Evidence that the Effect of Bicycle Exercise on Blood Mononuclear Cell Proliferative Responses and Subsets is Mediated by Epinephrine

Abstract

The present study was designed to test the hypothesis that the exercise-induced changes in blood mononuclear cell (BMNC) subsets, BMNC proliferative responses and lymphokine activated killer (LAK) cell activity are mediated by increased epinephrine concentrations. Healthy male volunteers 1) exercised on a bicycle ergometer (75% of VO2max, 1 h) and 2) on another day were given epinephrine as an intravenous infusion to obtain plasma epinephrine concentrations comparable with those seen during exercise. Blood samples were collected in the basal state, during the last minutes of exercise or epinephrine infusion and 2 h later. During both perturbations the %CD3+ and %CD4+ T cells declined and the %CD16+ NK cells increased. Two h afterwards the CD14+ monocytes increased, while no changes were observed in %CD8+ T cells or %CD20+ B cells. The phytohemagglutinin (PHA) response declined during both epinephrine infusion and exercise experiments. The changes in interleukin-2 (IL-2) effect on proliferation and cytotoxic activity (LAK cell activity) were more pronounced in exercise experiments than during epinephrine. Exercise and epinephrine caused increase in concentrations of lymphocytes and neutrophils, but the changes were more pronounced in exercise experiments. The results indicate that, in response to physical exercise, the rise in plasma epinephrine may contribute to the changes in cellular immunity.

Attenuation of natural killer cell activity during 2-h exercise in individuals with spinal cord injuries

“…18,19 Previous studies showed that prostaglandins from activated monocytes and neutrophils that have migrated into damaged tissue might contribute to the reduction of NKCA. 9,11 In the present study, prostaglandins significantly increased after exercise in SCI subjects but not in able-bodied persons. Since the intensity of exercise in SCI subjects was similar to that of able-bodied subjects, we suggest that arm cranking during ergometer exercise in SCI subjects could result in compression of the tissue in paralyzed trunk, hip and lower limbs and induce distress and/or microdamage in the paralyzed area.…”

“…12,13 NKCA is stimulated by adrenaline, 3 suppressed by cortisol 10 and inhibited by prostaglandins. 9,11 The purpose of this study was to investigate the pattern of NKCA during exercise in SCI persons and to determine the mechanism(s) of any exerciseinduced change in NKCA, including the effects of adrenaline, PGE 2 and cortisol. For this purpose, we examined NKCA response to 2-h arm ergometer exercise at 60% of maximum oxygen consumption (VO 2max ) in SCI and ablebodied persons.…”

Selective Mobilization of Cytotoxic Leukocytes by Epinephrine

“…We show that stresslike increases in epinephrine concentrations invoke a specific increase in immune subpopulations with cytotoxic effector potential, namely, effector CD8 + T cells It has been repeatedly demonstrated that the number of immune cells increases after physical exercise or mental stress, with the most pronounced increases occurring in NK cell and CD8 + cytotoxic T cell counts (3,5,16,34), whereas both populations are decreased when endogenous catecholamines are suppressed by stellate ganglion block (40). These effects are caused by adrenal medullary epinephrine binding to b2-adrenoceptors on PBMCs, with high and intermediate levels of b2-adrenoceptor expression on NK cells and cytotoxic T cells, respectively (1,3,7,8,19,33,41). Our findings substantially expand these previous findings in showing that the epinephrine-induced increase in circulating immune cells is highly specific to cytotoxic effector subtypes, namely, effector CD8 + T cells, g/d T cells, NKT-like cells, cytotoxic NK cells, and proinflammatory monocytes, whereas no change is seen for cells lacking any cytotoxic potential, namely, CD4 + T cells, CD8 + T cells at their early stage of differentiation, immunomodulatory NK cells, and conventional monocytes.…”

“…epinephrine infusion at concentrations within the physiological normal range on 14 different T cell, NK cell, and monocyte subsets. Epinephrine was chosen because it is well-known, via binding with high affinity to the b2-adrenoceptor of PBMCs, to play a key role in mediating acute stress-induced leukocytosis (1)(2)(3)(32)(33)(34) + proinflammatory monocytes. Analysis of adhesion molecule and chemokine receptor expression reveals a specific profile in these cells, characterized by high expression of CD11a and CX3CR1 (fractalkine receptor).…”

Exercise-induced modulation of macrophage function

“…25 Second, injection of epinephrine induced monocytosis similar to exercise. 26 Last, one study has demonstrated that administration of propranolol can abrogate the exerciseinduced rise in blood monocytes. 27 This finding needs to be repeated.…”