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Objective: This study examined the effects of acute psychological stress and exhaustive exercise on the expression and density of adhesion molecules (L-selectin, lymphocyte function antigen-1 [LFA-1], and intracellular adhesion molecule-1 [ICAM-1]) on monocytes, granulocytes, and lymphocytes., Methods: Forty-five healthy volunteers performed a 15-minute public speaking task and a 15- to 18-minute bicycle ergometer challenge., Results: In general, both the exercise and speaking tasks led to increases in the number of circulating leukocytes and lymphocyte subsets. The density of L-selectin (CD62L) on mixed lymphocytes and T lymphocytes was decreased in response to exercise (p values < .001). Both stressors led to an increased density of LFA-1 (CD11a) on mixed lymphocytes (p values < .01), whereas CD11a density on monocytes and granulocytes remained unchanged. ICAM-1 (CD54) density was unaffected, but the number of lymphocytes, monocytes, and granulocytes expressing CD54 increased in the circulation on both stressors., Conclusions: The data indicate that both psychological stress and exercise have significant effects on cellular expression of adhesion molecules on circulating leukocytes. Given the crucial role that adhesion molecules on circulating cells play in inflammation and disease, these findings may have clinical relevance in sympathetic nervous system-induced immune activation.

Objective: The aim of the study was to assess the effects of three different methods of acute activation of the sympathetic nervous system on lipopolysaccharide-induced in vitro production of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha)., Methods: Thirty-two healthy volunteers performed speech and exercise tasks and underwent a 30-minute infusion of isoproterenol., Results: As expected, acute activation of the sympathetic nervous system led to leukocytosis, including increases in lymphocyte, monocyte, and granulocyte populations (p values <.05). Lipopolysaccharide-induced IL-6 production was increased after both the speaking and exercise tasks (p values <.001), whereas TNF-alpha production was elevated only after exercise (p<.05). In contrast, infusion of isoproterenol inhibited TNF-alpha production (p<.001) and caused no change in IL-6 production., Conclusions: In response to the challenges, IL-6 and TNF-alpha production showed different profiles. Purely beta-agonist stimulation led to downregulation of TNF-alpha production, providing evidence of the antiinflammatory effect of in vivo beta-receptor activation. The enhanced production of both cytokines after exercise, and of IL-6 after the speech task, can be best explained by a simultaneous upregulation of proinflammatory and inflammation-responding mediators. These effects may have an important role in controlling the immune response to acute psychological and physical stress.