title: Polyethylene glycol but not mifepristone prevents intestinal lymphocyte loss following treadmill exercise in mice.
abstract: Circulating lymphocyte numbers decrease following intense physical activity, possibly due to exercise-induced apoptosis. Increased reactive oxygen species (ROS) and glucocorticoids (GC) following exercise contribute to lymphocyte apoptosis. Intestinal lymphocyte (IL) numbers also decrease following exercise.
  
  
  OBJECTIVE
  The purpose of this study was to determine the contribution of GC to exercise-induced IL loss.
  
  
  METHODS
  Female C57BL/6 mice (n = 178) were randomized to five drug conditions: (1) single injection of the glucocorticoid receptor antagonist mifepristone (MIF) solubilized in polyethylene glycol (PEG); (2) three injections of MIF (repeated MIF) PEG; (3) single injection of PEG (PEG); (4) three injections of PEG (repeated PEG); or (5) repeated injections of saline (SAL). Within each drug group mice were further randomized to exercise conditions: (1) control condition (non-exercised); (2) treadmill running with sacrifice immediately following the exercise; or (3) treadmill running with sacrifice 24 h after completion of the exercise.
  
  
  RESULTS
  There was a significant exercise effect, across all T lymphocyte subsets, in SAL (P < 0.01), PEG (P < 0.01) and MIF (P < 0.01) treated mice but not in mice given repeated PEG or repeated MIF exposure. The exercise effect was due to reduced IL numbers 24 h post-exercise compared with non-exercised controls.
  
  
  CONCLUSIONS
  These results suggest that GC are not directly responsible for IL cell loss following exercise. Repeated exposure to PEG may confer protection in the gastrointestinal tract from exercise-induced lymphocyte depletion. Because PEG inhibits ROS generation in experimental cell injury, the mechanisms for IL loss after exercise may involve oxidative stress.
authors.affiliation: Department of Health Studies and Gerontology, Faculty of Applied Health Sciences, University of Waterloo, Waterloo, Ontario, Canada.
authors.forename: J
authors.initials: J
authors.lastname: Quadrilatero
authors.forename: J
authors.initials: J
authors.lastname: Guan
authors.forename: J
authors.initials: J
authors.lastname: Boudreau
authors.forename: S
authors.initials: S
authors.lastname: Marra
authors.forename: L
authors.initials: L
authors.lastname: Hoffman-Goetz
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D017252:CD3 Complex / Q000276:immunology; D003345:Corticosterone / Q000097:blood; D005260:Female; D006727:Hormone Antagonists / Q000494:pharmacology*; D007422:Intestines / Q000187:drug effects / Q000276:immunology; D007694:Killer Cells, Natural / Q000276:immunology; D018655:Lymphocyte Count; D051379:Mice; D008810:Mice, Inbred C57BL; D015735:Mifepristone / Q000494:pharmacology*; D018384:Oxidative Stress / Q000502:physiology; D010641:Phenotype; D010805:Physical Conditioning, Animal / Q000502:physiology*; D011092:Polyethylene Glycols / Q000494:pharmacology*; D017382:Reactive Oxygen Species / Q000378:metabolism; D011965:Receptors, Glucocorticoid / Q000037:antagonists & inhibitors*; D012997:Solvents / Q000494:pharmacology; D016176:T-Lymphocyte Subsets / Q000187:drug effects; D013601:T-Lymphocytes / Q000187:drug effects*
chemical_list: D017252:CD3 Complex; D006727:Hormone Antagonists; D017382:Reactive Oxygen Species; D011965:Receptors, Glucocorticoid; D012997:Solvents; D015735:Mifepristone; D011092:Polyethylene Glycols; D003345:Corticosterone