EXCITATION FAILURE IN ECCENTRIC CONTRACTION-INDUCED INJURY OF MOUSE SOLEUS MUSCLE

1. Histological evidence suggests that the force deficit associated wi th eccentric contraction-induced muscle injury is due to structural da mage to contractile elements within the muscle fibre. Alternatively, t he force deficit could be explained by an inability to activate the co ntractile proteins. It was the objective of this study to investigate the latter possibility. 2. Mouse soleus muscles were isolated, placed in an oxygenated Krebs-Ringer buffer at 37-degrees-C, and baseline mea surements were made. The muscle then performed one of three contractio n protocols: (1) twenty eccentric (n = 10 muscles); (2) ten eccentric (n = 12); or (3) twenty isometric (n = 10) contractions. At the end of the injury protocol, measurements were made during performance of a p assive stretch, twitch and tetanus. Next, force was recorded during ex posure of the muscle to buffer containing 50 mm caffeine. 3. Decrement s in maximal isometric tetanic force (P0) observed for muscles in the twenty eccentric, ten eccentric, and twenty isometric contraction prot ocols were 42-6 +/- 4.2, 20.0 +/- 2.3 and 3-9 +/- 2.4%, respectively. However, the caffeine-elicited forces in muscles from the three protoc ols were not different when corrected for initial differences in P0 (6 4-9 +/- 1.3, 64.2 +/- 2.1 and 68.9 +/- 2.5% of pre-injury P0). The pea k caffeine-elicited force Was 118.4 +/- 8.6% of post-injury P0 for the muscles in the twenty eccentric contraction protocol, which was signi ficantly different from that observed for the other protocols (71.8-80 .2 % post-injury P0). These findings indicate that the force deficit i n this muscle injury model results from a failure of the excitation pr ocess at some step prior to calcium (Ca2+) release by the sarcoplasmic reticulum. 4. In an attempt to locate the site of failure, intracellu lar measurements were made in injured muscles to test whether injury t o the sarcolemma might have resulted in a shift of the resting membran e potential of the muscle fibre. However, microelectrode measurements of resting membrane potential for muscles in the twenty eccentric cont raction protocol (-74.4 +/- 0.6 mV) were not different from muscles in the twenty isometric contraction protocol (-73.4 +/- 1.0 mV). These d ata suggest that membrane resting conductances were normal and are com patible with the idea that the ability of the injured fibres to conduc t action potentials was probably not impaired.