Force, not sarcomere length, correlates with prolongation of isosarcometric contraction

1995 ◽  
Vol 269 (2) ◽  
pp. H676-H685 ◽  
Author(s):  
P. M. Janssen ◽  
W. C. Hunter
Keyword(s):  
Time Course ◽  
Sarcomere Length ◽  
Laser Diffraction ◽  
Common Mechanism ◽  
Thin Filaments ◽  
Twitch Force ◽  
Subsequent Time ◽  
Systolic Phase ◽  
Cross Bridges ◽  
Highly Correlated

Recent studies have emphasized the importance of the late systolic phase for understanding ventricular ejection. To examine the myocardial factors controlling this phase, we studied the timing of twitch contraction in nine excised rat trabeculae contracting isosarcometrically. By varying both sarcomere length (SL) and extracellular Ca2+ concentration ([Ca2+]) we determined which of these factors or the developed peak twitch force correlated better with the prolongation of contraction. We focused on the period from just before the peak of force to the time of half relaxation. SL was measured by laser diffraction and kept constant using adaptive control. Peak twitch force was the factor most tightly correlated with prolongation of contraction: as force rose from 10 to 100 mN/mm2, duration tripled from 100 to 300 ms. When the trend with force was removed, however, no separate influence of SL remained. Increase in [Ca2+]o abbreviated contraction equally at all force levels. Prolongation of late systolic contraction was also highly correlated with prolongation of the time constant for late relaxation, suggesting a common mechanism by which peak twitch force lengthens the entire subsequent time course of a twitch. We hypothesize that 1) increased force correlates with prolonged Ca2+ binding to troponin-C, and/or 2) attached cross bridges act cooperatively to oppose the inhibiting effects of tropomyosin as Ca2+ is lost from the thin filaments.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Polarization of Tryptophan Fluorescence from Single Striated Muscle Fibers

1972 ◽  
Vol 59 (1) ◽  
pp. 103-120 ◽  
Author(s):  
C. G. dos Remedios ◽  
R. G. C. Millikan ◽  
M. F. Morales
Keyword(s):  
Sarcomere Length ◽  
Striated Muscle ◽  
Muscle Fibers ◽  
Tryptophan Fluorescence ◽  
Thin Filaments ◽  
A Value ◽  
Striated Muscle Fibers ◽  
Types Of Muscle Fibers ◽  
Cross Bridges ◽  
Contraction And Relaxation

Instrumentation has been developed to detect rapidly the polarization of tryptophan fluorescence from single muscle fibers in rigor, relaxation, and contraction. The polarization parameter (P⊥) obtained by exiciting the muscle tryptophans with light polarized perpendicular to the long axis of the muscle fiber had a magnitude P⊥ (relaxation) > P⊥ (contraction) > P⊥ (rigor) for the three types of muscle fibers examined (glycerinated rabbit psoas, glycerinated dorsal longitudinal flight muscle of Lethocerus americanus, and live semitendinosus of Rana pipiens). P⊥ from single psoas fibers in rigor was found to increase as the sarcomere length increased but in relaxed fibers P⊥ was independent of sarcomere length. After rigor, pyrophosphate produced little or no change in P⊥, but following an adenosine triphosphate (ATP)-containing solution, pyrophosphate produced a value of P⊥ that fell between the contraction and relaxation values. Sinusoidal or square wave oscillations of the muscle of amplitude 0.5–2.0% of the sarcomere length and frequency 1, 2, or 5 Hz were applied in rigor when the myosin cross-bridges are considered to be firmly attached to the thin filaments. No significant changes in P⊥ were observed in either rigor or relaxation. The preceding results together with our present knowledge of tryptophan distribution in the contractile proteins has led us to the conclusion that the parameter P⊥ is a probe of the contractile state of myosin which is probably sensitive to the orientation of the myosin S1 subfragment.

Unstimulated force during hypoxia of rat cardiac muscle: stiffness and calcium dependence

1990 ◽  
Vol 258 (3) ◽  
pp. H861-H869 ◽  
Author(s):  
W. J. Leijendekker ◽  
W. D. Gao ◽  
H. E. ter Keurs
Keyword(s):  
Oxidative Phosphorylation ◽  
Strain Gauge ◽  
Sarcomere Length ◽  
Muscle Length ◽  
Laser Diffraction ◽  
Muscle Stiffness ◽  
Rapid Cycling ◽  
Cross Bridges ◽  
Passive Muscle

The stiffness of rat cardiac trabeculae was measured in vitro to distinguish between an increase in unstimulated force (Fu) caused by rapid cycling of cross bridges or caused by rigor bridges during hypoxia. The force was measured with a strain gauge, the sarcomere length was determined by laser diffraction techniques, and muscle length was controlled by means of a motor. Stiffness was analyzed by using small (less than 1% of muscle length) sinusoidal length perturbations of 1 and 100 Hz. The stiffness at 100 Hz increased linearly with force during tetani at a varied [Sr2+] (0.25-10 mM) in the Krebs-Henseleit (K-H) buffer, but remained virtually unchanged at 1 Hz. In contrast, the stiffness of both the passive muscle and the muscle exposed to either CN- or to PO2 less than 1.5 mmHg up to development of maximal Fu (Fumax) was similar at 1- and 100-Hz perturbations. Less profound hypoxia (PO2 6-10 mmHg) resulted in spontaneous sarcomere activity during the rise in Fu, and an increase in the ratio of stiffness at 100 Hz to stiffness at 1 Hz was detected. When oxidative phosphorylation was inhibited by CN- (2 mM) while the muscle was stimulated in the absence of both Ca2+ and Na+ (choline+substituted), the addition of Na+ at the time at which Fu had reached 30-40% of Fumax did not affect the rate of rise of Fu. These results show that the development of Fu during more complete anoxia in rat trabeculae is completely due to the formation of rigor links and that Ca2(+)-dependent cross-bridge activation can contribute to the rise in Fu during less severe hypoxia.

scholarly journals Developmental increase in β-MHC enhances sarcomere length–dependent activation in the myocardium

2019 ◽  
Vol 151 (5) ◽  
pp. 635-644 ◽  
Author(s):  
Sherif M. Reda ◽  
Sampath K. Gollapudi ◽  
Murali Chandra
Keyword(s):  
Guinea Pig ◽  
Cardiac Muscle ◽  
Sarcomere Length ◽  
Contractile Function ◽  
Thin Filaments ◽  
Cooperative Effects ◽  
Mediated Effects ◽  
Contractile Parameters ◽  
Cross Bridges ◽  
Length Dependent Activation

Shifts in myosin heavy chain (MHC) isoforms in cardiac myocytes have been shown to alter cardiac muscle function not only in healthy developing hearts but also in diseased hearts. In guinea pig hearts, there is a large age-dependent shift in MHC isoforms from 80% α-MHC/20% β-MHC at 3 wk to 14% α-MHC/86% β-MHC at 11 wk. Because kinetic differences in α- and β-MHC cross-bridges (XBs) are known to impart different cooperative effects on thin filaments, we hypothesize here that differences in α- and β-MHC expression in guinea pig cardiac muscle impact sarcomere length (SL)–dependent contractile function. We therefore measure steady state and dynamic contractile parameters in detergent-skinned cardiac muscle preparations isolated from the left ventricles of young (3 wk old) or adult (11 wk old) guinea pigs at two different SLs: short (1.9 µm) and long (2.3 µm). Our data show that SL-dependent effects on contractile parameters are augmented in adult guinea pig cardiac muscle preparations. Notably, the SL-mediated increase in myofilament Ca2+ sensitivity (ΔpCa50) is twofold greater in adult guinea pig muscle preparations (ΔpCa50 being 0.11 units in adult preparations but only 0.05 units in young preparations). Furthermore, adult guinea pig cardiac muscle preparations display greater SL-dependent changes than young muscle preparations in (1) the magnitude of length-mediated increase in the recruitment of new force-bearing XBs, (2) XB detachment rate, (3) XB strain-mediated effects on other force-bearing XBs, and (4) the rate constant of force redevelopment. Our findings suggest that increased β-MHC expression enhances length-dependent activation in the adult guinea pig cardiac myocardium.

Uncontrolled sarcomere shortening increases intracellular Ca2+ transient in rat cardiac trabeculae

1997 ◽  
Vol 272 (4) ◽  
pp. H1892-H1897 ◽  
Author(s):  
P. M. Janssen ◽  
P. P. de Tombe
Keyword(s):  
Time Course ◽  
Sarcomere Length ◽  
Calcium Transient ◽  
Feedback System ◽  
Laser Diffraction ◽  
Calcium Handling ◽  
Fura 2 ◽  
Intracellular Calcium Transient ◽  
Central Segment ◽  
The Impact

Isolated cardiac muscle preparations suffer from damaged-end compliance that allows for substantial shortening of central sarcomeres during contractions in which the overall length of muscle is kept constant. The impact of uncontrolled sarcomere shortening during a twitch on the intracellular calcium transient in myocardium is unknown. Accordingly, in the present study we developed an iterative laser-diffraction feedback system that allowed for the accurate control of central-segment sarcomere length and simultaneous measurement of iontophoretically injected fura 2 fluorescence in isolated cardiac trabeculae. We compared fura 2 fluorescence signals recorded during regular twitches with twitches in which central sarcomere length (SL) was held constant by feedback control ("SL clamp" twitches). We found that uncontrolled sarcomere shortening was associated with a significant (P = 0.005) increase in the peak of the calcium transient and that the amount of this increase was directly correlated to the extent of central-segment sarcomere shortening (r2 = 0.92; P < 0.01). The time course of the calcium transient, however, was unaffected by the mode of contraction (P = 0.64). These findings have important implications for the interpretation of studies of myocardial calcium handling in which uncontrolled sarcomere shortening takes place during the twitch.

scholarly journals "Creep currents" in single frog atrial cells may be generated by electrogenic Na/Ca exchange.

1986 ◽  
Vol 87 (6) ◽  
pp. 857-884 ◽  
Author(s):  
J R Hume ◽  
A Uehara
Keyword(s):  
Voltage Clamp ◽  
Time Course ◽  
Single Cells ◽  
Mechanical Activity ◽  
Common Mechanism ◽  
Mechanical Relaxation ◽  
Equilibrium Conditions ◽  
Atrial Cells ◽  
Current Voltage ◽  
Wide Range

The objective of these experiments was to test the hypothesis that the "creep currents" induced by Na loading of single frog atrial cells (Hume, J. R., and A. Uehara. 1986. Journal of General Physiology. 87:833) may be generated by an electrogenic Na/Ca exchanger. Creep currents induced by Na loading were examined over a wide range of membrane potentials. During depolarizing voltage-clamp pulses, outward creep currents were observed, followed by inward creep currents upon the return to the holding potential. During hyperpolarizing voltage-clamp pulses, creep currents of the opposite polarity were observed: inward creep currents were observed during the pulses, followed by outward creep currents upon the return to the holding potential. The current-voltage relations for inward and outward creep currents in response to depolarizing or hyperpolarizing voltage displacements away from the holding potential all intersect the voltage axis at a common potential, which indicates that inward and outward creep currents may have a common reversal potential under equilibrium conditions and may therefore be generated by a common mechanism. Measurements of inward creep currents confirm that voltage displacements away from the holding potential rapidly alter equilibrium conditions. Current-voltage relationships of inward creep currents after depolarizing voltage-clamp pulses are extremely labile and depend critically upon the amplitude and duration of outward creep currents elicited during preceding voltage-clamp pulses. An optical monitor of mechanical activity in single cells revealed (a) a similar voltage dependence for the outward creep currents induced by Na loading and tonic contraction, and (b) a close correlation between the time course of the decay of the inward creep current and the time course of mechanical relaxation. A mathematical model of electrogenic Na/Ca exchange (Mullins, L.J. 1979. Federation Proceedings. 35:2583; Noble, D. 1986. Cardiac Muscle. 171-200) can adequately account for many of the properties of creep currents. It is concluded that creep currents in single frog atrial cells may be attributed to the operation of an electrogenic Na/Ca exchange mechanism.

scholarly journals Troponin C modulates the activation of thin filaments by rigor cross-bridges

1997 ◽  
Vol 72 (5) ◽  
pp. 2262-2267 ◽  
Author(s):  
P.W. Brandt ◽  
F.H. Schachat
Keyword(s):  
Troponin C ◽  
Thin Filaments ◽  
Cross Bridges

scholarly journals Interfering with calcium release suppresses I gamma, the "hump" component of intramembranous charge movement in skeletal muscle.

1991 ◽  
Vol 97 (5) ◽  
pp. 845-884 ◽  
Author(s):  
L Csernoch ◽  
G Pizarro ◽  
I Uribe ◽  
M Rodríguez ◽  
E Ríos
Keyword(s):  
Skeletal Muscle ◽  
Time Course ◽  
Calcium Release ◽  
Time Derivative ◽  
Ruthenium Red ◽  
Total Charge ◽  
Charge Movement ◽  
Release Channel ◽  
Release Flux ◽  
Highly Correlated

Four manifestations of excitation-contraction (E-C) coupling were derived from measurements in cut skeletal muscle fibers of the frog, voltage clamped in a Vaseline-gap chamber: intramembranous charge movement currents, myoplasmic [Ca2+] transients, flux of calcium release from the sarcoplasmic reticulum (SR), and the intrinsic optical transparency change that accompanies calcium release. In attempts to suppress Ca release by direct effects on the SR, three interventions were applied: (a) a conditioning pulse that causes calcium release and inhibits release in subsequent pulses by Ca-dependent inactivation; (b) a series of brief, large pulses, separated by long intervals (greater than 700 ms), which deplete Ca2+ in the SR; and (c) intracellular application of the release channel blocker ruthenium red. All these reduced calcium release flux. None was expected to affect directly the voltage sensor of the T-tubule; however, all of them reduced or eliminated a component of charge movement current with the following characteristics: (a) delayed onset, peaking 10-20 ms into the pulse; (b) current reversal during the pulse, with an inward phase after the outward peak; and (c) OFF transient of smaller magnitude than the ON, of variable polarity, and sometimes biphasic. When the total charge movement current had a visible hump, the positive phase of the current eliminated by the interventions agreed with the hump in timing and size. The component of charge movement current blocked by the interventions was greater and had a greater inward phase in slack fibers with high [EGTA] inside than in stretched fibers with no EGTA. Its amplitude at -40 mV was on average 0.26 A/F (SEM 0.03) in slack fibers. The waveform of release flux determined from the Ca transients measured simultaneously with the membrane currents had, as described previously (Melzer, W., E. Ríos, and M. F. Schneider. 1984. Biophysical Journal. 45:637-641), an early peak followed by a descent to a steady level during the pulse. The time at which this peak occurred was highly correlated with the time to peak of the current suppressed, occurring on average 6.9 ms later (SEM 0.73 ms). The current suppressed by the above interventions in all cases had a time course similar to the time derivative of the release flux; specifically, the peak of the time derivative of release flux preceded the peak of the current suppressed by 0.7 ms (SEM 0.6 ms). The magnitude of the current blocked was highly correlated with the inhibitory effect of the interventions on Ca2+ release flux.(ABSTRACT TRUNCATED AT 400 WORDS)

Losartan prevents contractile dysfunction in rat myocardium after left ventricular myocardial infarction

2001 ◽  
Vol 281 (5) ◽  
pp. H2150-H2158 ◽  
Author(s):  
Marcel C. G. Daniëls ◽  
Rebecca S. Keller ◽  
Pieter P. de Tombe
Keyword(s):  
Myocardial Infarction ◽  
Sarcomere Length ◽  
Contractile Function ◽  
Left Ventricular ◽  
Contractile Dysfunction ◽  
Treatment Results ◽  
Twitch Force ◽  
Rat Hearts ◽  
Myofilament Function ◽  
Active Peak

We studied the effects of chronic losartan (Los) treatment on contractile function of isolated right ventricular (RV) trabeculae from rat hearts 12 wk after left ventricular (LV) myocardial infarction (MI) had been induced by ligation of the left anterior descending artery at 4 wk of age. After recovery, one-half of the animals were started on Los treatment (MI+Los; 30 mg · kg−1 · day−1per os); the remaining animals were not treated (MI group). Rats without infarction or Los treatment served as controls (Con group). MI resulted in increases in LV and RV weight and unstressed LV cavity diameter; these were partially prevented by Los treatment. The active peak twitch force-sarcomere length relation was depressed in MI compared with either Con or MI+Los. Likewise, maximum Ca2+saturated twitch force was depressed in MI, whereas twitch relaxation and twitch duration were prolonged. Myofilament function, as measured in skinned trabeculae, was not significantly different among the Con, MI, and MI+Los groups. We conclude that Los prevents contractile dysfunction in rat RV trabeculae after LV MI. Our results suggest that the beneficiary effect of Los treatment results not from improved myofilament function but rather from improved myocyte Ca2+homeostasis.

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