Undaria pinnatifidaextract feeding increases exercise endurance and skeletal muscle mass by promoting oxidative muscle remodeling in mice

Abstract

Dietary habits can alter the skeletal muscle performance and mass, and Undaria pinnatifida extracts are considered a potent candidate for improving the muscle mass and function. Therefore, in this study, we aimed to assess the effect of U pinnatifida extracts on exercise endurance and skeletal muscle mass. C57BL/6 mice were fed a 0.25% U pinnatifida extract‐containing diet for 8 weeks. U pinnatifida extract‐fed mice showed increased running distance, total running time, and extensor digitorum longus and gastrocnemius muscle weights. U pinnatifida extract supplementation upregulated the expression of myocyte enhancer factor 2C, oxidative muscle fiber markers such as myosin heavy chain 1 (MHC1), and oxidative biomarkers in the gastrocnemius muscles. Compared to the controls, U pinnatifida extract‐fed mice showed larger mitochondria and increased gene and protein expression of molecules involved in mitochondrial biogenesis and oxidative phosphorylation, including nuclear respiratory factor 2 and mitochondrial transcription factor A. U pinnatifida extract supplementation also increased the mRNA expression of angiogenesis markers, including VEGFa, VEGFb, FGF1, angiopoietin 1, and angiopoietin 2, in the gastrocnemius muscles. Importantly, U pinnatifida extracts upregulated the estrogen‐related receptor γ and peroxisome proliferator‐activated receptor gamma co‐activator 1‐alpha (PGC‐1α)/AMP‐activated protein kinase (AMPK)/sirtuin 1 (SIRT1) networks, which are partially increased by fucoxanthin, hesperetin, and caffeic acid treatments. Collectively, U pinnatifida extracts enhance mitochondrial biogenesis, increase oxidative muscle fiber, and promote angiogenesis in skeletal muscles, resulting in improved exercise capacity and skeletal muscle mass. These effects are attributable to fucoxanthin, hesperetin, and caffeic acid, bioactive components of U pinnatifida extracts.

Sesamol Reverses Myofiber-Type Conversion in Obese States via Activating the SIRT1/AMPK Signal Pathway

“…Skeletal muscle fibers display a significant phenotypic plasticity in response to several stimulations, including hormones, exercise, and nutritional status. , Skeletal muscle-fiber-type conversion from type I toward type II can be induced by obesity, resulting in ectopic lipid deposition and insulin resistance in skeletal muscle, eventually accelerating systemic metabolic abnormalities . Different studies observed that the SIRT1/AMPK signal pathway was sensitive to nutritional status and regulated energy metabolism and the myofiber-type conversion. , According to the past research works, the SIRT1/AMPK signal pathway action stimulates glucose uptake, lipid oxidation, and mitochondrial biogenesis, and prompts myofiber-type switching from type II toward type I, consequently elevating the energy consumption metabolism, insulin sensitivity, and exercise endurance capacity. − Hence, the stimulation of the SIRT1/AMPK signal pathway in skeletal muscle might be a feasible curative strategy for obesity and its relevant diseases.…”

Chemical Composition, Antioxidant, and Anti-Inflammatory Activity of Essential Oil from Omija (Schisandra chinensis (Turcz.) Baill.) Produced by Supercritical Fluid Extraction Using CO2

“…For western blot analysis [ 32 ], RAW 264.7 cells (5 × 10 5 cells/well) were seeded into a 6-well plate and cultured for 24 h. After then, various concentration (12.5–100 μg/mL) of OMEO were treated with LPS (1 μg/mL) in each well for additional 24 h. Total protein was extracted using RIPA buffer supplemented with protease and phosphatase inhibitor (Thermo Fisher Scientific). The concentration of protein was determined using BCA method.…”

Estrogen-related Receptor Signaling in Skeletal Muscle Fitness

“…orientalis) that promote myofiber type and metabolic remodeling to an aerobic phenotype in the skeletal muscle simultaneously induce the expression of ERR and/or ERR transcripts in the skeletal muscle [56][57][58][59]. However, the detailed transcriptional mechanisms through which these compounds induce ERRs are lacking, as well as whether ERRs are responsible for muscle remodeling by the aforementioned compounds is unclear.…”