No effect of passive stretching on neuromuscular function and maximum force-generating capacity in the antagonist muscle

Abstract

Purpose The present study investigated whether or not passive stretching increases the force-generating capacity of the antagonist muscle, and the possible neuromuscular mechanisms behind. Methods To this purpose, the neuromuscular function accompanying the force-generating capacity was assessed in 26 healthy male volunteers after passive stretching and in a control session. Before and after passive intermittent static stretching of the plantar flexors consisting of five sets × 45 s + 15 s-rest, maximum voluntary isometric contraction (MVC) and surface electromyographic root mean square (sEMG RMS) were measured in the tibialis anterior (the antagonist muscle). Additionally, evoked V wave, H-reflex, and M wave were elicited by nerve stimulation at rest and during MVC. Ankle range of motion (ROM) and plantar flexors MVC and EMG RMS were measured to check for the effectiveness of the stretching manoeuvre. Results No change in MVC [p = 0.670; effect size (ES) − 0.03] and sEMG RMS/M wave during MVC (p = 0.231; ES − 0.09) was observed in the antagonist muscle after passive stretching. Similarly, no change in V wave (p = 0.531; ES 0.16), H-reflex at rest and during MVC (p = 0.656 and 0.597; ES 0.11 and 0.23, respectively) and M wave at rest and during MVC (p = 0.355 and 0.554; ES 0.04 and 0.01, respectively) was observed. An increase in ankle ROM (p < 0.001; ES 0.55) and a decrease in plantar flexors MVC (p < 0.001; ES − 1.05) and EMG RMS (p < 0.05; ES − 1.72 to − 0.13 in all muscles) indicated the effectiveness of stretching protocol. Conclusion No change in the force-generating capacity and neuromuscular function of the antagonist muscle after passive stretching was observed.

Is the Interpolated-Twitch Technique-Derived Voluntary Activation Just Neural? Novel Perspectives from Mechanomyographic Data

“…The current increase in dorsiflexion ROM and the simultaneous reduction in MVC and joint passive stiffness are due to both neuromuscular (36) and mechanical factors (16). The former include an alteration in the motor pathway potentially acting at central level that could depress the force-generating capacity in both limbs, as suggested here by the reduction in sEMG RMS/M-wave, in line with previous studies (23,37). Moreover, the decrease in joint passive stiffness could be also caused by a reduction in muscle tone associated with a decrease in nociceptive activity, increasing the stretch tolerance in both the stretched and the contralateral nonstretched limbs (38).…”