Andrew J. Young

Tyrosine supplementation mitigates working memory decrements during cold exposure.

In rats, dietary supplementation with the amino acid tyrosine (TYR) prevents depletion of central catecholamines observed during acute environmental stress. Concomitant changes in the animals behavioral responses to stress suggest that TYR might have similar effects on central catecholamines and cognition in humans exposed to environmental stress. This study aimed to determine if severe cold exposure impairs human cognition and if dietary supplementation with TYR would ameliorate such deficits. Volunteers (N=19) completed three test sessions on different days (35 degrees C control/placebo, approximately 10 degrees C/placebo, approximately 10 degrees C/TYR) using a double-blind, within subjects design. During each session, volunteers completed two 90-minute water immersions and consumed a food bar (150 mg/kg TYR or placebo) before each immersion (total TYR 300 mg/kg). Cognitive performance, mood, and salivary cortisol were assessed. Cortisol was elevated in the cold (p<.01). Volunteers made fewer correct responses on a Match-to-Sample memory measure (p<.05) and reaction time (RT) and errors increased on a choice RT test (p<.01) in the cold. Self-reported tension (p<.01), depression (p<.05) and confusion (p<.01) also increased in the cold. When volunteers consumed TYR, correct responses increased on a Match-to-Sample memory measure (p<.05) and study time for the sample was shorter (p<.05), indicative of more rapid and accurate information processing. Finally, RT on the memory measure revealed a similar pattern across immersions for TYR and thermoneutral conditions, but not cold/placebo (p<.05). This study demonstrates cold exposure degrades cognitive performance and supplementation with TYR alleviates working memory decrements.

The effects of exhaustive exercise on thermoregulatory fatigue during cold exposure

Abstract Cold exposure facilitates body heat losses that, unless mitigated by vasoconstriction or shivering, thermogenesis, will cause lower body temperatures. Fatigue associated with chronic overexertion altered both vasoconstriction and shivering responses causing core temperature to decrease when exposed to cold. The question we posed is: do the physiological mechanisms elicited to maintain core body temperature “fatigue”, such that shivering and vasoconstriction are blunted during subsequent cold stress? This overview will focus on findings examining whether multiple stressors (fatigue combined with energy deficit and sleep deprivation over 9 weeks or 72 h) or individual stressors, such as acute exercise (1 h), and chronic exertional fatigue (3–7 days), compromise the ability to maintain thermal balance in the cold. Laboratory studies employed experimental design controls to isolate the effect of exercise from other consequences of exertion (initial core temperature, hypoglycemia) in order to study the independent effect of fatigue on thermoregulatory responses to cold. Results suggest that prior physical exercise may predispose a person to greater heat loss and to experience a larger decline in core temperature when subsequently exposed to cold air. The combination of exercise intensity and duration studied in these experiments did not fatigue the shivering response to cold exposure. Cold-induced increments in circulating norepinephrine, a marker of sympathetic nervous stimulation, appear unaffected by acute or chronic exertional fatigue. However, the possibility that fatigue impairs thermoregulatory responses to cold by mechanisms related to blunted peripheral vasoconstriction to sympathetic nervous stimulation merits further study.