The origin of passive force enhancement in skeletal muscle

2008 ◽  
Vol 294 (1) ◽  
pp. C74-C78 ◽  
Author(s):  
V. Joumaa ◽  
D. E. Rassier ◽  
T. R. Leonard ◽  
W. Herzog
Keyword(s):  
Calcium Concentration ◽  
Force Production ◽  
Primary Source ◽  
Passive Force ◽  
Active Force ◽  
Force Enhancement ◽  
Bridge Formation ◽  
Calcium Dependent ◽  
Cross Bridge ◽  
High Calcium

The aim of the present study was to test whether titin is a calcium-dependent spring and whether it is the source of the passive force enhancement observed in muscle and single fiber preparations. We measured passive force enhancement in troponin C (TnC)-depleted myofibrils in which active force production was completely eliminated. The TnC-depleted construct allowed for the investigation of the effect of calcium concentration on passive force, without the confounding effects of actin-myosin cross-bridge formation and active force production. Passive forces in TnC-depleted myofibrils ( n = 6) were 35.0 ± 2.9 nN/ μm2 when stretched to an average sarcomere length of 3.4 μm in a solution with low calcium concentration (pCa 8.0). Passive forces in the same myofibrils increased by 25% to 30% when stretches were performed in a solution with high calcium concentration (pCa 3.5). Since it is well accepted that titin is the primary source for passive force in rabbit psoas myofibrils and since the increase in passive force in TnC-depleted myofibrils was abolished after trypsin treatment, our results suggest that increasing calcium concentration is associated with increased titin stiffness. However, this calcium-induced titin stiffness accounted for only ∼25% of the passive force enhancement observed in intact myofibrils. Therefore, ∼75% of the normally occurring passive force enhancement remains unexplained. The findings of the present study suggest that passive force enhancement is partly caused by a calcium-induced increase in titin stiffness but also requires cross-bridge formation and/or active force production for full manifestation.

Non-cross-bridge calcium-dependent stiffness in frog muscle fibers

2004 ◽  
Vol 286 (6) ◽  
pp. C1353-C1357 ◽  
Author(s):  
M. A. Bagni ◽  
B. Colombini ◽  
P. Geiger ◽  
R. Berlinguer Palmini ◽  
G. Cecchi
Keyword(s):  
Time Course ◽  
Frog Muscle ◽  
Static Stiffness ◽  
Bridge Formation ◽  
Calcium Dependent ◽  
Cross Bridge ◽  
Steady Level ◽  
Intracellular Ca ◽  
Butanedione Monoxime ◽  
Cross Bridges

At the end of the force transient elicited by a fast stretch applied to an activated frog muscle fiber, the force settles to a steady level exceeding the isometric level preceding the stretch. We showed previously that this excess of tension, referred to as “static tension,” is due to the elongation of some elastic sarcomere structure, outside the cross bridges. The stiffness of this structure, “static stiffness,” increased upon stimulation following a time course well distinct from tension and roughly similar to intracellular Ca2+ concentration. In the experiments reported here, we investigated the possible role of Ca2+ in static stiffness by comparing static stiffness measurements in the presence of Ca2+ release inhibitors (D600, Dantrolene, 2H2O) and cross-bridge formation inhibitors [2,3-butanedione monoxime (BDM), hypertonicity]. Both series of agents inhibited tension; however, only D600, Dantrolene, and 2H2O decreased at the same time static stiffness, whereas BDM and hypertonicity left static stiffness unaltered. These results indicate that Ca2+, in addition to promoting cross-bridge formation, increases the stiffness of an (unidentified) elastic structure of the sarcomere. This stiffness increase may help in maintaining the sarcomere length uniformity under conditions of instability.

scholarly journals Active force inhibition and stretch-induced force enhancement in frog muscle treated with BDM

2004 ◽  
Vol 97 (4) ◽  
pp. 1395-1400 ◽  
Author(s):  
Dilson E. Rassier ◽  
Walter Herzog
Keyword(s):  
Fiber Length ◽  
Isometric Force ◽  
Ringer Solution ◽  
Total Force ◽  
Passive Force ◽  
Force Enhancement ◽  
Cross Bridge ◽  
Length Relationship ◽  
Cross Bridges ◽  
Lumbrical Muscles

There is evidence that the stretch-induced residual force enhancement observed in skeletal muscles is associated with 1) cross-bridge dynamics and 2) an increase in passive force. The purpose of this study was to characterize the total and passive force enhancement and to evaluate whether these phenomena may be associated with a slow detachment of cross bridges. Single fibers from frog lumbrical muscles were placed at a length 20% longer than the plateau of the force-length relationship, and active and passive stretches (amplitudes of 5 and 10% of fiber length and at a speed of 40% fiber length/s) were performed. Experiments were conducted in Ringer solution and with the addition of 2, 5, and 10 mM of 2,3-butanedione monoxime (BDM), a cross-bridge inhibitor. The steady-state active and passive isometric forces after stretch of an activated fiber were higher than the corresponding forces measured after isometric contractions or passive stretches. BDM decreased the absolute isometric force and increased the total force enhancement in all conditions investigated. These results suggest that total force enhancement is directly associated with cross-bridge kinetics. Addition of 2 mM BDM did not change the passive force enhancement after 5 and 10% stretches. Addition of 5 and 10 mM did not change (5% stretches) or increased (10% stretches) the passive force enhancement. Increasing stretch amplitudes and increasing concentrations of BDM caused relaxation after stretch to be slower, and because passive force enhancement is increased at the greatest stretch amplitudes and the highest BDM concentrations, it appears that passive force enhancement may be related to slow-detaching cross bridges.

Skeletal and cardiac α-actin isoforms differently modulate myosin cross-bridge formation and myofibre force production

2013 ◽  
Vol 22 (21) ◽  
pp. 4398-4404 ◽  
Author(s):  
Julien Ochala ◽  
Hiroyuki Iwamoto ◽  
Gianina Ravenscroft ◽  
Nigel G. Laing ◽  
Kristen J. Nowak
Keyword(s):  
Force Production ◽  
Actin Isoforms ◽  
Bridge Formation ◽  
Cross Bridge

Sperm chemotaxis in siphonophores. II. Calcium-dependent asymmetrical movement of spermatozoa induced by the attractant

1984 ◽  
Vol 68 (1) ◽  
pp. 163-181
Author(s):  
M.P. Cosson ◽  
D. Carre ◽  
J. Cosson
Keyword(s):  
Calcium Ions ◽  
Calcium Concentration ◽  
Sea Water ◽  
Large Diameter ◽  
Chemotactic Response ◽  
Wide Area ◽  
Ionophore A23187 ◽  
Calcium Dependent ◽  
Sperm Chemotaxis ◽  
High Calcium

Spermatozoa from siphonophores have been shown to be attracted towards an extracellular structure, the cupule, which covers the predetermined site of fertilization of the egg. Observations on sperm behaviour during the chemotactic response show that spermatozoa describe trajectories of large diameter (700-1000 micron) while far from the cupule, and of smaller diameter (200 micron) in the cupule area. The transition between the two types of swimming occurs progressively when spermatozoa cross a 3 mm wide area around the cupule. After a few minutes 99% of the spermatozoa keep swimming around the attractant source, following circular paths 150–200 micron in diameter. In the absence of the attractant, comparable modifications of sperm trajectories are observed in the presence of the ionophore A23187 and high calcium concentrations. In the presence of 10(−2) M calcium ions, A23187-treated spermatozoa describe trajectories 200 micron in diameter, which increase up to 800 micron at lower calcium concentrations (10(−6) M). In the absence of calcium ions, spermatozoa swim across the cupule area without modification of their trajectories and no sperm accumulation can be detected. This requirement of the chemotactic response for calcium ions is observed either with fresh cupules stuck on the eggs, with cupules separated from the eggs, or with cupule extracts. Moreover, a soluble component fractionated from the cupule induces, when diluted in sea water, a reduction in the size of the sperm trajectories and this also requires calcium ions. The present data show that the chemotactic response of siphonophore sperm, which requires millimolar concentrations of calcium ions, occurs through a non-transient induction of increased asymmetry of the flagellar waveform. It is proposed that the natural attractant operates to produce an increase in the intraaxonemal calcium concentration.

Considerations on the history dependence of muscle contraction

2004 ◽  
Vol 96 (2) ◽  
pp. 419-427 ◽  
Author(s):  
Dilson E. Rassier ◽  
Walter Herzog
Keyword(s):  
Muscle Contraction ◽  
Isometric Force ◽  
Force Production ◽  
Passive Component ◽  
Force Enhancement ◽  
History Dependence ◽  
Cross Bridge ◽  
Force Depression ◽  
Length Relationship ◽  
Length Changes

When a skeletal muscle that is actively producing force is shortened or stretched, the resulting steady-state isometric force after the dynamic phase is smaller or greater, respectively, than the purely isometric force obtained at the corresponding final length. The cross-bridge model of muscle contraction does not readily explain this history dependence of force production. The most accepted proposal to explain both, force depression after shortening and force enhancement after stretch, is a nonuniform behavior of sarcomeres that develops during and after length changes. This hypothesis is based on the idea of instability of sarcomere lengths on the descending limb of the force-length relationship. However, recent evidence suggests that skeletal muscles may be stable over the entire range of active force production, including the descending limb of the force-length relationship. The purpose of this review was to critically evaluate hypotheses aimed at explaining the history dependence of force production and to provide some novel insight into the possible mechanisms underlying these phenomena. It is concluded that the sarcomere nonuniformity hypothesis cannot always explain the total force enhancement observed after stretch and likely does not cause all of the force depression after shortening. There is evidence that force depression after shortening is associated with a reduction in the proportion of attached cross bridges, which, in turn, might be related to a stress-induced inhibition of cross-bridge attachment in the myofilament overlap zone. Furthermore, we suggest that force enhancement is not associated with instability of sarcomeres on the descending limb of the force-length relationship and that force enhancement has an active and a passive component. Force depression after shortening and force enhancement after stretch are likely to have different origins.

Force enhancement after stretch in mammalian muscle fiber: no evidence of cross-bridge involvement

2014 ◽  
Vol 307 (12) ◽  
pp. C1123-C1129 ◽  
Author(s):  
Marta Nocella ◽  
Giovanni Cecchi ◽  
Maria Angela Bagni ◽  
Barbara Colombini
Keyword(s):  
Time Course ◽  
Sarcomere Length ◽  
Active Force ◽  
Force Enhancement ◽  
Mouse Muscle ◽  
Cross Bridge ◽  
Force Increase ◽  
Flexor Digitorum Brevis ◽  
Flexor Digitorum ◽  
Low Tension

Stretching of activated skeletal muscles induces a force increase above the isometric level persisting after stretch, known as residual force enhancement (RFE). RFE has been extensively studied; nevertheless, its mechanism remains debated. Unlike previous RFE studies, here the excess of force after stretch, termed static tension (ST), was investigated with fast stretches (amplitude: 3–4% sarcomere length; duration: 0.6 ms) applied at low tension during the tetanus rise in fiber bundles from flexor digitorum brevis (FDB) mouse muscle at 30°C. ST was measured at sarcomere length between 2.6 and 4.4 μm in normal and N-benzyl- p-toluene sulphonamide (BTS)-added (10 μM) Tyrode solution. The results showed that ST has the same characteristics and it is equivalent to RFE. ST increased with sarcomere length, reached a peak at 3.5 μm, and decreased to zero at ∼4.5 μm. At 4 μm, where active force was zero, ST was still 50% of maximum. BTS reduced force by ∼75% but had almost no effect on ST. Following stimulation, ST developed earlier than force, with a time course similar to internal Ca2+ concentration: it was present 1 ms after the stimulus, at zero active force, and peaked at ∼3-ms delay. At 2.7 μm, activation increased the passive sarcomere stiffness by a factor of ∼7 compared with the relaxed state All our data indicate that ST, or RFE, is independent of the cross-bridge presence and it is due to the Ca2+-induced stiffening of a sarcomeric structure identifiable with titin.

scholarly journals The effect of hyperosmolality on the rate of heat production of quiescent trabeculae isolated from the rat heart.

1996 ◽  
Vol 108 (6) ◽  
pp. 497-514 ◽  
Author(s):  
D S Loiselle ◽  
G J Stienen ◽  
C van Hardeveld ◽  
E T van der Meulen ◽  
G I Zahalak ◽  
...  
Keyword(s):  
Heat Production ◽  
Calcium Concentration ◽  
Thermal Response ◽  
Force Production ◽  
Active Force ◽  
Release Channel ◽  
The Face ◽  
Increased Activity ◽  
External Calcium ◽  
Ventricular Trabeculae

We have measured the rate of heat production of isolated, quiescent, right ventricular trabeculae of the rat under isosmotic and hyperosmotic conditions, using a microcalorimetric technique. In parallel experiments, we measured force production and intracellular calcium concentration ([Ca2+]i). The rate of resting heat production under isosmotic conditions (mean +/- SEM, n = 32) was 100 +/- 7 mW (g dry wt)-1; it increased sigmoidally with osmolality, reaching a peak that was about four times the isosmotic value at about twice normal osmotic pressure. The hyperosmotic thermal response was: (a) abolished by anoxia, (b) attenuated by procaine, (c) insensitive to verapamil, ouabain, and external calcium concentration, and (d) absent in chemically skinned trabeculae bathed in low-Ca2+ "relaxing solution." Active force production was inhibited at all osmolalities above isosmotic. Passive (tonic) force increased to, at most, 15% of the peak active force developed under isosmotic conditions while [Ca2+]i increased, at most, 30% above its isosmotic value. We infer that hyperosmotic stimulation of resting cardiac heat production reflects, in large part, greatly increased activity of the sarcoplasmic reticular Ca2+ ATPase in the face of increased efflux via a procaine-inhibitable Ca(2+)-release channel.

Force enhancement following stretching of skeletal muscle

2002 ◽  
Vol 205 (9) ◽  
pp. 1275-1283 ◽  
Author(s):  
W. Herzog ◽  
T. R. Leonard
Keyword(s):  
Structural Damage ◽  
Great Part ◽  
Force Production ◽  
Isometric Contractions ◽  
Total Force ◽  
Passive Force ◽  
Force Enhancement ◽  
Structural Element ◽  
Length Relationship ◽  
Relationship Of

SUMMARY We investigated force enhancement following stretching in the in situ cat soleus muscle on the ascending and descending limb of the force-length relationship by varying the amount and speed of stretching and the frequency of activation (5 Hz, 30 Hz). There was a small but consistent(P<0.05) amount of force enhancement following muscle stretching on the ascending limb of the force—length relationship for both stimulation frequencies. The steady-state active isometric forces following stretches of 9 mm on the descending limb of the force—length relationship were always equal to or greater than the corresponding forces from the purely isometric contractions at the length at which the stretch was started. Therefore, force production for these trials showed positive stiffness and was associated with stable behavior. Following active stretching of cat soleus on the descending limb of the force—length relationship,the passive forces at the end of the test were significantly greater than the corresponding passive forces for purely isometric contractions, or the passive forces following stretching of the passive muscle. This passive force enhancement following active stretching increased with increasing magnitude of stretch, was not associated with structural damage, and only disappeared once the muscle was shortened. For stretches of 6 mm and 9 mm, the passive force enhancement accounted for more than 50 % of the total force enhancement,reaching a peak contribution of 83.7 % for the stretches of 9 mm at a speed of 3 mm s-1. The results of this study suggest that a passive structural element provides a great part of the force enhancement on the descending limb of the force—length relationship of the cat soleus. Furthermore, the results indicate that mechanisms other than sarcomere length non-uniformity alone are operative.

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