The metabolic role of IL-6 produced during exercise: is IL-6 an exercise factor?
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanistic and physiological concepts
PubMed 15294041 · doi:10.1079/PNS2004338
What was done
This review summarizes physiological and biochemical evidence on muscle contraction-induced interleukin-6 (IL-6) production and release into the circulation. It evaluates the metabolic roles of muscle-derived IL-6 across other tissues (such as adipose tissue and liver) and examines how muscle glycogen content and carbohydrate intake during exercise regulate its gene expression and secretion.
What was found
The abstract provides no quantitative effect sizes or numerical values. It reports qualitatively that contracting skeletal muscle produces and releases IL-6, which acts to induce lipolysis, suppress tumor necrosis factor (TNF) production, and stimulate cortisol production. Activation of the IL-6 gene is enhanced under conditions of low muscle glycogen, while carbohydrate supplementation during exercise suppresses muscle IL-6 release, supporting the concept that muscle-derived IL-6 acts as an "exercise factor" or "myokine."
Why it matters
This paper helped establish the paradigm that skeletal muscle functions as an endocrine organ, defining muscle-secreted signaling molecules like IL-6 as "myokines" that mediate the systemic metabolic adaptations to exercise.
Limits
This is a narrative review without systematic search criteria, meta-analytic pooling, or new primary experimental data. The abstract reports only qualitative mechanistic summaries without sample sizes, effect magnitudes, or variance metrics.
Cited by
- supports IL-6 acts on adipose tissue to stimulate lipolysis and on the liver to stimulate glucose production.