ArticleBiophysical journal2003
Cycling cross-bridges increase myocardial stiffness at submaximal levels of Ca2+ activation.
Article in Biophysical journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 39 citations in OpenAlex.
- Myocardial composition and contractile function of right atrial trabeculae from type 2 diabetic and nondiabetic male patients.Physiological reports · 2025Article
- Stress relaxation rates of myocardium from failing and non-failing hearts.Biomechanics and modeling in mechanobiology · 2025Article
- Muscle short-range stiffness behaves like a maxwell element, not a spring: Implications for joint stability.PloS one · 2024Article
- Muscle preflex response to perturbations in locomotion:Frontiers in bioengineering and biotechnology · 2023Article
- The Super-Relaxed State and Length Dependent Activation in Porcine Myocardium.Circulation research · 2021Article
- A Dynamic Situation with Uncertainty: Multiscale Modeling of Cardiac Thin-Filament CaBiophysical journal · 2019Article
- Integrative model of coronary flow in anatomically based vasculature under myogenic, shear, and metabolic regulation.The Journal of general physiology · 2018Article
- The effects of pH and PThe Journal of experimental biology · 2017Article
- Contributions of Ca2+-Independent Thin Filament Activation to Cardiac Muscle Function.Biophysical journal · 2015Article
- Cell- and molecular-level mechanisms contributing to diastolic dysfunction in HFpEF.Journal of applied physiology (Bethesda, Md. : 1985) · 2015Review
- Increased myocardial short-range forces in a rodent model of diabetes reflect elevated content of β myosin heavy chain.Archives of biochemistry and biophysics · 2014Article
- A Drosophila melanogaster model of diastolic dysfunction and cardiomyopathy based on impaired troponin-T function.Circulation research · 2014Article
- Effect of muscle length on cross-bridge kinetics in intact cardiac trabeculae at body temperature.The Journal of general physiology · 2013Article
- Adaptive control of cardiac contraction to changes in loading: from theory of sarcomere dynamics to whole-heart function.Pflugers Archiv : European journal of physiology · 2011Review
- Evidence that actomyosin cross bridges contribute to "passive" tension in detrusor smooth muscle.American journal of physiology. Renal physiology · 2010Article
- Short-range mechanical properties of skeletal and cardiac muscles.Advances in experimental medicine and biology · 2010Review
- Myocardial short-range force responses increase with age in F344 rats.Journal of molecular and cellular cardiology · 2009Article
- Response to Bianco et al.: Interaction forces between F-actin and titin PEVK domain measured with optical tweezers.Biophysical journal · 2008Article
- Titin: physiological function and role in cardiomyopathy and failure.Heart failure reviews · 2005Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Permeabilized multicellular preparations of canine myocardium were subjected to controlled length changes to investigate the extent to which cross-bridges augment passive stiffness components in myocardium at low levels of Ca(2+) activation. When the preparations were immersed in pCa 9.0 solution (negligible free [Ca(2+)]) they behaved as simple elastic systems (i.e., tension increased proportionately with length). In contrast, when the muscles were stretched in Ca(2+) activating solutions, tension rose much more rapidly during the initial phase of the movement than thereafter. Several lines of evidence suggest that the nonlinear response represents the displacement of populations of cycling cross-bridges that are perturbed by interfilamentary movement and take some time to recover. 1), The stiffness of the initial phase increased proportionately with the level of Ca(2+) activation. 2), The magnitude of the short-range response increased with stretch velocity. 3), The initial response was reversibly reduced by 5-mM 2,3-butanedione monoxime, a known cross-bridge inhibitor. The initial stiffness of the passive elastic (pCa 9.0) response was equivalent to the Ca(2+) dependent component at 2% (pCa approximately 6.2) of the maximal (pCa 4.5) level. These results suggest that cross-bridges may significantly affect diastolic chamber stiffness.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.