4.4 Article

Acute effects of stretching on the neuromechanical properties of the triceps surae muscle complex

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EUROPEAN JOURNAL OF APPLIED PHYSIOLOGY
卷 86, 期 5, 页码 428-434

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SPRINGER-VERLAG
DOI: 10.1007/s00421-001-0565-1

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stretch-shortening; stiffness; stretching; jumping; elastic energy

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Previous research has shown that an acute bout of passive muscle stretching can diminish performance in certain movements where success is a function of maximal force and/or power output. Two possible mechanisms that might account for such findings are a change in active musculotendinous stiffness and a depression of muscle activation. To investigate the likelihood of these two mechanisms contributing to a post-stretch reduction in performance, we examined the acute effects of stretching on the active stiffness and muscle activation of the triceps surae muscle group during maximal single-joint jumps with movement restricted to the ankle joint. Ten males performed both static (SJ) and countermovement (CMJ) jumps before and after passively stretching the triceps surae. Electrical activity of the triceps surae during each jump was determined by integrating electromyographic recordings (IEMG) over the course of the movement. Triceps surae musculotendinous stiffness was calculated before and after stretching using a technique developed by Cavagna (1970). Following stretching, a significant decrease [mean (SD) 7.4 (1.9)%; P < 0.05] in jump height for the CMJ occurred, but for the SJ, no significant (P > 0.05) change in jump height was found. A small but significant decrease [2.8 (1.24)%; P < 0.05] in stiffness was noted, but the magnitude of this change was probably not sufficient for it to have been a major factor underlying the decline in CMJ performance. Paradoxically, after stretching, the SJ exhibited a significant (P < 0.05) decrease in IEMG, but the IEMG for the CMJ remained unchanged (P > 0.05). It appears that an acute bout of stretching can impact negatively upon the performance of a single-joint CMJ, but it is unlikely that the mechanism responsible is a depression of muscle activation or a change in musculotendinous stiffness.

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