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Updated: Aug 18, 2026

Treatment of Ligament Constructs with Exercise-conditioned Serum: A Translational Tissue Engineering Model
Published on: June 11, 2017
Increased IGF mRNA in human skeletal muscle after creatine supplementation
Louise Deldicque1, Magali Louis, Daniel Theisen
1Department of Physical Education and Rehabilitation, Faculty of Medicine, Catholic University of Louvain, Louvain-la-Neuve, Belgium.
Purpose:
We hypothesized that creatine supplementation would facilitate muscle anabolism by increasing the expression of growth factors and the phosphorylation of anabolic signaling molecules; we therefore tested the responses of mRNA for IGF-I and IGF-II and the phosphorylation state of components of anabolic signaling pathways p70(s6k) and 4E-BP1 to a bout of high-intensity resistance exercise after 5 d of creatine supplementation.
Methods:
In a double-blind cross-over design, muscle biopsies were taken from the m. vastus lateralis at rest and 3 and 24 h postexercise in subjects who had taken creatine or placebo for 5 d (21 g x d(-1)). For the first 3 h postexercise, the subjects were fed with a drink containing maltodextrin (0.3 g x kg(-1) body weight x h(-1)) and protein (0.08 g x kg(-1) body weight x h(-1)).
Results:
After creatine supplementation, resting muscle expressed more mRNA for IGF-I (+30%, P < 0.05) and IGF-II (+40%, P = 0.054). Exercise caused an increase by 3 h postexercise in IGF-I (+24%, P < 0.05) and IGF-II (+48%, P < 0.05) and by 24 h postexercise in IGF-I (+29%, P < 0.05), but this effect was not potentiated by creatine supplementation. The phosphorylation states of p70(s6k) and 4E-BP1 were not affected by creatine at rest; phosphorylation of both increased (150-400%, P < 0.05) to similar levels under placebo and creatine conditions at 3 h postexercise plus feeding. However, the phosphorylation state of 4E-BP1 was higher in the creatine versus placebo condition at 24 h postexercise.
Conclusion:
The increase in lean body mass often reported after creatine supplementation could be mediated by signaling pathway(s) involving IGF and 4E-BP1.

