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1 University of Alberta
2 University of New South Wales
3 University of British Columbia
4 Prince of Wales Medical Research Institute
* To whom correspondence should be addressed. E-mail: olle{at}ualberta.ca.
Neuromuscular electrical stimulation (NMES) generates contractions by activation of motor axons (peripheral mechanism), but the afferent volley also contributes by recruiting spinal motoneurons synaptically (central mechanism), which recruits motoneurons according to Henneman's size principle. Thus, we hypothesized that contractions that develop due to a combination of peripheral and central mechanisms will fatigue less rapidly than when electrically-evoked contractions are generated by the activation of motor axons alone. Plantar-flexion torque evoked by NMES over the triceps surae was compared in five able-bodied subjects before ('Intact') and during ('Blocked') a complete anesthetic block of the tibial and common peroneal nerves. In the Blocked condition plantar-flexion torque could only develop from the direct activation of motor axons beneath the stimulating electrodes. NMES was delivered using three protocols: A) constant 100 Hz for 30 sec; B) four 2 sec bursts of 100 Hz alternating with 20 Hz stimulation, and C) alternating 100 Hz bursts (1 sec on, 1 sec off) for 30 sec. The percent change in evoked plantar flexion torque from the beginning to the end of the stimulation differed (p < 0.05) between 'Intact' and 'Blocked' conditions for all protocols (Intact: protocol A = +125%, B = +230%, C = + 78%; Blocked: protocol A = -79%, B = -15 %, C = -35%). These results corroborate previous evidence that NMES can evoke contractions via the recruitment of spinal motoneurons in addition to the direct recruitment of motor axons. We now show that NMES delivered for periods of up to 30 sec generates plantar-flexion torque that decreases when only motor axons are recruited and increases when the central nervous system can contribute.
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