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.

SUMMARY We studied the influence of inotropic factors on the shape of the relation between tension and sarcomere length. Tension measurements were performed on thin trabeculae dissected from the right ventricle of the rat heart. Sarcomere length was measured by laser diffraction techniques and controlled by a servomotor system. The relations between tension and sarcomere length were derived from contractions at various extracellular calcium concentrations [Ca 2+ ] o . The time course of tension development was dependent on both sarcomere length and [Ca 2+ ] o . At all [Ca 2+ ] o , the tension attained during contraction was zero at sarcomere lengths of 1.55-1.60 pm and maximal at a sarcomere length of 2.35 /im. Neither a summit nor a descending limb was found in the sarcomere length-tension relation. At [Ca 2+ ] o = 0.5 mM, tension increased linearly with sarcomere length, whereas at [Ca 2+ ] o = 2.5 mM, it approached maximal tension exponentially with sarcomere length. The relations between tension and sarcomere length derived from isometric contractions of the muscle and of sarcomeres were identical, and this suggests that shortening of sarcomeres does not contribute significantly to the effect of [Ca 2+ ] o . The relations between tension and sarcomere length obtained at [Ca 2+ ] o = 0.5 mM from contractions 30 seconds after a potentiating burst of stimuli (4 seconds at 4 Hz) were identical to the relation between tension and sarcomere length at [Ca 2+ ] o = 2.5 mm. Our results are consistent with the hypothesis that cardiac muscle length affects contractile performance by its influence on excitation contraction coupling. CircRes 46: [703][704][705][706][707][708][709][710][711][712][713][714] 1980 THE shape of the relation between tension and sarcomere length in cardiac papillary muscle suggests length-dependent activation of the contractile system (Jewell, 1977). However, there are no data on the effect of inotropic interventions on this curve. Only muscle length-tension curves are available, and these give conflicting results (Jewell, 1977;Huntsman and Stewart, 1977;Sonnenblick, 1962;Bodem et al., 1976). It is known that during isometric contractions there is considerable shortening of sarcomeres in the central region of papillary muscle. This happens at the expense of stretch of damaged regions near the clamps holding the ends of the specimen (Krueger and Pollack, 1975;Pollack and Krueger, 1976;Julian et al., 1976;Julian and Sollins, 1975). The damaged regions as well as the normal region may be influenced by inotropic factors. The interpretation of results of isometric contractions of the muscle is therefore ambiguous. The purpose of the present study was to examine the effect of different calcium concentrations on the relations Supported by Grants 74022 and 77086 from the Netherlands Heart Foundation.Dr. ter Keurs is an Established Investigator of the Netherlands Heart Foundation.Address for reprints: Henk E.D.J. ter Keurs, Department of Cardiology, Medical Faculty, State Un...

SUMMARY1. Intracellular action potentials and isometric force were measured from thin trabeculae of the right ventricle of rat heart. Characteristic for the action potential of rat myocardium is a short plateau and a slow final repolarization phase. We have studied the influence of ionic composition ofthe medium and of stimulation frequency on the slow phase of repolarization and its relation to peak force.2. The results confirmed a positive correlation between peak force and the duration of the slow phase of repolarization, as has been reported for other species.3. An increase of [Ca2+]. caused a shortening of the slow phase of repolarization when peak force was kept constant. 5. In the presence of the Ca2+ entry blocker nifedipine the action potential duration and peak force were reduced. Low [Na+]. caused less shortening of the slow phase of repolarization and a greater increase of peak force. The slow phase of repolarization was prolonged transiently following reperfusion at normal [Na+]O, but only during a few beats.6. These results are in agreement with the hypothesis that the slow phase of repolarization is due to an inward current generated by Na+-Ca2+ exchange, as the latter mechanism is known to be sensitive to the intracellular and extracellular concentrations of both Na+ and Ca2+.

A system that makes control of muscle length (ML), sarcomere length (SL), and force (F) possible in striated muscle preparations is described. SL was measured by light diffraction techniques and two diffractometers. Control was performed by influencing ML with a penmotor system with a frequency response of 190 Hz. SL or F could be controlled by interrupting the internal position (i.e., ML) feedback of the motor and by closing the respective loop. Velocity feedback of the motor through an internal velocity coil was maintained in all cases for optimal damping. Steady-state error of the system was minimized by an integrating loop filter. The feedback path was selected by means of potentiometers or analog switches. Electronic stops in the circuit protected the muscle against excessive stretch and load. A microprocessor-based average-response computer could be used for feedforward control to eliminate noise or to analyze longitudinal uniformity of the muscle. Responses of rat cardiac trabeculae during SL and F control are shown. Transient behavior of SL and F during control and measures to eliminate the transients are discussed.

Purkinje (P)-fibres are cardiac myocytes that are specialized for fast conduction of the electrical signal. P-fibres are usually defined as having the following identifying features: lack of T tubules; frequent lateral cell junctions; deep indentations at the intercalated discs level; the CX40 isoforms of gap junction proteins and, in large mammals, paucity of myofibrils and abundance of glycogen. We have examined the ultrastructure of P-fibres in free running P-strands from right and left ventricles of small (mouse and rat) intermediate (rabbit) and large (dog) size mammals focusing on presence and distribution of the T tubules. In contrast with previous studies, we find that P-fibres do have T tubules which form normal dyadic associations with the sarcoplasmic reticulum and that the frequency of tubules varies with the size of the animal. Profiles of T tubules and dyads are present over short segments of individual P-cells flanked by totally T tubule-free segments. It is thought that lack of T tubules in P-cells is necessary to reduce capacitance and thus accelerate action potential spread. This may not be as important in a small heart.