Effect of Yamadazyma triangularis derived peptide XHY69AP on muscle fatigue via regulation of AMPK/PGC-1α and Nrf2/Keap1 pathways

The peptide XHY69AP was derived from Yamadazyma triangularis with a molecular weight of less than 3 kDa from our lab. The objective of this study was to explore the effect of XHY69AP on muscle fatigue in vivo. Exercising mice were given 100, 200, and 400 mg/kg∙d XHY69AP by gavage daily during four weeks of treadmill training. XHY69AP was found to increase treadmill exhaustion time and energy reserve (glycogen, adenosine triphosphate, and sodium-potassium pump), decrease the metabolite accumulations (lactic acid, urea nitrogen, lactate dehydrogenase, and creatine kinase) in serum, and attenuate morphological injury of gastrocnemius muscle. Meantime, XHY69AP reduced the malondialdehyde content and improved antioxidant enzyme activities (superoxide dismutase and glutathione peroxidase) in skeletal muscles and liver to decrease oxidative damage caused by excessive exercise. Moreover, RT-qPCR and western blotting results further verified that XHY69AP activated AMPK/PGCC-1α and Nrf2/Keap1 signal pathways to relieve muscle fatigue of mice.