Contraction shortened

The two issues that now require examination are whether the visually extended tether is kinetically free and whether the chain does in fact contract (shorten) as the FeS eenter moves from the Qo site of cytochrome b to the heme of cytochrome Ci. 

Muscle cells contain contractile elements, myofibrils, which are essentially bundles of proteins found in the sarcoplasm (Figure 2.23). Muscle myofibrils contain isotropic sections (I-bands about 0.8 xm long) and anisotropic sections (A-bands about 1.5 xm long). The I-band is interrupted by a Z-line about 80 nm wide. The low-density central part of the A-band of is the H-zone. The M-line is situated in the centre of the H-zone. The entire structural unit of myofibrils, which is the span between two Z-lines, is called the sarcomere. In a relaxed state (relaxed muscle), it is about 2.5 [am long. During muscle contraction (shortening) it is shorter, 1.7-1.8 p.m. 

Muscle tissue is unique in its ability to shorten or contract. The human body has three basic types of muscle tissue histologically classified into smooth, striated, and cardiac muscle tissues. Only the striated muscle tissue is found in all skeletal muscles. The type of cells which compose the muscle tissue are known as contractile cells. They originate from mesenchymal cells which differentiate into myoblasts. Myoblasts are embryonic cells which later differentiate into contractile fiber cells. 

Figure 14.11 The sliding filament model of muscle contraction. The actin (red) and myosin (green) filaments slide past each other without shortening.

FIGURE 2.18 Inotropic and lusitropic responses of guinea pig left atria to (3-adrenoceptor stimulation. Panels A to C isometric tension waveforms of cardiac contraction (ordinates are mg tension abscissae are msec), (a) Effect of 0.3 nM isoproterenol on the waveform. The wave is shortened due to an increase in the rate of diastolic relaxation, whereas no inotropic response (change in peak tension) is observed at this concentration, (b) A further shortening of waveform duration (lusitropic response) is observed with 3 nM isoproterenol. This is concomitant with positive inotropic response (increase maximal tension), (c) This trend continues with 100 nM isoproterenol, (d) Dose-response curves for ino tropy (filled circles) and lusitropy (open circles) in guinea pig atria for isoproterenol, (e) Dose-response curves for inotropy (filled circles) and lusitropy (open circles) in guinea pig atria for the P-adrenoceptor partial agonist prenalterol. Data redrawn from [6]. 

Although blood pressure control follows Ohm s law and seems to be simple, it underlies a complex circuit of interrelated systems. Hence, numerous physiologic systems that have pleiotropic effects and interact in complex fashion have been found to modulate blood pressure. Because of their number and complexity it is beyond the scope of the current account to cover all mechanisms and feedback circuits involved in blood pressure control. Rather, an overview of the clinically most relevant ones is presented. These systems include the heart, the blood vessels, the extracellular volume, the kidneys, the nervous system, a variety of humoral factors, and molecular events at the cellular level. They are intertwined to maintain adequate tissue perfusion and nutrition. Normal blood pressure control can be related to cardiac output and the total peripheral resistance. The stroke volume and the heart rate determine cardiac output. Each cycle of cardiac contraction propels a bolus of about 70 ml blood into the systemic arterial system. As one example of the interaction of these multiple systems, the stroke volume is dependent in part on intravascular volume regulated by the kidneys as well as on myocardial contractility. The latter is, in turn, a complex function involving sympathetic and parasympathetic control of heart rate intrinsic activity of the cardiac conduction system complex membrane transport and cellular events requiring influx of calcium, which lead to myocardial fibre shortening and relaxation and affects the humoral substances (e.g., catecholamines) in stimulation heart rate and myocardial fibre tension. 

Contraction is a general term that refers to the mechanically activated state of myofibrils which is usually caused by action potentials). Contracture means muscle shortening or tension development, which is not triggered by action potentials), e.g. K+ contracture, and caffeine or halothane contracture. The word is also used for deformity or distortion of fingers, hand or limb, such as Dupuytren s or Volkmann s contracture. 

Figure 4. When a muscle contracts isotonically or a constant resisting force is imposed on it during a contraction, the velocity at which it shortens quickly comes to a constant. The force-velocity curve shows the relationship between the force applied to a muscle and the steady-state velocity of shortening. As in all other muscles, the force-velocity curve of smooth muscle is a rectangular hyperbola for all positive shortening velocities. In order to compare the behavior of muscles of different lengths and diameters, it is common to normalize force and velocity by dividing each by its maximum value and expressing the result as a percentage, nd...

In terms of muscle function, muscle is very adaptable. Depending on the type of stimulation, muscle can either twitch or contract tetanically for a variable length of time. If the ends are held fixed, then it contracts isometrically and the force produced is maximal. If one or both ends of the muscle are not held fixed then the muscle is able to shorten. The muscle can shorten at a fixed load (isotonic contraction) where the velocity of shortening is also constant. Power output (force X velocity) is maximum where the velocity of shortening is about one third of the maximal rate. Finally, the muscle can shorten at maximum velocity (unloaded shortening). However, the molecular basis of the interaction of myosin with actin to produce force, or shortening, is the same in each case. 

The ability of S-2 to act as a flexible link also explained another problem in muscle contraction. When muscle contracts its volume remains constant. As a muscle shortens, and the filaments slide past each other, the spacing between the filaments increases as part of this constant volume behavior. Therefore, the crossbridges have to be able to interact with actin over a wide range of filament spacings. The presence of the flexible link in S-2 would allow this to occur. 

Even with the diborylacetylenes illustrated by structures 39a-c, XRD data again show a shortening of the B—C bond as more electronegative groups are affixed to the boron centers but only a modest contraction of the C=C bond36 ... 

---