Force enhancement following stretch in a single sarcomere

Leonard, Tim; DuVall, Mike; Herzog, Walter

doi:10.1152/ajpcell.00222.2010

Cited by 110 publications

(115 citation statements)

References 34 publications

Supporting

Mentioning

105

Contrasting

Order By: Relevance

“…The level of force enhancement, when observed, was 10.46 Ϯ 0.78%, smaller than that observed in larger preparations and similar conditions of stretch. Although our results are difficult to compare with larger preparations, another study that investigated force enhancement in sarcomeres from the rabbit psoas muscle showed contrastingly different results (28). Leonard et al (28) observed that the force produced after stretching the preparation from 2.4 to 3.4 m was 285% higher than that produced during isometric contractions at 3.4 m. We do not have an explanation for the large discrepancy between the studies, which is even more significant if we consider that several sarcomeres that we tested did not show a residual force enhancement.…”

Section: Discussioncontrasting

confidence: 65%

“…Furthermore, in several preparations, half-sarcomere nonuniformities were not observed and still showed a residual force enhancement after stretch, suggesting that it contains the participation of a sarcomeric structure. In recent years, it has been suggested that titin, responsible for most of the passive forces in muscle fibers and myofibrils, could be responsible for the residual force enhancement (23,28,29,33). Conceptually, there are three mechanisms by which titin could be independently tuned by Ca 2ϩ .…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Force produced by isolated sarcomeres and half-sarcomeres after an imposed stretch

Rassier

Pavlov

2012

American Journal of Physiology-Cell Physiology

View full text Add to dashboard Cite

Rassier DE, Pavlov I. Force produced by isolated sarcomeres and half-sarcomeres after an imposed stretch. Am J Physiol Cell Physiol 302: C240 -C248, 2012. First published October 12, 2011 doi:10.1152/ajpcell.00208.2011.-When a stretch is imposed to activated muscles, there is a residual force enhancement that persists after the stretch; the force is higher than that produced during an isometric contraction in the corresponding length. The mechanisms behind the force enhancement remain elusive, and there is disagreement if it represents a sarcomeric property, or if it is associated with length nonuniformities among sarcomeres and half-sarcomeres. The purpose of this study was to investigate the effects of stretch on single sarcomeres and myofibrils with predetermined numbers of sarcomeres (n ϭ 2, 3. . . , 8) isolated from the rabbit psoas muscle. Sarcomeres were attached between two precalibrated microneedles for force measurements, and images of the preparations were projected onto a linear photodiode array for measurements of half-sarcomere length (SL). Fully activated sarcomeres were subjected to a stretch (5-10% of initial SL, at a speed of 0.3 m·s Ϫ1 ·SL Ϫ1 ) after which they were maintained isometric for at least 5 s before deactivation. Single sarcomeres showed two patterns: 31 sarcomeres showed a small level of force enhancement after stretch (10.46 Ϯ 0.78%), and 28 sarcomeres did not show force enhancement (Ϫ0.54 Ϯ 0.17%). In these preparations, there was not a strong correlation between the force enhancement and half-sarcomere length nonuniformities. When three or more sarcomeres arranged in series were stretched, force enhancement was always observed, and it increased linearly with the degree of half-sarcomere length nonuniformities. The results show that the residual force enhancement has two mechanisms: 1) stretch-induced changes in sarcomeric structure(s); we suggest that titin is responsible for this component, and 2) stretch-induced nonuniformities of halfsarcomere lengths, which significantly increases the level of force enhancement. myofibrils; myosin; titin; cross-bridges THE NOTION OF SARCOMERE LENGTH (SL) nonuniformity has played a significant role in the study of muscle contraction. It has been directly associated with several experimental observations, including the force "creep" observed at long muscle lengths (11,16), the relation between force and filament overlap (11,17,19), the kinetics of force development and relaxation (9, 43), and the effects of muscle stretch in force production (7,8,13,18,36,37). The latest is particularly important: when a stretch is applied to skeletal muscles during activation, force increases significantly while the energy consumption decreases (1, 30). The force remains elevated after the stretch to reach a steady-state level that is higher than that produced during isometric contractions at corresponding lengths (8,24,38). The mechanisms responsible for this "residual force enhancement" remain elusive and there is substantial disagreement in the literature...

show abstract

Section: Discussioncontrasting

confidence: 65%

Section: Discussionmentioning

confidence: 99%

Force produced by isolated sarcomeres and half-sarcomeres after an imposed stretch

Rassier

Pavlov

2012

American Journal of Physiology-Cell Physiology

View full text Add to dashboard Cite

show abstract

“…This process would not occur at 32 mol/liter of Ca 2ϩ where all actin sites are already available. The above analysis assumes that passive elasticity is unaffected by [Ca 2ϩ ], which may be an oversimplification (22).…”

Section: Effect Of Sarcomere Length and Activation Level On Isometricmentioning

confidence: 99%

Stretch of Contracting Cardiac Muscle Abruptly Decreases the Rate of Phosphate Release at High and Low Calcium

Mansfield

West

Curtin

et al. 2012

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background: Phosphate is released by the cardiac actomyosin ATPase during contraction. Results: Stretching active cardiac muscle decreases phosphate release within milliseconds. Conclusion: Mechanical stimuli such as stretch cause an immediate change in actomyosin ATPase kinetics. Significance: Stretch facilitates a powerful contraction by increasing cross-bridges in a pre-power stroke state, and changes cytoplasmic phosphate flux, which may influence energetic homeostasis.

show abstract

“…Mechanisms of RFE are believed to be a combination of both active and passive properties of muscle force generating and transmitting structures (Herzog and Leonard, 2002). Force enhancement is evident in various preparations (Joumaa et al, 2008;Julian and Morgan, 1979;Leonard et al, 2010;Rassier et al, 2003;Rassier and Pavlov, 2012;Telley et al, 2006) and also in studies on humans (Lee and Herzog, 2002;Pinniger and Cresswell, 2007;Tilp et al, 2009). Whereas stretch leads to RFE, repeated unaccustomed lengthening contractions result in muscle damage, by decreasing force generation through mechanical disruption of sarcomeres (Hough, 1900) and impairing excitation contraction (E-C) coupling (Allen, 2001).…”

Section: Introductionmentioning

confidence: 95%