Immune changes in humans during cold exposure: effects of prior heating and exercise.
Level 3 - non-randomized controlled study
Small within-subject controlled crossover study without stated randomization in the abstract.
PubMed 10444630 · doi:10.1152/jappl.1999.87.2.699
What was done
Seven healthy young men (mean age 24.0 ± 1.9 years, peak VO2 45.7 ± 2.0 ml/kg/min) completed four separate experimental trials. Each trial involved a 1-hour pretreatment followed by 2 hours of seated cold exposure in a 5 °C climatic chamber. The four pretreatments were: 1) thermoneutral rest in 35 °C water, 2) passive heating in 38 °C water (core temperature increased by 1 °C), 3) exercise at 55% peak VO2 in 35 °C water (core temperature increased by 1 °C), and 4) exercise at 55% peak VO2 in 18 °C water (thermal clamping, core temperature remained stable). Circulating immune cell counts, natural killer cell activity, interleukin-6 (IL-6), and core temperature were assessed.
What was found
Core body temperature rose by 1 °C during passive heating and warm-water exercise, but stayed stable during exercise in 18 °C water. Across conditions, subsequent 2-hour cold exposure at 5 °C induced leukocytosis and granulocytosis, increased natural killer cell count and activity, and raised circulating IL-6 levels. Pretreatment with exercise in 18 °C water further augmented the leukocyte, granulocyte, and monocyte responses during cold exposure. The abstract reports directional changes and temperature values but does not provide exact numerical values or effect sizes for immune parameters.
Why it matters
The study shows that acute cold air stress transiently mobilizes innate immune markers and natural killer cell activity in humans, and that pre-exposure metabolic activity without prior core heating enhances this response.
Limits
The sample size was very small (n = 7) and restricted entirely to young, healthy men, limiting generalizability to females, older populations, or clinical cohorts. The abstract does not report exact numerical values, variance, or p-values for immune markers, nor does it state whether the four pretreatment conditions were randomized or counterbalanced. Long-term immune consequences and clinical infection risk were not measured.
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