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.

Hot water immersion induces an acute cytokine response in cervical spinal cord injury

“…As repeatedly shown following exercise (Foster et al 1986;Laing et al 2008;Rhind et al 1999) and hyperthermia (Brenner et al 1999;Kappel et al 1998;Walsh and Whitham 2006) interventions in AB populations, we report increased neutrophil, lymphocyte and monocyte numbers following hot water immersion. While increased neutrophil counts have been observed earlier following exercise interventions in CSCI populations, lymphocyte numbers remained unchanged in this population (Kouda et al 2012;Yamanaka et al 2010).…”

“…In line with this, blocking β-adrenergic receptors in AB (Foster et al 1986) has been demonstrated to reduce the post-exercise increase in lymphocyte numbers. Similarly, exercise in cold water to keep core temperature constant results in a blunted adrenaline response in AB, causing a reduced increase in lymphocyte numbers following exercise (Rhind et al 1999). Finally, α-or β-adrenergic blockade in mice demonstrates the importance of adrenergic mechanisms for T cell migration following exercise (Kruger et al 2008).…”

Thermoregulatory and Immune Responses During Cold Exposure: Effects of Repeated Cold Exposure and Acute Exercise

“…Our observation that total leukocyte, granulocyte and lymphocyte counts rise in response to underwater cycle ergometer exercise is consistent with the findings reported by other investigators in our laboratory (23,82). Similarly, thermal clamping attenuated this leukocyte and granulocyte response.…”

Increasing heat storage by wearing extra clothing during upper body exercise up-regulates heat shock protein 70 but does not modify the cytokine response

“…Animal studies further indicate that alpha adrenergic receptor-signalling pathways are involved in the increase of extracellular HSP70 (Johnson et al, 2005). Even though not directly measured in the current study, heat stress is associated with increases in sympathetic activity (Rhind et al, 1999;Starkie et al, 2005), which has been previously suggested to be a mechanism modulating immune responses (Rhind et al, 1999). The differences in the heart rate or ratings of perceived exertion between conditions indicate that INT was the more stressful condition that could be associated with increased sympathetic activity, which would further explain the difference in HSP70 elevations found between conditions.…”