PURPOSE: To examine the effect of post-resistance exercise alcohol ingestion on lipopolysaccharide (LPS)-stimulated production of IFNγ, TNF-α, IL-1β, IL-6, IL-8, and IL-10. METHODS: Recreationally resistance-trained men (n = 10, 25 ± 3 year, 177 ± 7 cm, 83.8 ± 15.7 kg, 14.8 ± 8.5% body fat) and women (n = 8, 23 ± 2 year, 161 ± 3 cm, 59.5 ± 6.0 kg, 26.5 ± 3.0% body fat) completed two identical heavy back squat sessions (6 × 10 at 80% 1 repetition maximum) followed by ingestion of either an alcohol (ALC; 1.09 g ethanol · kg fat-free mass(-1)) or water (PLA) drink. Blood samples were collected before exercise (PRE), and at 3 h (3 h), and 5 h (5 h) after exercise, stimulated with LPS, and analyzed for IFNγ, TNF-α, IL-1β, IL-6, IL-8, and IL-10 concentrations. RESULTS: There were no drink conditions by time effects for IFNγ, TNF-α, IL-1β, or IL-10. Regardless of condition, resistance exercise induce an increase in IFNγ, TNF-α, and IL-1β at 5 h compared to PRE but a decrease in IL-10 at 3 and 5 h compared to PRE. For ALC, IL-8 was reduced at 5 h compared to PLA. From PRE to 3 h, IL-6 was reduced for ALC but increased for PLA; resistance exercise induced an increase in IL-6 for both conditions at 5 h. CONCLUSIONS: Heavy resistance exercise increased production of IFNγ, TNF-α, IL-1β, and Il-6 and decreased production of IL-10. Alcohol ingestion after resistance exercise affected aspects of inflammatory capacity (IL-6 and IL-8 production). It appears that some of the effects previously observed for alcohol ingestion alone on the LPS-stimulated cytokine production were overwhelmed by the response to resistance exercise.
PURPOSE: To examine the effect of post-resistance exercise alcohol ingestion on lipopolysaccharide (LPS)-stimulated production of IFNγ, TNF-α, IL-1β, IL-6, IL-8, and IL-10. METHODS: Recreationally resistance-trained men (n = 10, 25 ± 3 year, 177 ± 7 cm, 83.8 ± 15.7 kg, 14.8 ± 8.5% body fat) and women (n = 8, 23 ± 2 year, 161 ± 3 cm, 59.5 ± 6.0 kg, 26.5 ± 3.0% body fat) completed two identical heavy back squat sessions (6 × 10 at 80% 1 repetition maximum) followed by ingestion of either an alcohol (ALC; 1.09 g ethanol · kg fat-free mass(-1)) or water (PLA) drink. Blood samples were collected before exercise (PRE), and at 3 h (3 h), and 5 h (5 h) after exercise, stimulated with LPS, and analyzed for IFNγ, TNF-α, IL-1β, IL-6, IL-8, and IL-10 concentrations. RESULTS: There were no drink conditions by time effects for IFNγ, TNF-α, IL-1β, or IL-10. Regardless of condition, resistance exercise induce an increase in IFNγ, TNF-α, and IL-1β at 5 h compared to PRE but a decrease in IL-10 at 3 and 5 h compared to PRE. For ALC, IL-8 was reduced at 5 h compared to PLA. From PRE to 3 h, IL-6 was reduced for ALC but increased for PLA; resistance exercise induced an increase in IL-6 for both conditions at 5 h. CONCLUSIONS: Heavy resistance exercise increased production of IFNγ, TNF-α, IL-1β, and Il-6 and decreased production of IL-10. Alcohol ingestion after resistance exercise affected aspects of inflammatory capacity (IL-6 and IL-8 production). It appears that some of the effects previously observed for alcohol ingestion alone on the LPS-stimulated cytokine production were overwhelmed by the response to resistance exercise.
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