Theory of muscle contraction II. Isotonic contraction

The theory of muscle contraction developed in Part I is extended to non-isometric cases. The basic feature of the approach is the strong viscous coupling of the movement of the counterionic (K⁺) layer with the movement of I-filaments. The surface conductance of the K⁺ layer governs the flux of H⁺ along the I-filaments which in turns regulates the rate of ATP hydrolysis. The energy output of the muscle becomes the function of its mechanical activity. By assuming linear dependence of the K⁺ layer's surface conductance on the velocity of shortening Hill's equation has been derived. With a set of reasonably chosen values of the basic parameters of the theory the values of Hill's constants have been computed. The theory has been also shown to provide the observed dependence of the isometric tension on the degree of the myofilamental overlap.     

Muscular contraction

A molecular theory of muscular contraction, based on the trigger action of the cross bridge between actin and myosin, is postulated. The formation of the cross bridge is followed by a transconformation in contractile protein producing work and liberating heat. The process possesses a mechanochemical character and utilizes the energy liberated by dephosphorylation of ATP. The equation of for tension dependence of muscle power is derived from the theory of reaction rates. The equation of is meaningful after elementary treatment; the physical meaning of the constants in these equations is explained. Quantitative analyses are corroborated by the experimental data.     

Theory of muscle contraction: I. Isometric contraction

For each molecule of ATP hydrolyzed by the ATPase at the subfragment 1 of the heavy meromyosin, one H⁺ is produced and remains associated with the myosin heads until a contact with the G-actins of the I-filaments is established. This contact is brought about by the calcium ions released in the sarcomeres by the sarcoplasmic reticulum at the arrival of nerve impulses. A rapid flux of protons along the I-filaments towards the Z-membrane down the concentration gradient leads to the buildup of a diffusion potential which in turn causes a charge-compensating movement of the diffused cationic layer around the I-filaments in the opposite direction. The latter movement exerts a viscous drag on the actins and tends to move the I-filaments deeper into the inter-A-filament spaces towards the M-line. A consistent and straightforward theory of muscular contraction is developed on these lines. The value of the isometric tension in striated muscle fiber of frog at slack length calculated on the basis of this theory agrees well with the measured value.     

Cell locomotion forces versus cell contraction forces for collagen lattice contraction: an in vitro model of wound contraction

Cultured human dermal fibroblasts suspended in a rapidly polymerizing collagen matrix produce a fibroblast-populated collagen lattice. With time, this lattice will undergo a reduction in size referred to as lattice contraction. During this process, two distinct cell populations develop. At the periphery of the lattice, highly oriented sheets of cells, morphologically identifiable as myofibroblasts, show cell-to-cell contacts and thick, actin-rich staining cytoplasmic stress fibers. It is proposed that these cells undergoing cell contraction produce a multicellular contractile unit which reorients the collagen fibrils associated with them. The cells in the central region, referred to as fibroblasts, are randomly oriented, with few cell-to-cell contacts and faintly staining actin cytoplasmic filaments. In contrast it is proposed that cells working as single units use cell locomotion forces to reorient the collagen fibrils associated with them. Using this model, we sought to determine which of these two mechanisms, cell contraction or cell locomotion, is responsible for the force that contracts collagen lattices. Our experiments showed that fibroblasts produce this contractile force, and that the mechanism for lattice contraction appears to be related to cell locomotion. This is in contrast to a myofibroblast; where the mechanism for contraction is based upon cell contractions. Fibroblasts attempting to move within the collagen matrix reorganize the surrounding collagen fibrils; when these collagen fibrils can be organized no further and cell-to-cell contacts develop, which occurs at the periphery of the lattice first, these cells can no longer participate in the dynamic aspects of lattice contraction.     

Potentiation of knee extensor contraction by antagonist conditioning contraction at several intensities

The purpose of this study was to examine the effect of graded conditioning contractions of the antagonist knee flexor muscles on the output characteristics of knee extensor muscles in healthy humans. Eight male university students performed maximum isometric contractions of knee extensors, preceded by isometric conditioning contractions of the antagonist knee flexors. The developed force and electromyographic (EMG) amplitudes of the knee extensors after the conditioning contraction were measured and compared with those of simple knee extension without conditioning. The forces of the conditioning flexor contraction were set at three levels: low (20% of maximum voluntary contraction: MVC), moderate (60% of MVC), and high (100% of MVC). The EMG amplitudes of the vastus medialis, vastus lateralis, and rectus femoris muscle were recorded and the root mean square amplitudes were calculated. The strongest enhancement of the extension force was obtained by moderate intensity conditioning contraction (108.95+/-1.87% of simple knee extension), although high intensity conditioning also induced a significant increase (105.41+/-2.69%). Low intensity conditioning did not cause a significant enhancement of the contraction force (103.17+/-2.99%). Similarly, the EMG amplitudes were significantly increased by moderate and/or high conditioning. These results suggest that antagonist conditioning contraction of moderate intensities is sufficient and may be optimal to potentiate knee extensor contraction.     

Myonemal contraction of Spirostomum. I. Kinetics of contraction and relaxation

A microphotometric method is introduced that allows measurement of the contraction-relaxation kinetics of Spirostomum in response to electrical stimulation. The time course of contraction includes a rapidly contracting phase of some 4–5 mS during which cells shorten at a rate in excess of 100 cell lengths sec^?1. While a stimulus strength-duration curve determines the threshold of the response, the response to above threshold stimuli of different strengths and to trains of stimuli suggest that contraction of Spirostomum may not be an all-or-none event. The kinetics of relaxation following high stimulating voltages and repetitive after contractions also induced by high voltages are explained by excitation-contraction coupling through a stimulus-dependent intermediate effector, possibly the release of calcium ions. Changes in resting membrane potential detected by intracellular recording do not influence the initiation of contraction, while microinjection of calcium buffers above 10^?5 M Ca²⁺ invariably induces contraction.     

Considerations on muscle contraction

The independent force generator and the power-stroke cross-bridge model have dominated the thinking on mechanisms of muscular contraction for nearly the past five decades. Here, we review the evolution of the cross-bridge theory from its origins as a two-state model to the current thinking of a multi-state mechanical model that is tightly coupled with the hydrolysis of ATP. Finally, we emphasize the role of skeletal muscle myosin II as a molecular motor whose actions are greatly influenced by Brownian motion. We briefly consider the conceptual idea of myosin II working as a ratchet rather than a power stroke model, an idea that is explored in detail in the companion paper.