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"Psychological Effects of Combat"

The Physiology of Close Combat

An understanding of the stress of close combat begins with an understanding of the physiological response to close-range interpersonal aggression. The traditional view of combat stress is most often associated with combat fatigue and Post-Traumatic Stress Disorder, which are actually manifestations that occur after, and as a result of, combat stress. Bruce Siddle has defined combat stress as the perception of an imminent threat of serious personal injury or death, or the stress of being tasked with the responsibility to protect another party from imminent serious injury or death, under conditions where response time is minimal.

The debilitating effects of combat stress have been recognized for centuries. Phenomenon such as tunnel vision, auditory exclusion, the loss of fine and complex motor control, irrational behavior, and the inability to think clearly have all been observed as byproducts of combat stress. Even though these phenomena have been observed and documented for hundreds of years, very little research has been conducted to understand why combat stress deteriorates performance.

The key characteristic which distinguishes combat stress is the activation of the SNS. The SNS is activated when the brain perceives a threat to survival, resulting in a immediate discharge of stress hormones. This "mass discharge" is designed to prepare the body for fight-or-flight. The response is characterized by increasing arterial pressure and blood flow to large muscle mass (resulting in increased strength capabilities and enhanced gross motor skills--such as running from or charging into an opponent), vasoconstriction of minor blood vessels at the end of appendages (which serves to reduce bleeding from wounds), pupil dilation, cessation of digestive processes, and muscle tremors. Figure 2(below) presents a schematic representation of the effects of hormone induced heart rate increase resulting from SNS activation.

The activation of the SNS is automatic and virtually uncontrollable. It is a reflex triggered by the perception of a threat. Once initiated, the SNS will dominate all voluntary and involuntary systems until the perceived threat has been eliminated or escaped, performance deteriorates, or the parasympathetic nervous system activates to reestablish homeostasis.

The degree of SNS activation centers around the level of perceived threat. For example, low-level SNS activation may result from the anticipation of combat. This is especially common with police officers or soldiers minutes before they make a tactical assault into a potential deadly force environment. Under these conditions combatants will generally experience increases in heart rates and respiration, muscle tremors, and a sense of anxiety.

In contrast, high-level SNS activation occurs when combatants are confronted with an unanticipated deadly force threat and the time to respond is minimal. Under these conditions the extreme effects of the SNS will cause catastrophic failure of the visual, cognitive, and motor control systems. Although there are endless variables that may trigger the SNS, there are six key variables that have an immediate impact of the level of SNS activation. These are the degree of malevolent, human intent behind the threat; the perceived level of threat, ranging from risk of injury to the potential for death; the time available to response; the level of confidence in personal skills and training; the level of experience in dealing with the specific threat; and the degree of physical fatigue that is combined with the anxiety.

Once activated, the SNS causes immediate physiological changes, of which the most noticeable and easily monitored is increased heart rate. SNS activation will drive the heart rate from an average of 70 beats per minute (BPM) to more than 200 BPM in less than a second. As combat stress increases, heart rate and respiration will increase until catastrophic failure or until the parasympathetic nervous system is triggered.effects of hormone induced heart rate increase

In 1950, S.L.A. Marshall's The Soldier's Load and the Mobility of a Nation was one of the first studies to identify how combat performance deteriorates when soldiers are exposed to combat stress. Marshall concluded that we must reject the superstition that under danger men can be expected to have more than their normal powers, and that they will outdo their best efforts simply because their lives are in danger. Indeed, in many ways the reality is just the opposite, and individuals under stress are far less capable of doing anything other than blindly running from or charging toward a threat. Humans have three primary survival systems: vision, cognitive processing, and motor skill performance. Under stress, all three break down.

Bruce K. Siddle's landmark research at PPCT involved monitoring the heart rate responses of law enforcement officers in interpersonal conflict simulations using paintball-type simulation weapons. This research has consistently recorded heart rate increases to well over 200 beats per minute, with some peak heart rates of up to 300 beats per minute. These were simulations in which the combatants knew that their life was not in danger. The combatant,in a true life-and-death situation (whether soldier or law enforcement officer), faces the ultimate universal human phobia of interpersonal aggression and will certainly experience a physiological reaction even greater than that of Siddle's subjects. The fundamental truth of modern combat is that the stress of facing close-range interpersonal aggression is so great that, if endured for months on end without any other means of respite or escape, the combatant will inevitably become a psychiatric casualty.

Even greater than the resistance to being the victim of close-range aggression is the combatant's powerful aversion to inflicting aggression on fellow human beings. At the heart of this dread is the average healthy person's resistance to killing one's own kind.

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Encyclopedia of Violence, Peace, and Conflict, Volume 3, p.159
© 1999 by Academic Press. All rights of reproduction in any form reserved.


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