TY - JOUR
T1 - Age-related loss of associations between acute exercise-induced IL-6 and oxidative stress
AU - Sacheck, Jennifer M.
AU - Cannon, Joseph G.
AU - Hamada, Koichiro
AU - Vannier, Edouard
AU - Blumberg, Jeffrey B.
AU - Roubenoff, Ronenn
PY - 2006
Y1 - 2006
N2 - IL-6 mediates many aspects of the exercise-induced acute-phase response, including upregulation of antioxidant defenses. Moreover, IL-6 synthesis is regulated in part by oxidative stress. This investigation tested the hypothesis that an IL-6-mediated acute-phase response after exercise provides negative-feedback protection against exercise-induced oxidative stress. Healthy young (n = 16, 26.4 ± 1.8 yr) and older men (n = 16, 71.1 ± 2.0 yr) ran downhill for 45 min at 75% maximal oxygen consumption before and after a 12-wk period of supplementation with vitamin E (1,000 IU/day) or placebo. Circulating IL-6 and soluble IL-6 receptors, peripheral mononuclear cell production of IL-6, and IL-6 transcripts in muscle were measured before and within a 72-h time window after each acute exercise bout. At all time points plasma IL-6, IL-6 bioavailability, and C-reactive protein were higher in the older men; yet in response to exercise, young and older subjects experienced similar increases in these factors. Although the magnitude of postexercise changes in acute-phase variables was independent of age, correlations among plasma, mononuclear cell, and muscle IL-6 and oxidative stress were evident only in young men (R2 = 0.64, 0.35, and 0.33, respectively). These changes in circulating IL-6 were closely associated with a prooxidant state (R2 = 0.47), whereas muscle IL-6 mRNA correlated with an antioxidant state (R2 = 0.65). Supplementation with vitamin E did not affect exercise-induced responses or differences between the young and old men in a consistent manner. Therefore, oxidative stress is linked to the acute-phase response after exercise in young men, but not in older men who had elevated acute-phase reactants, suggesting that further research is warranted to determine the basis for these differences.
AB - IL-6 mediates many aspects of the exercise-induced acute-phase response, including upregulation of antioxidant defenses. Moreover, IL-6 synthesis is regulated in part by oxidative stress. This investigation tested the hypothesis that an IL-6-mediated acute-phase response after exercise provides negative-feedback protection against exercise-induced oxidative stress. Healthy young (n = 16, 26.4 ± 1.8 yr) and older men (n = 16, 71.1 ± 2.0 yr) ran downhill for 45 min at 75% maximal oxygen consumption before and after a 12-wk period of supplementation with vitamin E (1,000 IU/day) or placebo. Circulating IL-6 and soluble IL-6 receptors, peripheral mononuclear cell production of IL-6, and IL-6 transcripts in muscle were measured before and within a 72-h time window after each acute exercise bout. At all time points plasma IL-6, IL-6 bioavailability, and C-reactive protein were higher in the older men; yet in response to exercise, young and older subjects experienced similar increases in these factors. Although the magnitude of postexercise changes in acute-phase variables was independent of age, correlations among plasma, mononuclear cell, and muscle IL-6 and oxidative stress were evident only in young men (R2 = 0.64, 0.35, and 0.33, respectively). These changes in circulating IL-6 were closely associated with a prooxidant state (R2 = 0.47), whereas muscle IL-6 mRNA correlated with an antioxidant state (R2 = 0.65). Supplementation with vitamin E did not affect exercise-induced responses or differences between the young and old men in a consistent manner. Therefore, oxidative stress is linked to the acute-phase response after exercise in young men, but not in older men who had elevated acute-phase reactants, suggesting that further research is warranted to determine the basis for these differences.
KW - C-reactive protein
KW - F -isoprostanes
KW - Glycoprotein 130
KW - Interleukin-6
KW - Oxygen radical absorbance capacity
KW - Soluble interleukin-6 receptors
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U2 - 10.1152/ajpendo.00052.2005
DO - 10.1152/ajpendo.00052.2005
M3 - Article
C2 - 16507605
AN - SCOPUS:33745868692
SN - 0193-1849
VL - 291
SP - E340-E349
JO - American Journal of Physiology - Endocrinology and Metabolism
JF - American Journal of Physiology - Endocrinology and Metabolism
IS - 2
ER -