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1 Kinesiology, University of Waterloo, Waterloo, Canada
2 Department of Kinesiology, University of Waterloo, Waterloo, Canada
3 University of Waterloo, United States
* To whom correspondence should be addressed. E-mail: green{at}healthy.uwaterloo.ca.
To determine if exercise-induced depressions in neuromuscular function are altered with oral glucose supplementation, 15 untrained participants (VO2peak= 45 ± 2 ml· kg-1· min-1; mean±SE) performed prolonged cycle exercise at ~ 60% VO2peak on two occasions: without glucose supplementation (NG), and with oral glucose supplementation (G). The oral G began at 30 min of exercise and was administered every 15 min (total ingested = 1.23 ± 0.11 g CHO/kg body mass). Quadriceps isometric properties and membrane excitability were assessed prior to exercise, after 90 min of exercise, and at fatigue. Cycle time to fatigue was greater (P< 0.05) in G compared to NG (13±7 vs 115±6 min). Progressive reductions (P< 0.05) in maximal voluntary contraction (MVC, N) were observed for NG at 90 min (441 ± 29) and at fatigue (344 ± 33) compared to pre-exercise (666 ± 30) At fatigue in G, the reduction in MVC was not as pronounced (P<0.05) as in NG. Motor unit activation assessed with the interpolated twitch technique during an MVC following exercise was not different between conditions. During cycling, the G condition also resulted in a higher (P<0.05) muscle compound potential (M-wave) amplitude (mV) at both 90 min (+ 50%) and at fatigue (+87%) compared to NG. Similar effects were also found M-wave area (mV/ms). These results suggest that the ergogenic effect of glucose supplementation occurs not as a result of decreased neural activation but to improved muscle function, possibly as a consequence of protection of muscle membrane excitability.
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