Background. Contracting skeletal muscle is capable of producing a metabolic response involving the production of large amounts of intracellular messengers known as cytokines. IL-6 is one cytokine known to be released in response to muscular contraction. Plasma IL-6 concentrations have been shown to increase significantly followed intense resistive exercise, and muscle-derived IL-6 is capable of reducing the inflammatory response of blood mononuclear cells. Purpose. To examine the effects of an acute bout of resistive exercise on inflammatory markers in the blood, 23 obese, postmenopausal women performed a high intensity resistive exercise session and the effects of contraction-induced IL-6 on LPS-stimulated TNF-α and IL-1β production were measured. Methods. Obese, postmenopausal (65.65 ± 3.89 years) women (N=23) were acclimated to resistive exercise over a three day period. After the acclimation period, participants were randomized into one of two groups: non-exercising control group (CON; N=11) or exercise group (EX; N=12). At least three days after the third acclimation day, participants reported to the lab and either completed a resistive exercise session (EX) at 80% of their estimated 1-RM, or rested quietly in the lab (CON). Blood samples were obtained pre, post, 2 hours-post, and 24 hours-post exercise. Similar time points were used in the CON group. Blood samples were analyzed using ELISA for plasma IL-6 concentrations. Whole blood samples were stimulated with LPS endotoxin and incubated for 24 hours in physiological conditions (37°C, 5% CO₂). LPS-stimulated production of TNF-α and IL-1β were measured in the stimulated supernatants to assess immunocreativity of blood mononuclear cells. Results. Plasma IL-6 increased significantly following the exercise session (p<0.019), although the difference compared to CON at PO was not significant. Significant leukocytosis occurred following the exercise session. Total white blood cells were increased, as well as numbers of circulating monocytes, neutrophils and lymphocytes immediately following exercise. LPS-stimulated cytokine production was not significantly affected by the exercise session. Plasma cortisol pattern of release was unchanged in the CON group, while the diurnal decrease in cortisol was delayed immediately post-exercise in the EX group. Cortisol remained below baseline values at the 24H sample in EX (p=0.00). Conclusion. Resistive exercise is capable of generating an immune response in elder, postmenopausal women as seen in the significant increase in plasma IL-6 and systemic leukocytosis. Plasma IL-6 exerted its effects on plasma cortisol and mitogenstimulated, whole blood cultures. The typical decrease in cortisol was not seen in the EX group, likely because of the contraction-induced changes in plasma IL-6. Unfortunately we did not find any significant difference between LPS-stimulated samples, although there was a tendency for significance at PO, indicating that plasma IL-6 was inhibiting pro-inflammatory cytokine release to some degree.