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...