Modification of myo-electric power spectrum in fatigue from 15% maximal voluntary contraction of human elbow flexor muscles, to limit of endurance: reflection of conduction velocity variation and/or centrally mediated mechanisms?

Isometric flexion of the right elbow at 15% of the maximal voluntary contraction (MVC) was maintained to the limit of endurance (elbow angle 135 degrees). The surface electromyogram (EMG) of the brachioradialis (BR) and biceps brachii (BB) muscles was recorded for calculation of conduction velocity (CV) by the cross-correlation method, and determination of median frequency (fm) and root mean square (rms) amplitude. Perceived exertion was rated for both muscles, and heart rate and blood pressure were measured. The EMG of ten brief 15% MVC contractions distributed over a 30-min recovery period was also recorded. Eleven males in their twenties volunteered for the investigation. The average endurance time was 906 (SD 419) s. Mean CV for the unfatigued muscles was 4.2 (SD 0.41) m.s-1 (BR), and 4.3 (SD 0.29) m.s-1 (BB). The contraction caused a significant decrease in CV of BR (12%, P less than 0.001) whereas CV variation of BB remained insignificant. Concurrently the mean fm of both muscles dropped to approximately 66% of their initial values and their average rms amplitudes grew by approximately 380% (BR and BB: P less than 0.001, both parameters). The 1st min of recovery lowered the rms amplitudes by approximately 60% (BR and BB: P less than 0.01), while the fm increased to approximately 88% of the initial recording (BR, P less than 0.01; BB, P less than 0.05). The accompanying small increases in CV were beyond the level of significance. Over the next 29 min a significant parallel restitution in fm and CV took place; changes in fm evidenced a simple one to one reflection of relative CV variation. A similar uncomplicated linear causality between relative changes in CV and fm was hypothesized for the endurance contraction. Consequently, the 12% CV decrease of the BR accounted for only one-third of the fatigue induced fm reduction of 33%, while two-thirds were assumed to be attributable to centrally mediated regulatory interventions in motor unit (MU) performance. Independent of contributions from the virtually unchanged CV, the fm of the BB muscle decreased by 35%; from one subject exhibiting a remarkably manifest burst-type pattern of MU activity it is argued that synchronization/grouping of MU firing predominantly determined the power redistribution in the BB spectrum.