Effect of Intense Exercise on Inflammatory Cytokines and Growth Mediators in Adolescent Boys

Abstract

Objective. Exercise can enhance growth and development in children, but recent investigations have revealed an intriguing paradox. Namely, the early (4–5 weeks) response to training programs in children lead to a catabolic, growth hormone (GH)-resistant state rather than the expected anabolic activation of the GH→insulin-like growth factor-I (IGF-I) axis. This paradox led us to hypothesize that single bouts of exercise in children could stimulate proinflammatory cytokines known to inhibit directly anabolic activity of the GH→IGF-1 axis (interleukin [IL]-6, IL-1β, and tumor necrosis factor-α [TNF-α]). Methods. Eleven healthy high school-age boys, age 14 to 18.5 years, performed a single, typical, 1.5-hour wrestling practice session. Blood was sampled before and after the session. Results. We found significant decreases in anabolic mediators: total IGF-I (−11.2 ± 2.3%), bound IGF-I (−11.2 ± 2.4%), and insulin (−42 ± 10%. However, there was no change in unbound IGF-I. Remarkable increases were found in proinflammatory cytokines IL-6 (795 ± 156%), TNF-α (30 ± 12%), and IL-1β (286 ± 129%) and in IGF-binding protein-1 (835 ± 234%), which itself is stimulated by inflammatory cytokines and is known to inhibit IGF-I. Evidence for compensatory mechanisms to counter the antianabolic inflammatory response to acute exercise were also noted: IL-1ra increased (80 ± 20%) and IGF-binding protein-3 proteolysis (which can maintain unbound, biologically active IGF-I despite losses in total IGF-I) increased significantly (101 ± 39%) as well. Conclusions. These data demonstrate that an intense exercise bout in male adolescents leads to reductions in anabolic mediators and profound increases in inflammatory cytokines. This might explain the development of what seems to be a paradoxical catabolic state in the initial phases of exercise training programs.