Cross-correlating two surface EMG signals detected at two different locations along the path of flow of action potential enables the measurement of the muscle fiber average conduction velocity in those active motor units monitored by the electrodes. The position of the peak of the cross-correlation function is the time delay between the two signals and hence the velocity may be deduced. The estimated velocity using this technique has been observed previously to depend on the location of the electrodes on the muscle surface. Different locations produced different estimates. In this paper we present a measurement system, analyze its inherent inaccuracies and use it for the purpose of investigating the reliability of measurement of conduction velocity from surface EMG. This system utilizes EMG signals detected at a number of locations on the biceps brachii, when under light tension, to look for any pattern of variations of velocity as a function of location and time. It consists of a multi-electrode unit and a set of eight parallel on-line correlators. The electrode unit and the parallel correlators ensure that these measurements are carried out under the same physical and physiological conditions of the muscle. Further, the same detected signals are used in different measurement configurations to try to understand the reasons behind the observed variations in the estimated velocity. The results obtained seem to suggest that there will always be an unpredictable random component superimposed on the estimated velocity, giving rise to differences between estimates at different locations and differences in estimates with time at the same location. Many factors contribute to this random component, such as the non-homogeneous medium between the muscle fibers and the electrodes, the non-parallel geometry and non-uniform conduction velocity of the fibers, and the physical and physiological conditions of the muscle. While it is not possible to remove this random component completely from the measurement, the user must be aware of its presence and how to reduce its effects.
Compelling evidences posited that high level of saturated fatty acid gives rise to mitochondrial dysfunction and inflammation in the development of insulin resistance in skeletal muscle. Celastrol is a pentacyclic triterpenoid derived from the root extracts of Tripterygium wilfordii that possesses potent anti-inflammatory properties in a number of animal models with metabolic diseases. However, the cellular mechanistic action of celastrol in alleviating obesity-induced insulin resistance in skeletal muscle remains largely unknown. Therefore, the present investigation evaluated the attributive properties of celastrol at different concentrations (10, 20, 30 and 40nM) on insulin resistance in C2C12 myotubes evoked by palmitate. We demonstrated that celastrol improved mitochondrial functions through significant enhancement of intracellular ATP content, mitochondrial membrane potential, citrate synthase activity and decrease of mitochondrial superoxide productions. Meanwhile, augmented mitochondrial DNA (mtDNA) content with suppressed DNA oxidative damage were observed following celastrol treatment. Celastrol significantly enhanced fatty acid oxidation rate and increased the level of tricarboxylic acid (TCA) cycle intermediates in palmitate-treated cells. Further analysis revealed that the improvement of glucose uptake activity in palmitate-loaded myotubes was partly mediated by celastrol via activation of PI3K-Akt insulin signaling pathway. Collectively, these findings provided evidence for the first time that the protection from palmitate-mediated insulin resistance in C2C12 myotubes by celastrol is likely associated with the improvement of mitochondrial functions-related metabolic activities.