Muscle maximizing function

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. 

Figure 6. Glycogen content in the vastus lateralis muscle as a function of cycling time at 75-80% of maximal oxygen uptake (VO2 max). Data points are mean values from 10 subjects. For each subject, exercise was performed repeatedly in periods of 15 min separated by 15 min rest periods. At the point of exhaustion and muscle fatigue, muscle glycogen stores were depleted. From Bergstrom and Hultman (1967) with permission from the publisher.

The plasma level of fatty acids in a fed subject is between 0.3 and 0.5 mmol/L. As discussed above, the maximal safe level is about 2 mmol/L. This is not usually exceeded in any physiological condition since, above this concentration, that of the free (not complexed with albumin) fatty acids in the blood increases markedly. This can then lead to the formation of fatty acid micelles which can damage cell membranes the damage can cause aggregation of platelets and interfere with electrical conduction in heart muscle (Chapter 22). The cells particularly at risk are the endothelial cells of arteries and arterioles, since they are directly exposed to the micelles, possibly for long periods of time. Two important roles of endothelial cells are control of the diameter of arterioles of the vascular system and control of blood clotting (Chapter 22). Damage to endothelial cells could be sufficiently severe to interfere with these functions i.e. the arterioles could constrict, and the risk of thrombosis increases. Both of these could contribute to the development of a heart attack (Chapter 22) (Box 7.4). 

The lifestyles of modern humans are different from those of our hominid ancestors, but biological functions have remained the same a stress -induced state of maximal work capacity, albeit without energy-consuming muscle activity. 

Kinesin hydrolyzes ATP at a rate of approximately 80 molecules per second. Thus, given the step size of 80 A per molecule of ATP, kinesin moves along a microtubule at a speed of 6400 A per second. This rate is considerably slower than the maximum rate for myosin, which moves relative to actin at 80,000 A per second. Recall, however, that myosin movement depends on the independent action of hundreds of different head domains working along the same actin filament, whereas the movement of kinesin is driven by the processive action of kinesin head groups working in pairs. Muscle myosin evolved to maximize the speed of the motion, whereas kinesin functions to achieve steady, but slower, transport in one direction along a filament. 

The Ca " content of the sr is determined by a balance between the activity of the Ca -ATPase pump and mechanisms which release Ca " from the store (Fig. 9.3). These mechanisms include the opening of ion channels in the sr membrane in response to IP3 and passive leak of Ca out of the sr. Both of these processes involve the movement of Ca " " from the high concentration within the store, estimated to be 5 mM Ca (Leijten and van Breemen, 1984), to the low concentration (100 nM) within the cytosol. Functional studies in vascular smooth muscle have demonstrated that the quantity of Ca " " stored in the sr is sufficient to activate maximal... 

The functional residual capacity (FRC) is the volume of air remaining in the lungs at the end of a quiet expiration. FRC is the normal resting position of the lung and occurs when there is no contraction of either inspiratory or expiratory muscles and is normally 40% of TLC. Inspiratory capacity (IC) is the maximal volume of air that can be inhaled from the end of a quiet expiration and represents the sum ofVT and IRV. 

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