Why the study?
Does neuromuscular electrical stimulation during resistance training alter the spinal reflex circuit in healthy adults?
Does neuromuscular electrical stimulation during resistance training alter the spinal reflex circuit in healthy adults?
Neuromuscular electrical stimulation during resistance training induces proprioceptive input that inhibits resting muscle and excites voluntarily activated muscle via spinal and/or supraspinal pathways.
NMES with resistance training modulates spinal reflexes in healthy adults; extends RCT evidence for its proprioceptive effects on reflex circuits.
The purpose of the study was to examine the changes in soleus Hoffmann (H)-reflex and volitional (V)-wave after resistance training (RT) with and without neuromuscular electrical stimulation (NMES). Fourteen participants were randomly allocated to receive RT with NMES (RT+NMES, n = 7) or RT without NMES (RT, n = 7). Each participant trained for 10 sessions of right leg standing calf-raise for 2 weeks. For the RT+NMES group, NMES was applied to the tibial nerve using rectangular pulses (400 µsec duration, 75-Hz trains). Stimulation intensity was set at the maximal tolerable level. The H-reflex was elicited just above motor threshold during rest and during maximal voluntary isometric contraction (MVIC) conditions. The H-reflex and V-wave were normalized to the maximal motor response (Mmax). There was a significant interaction between time (pre/post) and group in the H-reflex during rest and during the MVIC condition (P = 0.05), but no significant difference in plantar torque, Mmax or V-wave. The H-reflex during rest decreased from 0.54 to 0.38 in the RT+NMES group (P = 0.01) but did not change in the RT group (from 0.48 to 0.47, P = 0.79). During MVIC, the H-reflex increased from 0.23 to 0.76 in the RT+NMES group (P = 0.02), but did not change in the RT group (from 0.44 to 0.58, P = 0.12). The results indicate that NMES-induced proprioceptive input during RT has an inhibitory effect in the resting muscle and an excitatory effect in the voluntarily activated muscle via spinal and/or supraspinal pathways.
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Egawa et al. (2013) studied this question.
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