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Background: One of the most challenging environmental extremes is immersion in cold/icy water, and consequent common assumption is that even a brief exposure to cold can lead to cold-related illnesses. The increase in the concentrations of the stress hormones cortisol, epinephrine (Epi), and norepinephrine (NE) in response to acute cold stress are thought to suppress the release of proinflammatory cytokines. No previous study has explored the residual consequences of whole-body short-term cold-water immersion (CWI; 14 °C for 10 min) on the immune response in healthy non-acclimated young adult men (aged 20–30 years). Materials and methods: In the current study, we tested the hypothesis that short-term acute whole-body CWI would induce high blood levels of cortisol, NE, and Epi, which in turn would increase circulating leukocyte numbers and delay the production of proinflammatory cytokines (tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), and IL-6). Results: Short-term whole-body CWI produced a stressful physiological reaction, as manifested by hyperventilation and increased muscle shivering, metabolic heat production, and heart rate. CWI also induced the marked release of the stress hormones Epi, NE, and cortisol. The change in IL-6 concentration after CWI was delayed and TNF-α production was decreased, but IL-1β was not affected within 48 h after CWI. A delayed increase in neutrophil percentage and decrease in lymphocyte percentage occurred after CWI. Conclusion: These findings suggest that, even though CWI caused changes in stress and immune markers, the participants showed no predisposition to symptoms of the common cold within 48 h after CWI.

Background: Although acute thermal stress appears to be one of the most effective stressors that increase the intra- and extracellular concentrations of heat shock protein 72 (Hsp72), 17β-estradiol has been shown to inhibit heat-induced Hsp72 expression. Materials and Methods: To determine whether severe whole-body hyperthermia (increase in rectal temperature up to 39.5 °C) induced by lower-body heating is a sufficient stimulus to modulate hormonal (17β-estradiol, progesterone, prolactin, epinephrine, and norepinephrine) and extracellular Hsp72 responses, we investigated young adult women (21 ± 1 yr). Results and Conclusions: In the present study, we show that a severe whole-body hyperthermia (increase in rectal temperature of approximately 2.6 °C and heart rate of approximately 80 bpm from baseline) was sufficient to increase 17β-estradiol, progesterone, and prolactin and catecholamine norepinephrine concentration. Moreover, we show that the concentration of extracellular Hsp72 and catecholamine epinephrine were not affected by severe whole-body hyperthermia in young adult women. From the functional point of view, expression of ovarian hormones induced by passive heat stress may have therapeutic potential for young adult women in, for example, estrogen treatment and overall women’s health.

Healthy aging is associated with a progressive decline in motor performance and thermoregulatory efficiency. Functional consequences of severe whole-body hyperthermia on neurophysiological functions in healthy aged men have not been investigated. To determine whether severe whole-body hyperthermia (increase in rectal temperature of about 2.5 °C) induced by lower-body heating in older men (64–80 years, n = 9) would suppress excitability of reflexes, voluntarily and electrically induced ankle plantar flexor contractile properties were compared with those in young men (19–21 years, n = 11). Though no aging effect on hyperthermia-induced reflex amplitudes was observed, a decrease in maximal H-reflex and V-wave latencies was found to be greater in older than in young men. In older men, lower-body heating was accompanied by a significant increase in twitch and tetani test torque in parallel with a greater decrease in muscle contraction time. There was no temperature-depended aging effect on the voluntary activation and maximal voluntary torque production. Despite delayed and weakened thermoregulation and age-related decline in neuromuscular function, motor performance in whole-body severe hyperthermia is apparently preserved in healthy aging.