Study of Mechanism on Muscle Injury Induced by Static Load

摘要

In order to study the mechanisms of muscle injury induced by static load the intracellular Ca~(2+) concentrations, Ca~(2+)-Mg~(2+)-ATPase activity in mitochondria (MR) and sarcoplasmic reticulum (SR), content of malondialdehyde(MDA), activity of serum creatine kinase(CK) and alterations of energy supply were measured after static load. The results showed that muscular ATP content in treated groups decreased on the 4th day,6th day and 8th day respectively,and was significantly lower than that of controls on the 8th day( P < 0.05). The content of PCr and glycogen showed a tendency of decreasing, but PCr was significantly lower than that of control group on the 6th day and 8th day(P<0.05, P<0. 01) while glycogen was significantly lower on the 8th day. The activity of serum CK was significantly higher than that of control group during the whole experiment period( P < 0. 01) . Intracellular Ca~(2+) concentration increased significantly on the 4th day(P<0.05). The content of Ca~(2+) in both SR and MR decreased but that of SR was significantly lower on the 6th day and 8th day(P<0.01) . The activity of Ca~(2+) -Mg~(2+) -ATPase in MR and SR decreased significantly on the 6th day and 8th day(P<0. 05). The MDA content in MR increased on the 4th day while that of SR increased from the 6th day respectively, both showed significant difference from the controls(P<0. 01, P<0. 05). The results of those biochemical parameters demonstrated that in the process of static load the decrement of energy supply, alterations of intracellular Ca~(2+) homeostasis, and enhancement of lipid hyperoxidation may play etiologic roles in muscle injury. However, relationships between those noxious factors remain to be further studied.