Effect of amino acids on IGF1 gene expression in human myotubes and skeletal muscle
Egor M.Lednev Growth Hormone & IGF Research Volumes 53–54, August–October 2020,
Highlights
• In human myotubes, amino acids (AAs) increase expression of IGF1.
• In athletes, long-term AAs administration increased blood levels of IGF1 (~50%).
• Long-term AAs administration is associated with a decrease in muscle membrane damage.
Objective
Insulin-like growth factor I (IGF1) is an important regulator of collagen and extracellular matrix protein expression. We aimed to evaluate the effect of amino acids (AAs) on expression of IGF1 and IGF1-dependent genes in human myotubes and skeletal muscle and supposed that AAs administration increases IGF1 levels in blood and expression of IGF1 and IGF1-dependent genes in trained skeletal muscle, thereby reducing training-induced muscle damage.
Design
Human myotubes were incubated with Arg and Leu for 24 h. Then, the effects of long-term branched chain AAs administration (10 weeks, 0.1 g/kg body mass/day) to volunteers (six subjects per AAs and placebo groups) performing large training volumes regularly (cross country skiers, training twice a day) were examined.
Results
Incubating the myotubes with AAs increases expression of IGF1 mRNA isoforms and IGF1 secretion by 2–3 times. In athletes, long-term AAs administration increased basal blood levels of IGF1 (~50%) and expression of IGF1Ea mRNA slightly in skeletal muscle. There is no marked increase in expression of COL1A1, COL3A1, COL5A1, and LOX genes in skeletal muscle after AAs administration. However, expression of these genes in the combined group (placebo + AAs; n = 12) significantly correlated with the expression of IGF1Ea mRNA in muscle and did not correlate with IGF1 levels in the blood.
Conclusions
AAs administration increases IGF1 expression in vitro and in vivo. To obtain more pronounced changes in expression of IGF1 and IGF1-dependent genes in skeletal muscle, it may be necessary to increase the dose and/or duration of AAs administration.