Proposes a novel 'winding filament' hypothesis to explain activation- and force-dependent increases in titin stiffness during muscle contraction.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for titin force regulation in muscle; requires experimental validation before revising cardiac or skeletal models.
In Brief Several properties of muscle defy explanation solely based on the sliding filament-swinging cross-bridge theory. Indeed, muscle behaves as though there is a dynamic “spring” within the sarcomeres. We propose a new “winding filament” mechanism for how titin acts, in conjunction with the cross-bridges, as a force-dependent spring. The addition of titin into active sarcomeres resolves many puzzling muscle characteristics. This paper summarizes a novel hypothesis for activation- and force-dependent increases in titin stiffness and implications for understanding muscle contraction.
No takes yet. Share an insight, caveat, or question.
Monroy et al. (2011) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: