Energy stored and dissipated in skeletal muscle basement membranes during sinusoidal oscillations

Abstract

We subjected single skeletal muscle cells from frog semitendinosus to sinusoidal oscillations that simulated the strain experienced as the cells near the end of passive extension and begin active contraction in slow swimming. Other cells from which the basement membrane was removed by enzymatic and mechanical procedures were tested identically. Effectiveness of the basement membrane removal technique was evaluated by electron microscopy, by an electrophoretic and lectin-binding assay for depletion of cell surface glycoproteins, and by confirmation by means of electrophoretic and immunologic analyses that major intracellular, cytoskeletal proteins were not disrupted. Measurements of maximum stress, maximum strain, and phase lag between these maxima enabled the complex modulus (dynamic stiffness) and loss tangent (relative viscous losses to elastic energy storage) to be calculated for each mechanically tested preparation. We also calculated the amounts of energy stored and dissipated in each preparation. These calculations indicate that cells with intact basement membranes have complex moduli significantly greater than those of cells without basement membranes, and that cells with basement membrane store significantly more elastic energy than basement membrane depleted cells. However, when subjected to identical sinusoidal strains, energy dissipation in cells with intact basement membranes is over three times greater than dissipation in cells without basement membrane. The relative magnitudes of energy losses to energy storage, called the specific loss, is nearly three times greater for intact cells than for basement membrane depleted cells. Basement membranes may thereby serve as a brake for slowing passive extension of muscle before contraction begins.

Electromechanical delay components during skeletal muscle contraction and relaxation in patients with myotonic dystrophy type 1

“…The resultant elastic force, acting in a direction opposite to that of the myofilaments, is expected to be greatest during a maximum contraction, i.e., when cross-bridges are mostly engaged and can therefore overcome the initial "myotonic" forces during the first phase of muscle relaxation, when the cross-bridges begin to disengage. By contrast, elastic forces, which are attenuated when myofilaments return to their resting state, would yield to the "myotonic" forces in the last phase of relaxation [42].…”

“…Some authors hypothesized two different mechanisms to describe the cross-bridges and SEC behaviour of a muscle presenting the myotonic phenomenon [5,42]. The first mechanism implies two populations of muscle fibres: (i) normally relaxing fibres, and (ii) slowly relaxing fibres.…”

“…The normally relaxing fibres drive the initial relaxation phase, but once they have fully relaxed, the slowly relaxing fibres dominate and drive the terminal relaxation phase [5]. The second mechanism is related to SEC elastic properties [42].…”

Before programs: The physical origination of multicellular forms

“…This is not a major effect in the liquid-like tissues described above in relation to differential adhesion; the mobility of cells within those aggregates dissipate most mechanical perturbations. However, the complex basement membranes (Lindblom and Paulsson, 1996) of epithelia confer stiffness to these tissues (Danielsen, 2004), which facilitate the storage of mechanical energy (Tidball, 1986). In combination with the biochemically excitable cellular component and the mechanical continuity fostered by cell surface-cytoplasmic linkage (Ingber et al, 1994), embryonic epithelia become capable of exhibiting tension-dependent collective cell movement (Beloussov et al, 2000) leading to complex folding, branching and bucking behaviors (Beloussov, 1998).…”

Mechanical factors in the initiation of eccentric contraction‐induced injury in rat soleus muscle.

“…It is generally recognized that this type of injury is associated with eccentric contractions (for review, see Armstrong, 1984;Ebbeling & Clarkson, 1989;Stauber, 1989); some have hypothesized that one or more mechanical aspects of the eccentric contraction that distinguish it from isometric or concentric contractions may be responsible for initiation of the injury. For example, the degree of eccentric contraction-induced injury has been reported to be related to the specific tension produced during the contraction (Katz, 1939;McCully & Faulkner, 1985, 1986, which can be twice that produced during an isometric or concentric contraction (Woledge, Curtin & Homsher, 1985). It has also been reported that the degree of injury produced during eccentric contraction is related to the muscle length prior to the contraction (Katz, 1939;Newham, Jones, Ghosh & Aurora, 1988).…”