Mechanisms of Exercise-Induced Leukocytosis: Contribution of Exertional Hyperthermia to Sympathoadrenal-Mediated Lymphocyte Subset Redistribution


  1. Rhind, S.G.
  2. Gannon, G.A.
  3. Shek, I.K.M.
  4. Brenner, Y.
  5. Severs, J.
  6. and others
Corporate Authors
Defence and Civil Inst of Environmental Medicine, Downsview ONT (CAN)
Contribution of exertional hyperthermia to sympathoadrenal-mediated lymphocyte subset redistribution. J. Appl. Physio. 87(3): 1178-1185, 1999. - The contribution of hyperthermia to the differential leukocytosis of exercise remains obscure. This study examined changes in circulating sympathaodrenal hormone concentrations and patterns of leukocyte subset (CD3(+), CD4(+), CD8(+), CD19(+), CD3(-)16(+)/56(+)) redistribution during exercise, with and without a significant rise of rectal temperature (Tre). Ten healthy men (age 26.9 + or - 5.7 (SD) yr, body mass 76.0 + or - 10.9 kg, body fat 13.9 + or - 4.6%, peak O2 consumption: 48.0 + or - 12.4 ml-kg1(-)-min1(-) exercised for 40 min (65% peak O2 consumption) during water immersion at 39 or 18C. Tre increased from 37.2 to 39.3C (P<0.0001) after 40 min of exercise in 39C water but was held constant to an increment of 0.5C during exercise in 18C 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 Tre had no direct association with lymphocyte subset mobilization but was significantly (P<0.0001) correlated with hormone levels.
Natural killer cells;Immune function;Cortisol;Epinephrine;Norepinephrine;Lymphocytosis;Thermal physiology;Water immersion
Report Number
DCIEM-98-P-84 — Paper
Date of publication
04 Nov 1999
Number of Pages
Hardcopy;Document Image stored on Optical Disk

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