To study the effects of exercise on natural killer (NK) cell number and activity (NKCA) healthy male (n = 32) and female (n = 32) subjects were randomly assigned to an exercise or control condition. Exercise involved a continuous incremental protocol consisting of cycling for three periods of 6 min at work rates corresponding to 55%, 70% and 85% peak oxygen uptake (VO2peak). Blood samples were drawn at baseline, at 6 min, 12 min and 18 min during exercise, and at 2 h following completion of exercise. Relative to both baseline and control conditions, exercise resulted in an increase in the number of circulating lymphocytes. The proportion of T cells (CD3+) and B cells (CD19+) significantly decreased, and NK cells (CD3-CD16+CD56+) increased throughout exercise. NKCA increased (P < 0.001) during the initial 6 min of exercise with no further changes observed, despite increases (P < 0.001) in the number and proportion of circulating NK cells during exercise at 70% and 85% VO2peak. Plasma epinephrine and norepinephrine increased (P < 0.001) above baseline at 12 min and 18 min. The changes in NK cell number and function were independent of gender. The results indicate that short-duration low-intensity exercise can significantly increase NK cell number and activity. However, alterations in NK cell number are not accompanied by changes of a similar magnitude in NKCA.

This study examined the effects of acute continuous incremental exercise on lymphocyte mitogenic function and cytokine production in physically active and sedentary males and females. Physically active (n = 32) and sedentary (N = 32) male and female subjects were randomly assigned to an exercise or control condition. Exercise involved a continuous incremental protocol consisting of cycling for 3 periods of 6 min at workrates corresponding to 55%, 70% and 85% VO2peak. Blood samples were drawn from a venous catheter at baseline, 6 min, 12 min and 18 min, and 2 h following completion of exercise. Relative to baseline and control condition the percentage of T (CD3+) and B cells (CD19+) significantly decreased, and the percentage of NK cells (CD3-CD16+CD56+) increased (p < 0.001) during each stage of the incremental exercise test. The proliferative response to ConA was suppressed, enhanced, or unchanged using 1.25 micrograms/ml, 2.5 micrograms/ml and 5.0 micrograms/ml ConA, respectively. The in-vitro production of IL-1 and IFN-gamma increased during each workload. In contrast IL-4 production did not change during exercise. The resting and exercise induced alterations in lymphocyte function and cytokine production were independent of gender and fitness level, and returned to baseline 2 h into recovery. The in-vitro production of IFN-gamma and IL-4 suggests that physical activity may alter the balance of TH1 and TH2 lymphocytes.

To study the effects of exercise on circulating leukocytes and leukocyte subsets, physically active (n = 32) and sedentary (n = 32) male and female subjects were randomly assigned to an exercise or control condition. Exercise involved a continuous incremental protocol consisting of cycling for three periods of 6 min at power outputs corresponding to 55%, 70% and 85% maximal oxygen uptake (VO2max). Blood samples were drawn from a venous catheter at baseline, and at 6 min, 12 min, and 18 min after beginning the exercise and 2 h following completion of exercise. Resting- and exercise-induced alterations in total leukocytes were independent of gender and subject fitness level. Relative to baseline, each increment in workload resulted in a rapid increase in the number of circulating leukocytes. Increases in neutrophils, lymphocytes and monocytes accounted for the exercise-induced leukocytosis. With regard to lymphocytes, exercise resulted in a significant increase in the number of T cells (CD3+), T helper cells (CD4+), T suppresser (CD8+) and natural killer (NK) cells (CD3-/CD16+/CD56+). The largest percentage increase occurred in the NK cell population. The CD4+: CD8+ ratio decreased (P < 0.001) throughout exercise due to a larger increase in the number of CD8+ cells relative to CD4+ cells. An exercise-induced neutrophilia, lymphocytopenia, and eosinophelia was observed 2 h into recovery. Exercise resulted in significant increases in plasma epinephrine and norepinephrine levels. There was no indication of a hypothalamic-pituitarty-adrenal response during exercise. The results indicate that the rapid, albeit transient, alteration in the number of circulating leukocytes during and following an acute progressive incremental exercise test are independent of gender and fitness.

It is well established that the route of infection affectsRespiratory enteric orphan virus (reovirus) has been used as a model viral pathogen to study virus-host interactions at mucosal surfaces and in the periphery. Reovirus is a nonenveloped, segmented double-stranded RNA virus (31) that replicates and elicits both humoral and cell-mediated immunity following oral or parenteral infection (7,13,14,16,25). After gaining access to the intestinal tissue via the M cells of the Peyer's patches (PP) (46), reovirus serotype 1 strain Lang (T1/L) infection of immunocompetent mice causes a self-limited disease of enterocytes of the crypts of Lieberkuhn adjacent to the PP of the distal ileum (37). In response, virus-specific cytotoxic T lymphocytes (CTLs) are induced within the PP (25). CTLs migrate via efferent lymphatic vessels to the mesenteric lymph nodes and then through the thoracic duct lymph and the systemic circulation to the spleen (25) or to intestinal mucosal sites, such as the intestinal intraepithelial lymphocyte (IEL) compartment (8, 9, 24). Parenteral infection with reovirus induces virus-specific CTLs in the draining peripheral lymph nodes and spleen (22,45).Although the humoral immune response to reovirus is influenced by microenvironmental or cellular factors at the anatomic site of infection (7,26,44), it is not known whether intestinal reovirus infection results in a CTL response distinct from that following parenteral infection. Most reovirus-specific CTLs are CD8␣␤ϩ TCR␣␤ ϩ Thy-1 ϩ and major histocompatibility complex (MHC) class I restricted (25). In addition, reovirus-specific CD8 ϩ CTLs induced in the PP following enteric infection and in the lung following respiratory infection express the unusual cell surface marker called germinal center and T antigen (23,44). Intratracheal instillation of reovirus elicits an unusual population of cytotoxic CD4 ϩ CD8␣␤ ϩ TCR␣␤ ϩ T cells (34), suggesting that unique CTL populations might be induced by infection at distinct anatomic locations. Furthermore, enteric reovirus T1/L infection of C3H mice has been shown to elicit CD8␣␤ ϩ CTL populations expressing V␤12 and V␤17, with minor populations expressing V␤2, V␤7, V␤9, and V␤14 among the IELs (8). These CTL populations were thought to be representative of the CTL response primed in the PP following oral infection with reovirus T1/L (9), although some might have been derived in situ, given the uncertain ontogeny of the IEL.There are several reasons why CTLs induced following oral infection could be different from those induced parenterally. During enteric reovirus infection, the ingested virions undergo pancreatic chymotryptic proteolysis of the outer coat proteins in the duodenum to yield infectious intermediate subviral particles (3). This processing within the lumen of the small intestine could potentially generate antigenic determinants distinct from those generated in the systemic periphery. Additionally, cleaved viral antigens might be taken up by intestinal absorptive epithelial cells (32,42), which expr...

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