Non-crossbridge stiffness in active muscle fibres

Abstract

Stretching of an activated skeletal muscle induces a transient tension increase followed by a period during which the tension remains elevated well above the isometric level at an almost constant value. This excess of tension in response to stretching has been called 'static tension' and attributed to an increase in fibre stiffness above the resting value, named 'static stiffness'. This observation was originally made, by our group, in frog intact muscle fibres and has been confirmed more recently, by us, in mammalian intact fibres. Following stimulation, fibre stiffness starts to increase during the latent period well before crossbridge force generation and it is present throughout the whole contraction in both single twitches and tetani. Static stiffness is dependent on sarcomere length in a different way from crossbridge force and is independent of stretching amplitude and velocity. Static stiffness follows a time course which is distinct from that of active force and very similar to the myoplasmic calcium concentration time course. We therefore hypothesize that static stiffness is due to a calcium-dependent stiffening of a noncrossbridge sarcomere structure, such as the titin filament. According to this hypothesis, titin, in addition to its well-recognized role in determining the muscle passive tension, could have a role during muscle activity.

Phosphate increase during fatigue affects crossbridge kinetics in intact mouse muscle at physiological temperature

“…; Colombini et al . ). Static tension was independent of crossbridges and was attributed to stretching of titin filaments stiffened by the increase of intracellular [Ca 2+ ] following activation (Bagni et al .…”

Bed Rest, Exercise Countermeasure and Reconditioning Effects on the Human Resting Muscle Tone System

“…Apart from the noteworthy exercise-induced preservation of the intramuscular collagen network density in postural soleus in bed rest shown here and suggested previously for the myofascial tissue ( Schleip et al, 2006 ), work in the literature offers several molecular structural elements as candidates generating the resting muscle tone. Possible elements include intrinsic forces of acto-myosin cross-bridging ( Campbell and Lakie, 1998 ), the non-crossbridge stiffness and spring-like sarcomeric giant proteins titin ( Labeit et al, 2003 ; Colombini et al, 2016 ) and nebulin ( Horowits et al, 1986 ), contractile myofibroblast cells (i.e., α-smooth muscle actin immunopositive stress-fiber bundles) found in superficial body fascia ( Staubesand and Li, 1996 ). Further possible candidates are the viscoelastic properties of the extracellular matrix including proteoglycans and glycosaminoglycans, collagen fiber cross-links, and non-collagenous link proteins ( Proske and Morgan, 1999 ).…”

Human Postural Control

“…For instance, static stiffness relies on calcium-dependent stiffening of the activated fibers, independent of crossbridge formation, and titin appears to have all the characteristics required to account for the static stiffness properties (Colombini et al, 2016 ). Force enhancement may also result from an interaction between an elastic element in muscle sarcomeres and the cross-bridges, which, in turn, interact with the elastic elements to regulate their length and stiffness.…”