Prof. J.P.N. Mishra
When a nerve impulse reaches in neuromuscular junction, about 300 vesicles of acetylcholine are released by the terminals into the synaptic clefts and sub-neural clefts. This release of vesicles is caused by movement of calcium ions from the extra-cellular fluid into the terminals when the action potential depolarizes their membranes. In the absence of calcium or in the presence of excess magnesium in the extra-cellular fluid, the release of acetylcholine is greatly depressed.
Within approximately 2 to 3 milliseconds after acetylcholine is released into the cleft, a small portion of it diffuses out of the gutter and no longer acts on the muscle fiber membrane, but the greater bulk of it is destroyed by the cholinesterase on the surface of the sub-neural clefts. The very short period of time that the acetylcholine remains in contact with the muscle fiber membrane - 2 to 3 milliseconds- is almost always sufficient to excite the muscle fiber, and yet the rapid removal of the acetylcholine prevents re-excitation after the muscle fiber has recovered from the. first action potential.
Even though the acetylcholine released into the space between the end-plate and the muscle membrane lasts for only a minute fraction of a second, during this period of time it can affect the muscle membrane sufficiently to open large pores with diameters of 0.6 to 0.7 nanometers (6 to 7 Angstroms) in the membrane. This makes the membrane very permeable to sodium ions (as well as most other ions), allowing rapid influx of sodium into a muscle fiber. As a result, the membrane potential rises in the local area of the end-place as much as 50 to 75 millivolts, creating a local potential called the end-plate potential.
The mechanism by which acetylcholine increases the permeability of the muscle membrane is probably the following: it believed that the muscle membrane contains a special protein molecule called an acetylcholine receptor substance to which the acetylcholine binds. Under the influence of the acetylcholine this receptor supposedly undergoes a conformational change that increases the permeability of the membrane to ions. Rapid influx of sodium ions ensures, and this elicits the end- plate potential that is responsible for initiation of the action potential at the muscle fiber membrane.
Ordinarily, each impulse that arrives at the neuromuscular junction creates an end-plate current flow about three to four times that required to stimulate the muscle fiber. Therefore, the normal neuromuscular junction is said to have a very high safety factor. However, artificial stimulation of the nerve fiber at rates greater than 100 times per seconds for several minutes often diminishes the number of vesicles of acetylcholine released with each impulse so much that impulses then often fail to pass into the muscle fiber. This is called fatigue of the neuromuscular junction. However, under normal functioning conditions such fatigue rarely occurs and more so following the relaxation and meditation the muscle excitation further decreases discarding any possibility of fatigue. This happens because almost significantly reduced nervous stimulation from spinal nerves as well as sympathetic nerves. Similar mechanism of action has been postulated by Guyton 1982; Madanmohan 2008 8c 1992; and Chan 2003.
Chemical studies have shown that actin and myosin filaments, particularly derived from smooth muscles interact with each other in the same way as do actin and myosin derived from skeletal muscle. Furthermore, the contractile process is activated b calcium ions, and ATP is degraded to ADP to provide the energy for contraction.
On the other hand, there are major differences in the physical organization of smooth muscle and skeletal muscle, as well as differences in other aspects of smooth muscle function such as excitation- contraction coupling, control of the contractile process by calcium ions, duration of contraction, and amount of energy required for the contractile process.
The physical organization of the smooth muscle cell shows large numbers of actin filaments attached to so-called dense bodies. Some of these bodies in turn are attached to the cell membrane, while others are dispersed throughout the sarcoplasm. There also appears to be enough cross attachments from one dense body to another to hold them in relatively fixed positions within the cell. Interspersed among the actin filaments are a few thick filaments about 2.5 times the diameter of the thin actin filaments. These are assumed to be myosin filaments. However, there are only one-twelfth of one fifteenth as many of these "myosin filaments" as filaments. Despite the relative paucity of myosin filaments, it is assumed that they have sufficient cross-bridge to attract the many actin filaments and cause contraction by the sliding filaments and cause contraction by the sliding filaments mechanism in essentially the same was as in skeletal muscle. And it is especially interesting that the maximum
strength of contraction of smooth muscle is approximately equal to that of skeletal muscle, about 2 to 3 kilograms per square centimeter of cross-sectional area of the muscle.
A typical smooth muscle tissue begin to contract 50 to 100 milliseconds after it is excited and will reach full contraction about half a second later. Then the contraction declines in another 1 to 2 seconds, giving a total contraction time of 1 to 3 seconds, which is about 30 times as long as the single contraction of skeletal muscle.
As little as one five-hundredth as much energy is required to sustain the same tension of contraction in smooth muscle as in skeletal muscle. This presumably results from the very slow activity of smooth muscle myosin ATP-ase and also from the fact that there are far fewer myosin filaments in smooth muscle than in skeletal muscle.
This economy of energy utilization by smooth muscle is exceedingly important to overall function of the body, because organs such as the intestines, the urinary bladder, the gallbladder and other viscera must maintain moderate degrees of muscle contractile tone day in and day out. (Guyton 1982, Seeley et al 2003, Choudhary 2001).
All such processes in muscular activities are related with the metabolic rate. Our experimental intervention has greatly influenced the rate of metabolism which was reduced up to significant mark thereby reducing the muscular contraction rate and thus, manifested in a level of complete relaxation.
The alteration in muscles strength to maintain force of contraction is termed as fatigue. Before actual muscle fatigue occurs, a person may have feelings of tiredness and the desire to cease activity. This response called central fatigue. Although its exact mechanism is unknown, it may be a protective mechanism to stop a person from exercising before muscles become damaged. As you will see, certain types of skeletal muscle fibers fatigue more quickly than others.
Although the precise mechanisms that cause muscle fatigue are still not clear, several factors are thought to contribute. One is inadequate release of calcium ions from the SR (Sarcoplasmic Reticulum), resulting in a decline of CA2+ concentration in the sarcoplasm. Depletion of creatine phosphate also is associated with fatigue, but surprisingly, the ATP levels in fatigued muscle often are not much lower than those in resting muscle. Other factors that contribute to muscle fatigue include insufficient oxygen, depletion of glycogen and other nutrients, buildup of lactic acid and ADP, and failure of action potentials in the motor neuron to release enough acetylcholine.
During prolonged periods of muscle contraction, increases in breathing rate and blood flow enhance oxygen delivery to muscle tissue. After muscle contraction has stopped, heavy breathing continues for a while, and oxygen consumption remains above the resting level. Depending on the intensity of the exercise, the recovery period may be just a few minutes, or it may last as long as several hours. The term oxygen debt refers to the added oxygen, over and above the resting oxygen consumption, that is taken into the body after exercise. This extra oxygen is used to "pay back" or restore metabolic conditions to the resting level in three ways: (1) to convert lactic acid back into glycogen stores in the liver, (2) to re-synthesize creatine phosphate and ATP in muscle fibers and (3) to replace the oxygen removed from myoglobin.
The metabolic changes that occur during exercise can account for only some of the extra oxygen used after exercise. Only a small amount of glycogen re synthesis occurs from lactic acid. Instead,
most glycogen is made much later from dietary carbohydrates. Much of the lactic acid that remains after exercise is converted back to pyruvic acid and used for ATP production via aerobic cellular respiration in the heart, liver, kidneys, and skeletal muscle. Oxygen use after exercise also is boosted by ongoing changes. First, the elevated body temperature after strenuous exercise increases the rate of chemical reactions throughout the body. Faster reactions use ATP more rapidly, and more oxygen is needed to produce the ATP. Second, the heart and the muscles used in breathing are still working harder than they were at rest, and thus they consume more ATP. Third, tissue repair processes are occurring at an increased pace. For these reasons, recovery oxygen uptake is a better term than oxygen debt for the elevated use of oxygen after exercise. (Tortora and Derrickson 2006).
Yoga and Preksha Meditation intervention improves the oxygen supply which ultimately enhances the ATP availability thereby reducing the oxygen debt. This results in enhancement of oxygen level in blood and further modulation in metabolic rate. The impact of such change is exhibited in terms of muscle relaxation, reduction in heart rate and blood pressure along with positive improvement in various components of respiratory functions as observed in the results of the present study.
