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It has been proposed, but not confirmed, that environmental stressors alter immune function and increase the risk of viral infection among healthy individuals. We evaluated this hypothesis, examining the relationship among stress, immune function, and illness in 96 first-year U.S. Air Force Academy cadets during orientation and 4 weeks later during the stressful environment of Basic Cadet Training (BCT). Perceived stress and well-being levels of cadets were assessed via questionnaire. Immune responsiveness was analyzed by PHA-stimulated thymidine uptake in mononuclear leucocytes and by serologic evidence of reactivation of the Epstein-Barr virus (EBV). We documented significant declines in in vitro PHA-induced lymphocyte transformation (-35%; p less than 0.05) and subjective well-being (-19%; p less than 0.05) from orientation to BCT with corresponding, significant increases in perceived stress (+32%; p less than 0.05). Despite significantly altered in vitro immune responsiveness, there was no serologic evidence of EBV reactivation nor was there an association between these measures and risk of illness as determined by medical chart review and self-reported symptoms. These results suggest that reduced in vitro immune responsiveness during a moderate stressor may not necessarily lead to an increased risk of infection and/or reactivation of EBV in normal individuals.

Intraocular pressures, retinal vascular diameters, and visual acuities of nine men (ages 19-29), were repeatedly measured while the subjects were tilted 10 degrees head-down for 48 h and while they were seated before (baseline), and after the tilt. An immediate increase in intraocular pressure, measured by pneumatonometer (4.7 +/- 0.6 mm Hg, p less than 0.001) was recorded when subjects assumed the head-down position, and diurnal variations in intraocular pressures were observed for the 48 h. The initial and final head-down intraocular pressures were not significantly different (18.9 +/- 1.2 mm Hg vs. 17.9 +/- 1.4 mm Hg, respectively). However, when subjects resumed the sitting position, intraocular pressures fell below the initial sitting values (14.2 +/- 0.9 pre vs. 11.2 +/- 0.5 post, p less than 0.04). Computer image analysis of the retinal vasculature detected a 6% and 2% reduction in the caliber of arteries and veins, respectively, as compared with sitting baseline values. No changes in visual acuity were documented during the 48 h of head-down tilt. Our data suggest that the choroidal blood reservoir increases in volume over 48 h at continuous head-down position with a compensatory decrease in aqueous volume. These findings may explain intraocular pressure changes noted in astronauts during previous space missions and in studies associated with change in body position.

The effect of hypoxia (H) on plasma renin (PRA), aldosterone (PA), and arginine vasopressin levels (AVP) was evaluated during 6 h of mild exercise (treadmill: 0 grade, 1 mph). A crossover study was performed on seven male volunteers during steady state conditions of H2O, Na+ and K+ balance while breathing 12.5% O2 (PaO2 42 +/- 3 mm Hg) and room air (N, 21% O2). After exercise there were no significant differences in body weight, hematocrit, calculated plasma volumes, serum or urine osmolality, urine Na+ or K+ excretion or AVP. Mean arterial pressure (MAP) while exercising was reduced during hypoxia (86 +/- 2 vs. 92 +/- 4 mm Hg), p less than 0.05. Normal diurnal variation in serum cortisol was lost during exercise (N and H). Plasma renin and aldosterone levels fell with exercise in both groups: PRA N 3.3 to 2.4 vs. H 4.9 to 2.3 ng X ml-1 X h-1; PA N 6.5 to 2.8 vs. H 9.3 to 2.3 ng X dl-1 (p less than 0.05). Hypoxia per se did not exert influence beyond mild exercise regarding serum osmolality, urine osmolality or Na+ or K+ excretion. Sustained hypoxia during 6 h of mild exercise despite a lower MAP failed to elevate PRA, aldosterone, or AVP levels when normal hydration is maintained.

We wished to determine in a field study the effectiveness of dexamethasone for prevention and treatment of acute mountain sickness (AMS). Prevention Trial: We transported 15 subjects from sea level to 4,400 m (PB = 400 mm Hg) on Denali (Mt. McKinley) by means of a 1-h helicopter flight. In a randomized, double-blind fashion we gave eight subjects a placebo and seven subjects 2 mg dexamethasone orally every 6 h, starting 1 h before take-off. The entire placebo group and five of the dexamethasone group developed AMS within 5 h, and became progressively more ill until 12 h when the trial was terminated. We concluded that 2 mg of dexamethasone every 6 h did not prevent AMS in active soldiers rapidly transported to high altitude. Treatment Trial: We treated 11 of those with moderate to severe AMS (symptom score 4.5 +/- 0.7, range 3 to 11) with 4 mg of dexamethasone every 6 h orally or intramuscularly for 24 h. All were markedly improved at 12 h (symptom score 1.0 +/- 0.3, p less than 0.001, range 0 to 3), but symptoms increased after the drug was discontinued at 24 h (symptom score = 2.4 +/- 0.5). We conclude that dexamethasone in a dosage of 4 mg PO or IM every 6 h is an effective treatment for AMS, but that illness may recur with abrupt discontinuation of the drug.