Abstract
Skeletal muscles exhibit high plasticity, such as overload-induced hypertrophy or immobilization-induced atrophy. During sports, skeletal muscle hypertrophy is induced by training to improve performance. Spermidine is a type of polyamine and oral intake of spermidine exerts many beneficial effects on health through various mechanisms, such as promoting autophagy and improving mitochondrial function. In a recent study, we showed that spermidine intake activates mTOR signaling and significantly increases the mean fiber cross-sectional area (CSA) 14 days after injury. This suggests that spermidine promotes the anabolic growth of differentiated muscle (i.e., muscle hypertrophy); however, calorie restriction, which has been reported to have effects on the same molecular mechanisms as spermidine (promoting autophagy and improving mitochondrial function), promotes skeletal muscle regeneration, while inhibiting skeletal muscle hypertrophy. Therefore, we evaluated the effect of spermidine intake on skeletal muscle hypertrophy in mice using a synergistic ablation-induced muscle hypertrophy model. Our results showed that spermidine intake significantly decreased mean myofiber of CSA, but this was not consistent with the change in skeletal muscle wet weight. We also analyzed autophagy, mTOR signaling, inflammation, and mitochondria, but no significant effects of spermidine intake were observed at most protein expression levels. Therefore, spermidine intake does not affect overload-induced skeletal muscle hypertrophy, and even if it does, the effect is suppressive.