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The use of nutrients to enhance performance may be one strategy for increasing the combat effectiveness of soldiers.

One nutrient that may prevent performance decrements caused by exposure to highly stressful environmental or operational conditions is the amino acid tyrosine. This substance is the precursor of several key brain neurotransmitters and may protect against the severe mental fatigue associated with exposure to life-threatening stressors that can occur in combat and certain other critical military operations. Tyrosine does not appear to have the stimulant-like activity of caffeine, so it is not likely to be useful in situations in which performance is degraded by boredom or sleepiness.

Tyrosine, a large neutral amino acid (LNAA) normally present in protein-containing foods, is the precursor of the catecholamine (CA) neurotransmitters dopamine (DA), norepinephrine (NE), and epinephrine.

There are no known adverse effects from tyrosine administration.

The ability of tyrosine supplementation to enhance the synthesis of CAs in and their release from rapidly firing neurons but not from relatively quiescent cells has been demonstrated by using a variety of experimental manipulations (for a review, see Milner and Wurtman [1986]). Tyrosine administration increases brain levels of the norepinephrine metabolite methoxyhydroxyphenylethylgylcol sulfate (MHPG-SO4) in cold-stressed rats (Gibson and Wurtman, 1978) and in the brains of spontaneously hypertensive rats (Sved et al., 1979) but not in those of control, normotensive animals.

The observation that the function of catecholaminergic neurons can be precursor dependent is the basis for the hypothesis that tyrosine mitigates the adverse effects of acute stress, because such neurons regulate, in part, the behavioral, cardiovascular, and neuroendocrine consequences of stress.

There is a great deal of evidence demonstrating that CA-containing neurons play a key role in the regulation of arousal level and anxiety.

Stressful conditions that can deplete central NE stores include cold, heat, restraint, exercise, and footshock (Stone, 1975). Acutely stressed animals become less responsive to their environment, explore less, are less aggressive and more submissive, cannot learn as readily, and generally seem debilitated (Maier and Seligman, 1976; Rapaport and Maier, 1978. The term learned helplessness has been applied to certain aspects of this syndrome because animals fail to respond appropriately (escape or avoid) to aversive stimuli when they are given the opportunity to do so (Maier and Seligman, 1976; Maier and Jackson, 1979; Minor et al., 1984; Weiss et al., 1976). This phenomenon has been used to model human clinical depression and posttraumatic stress disorder (Gray, 1982; van der Kolk et al., 1985).

Acutely stressed animals, for the most part, regardless of the specific nature of the stress, generally appear to be unable to function. Not only are complex stimulus-dependent behaviors like aggression, learning, and exploration depressed, but even eating and sleep are disturbed.

Many popular books and articles, as well as military histories, refer to the adverse consequences of combat stress on the performance of soldiers on the battlefield. In one of the few research studies conducted in a combat situation, the affect of Special Forces soldiers in an isolated outpost, deep in enemy territory during the earlier stages of the war in Vietnam, was assessed (Bourne et al., 1968). The primary symptom among these seasoned soldiers was hostility toward higher authorities at headquarters.

Efforts have also been made to formally describe the acute behavioral syndrome that occurs among some soldiers as a consequence of exposure to combat. It has been termed combat stress reaction (CSR), and its principal symptoms are anxiety, fear of death, helplessness, crying, and tiredness. Sleep is also disturbed (Solomon et al., 1989). The behavioral manifestations of the CSR syndrome appear to resemble the helplessness syndrome described in animals. It is likely that the underlying alterations in brain CA function documented in animals subjected to acute stress are also present in humans exposed to the life-threatening stress that characterizes combat.

One nutritional strategy to reduce the consequences of acute stress could be use of the dietary precursor of the CAs, tyrosine. In a number of studies, administration of tyrosine, either systemically just prior to initiation of the stress or as a dietary supplement, has been shown to partially protect animals from both the neurochemical and the behavioral consequences of the stress (Brady et al., 1980; Lehnert et al., 1984a,b; Lieberman et al., 1992; Luo et al, 1992; Rauch and Lieberman, 1990). After acute stress, animals pretreated with tyrosine more actively engage in a variety of normal behaviors in their environment compared with untreated but stressed control animals. Also, unlike stressed control animals not receiving tyrosine, the brain NE levels in treated animals were not depleted (Lehnert et al., 1984a,b).

it has been found to restore normal levels of aggressive behavior in animals that are subjected to cold-water stress (Brady et al., 1980). Additionally, in a stressful behavioral procedure sometimes considered to be a learned helplessness paradigm and used to screen drugs for their antidepressant activities (the Porsolt swim test [Porsolt et al., 1978]), significant dose-related potentiation of escape behavior following tyrosine administration has been observed (Gibson et al., 1982). The Porsolt test is conducted by placing the animal in a cylinder containing cold water for 3 min and assessing the duration of time that they spend actively swimming versus the amount of time that they maintain a characteristic immobile posture. Animals pretreated with tyrosine and phenylalanine (which is metabolized to tyrosine) continued to swim significantly longer than placebo-treated controls.

In the initial study of cold-induced stress (Rauch and Lieberman, 1990), rats were pretreated with 400 mg of tyrosine per kg, and their core body temperature was lowered to 30°C by immersing the animals in a cold-water bath for approximately 30 min. The Porsolt swim test was then used to assess the effects of tyrosine and cold-induced stress. As shown in Figure 15–1, the mean duration of immobility in this task increased as the core body temperature was reduced. This demonstrates that as the intensity of cold-induced stress increases, animals are less responsive to the environment. Figure 15–2 shows that when rats were pretreated with tyrosine, the duration of immobility declined significantly. In fact, tyrosine restored performance to the normal level typically observed in animals not exposed to cold-induced stress. Luo et al. (1992) replicated the findings of Rauch and Lieberman (1990) and demon strated that the effects of tyrosine on cold-stressed animals are dose dependent (Figure 15–3).