title: Exercise and lymphocyte activation following chemotherapy for breast cancer.
abstract: OBJECTIVE
  To determine whether exercise training would increase lymphocyte activation in patients with breast cancer following chemotherapy. Activation was determined by the presence of CD4(+)CD69(+) T-helper lymphocytes, mitogen-induced proliferation, and levels of cytokines produced by mitogen-stimulated lymphocytes and in the patients' plasma.
  
  
  METHODS
  Patients with breast cancer (N = 28) who participated in a 6-month exercise program were compared with patients (N = 21) who did not exercise. Following chemotherapy, and 3 and 6 months later, patients underwent fitness evaluations and had blood drawn. The exercise program consisted of resistance training and aerobic activity at 60-75% functional capacity three times a week with a personal trainer. Immunochemistry and flow cytometry were used to measure the number of CD4(+)CD69(+) blood lymphocytes. Whole blood was stimulated with concanavalin A (ConA), phytohemagglutin (PHA), or pokeweed mitogen (PWM) to determine proliferation potential. Enzyme-linked immunosorbent assays (ELISA) were used to determine the concentration of interferon-gamma (IFN-gamma) and interleukin-6 (IL-6) in the culture medium of mitogen-stimulated lymphocytes as well as the plasma concentrations of IL-6, soluble IL-6 receptor, soluble gp130, and IFN-gamma. Analysis of groups across time was done using the Wilcoxon signed rank test, and comparisons of groups were done using the Mann-Whitney U test.
  
  
  RESULTS
  The exercising patients showed increases in maximal oxygen uptake and upper body strength. This group also showed a greater percentage of CD4(+)CD69(+) cells and a greater level of tritiated thymidine incorporation (DNA synthesis) when stimulated with ConA, PHA, and PWM at the end of the intervention. Plasma and mitogen-stimulated IL-6 and IFN-gamma production were similar in both groups.
  
  
  CONCLUSIONS
  Exercise may improve immune function by increasing lymphocyte activation in patients with breast cancer following treatment.
authors.affiliation: The Pennsylvania State University Department of Biochemistry and Molecular Biology, University Park, 16802, USA.
authors.forename: Natalie A
authors.initials: NA
authors.lastname: Hutnick
authors.forename: Nancy I
authors.initials: NI
authors.lastname: Williams
authors.forename: William J
authors.initials: WJ
authors.lastname: Kraemer
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Orsega-Smith
authors.forename: Richard H
authors.initials: RH
authors.lastname: Dixon
authors.forename: Aaron D
authors.initials: AD
authors.lastname: Bleznak
authors.forename: Andrea M
authors.initials: AM
authors.lastname: Mastro
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000032:analysis; D000945:Antigens, Differentiation, T-Lymphocyte / Q000032:analysis; D001943:Breast Neoplasms / Q000188:drug therapy / Q000276:immunology* / Q000473:pathology; D015496:CD4-Positive T-Lymphocytes; D049109:Cell Proliferation; D016207:Cytokines / Q000032:analysis; D005081:Exercise Therapy; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007150:Immunohistochemistry; D037181:Lectins, C-Type; D008213:Lymphocyte Activation; D008875:Middle Aged; D010809:Physical Fitness; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D016207:Cytokines; D037181:Lectins, C-Type; D000099192:CD69 Antigens