Electromechanical delay in biceps brachii assessed by ultrafast ultrasonography

Hug, François; Gallot, Thomas; Catheline, Stéfan; Nordez, Antoine

doi:10.1002/mus.21948

Cited by 37 publications

(43 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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.…”

Section: Discussionmentioning

confidence: 92%

“…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.…”

Section: Discussionmentioning

confidence: 99%

“…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)].…”

mentioning

confidence: 99%

See 2 more Smart Citations

New insights on contraction efficiency in patients with Duchenne muscular dystrophy

Lacourpaille

Hug

Guével

et al. 2014

Journal of Applied Physiology

Self Cite

View full text Add to dashboard Cite

The decrease in muscle strength in patients with Duchenne muscular dystrophy (DMD) is mainly explained by a decrease in the number of active contractile elements. Nevertheless, it is possible that other electrochemical and force transmission processes may contribute. The present study aimed to quantify the effect of DMD on the relative contribution of electrochemical and force transmission components of the electromechanical delay (i.e., time lag between the onset of muscle activation and force production) in humans using very high frame rate ultrasound. Fourteen patients with DMD and thirteen control subjects underwent two electrically evoked contractions of the biceps brachii with the ultrasound probe over the muscle belly. The electromechanical delay was significantly longer in DMD patients compared with controls (18.5 Ϯ 3.9 vs. 12.5 Ϯ 1.4 ms, P Ͻ 0.0001). More precisely, DMD patients exhibited a longer delay between the onset of muscle fascicles motion and force production (13.6 Ϯ 3.1 vs. 7.9 Ϯ 2.0 ms, P Ͻ 0.0001). This delay was correlated to the chronological age of the DMD patients (r ϭ 0.66; P ϭ 0.01), but not of the controls (r ϭ Ϫ0.45; P ϭ 0.10). No significant difference was found for the delay between the onset of muscle stimulation and the onset of muscle fascicle motion. These results highlight the role of the alteration of muscle force transmission (delay between the onset of fascicle motion and force production) in the impairments of the contraction efficiency in patients with DMD. myopathy; force; ultrasound; electromechanical delay DUCHENNE MUSCULAR DYSTROPHY (DMD) is one of the most severe degenerative muscle diseases characterized by a lack of dystrophin (14). Dystrophin is a protein that has a role, with other proteins, to laterally link actin filaments through the sarcolemma to the extracellular matrix (10). It is essential for the transmission of the force generated by contractile proteins (34,35). An absence of dystrophin ultimately leads to contractile tissue wastage (27) and thus to a dramatic decrease in maximal force-generating capacity (21). This is even observed when maximal strength is normalized to muscle contractile cross-sectional area, illustrating an impairment of muscle quality (37). This alteration is mainly explained by a decrease in the number of active contractile elements for a given muscle volume, due to fiber necrosis (1). Still, it is plausible that other electrochemical and mechanical processes might further alter the contraction efficiency.In addition to the main muscle structural consequence of DMD, it has been shown that both muscle (12) and tendon (32) mechanical properties are altered in X-linked muscular dystrophy mice model (mdx). As both structural and mechanical properties may play an important role in force transmission (12,17,32), the efficiency of force transmission from the actomyosin cross bridges to the tendons is presumed to be altered in patients with DMD (24). The alteration of contraction efficiency in DMD patients might also be related to an alter...

show abstract

Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

New insights on contraction efficiency in patients with Duchenne muscular dystrophy

Lacourpaille

Hug

Guével

et al. 2014

Journal of Applied Physiology

Self Cite

View full text Add to dashboard Cite

show abstract

“…It reflects both electro-chemical processes (i.e., synaptic transmission, propagation of the action potential, excitation-contraction coupling) as well as mechanical processes (i.e., force transmission along the active and the passive part of the series elastic component, SEC) [1]. The relative contributions of both electro-chemical and mechanical processes involved in EMD has recently been characterized on gastrocnemius medialis [2] and biceps brachii [3], [4] using very high frame rate ultrasound. More precisely, the delay between the muscle electrical stimulation and the onset of muscle fascicles motion has been mainly attributed to electro-chemical processes and the delay between the onset of fascicles motion and the onset of both the myotendinous junction motion and the force production has been attributed to mechanical processes [2], [3], [4].…”

Section: Introductionmentioning

confidence: 99%

“…The relative contributions of both electro-chemical and mechanical processes involved in EMD has recently been characterized on gastrocnemius medialis [2] and biceps brachii [3], [4] using very high frame rate ultrasound. More precisely, the delay between the muscle electrical stimulation and the onset of muscle fascicles motion has been mainly attributed to electro-chemical processes and the delay between the onset of fascicles motion and the onset of both the myotendinous junction motion and the force production has been attributed to mechanical processes [2], [3], [4]. While the study of gastrocnemius medialis reported a delay of about 2.4 ms between the onset of muscle fascicles motion and the onset of myotendinous junction motion (i.e., the delay to transmit force along the aponeurosis) [2], fascicles and myotendinous junction motion occurred concomitantly in biceps brachii [3], [4].…”

Section: Introductionmentioning

confidence: 99%

Influence of Passive Muscle Tension on Electromechanical Delay in Humans

2013

Self Cite

View full text Add to dashboard Cite

BackgroundElectromechanical delay is the time lag between onsets of muscle activation and muscle force production and reflects both electro-chemical processes and mechanical processes. The aims of the present study were two-fold: to experimentally determine the slack length of each head of the biceps brachii using elastography and to determine the influence of the length of biceps brachii on electromechanical delay and its electro-chemical/mechanical processes using very high frame rate ultrasound.Methods/ResultsFirst, 12 participants performed two passive stretches to evaluate the change in passive tension for each head of the biceps brachii. Then, they underwent two electrically evoked contractions from 120 to 20° of elbow flexion (0°: full extension), with the echographic probe maintained over the muscle belly and the myotendinous junction of biceps brachii. The slack length was found to occur at 95.5 ± 6.3° and 95.3 ± 8.2° of the elbow joint angle for the long and short heads of the biceps brachii, respectively. The electromechanical delay was significantly longer at 120° (16.9 ± 3.1 ms; p<0.001), 110° (15.0 ± 3.1 ms; p<0.001) and 100° (12.7 ± 2.5 ms; p = 0.01) of elbow joint angle compared to 90° (11.1 ± 1.7 ms). However, the delay between the onset of electrical stimulation and the onset of both muscle fascicles (3.9 ± 0.2 ms) and myotendinous junction (3.7 ± 0.3 ms) motion was not significantly affected by the joint angle (p>0.95).ConclusionIn contrast to previous observations on gastrocnemius medialis, the onset of muscle motion and the onset of myotendinous junction motion occurred simultaneously regardless of the length of the biceps brachii. That suggests that the between-muscles differences reported in the literature cannot be explained by different muscle passive tension but instead may be attributable to muscle architectural differences.

show abstract