Page 187 - Biobehavioral Resilence to Stress

164 Biobehavioral Resilience to Stress

endogenous antioxidant pathways and thus promote resilience to the eff ects
of chronic stress. Repeated damage and oxidative stress leads to long-term
loss of muscle function, but proper exercise training provides specifi c protec-
tive benefits that may be mediated through heat shock protein stimulation of

the skeletal muscle antioxidant, glutathione (Koh, 2002). Recent studies have
also demonstrated the importance of exercise-induced stimulation of brain-
derived neurotrophic factor (BDNF) in the hippocampus and elsewhere, and
this effect appears to be mediated by astrocytes (Adlard & Cotman, 2004;

Zaheer et. al., 2006).
Attempts to extend performance limits through metabolic manipulation

are often frustrated by mechanisms that protect individuals from metaboli-
cally running amok with every meal. For example, there is a theoretical basis
to consider that l-carnitine ingestion increases fatty acid oxidation, which
could serve to tilt metabolism towards fat metabolism. Th eoretically, this
could be used as a strategy to protect lean mass in a semistarvation environ-
ment or to increase the availability of energy during high-intensity exercise.
However, except for rare individuals with a carnitine deficiency, this strategy

simply does not work. Protective mechanisms include limited gut absorp-
tion, inhibitory metabolic feedback loops, and mitochondrial energy fl ux
limitations. Effective nutritional supplements are substrates such as basic

fuels that are involved in rate-limiting processes. For example, carbohy-
drates improve physical resilience in extreme environments by extending
endurance exercise time (CMNR, 2006), reducing the incidence of AMS in
hypobaric hypoxia (Fulco et al., 2005), and improving performance in cold
environments (Haman, Legault & Weber, 2004).

Creatine is another energy substrate that can affect specialized types of
performance related to short burst strength. However, creatine has failed to
provide the benefits originally theorized for brain function (e.g., in hypoxia)

and chronic oxidative damage. Likewise, protective mechanisms prevent
benefi cial eff ects of direct neurotransmitter administration on the activity
of relevant neural pathways. However, it is possible to achieve an eff ect by
providing a substrate for rate-limited resynthesis of neurotransmitters, at
least in the case of tyrosine. This may be helpful in high-stress environ-

ments, where there occurs substantial depletion of the catecholamines that
are synthesized from tyrosine. Cold, wet rats subjected to hypoxia achieve
stress levels high enough to reduce the epinephrine content of their adre-
nals by nearly half (Kiang-Ulrich, 1977). Tyrosine ingestion in stressed rats
increases brain resynthesis of NE (Rauch & Lieberman, 1990). Because high
levels of stress are required to demonstrate such effects, it is a diffi cult scien-

tific and ethical challenge to demonstrate the efficacy of such interventions
in human subjects.
Kosslyn et al. (2002) present convincing evidence for the importance of
individual differences in stress response, activation of the autonomic nervous

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