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1 Defence and Civil Institute of Environmental Medicine, Toronto, M3M 3B9; 3 Faculty of Physical Education and Health and 4 Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario M5S 1A1 Canada; and 2 United States Army Research Institute of Environmental Medicine, Natick, Massachusetts 01760
This study tested the
hypothesis that exercise elicits monocytic cytokine expression and that
prolonged cold exposure modulates such responses. Nine men (age,
24.6 ± 3.8 y;
O2 peak, 56.8 ± 5.6 ml · kg
1 · min
1) completed
7 days of exhausting exercise (aerobic, anaerobic, resistive) and
underwent three cold, wet exposures (CW). CW trials comprised
6 h
(six 1-h rest-work cycles) exposure to cold (5°C, 20 km/h wind) and
wet (5 cm/h rain) conditions. Blood samples for the determination of
intracellular and serum cytokine levels and circulating hormone
concentrations were drawn at rest (0700), after exercise (~1130), and
after CW (~2000). Whole blood was incubated with (stimulated) or
without (spontaneous) lipopolysaccharide (LPS; 1 µg/ml) and stained
for CD14 monocyte surface antigens. Cell suspensions were stained for
intracellular cytokine expression and analyzed by flow cytometry. The
proportion of CD14+ monocytes exhibiting spontaneous and
stimulated intracellular expression of interleukin (IL)-1
, IL-6, and
tumor necrosis factor (TNF)-
increased after exercise, but these
cells produced less IL-1
and TNF-
after CW when CW was preceded
by exhausting exercise. Serum cytokine concentrations followed
a parallel trend. These findings suggest that blood monocytes
contribute to exercise-induced cytokinemia and that cold exposure can
differentially modulate cytokine production, upregulating expression of
IL-6 and IL-1 receptor antagonist but downregulating IL-1
and
TNF-
. The cold-induced changes in cytokine expression appear to be
linked to enhanced catecholamine secretion associated with cold exposure.
catecholamines; cortisol; flow cytometry; immune; interleukin; thermal stress
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