Abstract
Past contraction-induced skeletal muscle injury reduces the degree of subsequent injury; this phenomenon is called the "repeated bout effect (RBE)." This study addresses the mechanisms underlying the RBE, focusing on primary calcium-dependent injury pathways. Wistar rats were subdivided into single injury (SI) and repeated injury (RI) groups. At age 10 weeks, the right gastrocnemius muscle in each rat in the RI group was subjected to strenuous eccentric contractions (ECs). Subsequently, mild ECs were imposed on the same muscle of each rat at 14 weeks of age in both groups. One day after the exercise, the RI group showed a lower strength deficit than did the SI group, and neither group manifested any increase in membrane permeability. The concentration of protein carbonyls and activation of total calpain increased after ECs given at the age of 14 weeks. Nonetheless, these increases were lower in the RI group than in the SI group. Furthermore, calcium-dependent autolysis of calpain-1 and calpain-3 in the RI group was diminished as compared with that in the SI group. Although peak ankle joint torque and total force generation during ECs at the age of 14 weeks were similar between the two groups, phosphorylation of JNK (Thr183 /Tyr185 ), an indicator of mechanical stress applied to a muscle, was lower in the RI group than in the SI group. These findings suggest that activation of the primary calcium-dependent injury pathways is attenuated by past injurious exercise, and mechanical stress applied to muscle fibers during ECs may decrease in the RBE.