title: Contribution of exertional hyperthermia to sympathoadrenal-mediated lymphocyte subset redistribution.
abstract: 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 x kg(-1) x min(-1)] exercised for 40 min (65% peak O(2) consumption) during water immersion at 39 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. 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.
authors.affiliation: Defence and Civil Institute of Environmental Medicine, Toronto, Ontario M3M 3B9, Canada.
authors.forename: S G
authors.initials: SG
authors.lastname: Rhind
authors.forename: G A
authors.initials: GA
authors.lastname: Gannon
authors.forename: P N
authors.initials: PN
authors.lastname: Shek
authors.forename: I K
authors.initials: IK
authors.lastname: Brenner
authors.forename: Y
authors.initials: Y
authors.lastname: Severs
authors.forename: J
authors.initials: J
authors.lastname: Zamecnik
authors.forename: A
authors.initials: A
authors.lastname: Buguet
authors.forename: V M
authors.initials: VM
authors.lastname: Natale
authors.forename: R J
authors.initials: RJ
authors.lastname: Shephard
authors.forename: M W
authors.initials: MW
authors.lastname: Radomski
mesh_terms: D000311:Adrenal Glands / Q000502:physiology*; D000328:Adult; D001810:Blood Volume / Q000502:physiology; D001831:Body Temperature / Q000502:physiology*; D002395:Catecholamines / Q000097:blood; D015444:Exercise / Q000502:physiology*; D005080:Exercise Test; D006400:Hematocrit; D006454:Hemoglobins / Q000378:metabolism; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007101:Immersion; D016130:Immunophenotyping; D008297:Male; D013564:Sympathetic Nervous System / Q000502:physiology*; D016176:T-Lymphocyte Subsets / Q000502:physiology*
chemical_list: D002395:Catecholamines; D006454:Hemoglobins; D006854:Hydrocortisone