Uncoupling of in vivo torque production from EMG in mouse muscles injured by eccentric contractions

1. The main objective of this study was to determine whether eccentric cont raction-induced muscle injury causes impaired plasmalemmal action potential conduction, which could explain the injury-induced excitation-contraction coupling failure. Mice were chronically implanted with stimulating electrod es on the left common peroneal nerve and with electromyographic (EMC) elect rodes on the left tibialis anterior (TA) muscle. The left anterior crural m uscles of anaesthetized mice were stimulated to perform 150 eccentric (ECC) (n = 12 mice) or 150 concentric (CON) (n = 11 mice) contractions. Isometri c torque, EMG root mean square (RMS) and M-wave mean and median frequencies were measured before, immediately after, and at 1, 3, 5 and 14 days after the protocols. In parallel experiments, nicotinic acetylcholine receptor (A ChR) concentration was measured in TA muscles to determine whether the exci tation failure elicited a denervation-like response. 2. Immediately after the ECC protocol, torque was reduced by 47-89%, while RMS was reduced by 9-21%; the RMS decrement was not different from that obs erved for the CON protocol, which did not elicit large torque deficits. One day later, both ECC and CON RMS had returned to baseline va,lues and did n ot change over the next 2 weeks. However, torque production by the ECC grou p showed a, slow recovery over that time and was still depressed by 12-30% after 2 weeks. M-wave mean and median frequencies were not affected by perf ormance of either protocol. 3. AChR concentration was elevated by 79 and 368% at 3 and 5 days, respecti vely, after the ECC protocol; AChR concentration had returned to control le vels 2 Reeks after the protocol. At the time of peak AChR concentration in the ECC protocol muscles (i.e. 5 days), AChR concentration in CON protocol muscles was not different from the control level. 4. In conclusion, these data demonstrate no major role for impaired plasmal emmal action potential conduction in the excitation-contraction coupling fa ilure induced by eccentric contractions. Additionally, a muscle injured by eccentric contractions shows a response in AChR concentration similar to a transiently denervated muscle.