Force velocity relationship smooth muscle contraction

Muscle Physiology - Functional Properties

force velocity relationship smooth muscle contraction

Muscle contraction is the activation of tension-generating sites within muscle fibers. Unlike skeletal muscle, the contractions of smooth and cardiac muscles are .. Force–velocity relationship relates the speed at which a muscle changes its. The isometric length-tension curve represents the force a muscle is capable of of the cross-bridges which cycle during muscle contraction. Force-velocity curve: muscle: Mechanical properties: force is characterized by the force-velocity relationship. however, the smooth muscle force-velocity relationship differs from that of striated muscle representation of muscle contraction.

Journal of Applied Physiology, 68 2 Effects of load and contraction velocity during three-week biceps curls training on isometric and isokinetic performance. International Journal of Sports Medicine. Comparison of treadmill and cycle ergometer measurements of force-velocity relationships and power output.

International Journal of Sports Medicine, 20 3 Effect of countermovement on power—force—velocity profile. European Journal of Applied Physiology, 11 Effectiveness of an individualized training based on force-velocity profiling during jumping. Frontiers in Physiology, 7, Training effect of different loads on the force-velocity relationship and mechanical power output in human muscle.

Scandinavian Journal of Sports Science, 5 2 Specificity of speed of exercise. Physical Therapy, 50 12 Direct measurement of power during one single sprint on treadmill. Journal of Biomechanics, 43 10 Effects of maximal effort strength training with different loads on dynamic strength, cross-sectional area, load-power and load-velocity relationships. Age-and sex-related differences in force-velocity characteristics of upper and lower limbs of competitive adolescent swimmers.

Journal of Human Kinetics, 32, The effectiveness of a mini-cycle on velocity-specific strength acquisition. European Journal of Applied Physiology, 84 3 Importance of upper-limb inertia in calculating concentric bench press force. Journal of strength and conditioning research, 22 2 Variable resistance training promotes greater strength and power adaptations than traditional resistance training in elite youth rugby league players.

Specificity of strength gains after 12 weeks of isokinetic eccentric training in healthy men. Isokinetics and Exercise Science, 19 3 Voluntary strength and muscle characteristics in untrained men and women and male bodybuilders. Journal of Applied Physiology, 62 5 Optimal force-velocity profile in ballistic movements—altius: International Journal of Sports Medicine, 35 6 Assessing the force-velocity characteristics of the leg extensors in well-trained athletes: Force-velocity and power-velocity relationships during maximal short-term rowing ergometry.

Evaluation of force—velocity and power—velocity relationship of arm muscles.

Force velocity relationships in vascular smooth muscle. The influence of temperature.

Force-velocity relationship and maximal power on a cycle ergometer. Acta Physiologica Scandinavica, 1 Muscle architecture and force-velocity relationships in humans. A single thin filament is composed of to actin molecules and 40 to 60 troponin and tropomyosin molecules. Actin is a small, nearly spherical molecule that is arranged in the filament into two helical strands, as shown in Figurewith about 13 actin molecules per complete turn of the helix.

Troponin and tropomyosin are sometimes called regulator proteins because of their central role in regulating muscle contraction. Tropomyosin is a filamentous protein that is thought to form two strands that lie in the grooves formed between the actin strands. Troponin, a globular protein, binds to tropomyosin at only one site and therefore is thought to sit astride the tropomyosin molecule strand at regular intervals approximating 40 nm.

Muscle contraction - Wikipedia

Figure shows the relationships between the three proteins as they are currently thought to exist. The thin filaments attach to the Z disc, a flat protein structure. Thin filaments may be connected end-to-end in the H band by slender threadlike processes.

Organization of the sarcomeres. Pattern of cross-striation in skeletal muscle with bands labeled. Arrangement of thick and thin filaments that accounts for the pattern of cross-striations. Hexagonal arrays of thick and thin filaments in cross sections through the sarcomere in the A band, H band and I band. The relatively high anisotropicity of the A band results from the presence of both thin and thick filaments shown in longitudinal section in the upper part and cross-section in the lower part of Fig.

The I band is only slightly anisotropic because it contains only thin filaments. The H band is not optically as dense as the rest of the A band because it does not contain any thin filaments when the muscle is at rest. As can be seen in the cross section of Figurethe thin filaments are organized into regular hexagonal arrays within the myofibrils, with a thick filament at the center of each array in the A band. Three thick filaments are equidistant from each thin filament, whereas six thin filaments are equidistant from each thick filament as shown in the left panel.

A cross section through the I band shows only the thin filament array; a section through the H band shows only the thick filament array plus the slender, thread-like processes interconnection thin filaments. Proposed structure of thin filament with relative positions of actin, troponin and tropomyosin indicated. Quart Rev Biophys 2: Because they are staggered around the thin filament at 60 intervals, each projects in the direction of a thin filament, and each thin filament has projections toward it from three thick filaments.

These projections have been termed either cross-bridges or cross-projectionsdepending upon whether the heads are thought to contact and bind thin filaments or not. As we shall see, there are two schools of thought, in fact, two different mechanisms proposed to account for the generation of the mechanical force of contraction. Three-dimensional reconstruction of skeletal muscle illustrating organizatin of myofibrils, sarcoplasmic reticulum and T tubules.

Gray's Anatomy, 35th British ed, Philadelphia, W. Saunders, T tubules and sarcoplasmic reticulum Muscle cells have a unique membrane structure, called the transverse tubule or simply the T tubule. The T tubule is an invagination of the muscle membrane, much like the invagination produced in a balloon by pushing a finger into its side without puncturing it, but the T tubules are long and tortuous.

The T tubule system forms a ring around every myofibril either at the Z line, in which case there is one per sarcomere, or at the A-I-band junction, in which case there are two per sarcomere. These perifibrillar rings are inter-connected, forming a kind of honeycomb arrangement, as shown in Figure The position of the T tubule with respect to the sarcomere is somewhat species specific; frog skeletal muscle has only one tubule per sarcomere, whereas human skeletal muscle has two.

force velocity relationship smooth muscle contraction

It should be noted that in human cardiac muscle there is only one tubule per sarcomere as shown in Figure The inside of the T tubule is continuous with the extracellular space and presumably contains a fluid like extracellular fluid, but, because the tubular space is small and not well stirred, it is likely that ionic movements across the tubule membrane produce significant changes in ionic concentration, at least on a short-term basis.

Fortuitous sections through triads, one at right angles to the other. Relative positions of T tubules and sarcoplasmic reticula at the triad are shown clearly. Another intracellular structure with special significance for contraction is the sarcoplasmic reticulum, the muscle cell version of the endoplasmic reticulum. The sarcoplasmic reticulum is made up of tubules that run parallel to the sarcomeres from T tubule to T tubule see Figures and ; thus, there are two sets of sarcoplasmic reticulum tubules per sarcomere in muscles with two sets of T tubules per sarcomere.

The sarcoplasmic reticulum is a sack with its ends expanded the cisternae adjacent to the T tubules and with narrow, longitudinal channels connecting these expansions, one at each end. In fortuitous sections, one can find a section of T tubule bounded on two sides by sort of dumb-bell-shaped sarcoplasmic reticula as illustrated in Figure The T tubule with its two adjacent regions of sarcoplasmic reticulum is often called a triad. Because the T tubules and the cisternae of the sarcoplasmic reticulum run together for such a long way, a large proportion of the sarcoplasmic reticulum is in contact with the sarcolemma.

There is a space of about 12 nm between the membranes which, in electron micrographs, appears to be traversed at regular intervals by structures that have been suggested to be channels coupling the T tubule with the sarcoplasmic reticulum. However, large molecules such as ferritin cannot cross between the two structures, and the lumen of the sarcoplasmic reticulum contains a fluid like sarcoplasm, not like extracellular fluid. In addition, electrical measurements indicate that the sarcoplasmic reticulum does not communicate with the T tubule through low resistance pathways.

force velocity relationship smooth muscle contraction

A model of the opening of the Ca channel by the action potential is the T tubule of the skeletal muscle fiber. One model has a mechanical plug that closes the Ca channel, preventing calcium from leaving the sarcoplasmic reticulum. Hypopolarization of the T tubule somehow pulls the plug out of the channel opening, allowing Ca to enter the sarcoplasm.

In Figurethe plug is show in red ladle-shaped piece and the Ca channel in purple cut cylinder. Presumably, the plug is a dipole whose position is altered by altering the membrane polarization.

In any case, Ca efflux from the sarcoplasmic reticulum starts the muscle contraction. In recently active muscle, the calcium is found in the narrowed, longitudinal portion from which it moves to the triad as time passes. Sliding filament model Fig. Sliding filament model of muscle contraction.

Force velocity relationships in vascular smooth muscle. The influence of temperature.

A single sarcomere is shown stretched, with little overlap between thick and thin filaments Awith greater overlap Bwith complete overlap Cand extremely shortened with thin filaments shown buckled D. Another possibility, not shown, is that at extreme shortening, the buckling occurs at the Z line. Observations that during muscle contraction, the sarcomere, the I and H bands become narrower, while the A band does not, coupled with the observation that thick and thin filaments do not shorten although at very short lengths the thin filaments may either push through the Z line or fold up like an accordionsuggested the sliding filament model of contraction.

According to the model, the thick and thin filaments simply slide past each other. Figure shows several positions in the shortening of the muscle, illustrating the sliding of the filaments.

A modified force-velocity equation for smooth muscle contraction.

At the maximum length there is little or no overlap of the filaments Abut as the muscle shortens there is more and more overlap until the fibers completely overlap D. There is general agreement that the sliding filament model is an accurate description of what happens during muscle contraction.

According to the sliding filament hypothesis, thick and thin filaments simply slide past each other to produce shortening. Events leading to contraction Fig. The skeletal muscle action potential. The spike is followed by a depolarizing tail that lasts 4 to 5 msec. Although muscle contraction can be initiated by direct electrical stimulation of the muscle, it usually results from activity in the motoneurons innervating the muscle.

An action potential initiated in an alpha-motoneuron propagates into the motoneuron terminals and releases acetylcholine into the synaptic cleft. The acetylcholine induces an end-plate potential in the muscle which, in normal muscle, always leads to an action potential in the muscle. The muscle spike is very much like the nerve spike but longer in duration and with a hypopolarizing tail on the falling phase that prolongs the spike by msec.

An example of a muscle spike is shown in Figure The mechanism of generation of the spike in mammalian striated muscle is the same as that described for nerve in Chapter 3.

The long msec hypopolarizing tail of the muscle action potential is probably the electrotonic reflection of the action potential as it conducts into the T tubules. At least, the tail disappears from the spike when the muscle is treated with glycerol and then returned to Ringer's solution, a treatment that more or less specifically ruptures T tubules, leaving the surface membrane and resting potential intact.

Force-velocity relationship

The muscle still generates a spike but does not contract. Conduction of the spike into the T tubules is probably an active process as elsewhere on the membrane, and it is the hypopolarization of the T tubule that leads to contraction. It is reasonable to ask why there exists such an elaborate system of tubules in striated muscle. The answer may lie in the synchronization of contraction of sarcomeres along the length of the muscle and in its depths.

The myofibrils are located throughout the muscle fiber, but in mammalian muscle there is usually only one neuromuscular junction per fiber. If there were no way for the hypopolarization of the spike to get into the center of the fiber, the myofibrils on the surface would contract before those in the center.

With the T-tubule system, the spike is conducted rapidly to all parts of the cell, reaching all of the myofibrils at nearly the same time. In the absence of such a mechanism, contracting segments of the myofibrils would stretch the non-contracting ones, lessening the force transmitted to the ends of the fibers and, therefore, to the joints. The hypopolarization of the T tubules opens special voltage-gated channels in opposing regions of the sarcoplasmic reticulum membrane.

By an as yet incompletely understood mechanism, this leads to a release of calcium from the cisternae of the sarcoplasmic reticulum into the region of the myofilaments. This is an essential step in the contraction mechanism; muscles depleted of calcium do not contract. The calcium diffuses to the thin filaments and binds to troponin. Production of force according to the cross-bridge theory.