Abstract
To observe the changes of Prohibitin1(PHB1) contents in rat brain, heart, skeletal muscle tissue and mitochondria with acute exhaustive exercise and the effects of acute exhaustive exercise on mitochondrial function in rats, to explore the relationship among PHB1 and mitochondrial function and energy metabolism. Acute exhaustive exercise model:The rats carried acute exhaustive exercise after 8 weeks of feeding. The heart, brain and skeletal muscle samples were collected and the mitochondria were collected to detect the changes of respiratory function and reactive oxygen species(ROS). The expression of PHB1 protein in tissues and mitochondria was detected by Western blot. The ATP content in the organs and the activity of complexes (ATP synthase activity) in mitochondria were measured by spectrophotometer. ① The ATP contents of brain, myocardium and skeletal muscle were decreased significantly after acute exhaustive exercise. ②The activities of complex V, respiratory control rates (RCR) and ROS in mitochondria of brain, myocardium and skeletal muscle were decreased significantly after acute exhaustive exercise, respiration rate state 4(ST4) was increased significantly, at the same time, respiration rate state 3(ST3) had no significant difference. ③ The expression of PHB1 in mitochondria of skeletal muscle was decreased significantly after acute exhaustive exercise, while there was no significant change in PHB1 in myocardial tissue and mitochondria. ④ The correlation analysis showed that the ATP contents in the brain, myocardium and skeletal muscle were positively correlated with the activity of complex V and the expression of PHB1 after acute exhaustive exercise. After acute exhaustive exercise, the mitochondrial oxidative phosphorylation was reduced, the ROS production was increased, the expression of PHB1 was decreased, the ATP content and the activity of complex V were decreased in the brain and skeletal muscle of rats. Acute exhaustive exercise reduced the expression of PHB1 in mitochondria, decreased mitochondrial function, and reduced energy metabolism.
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