title: Exercise training-induced adaptations of immune response are mediated by beta-adrenergic receptors in aged but not young mice.
abstract: Beta-adrenergic blockade was used to determine whether the exercise training-induced adaptations of immune response to viral infection were mediated by catecholamines in young and old mice. Young (2 mo) and older (16 mo) male BALB/c mice were randomly assigned to an exercise or control group, and half of the mice in each group received the beta-adrenergic receptor antagonist nadolol. After 8 wk of moderate exercise training, mice were challenged with herpes simplex virus (HSV) 24 h postexercise. The results showed that exercise treatment increased anti-HSV IgM antibody, enhanced IL-10, and altered the kinetics of IFN-gamma and IL-2 production in young and old mice. Unique to older mice, exercise decreased mitogen-induced proliferation, increased splenocytes, and tended to decrease memory cells (CD44(hi+)). In contrast, exercise increased mitogen-induced proliferation but decreased the number of splenic lymphocyte and CD4+ cells in young mice. beta-Adrenergic blockade blunted the exercise-induced changes in anti-HSV IgM, IL-2, IFNgamma, and mitogen-induced proliferation in old but not young mice. The findings suggest that some of the immunomodulatory effects of chronic exercise are mediated via beta-adrenergic receptors and that the role of beta-adrenergic receptors is age dependent.
authors.affiliation: Department of Health and Human Performance, Iowa State University, Ames, IA 50011, USA. mkohut@iastate.edu
authors.forename: Marian L
authors.initials: ML
authors.lastname: Kohut
authors.forename: James R
authors.initials: JR
authors.lastname: Thompson
authors.forename: Wanglok
authors.initials: W
authors.lastname: Lee
authors.forename: Joan E
authors.initials: JE
authors.lastname: Cunnick
mesh_terms: D000222:Adaptation, Physiological; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000375:Aging / Q000502:physiology*; D000818:Animals; D000914:Antibodies, Viral / Q000097:blood; D000917:Antibody Formation / Q000502:physiology; D002395:Catecholamines / Q000378:metabolism; D002455:Cell Division / Q000187:drug effects; D003208:Concanavalin A / Q000494:pharmacology; D006561:Herpes Simplex / Q000276:immunology; D018259:Herpesvirus 1, Human / Q000276:immunology; D007107:Immune System / Q000502:physiology*; D007075:Immunoglobulin M / Q000097:blood; D007371:Interferon-gamma / Q000096:biosynthesis; D016753:Interleukin-10 / Q000096:biosynthesis; D007376:Interleukin-2 / Q000096:biosynthesis; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009248:Nadolol / Q000494:pharmacology; D010805:Physical Conditioning, Animal; D010835:Phytohemagglutinins / Q000494:pharmacology; D011897:Random Allocation; D011943:Receptors, Adrenergic, beta / Q000502:physiology*; D013154:Spleen / Q000166:cytology
chemical_list: D000319:Adrenergic beta-Antagonists; D000914:Antibodies, Viral; D002395:Catecholamines; D007075:Immunoglobulin M; D007376:Interleukin-2; D010835:Phytohemagglutinins; D011943:Receptors, Adrenergic, beta; D003208:Concanavalin A; D016753:Interleukin-10; D009248:Nadolol; D007371:Interferon-gamma