Muscle action

The essential contractile components of muscle are the microfibrils which consist principally of two filamentous proteins called actin and myosin, together with another protein, troponin. The detailed processes involved in the contraction and relaxation of muscle are very complicated and will not be dealt with here. They involve the sliding back and forth over each other of the actin and myosin filaments, the binding and releasing of Ca + and the utilisation of ATP as the source of energy. 

Contraction can be indicated as in Equation 11.87, where the sliding process involves dissociation of an actin-myosin complex. When relaxation occurs the sliding process is reversed and the complex is re-formed, again utilising energy from the ATP. 

The supply of ATP is maintained by the stored creatine phosphate (11.50) and to an extent by reaction (11.88). When the stored ATP is exhausted the latter supply is insufficient and the muscle becomes temporarily tired. 

---

Plasma membrane channels. The most common mechanism for the movement of into smooth muscle cells Ifom the extracellular space is the electrodiffusion of Ca " ions through highly selective channels. This movement can be significant in two quite different ways. First, Ca ions carry two positive charges and, in fact, most of the inward charge movement across the plasma membrane of smooth muscle myocytes is carried by Ca. Most smooth muscle action potentials are known to be Ca " action potentials. And second, the concentration of intracellular free calcium, the second messenger, is increased by inward calcium movement. 

Action potentials, self-propagating. Action potentials of smooth muscle differ from the typical nerve action potential in at least three ways. First, the depolarization phases of nearly all smooth muscle action potentials are due to an increase in calcium rather than sodium conductance. Consequently, the rates of rise of smooth action potentials are slow, and the durations are long relative to most neural action potentials. Second, smooth muscle action potentials arise from membrane that is autonomously active and tonically modulated by autonomic neurotransmitters. Therefore, conduction velocities and action potential shapes are labile. Finally, smooth muscle action potentials spread along bundles of myocytes which are interconnected in three dimensions. Therefore the actual spatial patterns of spreading of the action potential vary. 

Not all toxic organophosphoms compounds have uses beneficial to humans. Sarin is an extremely toxic nerve gas that is lethal to humans. In March 1995 this substance was released in a terrorist attack on a Japanese subway, resulting in several deaths and many serious injuries. Sarin and related nerve gases bind an amino acid in the enzyme responsible for muscle action. When this enzyme is deactivated, muscles contract but cannot relax. Even a small dose can be lethal if the nerve gas reaches the muscles of the heart. 

Polymer gels In response to pH changes in their enviromnent, materials derived from poly(acrylonitrile) will swell or shrink in a slow analogy to muscle action, thought to have robotic applications. 

Polymer-metal composites Cationic mobility activated electrically in membranes of the Nafion (DuPont) and Flemion (Asahi Glass) type leads to a bending response, again mimicking muscle action. 

Enteric nerves control intestinal smooth muscle action and are connected to the brain by the autonomic nervous system. IBS is thought to result from dysregulation of this brain-gut axis. The enteric nervous system is composed of two gan-glionated plexuses that control gut innervation the submucous plexus (Meissner s plexus) and the myenteric plexus (Auerbach s plexus). The enteric nervous system and the central nervous system (CNS) are interconnected and interdependent. A number of neurochemicals mediate their function, including serotonin (5-hydroxytryptamine or 5-HT), acetylcholine, substance P, and nitric oxide, among others. 

Cadherins Transmembrane glycoproteins (352) promoting cellcell adhesion (353,354) linked to integrins (355) and via catenins to muscle action (356)... 

Slow-channel syndrome. Abnormally long-lived openings of mutant AChR channels result in prolonged endplate currents and potentials, which in turn elicit one or more repetitive muscle action potentials of lower amplitude that decrement. The morphologic consequences stem from prolonged activation of the AChR channel that causes cationic overload of the postsynaptic region - the endplate myopathy - with Ca2+ accumulation, destruction of the junctional folds, nuclear apoptosis, and vacuolar degeneration of the terminal. Some slow-channel mutations in the transmembrane domain of the AChR render the channel leaky by stabilization of the open state, which is populated even in the absence of ACh. Curiously, some slow-channel mutants can be opened by choline even at the concentrations that are normally present in serum. Quinidine, an open-channel blocker of the AchR, is used for therapy. 

CVSF = conduction velocity of slow = motor fibers dSCV = distal sensory nerve conduction velocity MAP k/a = proximal to distal amplitude ratio of muscle action potentials MMCV = maximal motor nerve conduction velocity MNCV = mixed nerve conduction velocity RL = residual latency of motor nerve conduction... 

Overall, the polymer of tomorrow will reach into inorganic, quasi metallic combinations on one side, and bio polymers of living tissue on the other. These will provide the widest interface in the science and the technology of matter. Both the wonderful spiral conformation of collagen, Fig. 23, and the subtle information content of its peptide components in muscle action are qualities to be sought in polymers made by people. 

Form constancy being one criteria of these movements which means that the phase distance of the muscle actions that participate in the movements remaining constant. Amplitude of movement and speech may change with intensity. The pattern remains recognizable the same. 

The translation of the term Instinktbewegung or Erbkoordination into fixed action pattern led to many misunderstandings. There is variation in the movement by intensity and speed. What is fixed is the score or script of the muscle actions. The movement may just occur as an intention movement or full blown, and it may run off fast or slow. What remains constant is the relative phase distance of the muscle actions involved. Form constancy, furthermore, is characteristic of any stereotyped movement and therefore not only a characteristic for a fixed action pattern. Innateness is the decisive characteristic. 

Other agents such as actinomycin D, C-Myc antisense, dexamethasone, and matrix metalloproteinase inhibitors, aimed at altering inflammatory and smooth muscle actions in the biological repair response to vascular injury, are being evaluated. The success of these devices depends upon multiple issues, including stent platform, carrier, drug properties, and pharmacokinetic profile (18-26). Large randomized, controlled trials, demonstrate a restenosis rate of 5% to 10% with DES (27). 

The nervous system controls muscle action. Norepinephrine and acetylcholine are important neurotransmitters at the neuromuscular junction. 

Chapter 13). Failure of central control of muscle action can also have severe consequences. Malfunctioning of some parts of the central control mechanism can result in failure of muscles to contract normally and in a coordinated manner, e.g. Parkinson s disease (Chapter 14) or result in excessive fatigue (chronic fatigue syndrome (Chapter 13)). 

---