Effect of dietary L-theanine supplementation on skeletal muscle fiber type transformation in vivo.

The aim of this study was to investigate the effect of dietary L-theanine supplementation on skeletal muscle fiber type transition in mice. Our data indicated that dietary 0.15% L-theanine supplementation significantly increased the mRNA expression levels of muscle fiber type related genes (MyHC I, MyHC IIa, PGC-1α, Sirt1, Tnnt1, Tnnc1, Tnni1, MEF2C) and the protein expression levels of MyHC IIa, myoglobin, PGC-1α, Sirt1 and Troponin I-SS, but significantly decreased the mRNA and protein expression levels of MyHC IIb. Dietary 0.15% L-theanine supplementation significantly increased the activities of SDH and MDH and decreased the activity of LDH. Furthermore, immunofluorescence demonstrated that dietary 0.15% L-theanine supplementation significantly increased the percentage of type I fibers, and significantly decreased the percentage of type II fibers. In addition, we found that dietary 0.15% L-theanine supplementation increased the fatigue-resistant, antioxidant capacity, mitochondrial biogenesis, and function in skeletal muscle of mice. Furthermore, dietary 0.15% L-theanine supplementation significantly increased the mRNA levels of prox1, CaN and NFATc1, the protein levels of prox1, CNA and NFATc1 and the activity of CaN in GAS muscle when compared with the control group. These results indicated that dietary L-theanine supplementation promoted skeletal muscle fiber transition from type II-type I, which might be via activation of CaN and/or NFATc1 signaling pathway.

Anti-fatigue effect of quercetin on enhancing muscle function and antioxidant capacity.

The aim of this study was to evaluate the anti-fatigue effect of quercetin in mice. Three-week-old male BALB/c mice, fed with/without 0.005% quercetin for 6 weeks, were randomly divided into two experimental sets (loaded swimming and non-loading swimming tests). Our data indicated that dietary quercetin supplementation prolonged the exhaustive swimming time. In addition, lactic acid (LD) and blood urea nitrogen (BUN) levels, lactate dehydrogenase (LDH) and creatine kinase (CK) activities in serum were significantly decreased, while the levels of non-esterified free fatty acids (NEFA) in serum and the content of liver glycogen and muscle glycogen were significantly enhanced in dietary quercetin supplementation group. Furthermore, dietary quercetin supplementation significantly enhanced the glutathione peroxidase (GPx) and catalase (CAT) activities in serum, liver and gastrocnemius muscle and enhanced the total superoxide dismutase (T-SOD) activity in gastrocnemius muscle, but decreased the malondialdehyde (MDA) content and reactive oxygen species (ROS) level. Meanwhile, dietary quercetin supplementation affected the mRNA expression of regulators factors involved in muscle damage and inflammation, glucose metabolism and gluconeogenesis, muscle mitochondrial fatty acid ß-oxidation and antioxidant related genes. Together, our data confirm that dietary quercetin supplementation can promote anti-fatigue capacity by promoting the antioxidant capacity and glycogen storage, as well as enhancing muscle function. PRACTICAL APPLICATIONS: Quercetin is a natural polyphenolic flavonoid substance. Here we confirm that quercetin has anti-fatigue activity. Our study indicates that quercetin may be used as natural anti-fatigue functional food or drugs.

Quercetin regulates skeletal muscle fiber type switching via adiponectin signaling.

This study aimed to investigate the role and underlying molecular mechanism of quercetin in regulating skeletal muscle fiber type transition. We found that dietary quercetin supplementation in mice significantly increased oxidative fiber-related gene expression, slow-twitch fiber percentage and succinic dehydrogenase (SDH) activity. By contrast, quercetin decreased lactate dehydrogenase (LDH) activity, fast MyHC protein expression, fast-twitch fiber percentage, and MyHC IIb mRNA expression. Furthermore, quercetin significantly increased serum adiponectin (AdipoQ) concentration, and the expression levels of AdipoQ and AdipoR1. However, inhibition of adiponectin signaling by AdipoR1 siRNA significantly attenuated the effects of quercetin on muscle fiber type-related gene expression, the percentages of slow MyHC-positive and fast MyHC-positive fibers, and metabolic enzyme activity in C2C12 myotubes. Together, our data indicated that quercetin could promote skeletal fiber switching from glycolytic type II to oxidative type I through AdipoQ signaling.