title: Swimming training prevents generation of suppressor macrophages during acute cold stress.
abstract: OBJECTIVE
  Acute cold stress induces suppressor macrophages expressing large numbers of receptors to Fc portion of immunoglobulin G (MAC-1+ Fc gammaRII/IIIbright cells), resulting in suppression of splenocyte mitogenesis. The generation of MAC-1+ Fc gammaRII/IIIbright cells is partly mediated by increased glucocorticoid levels during acute cold stress. The aim of the current study was to investigate the effect of swimming training on the generation of the MAC-1+ Fc gammaRII/IIIbright suppressor macrophages by acute cold stress.
  
  
  METHODS
  The trained mice underwent a 6-wk endurance swimming training (5 times/wk) in water at 35-36 degrees C for 90 min. The swimming training significantly increased brown adipose tissue mass, suggesting improved cold tolerance. Actually, when the swimming-trained mice were exposed to 5 degrees C for 3 h (acute cold stress), the rectal temperature was not decreased. The proportion of MAC-1+ Fc gammaRII/IIIbright cells in peritoneal exudate cells from swimming-trained mice was significantly lower than that from control mice. In addition, the proportion of MAC-1+ Fc gammaRII/IIIbright cells in peritoneal exudate cell population from swimming-trained mice was unaffected by the acute cold stress. The swimming training significantly attenuated the increases in serum corticosterone levels in response to acute cold stress. These results suggested that swimming training not only improves cold tolerance but also inhibits the generation of suppressor macrophages under acute cold stress as well as under normal conditions.
authors.affiliation: Department of Hygiene, National Defense Medical College, Tokorozawa, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Kizaki
authors.forename: S
authors.initials: S
authors.lastname: Haga
authors.forename: I
authors.initials: I
authors.lastname: Sakata
authors.forename: T
authors.initials: T
authors.lastname: Ookawara
authors.forename: M
authors.initials: M
authors.lastname: Segawa
authors.forename: T
authors.initials: T
authors.lastname: Sakurai
authors.forename: T
authors.initials: T
authors.lastname: Izawa
authors.forename: H
authors.initials: H
authors.lastname: Ohno
mesh_terms: D000064:Acclimatization / Q000502:physiology; D000208:Acute Disease; D000273:Adipose Tissue / Q000033:anatomy & histology; D000316:Adrenergic alpha-Agonists / Q000097:blood; D000818:Animals; D001831:Body Temperature / Q000502:physiology; D003080:Cold Temperature / Q000009:adverse effects*; D003345:Corticosterone / Q000097:blood; D016177:Macrophage-1 Antigen / Q000032:analysis; D008264:Macrophages / Q000276:immunology* / Q000473:pathology; D017737:Macrophages, Peritoneal / Q000276:immunology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008938:Mitosis; D009638:Norepinephrine / Q000097:blood; D010807:Physical Endurance / Q000502:physiology; D011961:Receptors, Fc / Q000032:analysis; D017452:Receptors, IgG / Q000032:analysis; D013154:Spleen / Q000276:immunology / Q000473:pathology; D013312:Stress, Physiological / Q000097:blood / Q000276:immunology* / Q000473:pathology; D013550:Swimming / Q000193:education / Q000502:physiology*
chemical_list: D000316:Adrenergic alpha-Agonists; D016177:Macrophage-1 Antigen; D011961:Receptors, Fc; D017452:Receptors, IgG; D003345:Corticosterone; D009638:Norepinephrine