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Resilience and Survival in Extreme Environments 157

effort can be achieved up to what appears to be a limit that is consistent

across mammalian species of approximately five times the resting metabolic

rate (Hoyt & Friedl, 2006). Higher levels of energy expenditure are limited by
a combination of biomechanical, thermoregulatory, and substrate availabil-
ity factors. However, motivated individuals usually are not stopped by these
factors. It appears that there exists some additional sort of central neural
mechanism that provides the normal limits. For example, while sleep depri-
vation causes selective hypometabolic changes in regions of the brain associ-
ated with specifi c types of cognition and emotion, it is also true that one of
the most reliable indicators of a sleep-deprived brain is a dramatically short-
ened sleep latency period (Balkin et al., 2004), which serves to protect against
continued wakefulness and resultant impairments in cognitive function.
Researchers in this area have suggested that a central protective mechanism
may be related to tissue proton accumulation, to an increase in brain levels of
5-hydroxytryptamine, or to some other type of central neural perceptual or
biochemical feedback (Abbiss & Laursen, 2005; Newsholme, Blomstrand &
Ekblom, 1992; Noakes, 1997).
Cold and hypoxia have been used individually and in combination as
stressors to accelerate brain NE secretion rates, and to impair cognition
and mood. Rat brain microdialysis studies have demonstrated hypother-
mia-induced elevated NE concentrations in the hippocampus (Rauch &
Lieberman, 1990; Yeghiayan, Luo, Shukitt-Hale & Lieberman, 2001), and
tyrosine dietary supplementation has been shown to reverse mood and cog-

nitive decrements in human subjects in cold conditions (Shurtleff et al., 1994)
and in cold and hypoxic conditions (Banderet & Lieberman, 1989). Taken
together, these studies suggest that the tyrosine substrate is the rate limiter in
conditions of extremely high physiological demand. If so, this would provide

another modifiable mechanism by which one can prevent or mitigate envi-
ronmental stress-related impairment. Dienstbier (1991) has suggested that
resilience (or “toughness”) is closely related to resistance to catecholamine
depletion in the brain, and that “catecholamine capacity” can be improved
by aerobic training, cold exposure, and psychological challenge.
Neural mechanisms that support resilience to stress may be grouped into
at least three areas: reward and motivation, fear responsiveness, and adap-
tive social behavior. A wide variety of neurochemicals and hormones align
with these key mechanisms (Charney, 2004), and deficiencies in each area

highlight the behavioral limiting actions of associated neural systems. Th us,
classically documented generalized stress-related increases in corticotropin-
releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and cor-
tisol during activation of the HPA axis exert interactive eff ects with other
neurobehavioral hormones that play a key role in limiting the motivation of
individuals who are under stress. For example, HPA axis activation has been
linked to the suppression of testosterone in men, with consequent reductions

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