATPase activity is different in the long- and short-sarcomere preparations. The maximum Ca(2+)-activated force (P0) of both short- and long-sarcomere fibres was quite insensitive to BDM compared with vertebrate muscle. Force decreased to 60.2 +/- 5.3% and 76.1 +/- 2.7% in the short- and long-sarcomere fibres respectively in the presence of 100 mmol l-1 BDM. The difference in the force depression between the long- and short-sarcomere fibres is statistically significant (p < 0.05). Fibre stiffness during maximum Ca(2+)-activation expressed as percentage maximum force per nm per half sarcomere was higher by a factor of 3.5 in short-sarcomere fibres than in long-sarcomere fibres suggesting that the compliance of the filaments in the long-sarcomere fibres is considerably higher than in the short-sarcomere fibres. Sr2+ could not activate the contractile apparatus to the same level as that seen by Ca2+ in either fibre type: the maximum Sr(2+)-activated force was (20 +/- 3%) and (63 +/- 3%) of the maximum Ca(2+)-activated force response in short- and long-sarcomere fibres, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)
Actins↗
YAP Promotes Microtubule Growth to Facilitate Sarcomere Disassembly in Adult Cardiomyocytes.
BACKGROUND: Mature mammalian cardiomyocytes (CMs) develop compact sarcomeric structures that inhibit proliferation. Consequently, CMs must dedifferentiate to a fetus-like state, which is accompanied by sarcomere disassembly, to enable successful cytokinesis. However, the regulation and coordination of CM dedifferentiation, cell cycle progression, and sarcomere reorganization remain unclear. METHODS: We generated adenovirus and adeno-associated virus (MyoAAV) vectors expressing YAP5SA and YAP5SA-S94A under Xon control for LMI070-inducible protein expression. We also developed MyoAAV-cTnT-Tuba1b-shRNA-miR30 for cardiomyocyte-specific knockdown of Tuba1b. These tools were used to investigate CM dedifferentiation and proliferation and sarcomere disassembly. We also performed Cleavage Under Targets and Release Using Nuclease to map the genome-wide binding sites of YAP5SA and YAP5SA-S94A in combination with RNA sequencing to identify YAP target genes. In addition, time-course live-imaging analysis was used to evaluate microtubule and sarcomere dynamics in adult CMs. RESULTS: We show that microtubule expression and network density decline with cardiac maturation. Overexpression of YAP5SA, a constitutively active YAP mutant, promotes microtubule growth by stabilizing microtubule dynamics, leading to CM dedifferentiation, cell cycle re-entry, and sarcomere disassembly. In contrast, colchicine blocks these processes and significantly attenuates YAP-induced cardiac regeneration. Live imaging reveals a distinct mode of sarcomere disassembly driven by enhanced microtubule polymerization, wherein microtubule plus-ends directly interact with α-actinin and displace α-actinin fragments, thereby facilitating sarcomere breakdown. Furthermore, the YAP5SA-S94A mutation, which disrupts the YAP and TEA domain interaction, significantly reduces YAP5SA-induced microtubule growth, sarcomere disassembly, and cell cycle activity. Mechanistically, cleavage under targets and release using nuclease combined with RNA sequencing identified direct YAP targets, including Ajuba and Tuba1b, which are critical for microtubule growth. CM-specific knockdown of Tuba1b attenuates YAP-driven sarcomere disassembly. CONCLUSIONS: These findings identify microtubule networks as an essential regulator modulating CM dedifferentiation and sarcomere reorganization, which is critical for CM cytokinesis and cardiac regenerative repair.
Animals↗
Functional adaptation of sarcomere number of normal cat muscle.
1. Physiological and histological data were obtained from soleus and tibialis anterior muscles of normal adult cats to study to what extent fibre length and sarcomere number varied between animals and how this was related to the physiological characteristics of the muscles. 2. For a given muscle, the variation in the sarcomere number of individual muscle fibres between animals was found to be about 25%. These difference could partly be explained by comparing the number of sarcomeres and the length of the fibula, which was chosen as an index of the size of the animal. The average sarcomere number in the tibialis anterior muscle was about 60% greater than in the soleus. The variations between animals and between the anterior tibialis and soleus muscles were significantly greater than the variations observed within the same muscle. 3. The sarcomere length is dependent upon the articular angle, that is to say, the length change imposed on the muscle. These length changes are more extensive in the soleus muscle (100%) than in the tibialis anterior muscle (60%). A very significant correlation was found between articular angle and sarcomere length (for soleus r = 0.98, for tibialis anterior r = 0.94). 4. Although fibre length did vary considerably within a given muscle, the sarcomere length showed only minor variations at any given angle. This suggests that sarcomere number is determined in each individual muscle fibre. Such an adaptation implies a concomitant adaptation of the tendinous part of the fibre. This adaptation, resulting in definite sarcomere length at a definite angle, has obvious physiological implications. 5. Conventional length vs. active tension curves were established for the soleus and the tibialis anterior muscles. It is suggested that the difference between the sarcomere number of the two muscles may result in the difference between the shape of curves of these two muscles. 6. Active torque-angle curves were established for the two muscles in situ. The shapes of the curves for soleus and tibialis anterior are similar in spite of the different mechanical conditions of the two muscles. This fact helps to explain why the two muscles, despite their similar articular range, had very different sarcomere number.
Adaptation, Physiological↗
Effect of small release on force during sarcomere-isometric tetani in frog muscle fibers.
We investigated the effect of small shortening imposed on frog muscle fibers during sarcomere-isometric tetani. Sarcomere length was initially kept constant, then slightly shortened (1%-5% of initial length) and clamped again for the remainder of the tetanus. Force level after the shortening was higher than the force level preceding the release. The size of the increase was larger than that predicted by the descending limb of the linear force-length relation. The difference between measured and predicted force levels increased with sarcomere length. At a sarcomere length of 3.2 microns, the force level after the shortening was higher by 50% than the force level expected from the linear descending limb. Dispersion of sarcomere-length within the sampled region was measured by two independent methods: striation imaging and analysis of the intensity profile of the first diffraction order. Sarcomere-length inhomogeneity in the sampled region was too small (standard deviation from the average sarcomere-length was +/- 0.03 microns) to account for the size of the increase in force. We studied the dependence of increase in tetanic force level after small sarcomere-length release on the size, velocity and timing of the release, as well as on initial sarcomere-length. Release size was the major determinant of the amount of increase in force. Release of 20 nm per half sarcomere was sufficient to produce an almost full force increase. Larger releases increased the force only moderately. Over the range studied, release velocity and timing had little or no effect.
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The relative contributions of the folds and caveolae to the surface membrane of frog skeletal muscle fibres at different sarcomere lengths.
The plasmalemmal area of striated muscle fibres is greater than the apparent surface area (A = circumference x length) because of variable folds and the invaginations of the caveolae and T-tubules. Freeze-fracture replicas of the surface membrane of sartorius and semitendinosus muscles from Rana pipiens have been used to determine the numbers and distribution of folds and caveolae at different sarcomere lengths. (1) The plasmalemma folds are variable in size and shape, but are always oriented perpendicular to the long axis of the fibre. The folds vary with stretch, being more prominent at short sarcomere lengths. The caveolae are elliptical invaginations of the plasmalemma which open to the outside by a narrow "neck" of approximately 20 nm. The caveolar lumen has an average long dimension of 81.6 +/- 11.7 nm and an average short dimension of 66.9 +/- 7.9 nm. The caveolar "necks" only can be seen in freeze-fracture replicas and these are distributed in two circumferential bands on either side of the Z-line, and in longitudinal bands separated by distances of 1-5 mum. In the sartorius muscle, at a sarcomere length of 2.8 mum, there is an average number of thirty-seven caveolae per square micrometer of fibre surface. (2) During passive stretch the opening of folds provides membrane for the necessary increase in surface area up to a sarcomere length of about 3.0 mum. This length is defined as the critical sarcomere length (Sc). The number of caveolae remains constant at all sarcomere lengths less than Sc and thus their "necks" have been used as membrane markers to determine the amount of folding at different sarcomere lengths. The membrane area contained in folds and caveolae is expressed as a fraction of the apparent surface area (A). For example, in the sartorius muscle, at a sarcomere length of 2.4 mum, the membrane area, excluding the T-tubules, is: A + 0.1A (folding) + 0.7A (caveolae) = 1.8A. (3) For stretch beyond Sc membrane is provided by the opening of caveolae. At a sarcomere length of about 8 mum all the caveolae are open and the fibres rupture with further stretch. (4) The relative contributions of folds and caveolae vary with sarcomere length in a way that is consistent with assumptions of constant volume and plasmalemma area. The maintenance of constant plasmalemma area, even after excessive stretch, suggests that the plasmalemma is relatively inelastic in this situation.
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The passive electrical properties of frog skeletal muscle fibres at different sarcomere lengths.
1. The passive electrical properties of frog skeletal muscle fibres have been measured at a number of different sarcomere lengths (from 2-1 to 4-0 micron). The geometrical outline of each fibre was determined from optical cross-sections and sarcomere length was measured by laser beam diffraction. 2. When fibres were stretched to long sarcomere lengths the membrane capacity, Cm, of both normal and detubulated (glycerol-treated) fibres was significantly less than the Cm of fibres at rest length. A significant reduction in membrane conductance of fibres held at long sarcomere lengths was only seen with detubulated fibres. 3. Membrane capacity and membrane conductance have a significant dependence on the cross-sectional area of normal fibres but are independent of cross-sectional area after detubulation. 4. It has been shown that membrane geometry depends on the sarcomere length of the fibre and it is suggested that the passive membrane properties are related to sarcomere length because they depend on membrane geometry. 5. The specific membrane capacity, calculated from the data from detubulated fibres, is 0-8 micronF/cm2. 6. The internal resistivity, Ri, of normal fibres, also depends on sarcomere length between 2-1 and 3-0 micron. At a sarcomere length of 2-1 micron the average Ri is 122 +/- 3 omega. cm (mean +/- S.E. of mean) and at a sarcomere length of 3-0 micron the average Ri is 210 +/- 17 omega. cm (mean +/- S.E. of mean). No further increase in Ri was observed with further increases in sarcomere length.
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Cross-bridge detachment and sarcomere 'give' during stretch of active frog's muscle.
1. A study has been made of the tension responses and sarcomere length changes produced by servo-controlled stretches applied to isometrically contracting frog muscle. Sarcomere lengths were monitored by cine-photography of diffiraction spectra obtained by illuminating a small area of muscle with a laser. 2. The tension increment produced by a ramp-and-hold stretch of approximately 1 mm (ca. 4% of the muscle length) comprises three phases whose limits are defined by two points, S1 and S2, where the slope of the response decreases abruptly. S1 and S2 correspond to extensions of 0.13 and 1.2% of the muscle length. 3. Movements of the first order spectra relative to the zero order recorded during stretch reveal that S2 coincides with an abrupt elongation of the sarcomeres. This is termed sarcomere 'give' and it occurs when the filaments are displaced by 11-12 nm from their steady-state (isometric) position. 4. The stiffness of the sarcomeres, Es, up to S2 decreases with increasing sarcomere length. The maximum force sustained by the muscle at S2, PS2, also shows an inverse dependence on sarcomere length. Both Es and PS2 fall to zero at an extrapolated sarcomere spacing of 3.6-3.7 micrometer, coinciding with the length at which the actin and myosin filaments no longer overlap. 5. The ratio PS2/P0 (where P0 = maximum isometric tension) varies with temperature and speed of stretch. It increases with increasing speeds of stretch until a certain critical velocity, Vc, is reached, beyond which it is almost independent of any further increase. Vc has a positive temperature coefficient, increasing 5-6 in the range 0-30 degrees C (Q10 = 1.8). There is a positive correlation between the maximum speed of isotonic shortening (Vmax.) and Vc in different muscles. 6. Sarcomere 'give' during stretch is considered to be due to forcible detachment of cross-bridges between the actin and myosin filaments. This results in recoil of the extended series elastic elements in the muscle at the expense of the sarcomers. The amount of filament displacement required to induce sarcomere 'give' (11-12 nm) is thought to represent the range of movement over which a cross-bridge can remain attached to actin during a stretch.
Actins↗
Sarcomere relaxation in intact cardiac muscle.
The process of tension decay in the absence of sarcomere motion was studied in intact heart muscle isolated from rats. Sarcomere length, observed by an infrared light diffraction technique, was controlled and the effect on force dissipation measured. Distribution of the diffracted light suggested that sarcomere length was uniform immediately after contraction than prior to the next. When sarcomeres - as distinct from the total muscle length - are kept isometric, the rate of tension decay (a) reaches its maximum sooner, and (b) appears to be constant throughout relaxation. Slow stretch (about 3% sarcomere length) prolonged cardiac muscle tension during early relaxation without direct evidence of sarcomere 'yielding'. The dynamics of isometric relaxation and the effect of stretch were qualitatively the same at external calcium concentrations of 0.6 and 1.9 mM. For a specified sequence of sarcomere length changes during relaxation, the dynamics of tension decay were independent of preloaded sarcomere length when the sarcomeres are kept isometric. The data suggest that lowering contractile tension enhanced relative relaxation rate (sec-1) at a sarcomere length of 2.0 micron. The results clarify the physiological mechanism regulating the dynamics of myocardial fiber relaxation.
Animals↗
The sarcomere length-tension relation in skeletal muscle.
Tension development during isometric tetani in single fibers of frog semitendinosus muscle occurs in three phases: (a) in initial fast-rise phase; (b) a slow-rise phase; and (c) a plateau, which lasts greater than 10 s. The slow-rise phase has previously been assumed to rise out of a progressive increase of sarcomere length dispersion along the fiber (Gordon et al. 1966. J. Physiol. [Lond.]. 184:143--169;184:170--192). Consequently, the "true" tetanic tension has been considered to be the one existing before the onset of the slow-rise phase; this is obtained by extrapolating the slowly rising tension back to the start of the tetanus. In the study by Gordon et al. (1966. J. Physiol. [Lond.] 184:170--192), as well as in the present study, the relation between this extrapolated tension and sarcomere length gave the familiar linear descending limb of the length-tension relation. We tested the assumption that the slow rise of tension was due to a progressive increase in sarcomere length dispersion. During the fast rise, the slow rise, and the plateau of tension, the sarcomere length dispersion at any area along the muscle was less than 4% of the average sarcomere length. Therefore, a progressive increase of sarcomere length dispersion during contraction appears unable to account for the slow rise of tetanic tension. A sarcomere length-tension relation was constructed from the levels of tension and sarcomere length measured during the plateau. Tension was independent of sarcomere length between 1.9 and 2.6 microgram, and declined to 50% maximal at 3.4 microgram. This result is difficult to reconcile with the cross-bridge model of force generation.
Animals↗
Capillary and fiber geometry in rat diaphragm perfusion fixed in situ at different sarcomere lengths.
To determine the potential range of diaphragm sarcomere lengths in situ and the effect of changes in sarcomere length on capillary and fiber geometry, rat diaphragms were perfusion fixed in situ with glutaraldehyde at different airway pressures and during electrical stimulation. The lengths of thick (1.517 +/- 0.007 microns) and thin (1.194 +/- 0.048 microns) filaments were not different from those established for rat limb muscle. Morphometric techniques were used to determine fiber cross-sectional area, sarcomere length, capillary orientation, and capillary length and surface area per fiber volume. All measurements were referenced to sarcomere length, which averaged 2.88 +/- 0.08 microns at -20 to -25 cmH2O airway pressure (residual volume) and 2.32 +/- 0.05 microns at +20 to +26 cmH2O airway pressure (total lung capacity). The contribution of capillary tortuosity and branching to total capillary length was dependent on sarcomere length and varied from 5 to 22%, consistent with that shown previously for mammalian limb muscles over this range of sarcomere lengths. Capillary length per fiber volume [Jv(c,f)] was significantly greater at residual volume (3,761 +/- 193 mm-2) than at total lung capacity (3,142 +/- 118 mm-2) and correlated with sarcomere length [l; r = 0.628, Jv(c,f) = 876l + 1,156, P less than 0.01; n = 18]. We conclude that the diaphragm is unusual in that the apparent in situ minimal sarcomere length is greater than 2.0 microns.(ABSTRACT TRUNCATED AT 250 WORDS)
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Muscle development in Caenorhabditis elegans: mutants exhibiting retarded sarcomere construction.
We have studied the structural changes within the body-wall muscle cells of Caenorhabditis elegans during postmitotic development. In wildtype, the number of sarcomeres progressively increases, and each sarcomere appears to grow in length and depth continuously during this period. In mature wild-type cells, the anterior-most body-wall muscle cells have 6--7 sarcomeres; the rest have 9--10 sarcomeres per cell. Twelve mutants in the unc-52 II gene exhibit markedly retarded sarcomere construction and progressive paralysis. Several unc-52 mutants, such as the severely paralyzed SU200, produced only 2--3 sarcomeres per body-wall muscle cell, while the other mildly paralyzed unc-52 mutants, such as SU250, build 3--4 sarcomeres per muscle cell. Other structures such as the pharynx and even the noncontractile organelles of the body-wall muscle cells do not appear to be structurally or functionally altered. The unc-52 body-wall sarcomeres become moderately disorganized as they are outstripped by cell growth; sufficient order is preserved, however, so that the majority of thick and thin filaments still interdigitate. The myosin heavy chains of SU200 body-wall muscle fail to accumulate normally, while the pharyngeal myosin heavy chains do not appear to be specifically affected. This biochemical result correlates well with the specificity of morphological changes in the mutant. A model is discussed in which the biochemical and morphological deficits are explained by a simple regulatory mechanism.
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Sarcomere length-resting tension relation in single frog atrial cardiac cells.
It generally has been thought that the relatively high resting tension characteristic of cardiac tissue resides in structures (collagen, elastin) external to the individual cardiac cells, but the evidence to support this conclusion has been indirect, since the resting tension of intact single cardiac cells has not been determined previously. The purpose of the present investigation was to determine the resting tension (stress)-sarcomere length relationships of single intact frog atrial cells. For tension determinations, a single cell was attached between two poly-L-lysine coated glass beams; one beam served as a compliant calibrated cantilevered force beam, and length changes were imposed on the cell by movement of the other beam. Coventional bright-field light microscope techniques were used to view the cell, the sarcomere pattern within the cell, and the position of the force beam. The resting tension of the intact cell increased from a value of about 10 nN at a sarcomere length of 2.35 microns to a value of about 130 nN at a sarcomere length of 3.45 microns. Lagrangian and Eulerian resting stress-sarcomere length relationships were computed from the resting tension-sarcomere length relationships. The Lagrangian stress increased from a value of about 0.6 mN/mm2 at a sarcomere length of 2.35 microns to a value of about 7 mN/mm2 at a sarcomere length of 3.45 microns. These values of stress are about 8- to 30-fold less than those previously reported for intact frog atrial tissue and indicate that the resting tension of intact frog atrial preparations resides primarily in structures external to the individual cardiac cell.
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The effect of denervation and dystrophy on the adaptation of sarcomere number to the functional length of the muscle in young and adult mice.
In young animals the elongation of the limb bones increases the functional lengths of the muscles. In adult animals the functional length of a muscle can be increased by immobilizing it in the lengthened position. In both cases the muscle adapts by adding on more sarcomeres in series. The role of the nerve supply in this adaptation has been investigated using denervated muscles and muscles from dystrophic animals where there is thought to be an abnormality of the nerve supply. Postnatal sarcomere addition in denervated muscles falls short of that of controls. Although this might mean that the nerve supply is necessary for normal addition of sarcomeres, it is just as likely that there is a change in gait resulting from denervation, which affects the sarcomere number. Sarcomere number in fully grown mice is not affected by denervation, nor is the ability of the muscle to adapt to immobilization in the lengthened position. This is true for fast-twitch as well as slow-twitch muscles. In dystrophic muscles postnatal sarcomere addition is normal, although the presence of a few short fibres in the muscle may mean that some muscle fibres cannot adapt to an increase in the functional length of the muscle accompanying bone growth. Adult dystrophic muscle is capable of adapting to immobilization in the lengthened position. However, although the total number of additional sarcomeres is the same as in normal immobilized muscle, they are added on at a slower rate. The experiments show that although denervated and dystrophic muscle fibres are in a state of atrophy they are still capable of adding on sarcomeres in series when the functional length of the muscle is increased. It would appear that the mechanism which enables the muscle to respond in this way to an increased functional length does not involve the nerve supply. This work was supported by a grant from the National Fund for Research into Crippling Diseases.
Age Factors↗
Editorial: Myocardial sarcomeres and the functioning mammalian heart.
Previously the length-tension properties of the isolated papillary muscle have been related to myocardial sarcomere lengths. Though past studies have relied upon fixed material, recentlly, living muscles have been used. Sarcomere lengths have now been measured on the same specimens in both living and fixed material and the sarcomere length at optimum muscle length established. These lengths are extremely uniform. Studies on the sarcomere lengths through the wall of the left ventricle have also been carried out. Surprisingly sarcomere lengths were relatively uniform from endocardium to epicardium over a wide range of intraventricular pressures. Furthermore, enddiastolic sacarcomere lengths were 91% to 94% of optimum sarcomere length over a physiologic pressure range. Since the papillary muscle in function has been shown to shorten by 23% (to 70% of optimum sarcomere length), these results suggest that the papillary muscle uses the entire ascending limb of the length-tension curve during function.
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Relationship between sarcomere length and active force in rabbit papillary muscle.
Isometric peak twitch force (stimulation frequency 0.5/s; 29.5-30.5 degrees C) was correlated with sarcomere length in isolated papillary muscles of the rabbit. Sarcomere length was measured from photographic recordings (1.5 ms exposure time) performed at rest between contractions and at the time of isometric peak twitch force. The sarcomere length at rest was found to be relatively uniform throughout the preparation and to be linearly related to the overall muscle length within the range Lmax-0.85Lmax. The distribution of sarcomere lengths increased considerably as the muscle went from rest to activity. Studies of surface markers showed different degrees of shortening (or elongation) of individual segments along the length of the preparation. The mean resting sarcomere length at Lmax (the optimum muscle length for force production) was 2.44 +/- 0.01 micron (grand mean +/- S.E., 7 muscles). The means active sarcomere length at Lmax was 2.29 +/- 0.04 micron. Active force declined steeply as the muscle length was reduced below Lmax. At a resting sarcomere length of 2.0 micron, active force was approximately 1/3 of the maximum. The observed differences between the length-tension relat-onships in myocardium (twitch responses) and skeletal muscle (tetanic contractions) are discussed on the basis of a length dependency of the activation process in cardiac muscle.
Animals↗
Sarcomere length-tension relations of frog skinned muscle fibres during calcium activation at short lengths.
1. Single twitch fibres were isolated from anterior tibial muscles of the frog, Rana pipiens. The relationship between sarcomere length and steady tetanic tension at 5 degrees C was obtained from these living fibres in the range of sarcomere lengths between about 2.2 and 1.3 microns . These fibres were then either mechanically or chemically skinned. 2. Segments were cut from the skinned fibres and mounted in an experimental chamber using a technique designed to minimize segment compliance at the points of attachment. A piece approximately 1 mm in length remained exposed to the bathing solution. 3. The segments were photographed through a light microscope at magnifications of about 460 or 110 X during activation and relaxation, so that the sarcomere lengths could be determined from a part or the whole of the segment. Activations were done with solutions of pCa either 5.49 or 6.09 and at a temperature of 5 degrees C. Fibre segments which developed striation pattern irregularities during contraction were rejected. 4. The sarcomere length-tension relation obtained from these segments in the sarcomere length range 1.3-2.2 microns was similar to that obtained from the same fibres while still living. The results were similar at the two values of pCa used. 5. These results do not support the view that sarcomere length dependent variation in the amount of calcium which is released during tetanic stimulation is a major determinant of the form of the length-tension relation in living muscle fibres at sarcomere lengths less than about 2.0 microns.
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Sarcomere length-tension relations in living rat papillary muscle.
Small papillary muscles about 2 mm long and 0.2 mm thick were dissected from the right ventricles of 16-19 day-old rats. Resting (between twitches) and active (at twitch peaks) striation patterns were photographed in living muscles using a light microscope. External muscle length was varied from Lmax, the length at which peak twitch tension was maximum, to 0.75Lmax, the length at which peak twitch tension was about 10% of maximum. Resting and active tension versus muscle length curves were similar to those obtained from other papillary muscle preparations. Resting average sarcomere length at Lmax was about 2.23 mu; it decreased with decreasing muscle length in the range between Lmax and 0.75Lmax. Near 0.75Lmax, resting average sarcomere length was about 1.5-1.6mu. Considerable internal shortening occurred during contractions, and the active average sarcomere lengths measured at the twitch peaks were less than the resting values. At Lmax, the active average sarcomere length was 1.98mu. At 0.75Lmax, there was only about a 3-6% decrease in average sarcomere length at the twitch peaks. However, at external muscle lengths between Lmax and 0.75Lmax more internal shortening was present than there was at Lmax, since average sarcomere length decreases of about 15% were observed. The finding that peak active tension decreases as sarcomere length decreases below about 2.0mu suggests that some of the factors limiting force generation at short lengths in skeletal muscle may also limit it in mammalian cardiac muscle.
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