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 (Tre). Ten healthy men [age 26.9 ± 5.7 (SD) yr, body mass 76.0 ± 10.9 kg, body fat 13.9 ± 4.6%, peak O2consumption: 48.0 ± 12.4 ml ⋅ kg−1⋅ min−1] exercised for 40 min (65% peak O2consumption) during water immersion at 39 or 18°C. Treincreased 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 Trehad 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.