Contribution of exertional hyperthermia to sympathoadrenal-mediated lymphocyte subset redistribution

Citation
Sg. Rhind et al., Contribution of exertional hyperthermia to sympathoadrenal-mediated lymphocyte subset redistribution, J APP PHYSL, 87(3), 1999, pp. 1178-1185
Citations number
50
Categorie Soggetti
Physiology
Journal title
JOURNAL OF APPLIED PHYSIOLOGY
ISSN journal
87507587 → ACNP
Volume
87
Issue
3
Year of publication
1999
Pages
1178 - 1185
Database
ISI
SICI code
8750-7587(199909)87:3<1178:COEHTS>2.0.ZU;2-K
Abstract
The contribution of hyperthermia to the differential leukocytosis of exerci se remains obscure. This study examined changes in circulating sympathoadre nal 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, bod y fat 13.9 +/- 4.6%, peak O-2 consumption: 48.0 +/- 12.4 ml.g(-1)min(-1)] e xercised for 40 min (65% peak. O-2 consumption) during mater immersion at 3 9 or 18 degrees C. T-re increased from 37.2 to 39.3 degrees C (P < 0.0001) after 40 min of exercise in 39 degrees C water but was held constant to an increment of 0.5 degrees C during exercise in 18 degrees C water. Applicati on of this thermal clamp reduced exercise-associated increments of plasma e pinephrine (Epi) and norepinephrine (NE) by >50% (P < 0.05) and abolished t he postexercise increase in cortisol. Thermal clamping also reduced the exe rcise-induced leukocytosis and lymphocytosis. Multiple regression demonstra ted 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 relationshi p 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) rela ted to NE. Cortisol was negatively associated with leukocytes, CD14(+) mono cytes, and CD19(+) B- and CD4(+) T-cell subsets but was positively related to granulocytes. We conclude that hyperthermia mediates exercise-induced im mune cell redistribution to the extent that it causes sympathoadrenal activ ation, with alterations in circulating Epi, NE, and cortisol.