Autocrine signaling may regulate exercise-induced interleukin-6 release from human skeletal muscle.
Jonas Osted Hvidemose, Beckey Trinh, Alexandra Vassilieva et al.
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In 30 seconds
This randomized, double-blind, placebo-controlled trial examined tissue exchange of interleukin-6 (IL-6) and soluble IL-6 receptor (sIL-6R) during moderate-intensity cycling in 30 young, well-trained men. Arteriovenous measurements were made across the leg, splanchnic region, and brain, with or without pharmacological IL-6 receptor blockade. Leg IL-6 release rose during exercise in both groups and was significantly greater with blockade, consistent with possible autocrine regulation. The splanchnic bed predominantly cleared IL-6 under control conditions, while the exercising leg released sIL-6R.
Key findings
- Exercise increased leg IL-6 release in both groups; release was significantly augmented by IL-6 receptor blockade.
- Under control conditions, the splanchnic bed was the predominant site of IL-6 clearance; blockade shifted its net balance from uptake to release.
- The exercising leg was a source of circulating sIL-6R during exercise, with no consistent exchange across the splanchnic bed or brain.
Why it matters
The findings help clarify how exercise-related IL-6 availability may be shaped by both muscle release and splanchnic clearance. They also suggest that IL-6 signaling can influence local muscle IL-6 release and that exercising muscle contributes to circulating sIL-6R. These tissue-specific mechanisms provide context for interpreting changes in circulating cytokines during exercise.
What to keep in mind
The study included only young, well-trained men performing moderate-intensity cycling, so the findings may not generalize to other populations or exercise conditions.