Dityrosine (Dityr) has been detected in commercial food
as a product
of protein oxidation and has been shown to pose a threat to human
health. This study aims to investigate whether Dityr causes a decrease
in lactic acid metabolism in the gastrocnemius muscle during endurance
exercise. C57BL/6 mice were administered Dityr or saline by gavage
for 13 weeks and underwent an endurance exercise test on a treadmill.
Dityr caused a severe reduction in motion displacement and endurance
time, along with a significant increase in lactic acid accumulation
in the blood and gastrocnemius muscle in mice after exercise. Dityr
induced significant mitochondrial defects in the gastrocnemius muscle
of mice. Additionally, Dityr induced serious oxidative stress in the
gastrocnemius muscle, accompanied by inflammation, which might be
one of the causes of mitochondrial dysfunction. Moreover, significant
apoptosis in the gastrocnemius muscle increased after exposure to
Dityr. This study confirmed that Dityr induced oxidative stress in
the gastrocnemius muscle, which further caused significant mitochondrial
damage in the gastrocnemius muscle cell, resulting in decreased capacity
of lactic acid metabolism and finally affected performance in endurance
exercise. This may be one of the possible mechanisms by which highly
oxidized foods cause a decreased muscle energy metabolism.