Electromechanical delay revisited using very high frame rate ultrasound

Abstract

Electromechanical delay (EMD) represents the time lag between muscle activation and muscle force production and is used to assess muscle function in healthy and pathological subjects. There is no experimental methodology to quantify the actual contribution of each series elastic component structures that together contribute to the EMD. We designed the present study to determine, using very high frame rate ultrasound (4 kHz), the onset of muscle fascicles and tendon motion induced by electrical stimulation. Nine subjects underwent two bouts composed of five electrically evoked contractions with the echographic probe maintained over 1) the gastrocnemius medialis muscle belly (muscle trials) and 2) the myotendinous junction of the gastrocnemius medialis muscle (tendon trials). EMD was 11.63 +/- 1.51 and 11.67 +/- 1.27 ms for muscle trials and tendon trials, respectively. Significant difference (P < 0.001) was found between the onset of muscle fascicles motion (6.05 +/- 0.64 ms) and the onset of myotendinous junction motion (8.42 +/- 1.63 ms). The noninvasive methodology used in the present study enabled us to determine the relative contribution of the passive part of the series elastic component (47.5 +/- 6.0% of EMD) and each of the two main structures of this component (aponeurosis and tendon, representing 20.3 +/- 10.7% and 27.6 +/- 11.4% of EMD, respectively). The relative contributions of the synaptic transmission, the excitation-contraction coupling, and the active part of the series elastic component could not be directly quantified with our results. However, they suggest a minor role of the active part of the series elastic component that needs to be confirmed by further experiments.

New insights on contraction efficiency in patients with Duchenne muscular dystrophy

“…Using very high frame rate ultrasound, the present study demonstrates that the delay between electrical stimulation and onset of muscle fascicle shortening (Dm) is not different in DMD patients compared with healthy controls. As this delay is principally attributed to synaptic transmission and excitation-contraction coupling (15,26), this result suggests that the efficiency of the excitation-contraction coupling might be affected independently of its duration. This is in line with a previous animal study showing that the time to release the maximal quantity of Ca 2ϩ is not affected (Ϸ4 ms; Ref.…”

“…As previously described in Lacourpaille et al (18,19), the detection of the onset of both muscle fascicle motion and external force production was defined visually. We defined the EMD as the time lag between the onset of the electrical stimulation (i.e., artifact of stimulation) and the onset of force production (15,18,19,26). Then delays between the onset of electrical stimulation and the onset of muscle fascicle motion (Dm) and between the onset of fascicle motion and the onset of force production (Tm) were calculated (Fig.…”

“…The relative contribution of both electrochemical (synaptic transmission, excitation-contraction coupling) and mechanical components (force transmission) to EMD has been recently characterized in humans using very high frame rate ultrasound (15,18,19,26) and mechanomyography (5,30,33). More precisely, the delay between muscle electrical stimulation and the onset of muscle fascicle motion is mainly attributed to electrochemical processes [referred to as time delay for muscle contraction (Dm)].…”

Repeated exercise stress impairs volitional but not magnetically evoked electromechanical delay of the knee flexors

“…Electromechanical delay is comprised of several events and the primary determinant of this latency is thought to comprise the time taken to stretch the SEC (Norman & Komi, 1979;Sasaki, Sasaki, Ishii, 2011). The aponeurosis and tendon has been estimated recently to account for approximately 48% of EMD when measured by means of very high frame rate ultrasound (Nordez et al, 2009). Thus the capability to generate contractile force might only partially influence EMD and it would seem that the interaction of exercise-related stress and the different assessment characteristics associated with evoked and volitional EMD might account for the disparate responses in the latter indices of the time needed to initiate muscle force.…”

In vivo maximal fascicle-shortening velocity during plantar flexion in humans

“…Although measurement of fascicle-shortening velocity is classically performed using ultrasound (13), the sampling frequency of conventional devices (i.e., the number of images per second, typically 30 -170 Hz) limits the investigations to relatively slow motion, far from the maximal velocities reached during human movements. In this context, ultrafast ultrasound (14, 55) could be used to overcome this limitation and analyze very fast movements (17,29,47). Using this technique, we measured fascicle-shortening velocity during maximal isokinetic plantar flexions performed at various submaximal preset angular velocities, from 30°/s up to 330°/s (29).…”