Contribution of exertional hyperthermia to sympathoadrenal-mediated lymphocyte subset redistribution
1 Defence and Civil Institute of Environmental Medicine, Toronto, Ontario M3M 3B9; 2 Faculty of Physical Education and Health, 3 Department of Laboratory Medicine and Pathobiology, and 4 Department of Public Health Sciences, University of Toronto, Toronto, Ontario, Canada M5G 1L57; 5 Centre de...
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| Published in: | Journal of applied physiology (1985) Vol. 87; no. 3; pp. 1178 - 1185 |
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| Main Authors: | , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
Bethesda, MD
Am Physiological Soc
01-09-1999
American Physiological Society |
| Subjects: | |
| Online Access: | Get full text |
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| Summary: | 1 Defence and Civil Institute
of Environmental Medicine, Toronto, Ontario M3M
3B9; 2 Faculty of Physical
Education and Health, 3 Department
of Laboratory Medicine and Pathobiology, and
4 Department of Public Health
Sciences, University of Toronto, Toronto, Ontario, Canada M5G 1L57;
5 Centre de Recherches du Service
des Santé des Armées, 38702 La Tronche, France; and
6 Hospital das Clínicas da
Faculdade de Medicina, da Universidade de São Paulo, 05403-0 Ribeirõ Preto, Brazil
The contribution of hyperthermia to the
differential leukocytosis of exercise remains obscure. This study
examined changes in circulating sympathoadrenal hormone concentrations
and patterns of leukocyte and lymphocyte subset
(CD3 + ,
CD4 + ,
CD8 + ,
CD19 + ,
CD3 16 + /56 + )
redistribution during exercise, with and without a significant rise of
rectal temperature (T re ). Ten
healthy men [age 26.9 ± 5.7 (SD) yr, body mass 76.0 ± 10.9 kg, body fat 13.9 ± 4.6%, peak O 2 consumption: 48.0 ± 12.4 ml · kg 1 · min 1 ]
exercised for 40 min (65% peak O 2
consumption) during water immersion at 39 or 18°C.
T re increased from 37.2 to
39.3°C ( P < 0.0001) after 40 min
of exercise in 39°C water but was held constant to an increment of
0.5°C during exercise in 18°C water. Application of this
thermal clamp reduced exercise-associated increments of plasma
epinephrine (Epi) and norepinephrine (NE) by >50%
( P < 0.05) and abolished the
postexercise increase in cortisol. Thermal clamping also reduced the
exercise-induced leukocytosis and lymphocytosis. Multiple regression
demonstrated that T re had no
direct association with lymphocyte subset mobilization but was
significantly ( P < 0.0001)
correlated with hormone levels. Epi was an important determinant of
total leukocytes, lymphocytes, and
CD3 + ,
CD4 + ,
CD8 + , and
CD3 CD16 + /56 +
subset redistribution. The relationship between NE and lymphocyte subsets was weaker than that with Epi, with the exception of
CD3 CD16 + /56 +
counts, which were positively ( P < 0.0001) related to NE. Cortisol was negatively associated with
leukocytes, CD14 + monocytes, and
CD19 + B- and
CD4 + T-cell subsets but was
positively related to granulocytes. We conclude that hyperthermia
mediates exercise-induced immune cell redistribution to the extent that
it causes sympathoadrenal activation, with alterations in circulating
Epi, NE, and cortisol.
catecholamines; cortisol; epinephrine; heat stress; hormones; immune; natural killer cells; lymphocytosis; norepinephrine; thermal
physiology; water immersion |
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| Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 |
| ISSN: | 8750-7587 1522-1601 |
| DOI: | 10.1152/jappl.1999.87.3.1178 |