Effects of prolonged exhaustive swimming on myocardial mitochondria membrane and free calcium of matrix in rats

Por: Lijuan Mao.

Athens 2004: Pre-olympic Congress

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Introduction

Exhaustive exercise appears to increase reactive oxygen species, which can result in damage to cells. The purpose of the present study was to investigate the effects of prolonged exhaustive swimming on myocardial mitochondria membrane and free calcium of matrix.

Methods

Male Spragu-Dawley rats (200-250g, n=18) were randomly assigned to an exhaustive swimming group or control group, Sulfhydryl (-SH), gluththione (GSH) of myocardial mitochondrion were separately measured by DTNB spectrophotometrically and a high-performance liquid chromatography method using COPC electrode, Myocardial mitochondrion phosphlipase A2 (PLA2) was measured according to Chen sifeng et al, Free calcium of myocardial mitochondrion was investigated according to Gunter et al.

Results

The results showed that -SH, GSH and Ca2+ content in myocardial mitochondrion after exhaustive exercise were significantly lower than that of the control group. Myocardial mitochondrion phosphlipase A2 (PLA2) was significantly increased after the exhausting exercise.

Discussion

According to results, the relationship between the oxidant reduction reaction of exercise induced reactive oxygen species, the changes of myocardial mitochondria membrane structure and the free calcium of matrix was discussed. It is suggested that the increase of PLA2 activity might be a key parameter of fatigue after prolonged exhaustive exercise. By means of further observation the molecules mechanism of prolonged exercise induced fatigue appearance could be further deeply understood.

References

[1] L. L., F. W. Stratman, and H.A.Larday. Enzymatic down regulation with exercise in rat skeletal muscle. Arch. Biochem. Biophys 263: 137-149, 1988
[2] Beatrice M. C., D.L.Stiers and D. R. Pfeiffer. The role of glutathione in retetention of Ca2+ by liver mitochondria. J. Biol.Chem. 259(2)1279-1289,1984
[3] Gutter, T.E., D. R. Pfeiffer Mechanisms by which mitochondria transpott cacium. Am. J. Physiol. 258:775-786, 1990.
[4] Zamzmi. N., Susin S.A., Marchectti. P., et al Mitochiondrial control of nuclear apoptosis. J. Exp. Med.,183:1533-1544,1996.

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