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Mental and Physical Training
Training comes in many forms depending the sport you have selected. For shooting the best physical training for the sport is swimming and Tai Chi. Swimming because it builds the upper chest and shoulders to the point that the shooter athlete has little difficulty in holding an 8 to 20 pound rifle or pistol to target for the completion of each one-shot-match. Swimming also strengthens the lungs including mastering mental control of lungs, which is most important. Swimming is advantages for two main reasons, first the center of balance of any human is located at the hips or pelvis and the legs provide the muscle strength (gained through kicking in swimming) for maintaining the body balance through out the shooting procedure, and secondly the upper shoulders and arm muscles are strengthened for holding the rifle or pistol in position while the head acts as controller of the upper body balance in position. Natural Tai Chi is used for perfecting mental control over the neuromuscular movements of each coordinated movement during the exercise. Tai Chi is not the marshal arts style of exercise but the Chinese exercise version used for the purpose of physical unity and the practice of mental control over the many neuro-muscular controlled movements during the exercise. Tai Chi is basically a physical exercise with integrated mental control over the neuromuscular system through intensive concentration. Putting the two methods of exercise together with mental practice and analysis teaches the mind what you want accomplished and how it is to be accomplished. This instructional method is there after placed into the mental memory for later use by the non-dominant mental entity (NDME).
The information filed into memory is for the use of the NDME during automatic functioning where the only information available to correct or affect some type of movement can be found in the memory files. If the necessary information is not found in the memory files then the NDME will take all the information available that it feels is similar and run analysis of all data facts for determining the correct response and then place it into effect. The NDME in such cases determines the correct response action by consensus rather than finding the correct response in the NDME memory files. This results in errors of procedure and usually prevents the shooting athlete from achieving the perfect-bull's-eye desired. The shooting athlete will through mental practice and analysis formulate the correct responses with validated actions and file same into the NDME memory files ready for use.
From here we address the important functioning elements of the mental processes.
1. The mental practice and analysis.
2. Mental practice with dryfiring.
3. Dryfiring with live firing augmented with mental practice.Phase 1. The mental practice and analysis as discussed above. Any given shooting function is minutely analyzed and filed into the non-dominant mental entity (NDME) for later use. It is during automatic functioning that the NDME extracts this data from memory and puts such required functions into effect.
The learning phase occurs during analysis and then filed into memory.
Phase 2. Mental practice is now used with dryfiring practice. During mental analysis we have analyzed the function and now we must exercise what we have learned and placed into memory. Dry firing is used for this purpose. After analyzing the function, we place it into external motor neuromuscular implementation. Through this effort the NDME is the master controller and the instructions is transmitted to the neuromuscular system for execution. During this phase the timing sequences is developed and smoothed. The effort also renews mental analysis for refinement of the overall shooting technique.
Phase 3. Dryfiring validation of technical elements required for live firing exercise. Live fire results is a report card of how well the shooting athlete is accomplishing the refined shooting technique and eliminating the errors previously found during the shooting practice sessions. The shooting athlete is that athletes sole competitor, No one else.
One other item that many do not understand is the short time the mind has to act upon any given function. It is very quick because of the BIO design of the mental entity. For instance you cannot hold mental attention on any given item for more than 6 to 10 seconds and this controls how long you can perform mental practice or training lasting about 15 minutes or less...When the time is stretched beyond this time it destroys the process and mental precision goes to Null. In other words, not a single shooter can hit a perfect bull-eye (10.9) after exceeding the mental time limit of 10 seconds, not even Wigger. Two things happen to us. We use the condition of heightened attention and then move to intensive concentration. Heightened attention is the state you normally use during the set up of position and natural point of aim. Intensive concentration occurs for the 4 seconds of the mental checklist to trigger pull time. Then you return to heightened attention which is not Intensive concentration...Are you confused now?
How mental practice affects the growth of the brain during mental analysis and practice.
An activity-dependent protein involves the initial beginning and continuing development of cells during mental practice events. The protein, which is present in brain cells, increases dendritic growth in neurons in the visual system. Dendrites are the branches of neurons through which neurons receive signals. The protein helps to regulate the normal development of dendrites. These results indicate that the growth-promoting gene is activated by stimulation of the brain. "It's been known that if signals from the retina are blocked from reaching the optic dorsal midbrain - the part of the brain that processes visual input - proper development of that part of the brain is stunted. To determine the cause of this phenomenon, and the role of synaptic activity in brain development, researchers went looking for genes that were 'turned on' by those signals". The protein is an activity-regulated, membrane-bound, growth-promoting protein that controls dendritic outgrowth of neurons in which it is expressed, as well as the dendritic growth of neighboring neurons, conferring exquisite spatial and temporal control of neuronal structure in the developing brain. Levels of the protein are normally highest while development is taking place (as in mental practice and analysis) and lower when development is complete.
To determine whether the protein functions increase dendritic growth, the researcher used a virus vector (vaccinia virus) to introduce the gene into cells in the optic dorsal midbrain so that the midbrain cells produce higher-than-normal levels of protein. As a result of the extra protein gene activity, dendritic growth in midbrain neurons was increased dramatically as observed by the growth of longer, more highly branched dendritic arbors. The control group that did not express protein did not show a similar increase in the length or number of dendritic branches.
Furthermore, the researchers observed high levels of dendritic growth in neurons which were adjacent to the ones expressing protein, but which did not express protein themselves. "It is possible that an intercellular signaling mechanism exists, through which protein controls the growth of neighboring neurons."For many years, neuroscientists have generated evidence that brain activity helps to shape brain architecture. During early development, synapses—the communication junctions among nerve cells—form and disappear, giving rise to the microscopic wiring patterns of the mature brain. But it has been difficult to observe how or when an individual nerve cell changes its shape in response to synaptic activity.
Now, scientists have used sophisticated imaging techniques to demonstrate that intense stimulation of specific synapses in cultured slices of brain tissue induces the growth of threadlike projections from dendrites. These filopodia, as they are called, form stable synapses as the brain matures. (Dendrites are the highly branched outgrowths of nerve cells that receive incoming electrochemical signals from the axons of other nerve cells. The sites of communication formed by the endings of an axon and the projections from a dendrite are synapses.) The observation that synaptic stimulation triggers the growth of filopodia supports the long-held notion that mental activity shapes the cellular architecture of the brain. "The finding is important because it is the first time we have been able to see morphological changes induced by synaptic stimulation in living brain tissue." "We were able to see something that many people believed must be there, but despite looking for many years had not been able to observe." The growth of dendritic filopodia observed in the recent experiments has three important properties. First, the period of growth is transient (occurring 5 to 15 minutes during and after stimulation), although the resulting elongation of the filopodia is long-lasting (hours or more). Second, the growth of filopodia from dendrites is local, meaning it only occurs close (within 50 microns) to the site of synaptic stimulation, not in distant parts of the dendritic tree. And third, the growth of filopodia requires the activation of synaptic N-methyl-D-aspartate (NMDA) receptors, which respond to the neurotransmitter glutamate. The phenomenon was quite amazing while we observed this very simple change in the structure of post-synaptic nerve cells with synaptic stimulation. It was a very clear, very large change right under our microscope."To determine whether synaptic activity can release morphological changes in neurons, the researchers stimulated specific nerve cell axons with a small glass electrode placed close to the dendrite of interest and watched. Filopodia on dendrites close to the active synapses grew dramatically, increasing significantly in number and length for a duration of 20 minutes after stimulation, and maintained their extended length for more than two hours. These experiments get us closer to understanding how the wiring of the brain is established and modified by mental analysis and experience. The glass electrode supplied the stimulus that might mimic a sensory "experience" such as light, sound, or touch. The results suggest that nearby synaptic stimulation can change the shapes and synaptic connections of nerve cells. Previous studies by many neuroscientists had indicated that NMDA receptors are important for the normal development of the central nervous system and the formation of memories. Researchers who monitor electrophysiological activity in brain slices had shown that synapses become stronger after electrical stimulation and that long-term synaptic strengthening depends on repetitive activation of the NMDA receptors. The new experiments help connect those observations; they allowed the researchers to observe in real time how nerve cells change their shape in response to synaptic stimulation.
Next is the complex task of showing whether the newly elongated filopodia form functional synapses, transform into another kind of dendritic projection—perhaps mushroom-shaped "spines"—or simply retract into the trunk of the dendrite. The researchers also want to understand the molecular mechanisms that underlie the growth of filopodia in the brain and determine whether the same mechanisms are at work in the adult brain. Researchers found that receptors for the excitatory neurotransmitter glutamate are rapidly transported when nearby nerve cells are stimulated. The unleashed receptors move from inside nerve cells to the surfaces of dendritic spines, tiny protrusions from brain neurons, where synapses are most common. And because synapses are the junctions for communication (kinesthetic feedback) among nerve cells, glutamate receptor delivery to synaptic sites may be a key molecular event for the increased synaptic transmission that occurs during learning and memory. Receptors Unleashed! Key Event in Learning and Memory May Be Receptor Delivery to Synapses "People have been trying to understand how synapses strengthen for a long time." This long-lasting increase in synaptic transmission is thought to underlie the formation of new memories, particularly in the hippocampus, an evolutionarily primitive part of the cerebral cortex. Many researchers also find that dendritic spines-stubby, mushroom-shaped projections from nerve cell branches called dendrites-are frequently the sites of synaptic contact between incoming nerve axons from other brain regions and nerve cells that reside in the hippocampus. The new reports are important because they represent the first direct observation of the movement of key neurotransmitter receptors to probable sites of synaptic contact during the kind of neural stimulation that simulates learning. In recent experiments, their colleagues observed the delivery to dendritic spines of a component of one kind of glutamate receptor, called AMPA receptors (for a-amino-3-hydroxy-5-methyl-4-isoxazole propionate). Specifically, the researchers found that the redistribution of the AMPA receptor subunit GluR1 (glutamate receptor subunit 1) requires the activation of a second kind of glutamate receptor called NMDA receptors (N-amino-D-aspartate). Among neuroscientists who study learning and memory, NMDA receptors have become notorious; many argue that their activation is required for inducing LTP and forming certain kinds of memories. The new findings provide a possible mechanism by which AMPA receptors in postsynaptic neurons also contribute to synaptic strengthening. Stimulation of presynaptic neurons, which release glutamate as a neurotransmitter may trigger the delivery of AMPA receptors to synaptic sites on postsynaptic neurons, thereby, providing more places for glutamate to bind to and excite the cells. "Seeing is believing." "You have glutamate receptors tagged with a label and can actually see them move, which is what people imagined must happen during LTP. But you don't believe it until you see it." To study the rapid deployment of glutamate receptors to dendritic spines following synaptic stimulation maintained slices of hippocampus in long-term culture. They visualized the movement of AMPA-type glutamate receptors by tagging GluR1 receptors with green fluorescent protein (GFP). The fusing of the genes encoding GFP and GluR1 in a way that allowed them to be incorporated into the non-pathogenic Sindbis virus and injected into cultured hippocampal slices. Neurons that became infected with the genetically altered virus then synthesized the glutamate receptor subunit tagged with the brightly fluorescent protein. Two to three days later, used time-lapse, two-photon laser scanning microscopy to see the labeled glutamate receptors in the living nerve cells. (Researchers developed the high-tech imaging system and used it, in another collaboration the growth of dendritic filopodia from hippocampal neurons. Initially, in unstimulated neurons of the CA1 region of the hippocampus, most (88 percent) of the tagged glutamate receptors were distributed intracellularly throughout the shafts of dendrites.
The researchers used two methods to observe the initial, even distribution of receptors: two-photon laser imaging of the fluorescence-tagged GluR1, and electron microscopy of immuno-gold labeled receptors. But within 15 minutes after the researchers delivering a brief, high frequency stimulus to nearby nerve cell axons, the fluorescently labeled glutamate receptors redistributed in two ways. Some moved to the surface membranes of dendritic spines and others formed clusters within the shafts of dendrites near the bases of spines. The clusters may represent "a local reserve of glutamate receptors" that will be delivered to the spines over time to maintain a greater number of receptors at synaptic sites. We have found this phenomenon about the rapid delivery of glutamate receptors to dendritic spines after high-frequency stimulation such as mental practice. We really want to be able to say that glutamate receptor movement contributes to an increased synaptic signal during LTP. The researchers wanted to show that if AMPA-type glutamate receptors are delivered to active synapses, their delivery makes the synapses stronger. Or, if no synapses preexist at those sites, to demonstrate that the arrival of the glutamate receptors creates an active synapse.
With the just completed text we have the understanding how the brain responds to stimulation such as mental practice and dryfiring training sessions. Typical stimulation can be originated externally or internally during training sessions. Learning memory is developed over a 5 to 30 minute period and will last in temporary memories from a 20-minute period to a 2-hour period. Long-term memory takes many repetitions of the aforementioned periods of mental practice and dryfiring periods. We have found this phenomenon about the rapid delivery of glutamate receptors to dendritic spines after high-frequency repetitive stimulation such as mental practice and dryfiring sessions. Dryfiring may be boring but if the shooting athlete does not mentally analyze every aspect of the shooting position and shooting technique, the above neurophysicologcal activity will not occur and shooter learning will never occur.
All mental analysis is to be conducted upon that which is correct or perfect and build upon this basic position of correctness. Never analyze that which is incorrect or wrong or in error to the accepted position form or technical procedure of the shooting technique. Practice the mental checklist of chapter 7 until the timing is smooth and the PBE are arriving in regular frequency.