文摘
Introduction Oxidative stress plays a pivotal role in the intense exercise-induced myocardium injury, and mitochondrial compartment is presumed as the main source and susceptible target of intracellular reactive oxygen species (ROS). Purpose The objective of this study was to evaluate the protective effect of quercetin, a naturally occurring flavonoids possessing antioxidant effect on repeated intense exercise-induced mitochondrial oxidative stress and dysfunction. Methods Adult male BALB/C mice were treated by quercetin (100?mg/kg bw) for 4?weeks and subjected to the exercise protocol on a treadmill (28?m/min at 5° slope for 90?min) for seven consecutive days concurrently at the fourth week. Results Intense exercise in mice resulted in the leakage of creatine kinase-MB (increased from 221.5?±?33.8 to 151.1?±?19.1?U/l, P?<?0.01) and ultrastructural malformation mainly evidenced by disrupted myofibrils and swollen mitochondria, which was overtly attenuated by quercetin prophylaxis. Quercetin pretreatment evidently alleviated mitochondrial oxidative stress by inhibiting glutathione depletion and aconitase inactivation, ROS over-generation, and lipid peroxidation in cardiac mitochondria of intense exercise mice. Furthermore, mitochondrial dysfunction manifested by decreased mitochondrial membrane potential (68.6?±?7.6 versus 100.0?±?7.7?%, P?<?0.01) and respiratory control ratio (5.03?±?0.55 versus 7.48?±?0.71, P?<?0.01) induced as a consequence of acute exercise was markedly mitigated by quercetin precondition. Conclusion Quercetin protects mouse myocardium against intense exercise injury, especially ultrastructural damage and mitochondrial dysfunction, probably through its beneficial antioxidative effect, highlighting a promising strategy for over-training injury by naturally occurring phytochemicals.