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In order to study the mechanisms of exercise-induced exhaustion and porteinuria, the experiment was designed to investigate exhaustive exercise-induced oxidative stress on the functions of kidney mitochondria. 30 male Sprague-Dawley rats were randomly divided into four groups control group, n = 7; immediate postexercise group, n = 7; 1 h postexercise group, n = 8 and 24 h postexercise group , n = 8, and the changes were measured that the content of MDA ATP syntheses activity and total calcium in the kidney mitochondria in the different phases were observed. The results are as follows: when compared with control group , the MDA content significantly rises immediately after exercise (p < 0.05) and it is the same to 1 h and 24 h postexercise group (p < 0.01); The ATP synthesis activity of kidney mitochondria of immediate postexercise, 1 h postexercise group individually declines extremely as compared with control group (p < 0.01) while it does not recover to a normal value 24 h after exercise; The mitochondria total calcium of 1 h and 24 h groups is markedly higher than the control group (p < 0.01; p < 0.05). The findings suggest that exhaustive swimming can lead to an increase of mitochondria lipid peroxidation, a decrease of ATP synthesis activity of kidney mitochondria and irregularity of the steady state of the mitochondria calcium while the mitochondria calcium accumulation probably results in the uncoupling of intramitochondria oxidative phosphorylation and anormality of kidney functions. It might be one of the important reasons of exercise-induced exhaustion and porteinuria.