Swimming training prevents generation of suppressor macrophages during acute cold stress

Citation
T. Kizaki et al., Swimming training prevents generation of suppressor macrophages during acute cold stress, MED SCI SPT, 32(1), 2000, pp. 143-148
Citations number
35
Categorie Soggetti
Medical Research General Topics
Journal title
MEDICINE AND SCIENCE IN SPORTS AND EXERCISE
ISSN journal
01959131 → ACNP
Volume
32
Issue
1
Year of publication
2000
Pages
143 - 148
Database
ISI
SICI code
0195-9131(200001)32:1<143:STPGOS>2.0.ZU;2-4
Abstract
Purpose: Acute cold stress induces suppressor macrophages expressing large numbers of receptors to Fc portion of immunoglobulin G (MAC-1(+)Fc gamma RI I/IIIbright cells), resulting in suppression of splenocyte mitogenesis. The generation of MAC-1(+)Fc gamma RII/IIIbright cells is paltry mediated by i ncreased glucocorticoid levels during acute cold stress. The aim of the cur rent study was to investigate the effect of swimming training on the genera tion of the MAC-1(+)Fc gamma RII/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 impr oved 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 gamma RII/IIIbright cells in perito neal exudate cells from swimming-trained mice was significantly lower than that from control mice. In addition, the proportion of MAC-1(+)Fc gamma RII /IIIbright cells in peritoneal exudate cell population from swimming-traine d mice was unaffected by the acute cold stress. The swimming training signi ficantly attenuated the increases in serum corticosterone levels in respons e to acute cold stress. These results suggested that swimming training not only improves cold tolerance bur also inhibits the generation of suppressor macrophages under acute cold stress as well as under normal conditions.