The main purpose of this study was to characterise neuromuscular fatigue induced by 30 contractions of the knee extensor muscles evoked by electromyostimulation (EMS). Twelve healthy subjects were tested before and after a typical EMS session (frequency: 75 Hz, on-off ratio: 6.25 s on-20 s off) used for quadriceps femoris muscle strengthening. Surface electromyographic (EMG) activity and torque obtained during maximal voluntary and electrically evoked contractions were analysed to distinguish peripheral from central fatigue. Maximal voluntary torque of the knee extensor muscles decreased approximately 20 % (p < 0.001) following EMS. In the same way, peak torque associated to single (p < 0.05) and paired (p < 0.001) stimuli as well as M-wave amplitude (p < 0.05) significantly decreased as a result of EMS. The raw EMG activity of both vastus lateralis and rectus femoris muscle recorded during maximal voluntary isometric contraction significantly decreased after the session (-17.3 and -14.5 %, respectively) whereas no changes were observed when EMG signals were normalised to respective M-wave amplitudes. Similarly, voluntary activation estimated by using the twitch interpolation technique was unchanged following EMS. In conclusion, a typical session of EMS of the knee extensor muscles mainly induced neuromuscular propagation failure while excitation-contraction coupling and neural mechanisms were not significantly affected. It is recommended to interpret surface EMG data together with the corresponding M wave, at least for the knee extensor muscles, in order to distinguish peripheral from central causes of fatigue.
Introduction: Myotonia congenita (MC) is caused by congenital defects in the muscle chloride channel CLC-1. This study used muscle velocity recovery cycles (MVRCs) to investigate how membrane function is affected. Methods: MVRCs and responses to repetitive stimulation were compared between 18 patients with genetically confirmed MC (13 recessive, 7 dominant) and 30 age-matched, normal controls. Results: MC patients exhibited increased early supernormality, but this was prevented by treatment with sodium channel blockers. After multiple conditioning stimuli, late supernormality was enhanced in all MC patients, indicating delayed repolarization. These abnormalities were similar between the MC subtypes, but recessive patients showed a greater drop in amplitude during repetitive stimulation. Conclusions: MVRCs indicate that chloride conductance only becomes important when muscle fibers are depolarized. The differential responses to repetitive stimulation suggest that, in dominant MC, the affected chloride channels are activated by strong depolarization, consistent with a positive shift of the CLC-1 activation curve.
Non-invasive excitability tests have been developed to appraise axonal membrane properties in peripheral nerves and are contributing to our understanding of neuropathies and neuronopathies. These techniques have been adapted to in vivo and in vitro rat models, but little data are available on mice, although mice provide more transgenic models of neurological disorders. This study was therefore undertaken to assess the suitability of mice to model human nerve excitability measurements and to document changes during maturation. Female mice, aged 4-19 weeks, were recorded under isoflurane anesthesia. Electrical stimuli were applied via surface electrodes to the caudal motor nerve and compound muscle action potentials (CMAPs) recorded from the tail with needle electrodes. Then, the sciatic nerve was stimulated above the ankle and CMAPs recorded from plantar muscles. The method was only minimally invasive, enabling the same animal to be tested up to eight times at weekly intervals. As in human studies, the multiple excitability program recorded stimulus-response, strength-duration, and current-threshold relationships; threshold electrotonus; and recovery cycle. The response waveforms were qualitatively similar to those from human axons. This resemblance was closer for the caudal nerve, which also showed more marked changes with age. Early hyperpolarizing electrotonus fell sharply from weeks 4 to 13 (p < 0.0001), while a progressive increase in superexcitability occurred throughout the period studied (p < 0.001). We conclude that multiple measures of nerve excitability can be performed reliably in mice in vivo, preferentially on the tail, and are suitable for longitudinal studies, but age matching is critical for younger animals.
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