JoCarol E. Shields, Jesus A. Hernandez-Sarabia, Alejandra Barrera-Curiel, Micheal J. Luera, Jason M. DeFreitas; Oklahoma State University, Stillwater Oklahoma

Performing unilateral contractions to exhaustion has been shown to lead to force deficits of both the exercised and unexercised limbs. It has been proposed that the contralateral force deficits are of neural origin, and not due to peripheral mechanisms of fatigue (e.g. glycogen depletion). While this proposed model appears likely, it remains speculative as the absence of peripheral factors to contralateral force deficits have not been verified. PURPOSE: Therefore, the purpose of the study was to quantify the changes in muscle glycogen content and maximal force of both limbs in response to unilateral fatigue. METHODS: Nineteen healthy subjects performed two maximal voluntary isometric (MVC) knee extensions of each leg before (PRE) and after (POST) a fatiguing protocol of the right leg. The fatiguing protocol consisted of repeated 56-second-long ramp contractions of the right leg at 30% MVC until failure. During the plateau phase of each contraction, ultrasound images were taken at the midpoint of the rectus femoris (RF). The echo intensity, which has been shown to be sensitive to acute changes in muscle glycogen content, was analyzed from each image of the RF muscle. RESULTS: A two-way repeated measures ANOVA showed a significant time × limb interaction (p < 0.001) for MVCs. Follow-up paired sample t-tests indicated that both limbs showed significant force loss. However, the right leg (-33%, from 773.36±191.79to 517.13±136.72, p <0.001) demonstrated a much larger force deficit than the left leg (-9.7%, from 803.07±215.32to 725.04±198.44, p = 0.002).For echo intensity, the right leg demonstrated a significant change (8.8%, from 48.64±7.70to52.58±8.68, p = 0.009) from PRE to POST. However, the left leg did not change (1.34%, from 53.93±7.65to 54.65±7.72, p = 0.621). It is worth noting the increase in echo intensity, such as seen with the right leg, represents a decrease in tissue density (e.g. decreased muscle glycogen content). CONCLUSION: Our findings suggest peripheral fatigue mechanisms, such as muscle glycogen content, were not responsible for the decreased force in the contralateral limb. This absence of peripheral, intracellular changes supports the original proposal that the contralateral force deficit is of a central, neural origin.

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