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Article Title

DOES IPSILATERAL MOTOR CORTEX ACTIVITY DURING UNILATERAL FATIGUE EXPLAIN THE DEFICITS IN THE NON-FATIGUED LIMB?

Abstract

Jesus A. Hernandez-Sarabia1, Alejandra Barrera-Curiel1, Micheal J. Luera1, Jason M. DeFreitas1; 1Oklahoma State University, OK

Performing unilateral contractions to exhaustion has been shown to lead to force deficits of both the exercised and unexercised limbs. Although limb muscles are controlled by the contralateral hemisphere of the brain, neuroimaging studies have also shown slight activation of the ipsilateral motor cortex during unilateral tasks. However, whether cortical activity of the ipsilateral hemisphere might, in part, be responsible for the force decrements in the non-fatigued limb remains unknown. PURPOSE: To quantify the relationship between changes in maximal voluntary contraction (MVC) of the non-fatigued limb, and oxyhemoglobin (HbO) changes in the ipsilateral motor cortex during a fatiguing task. METHODS: Eleven subjects (M±SD 20.8±1.14 yrs.) performed two maximal voluntary isometric knee extensions of the left leg before (MVCpre) and after fatiguing protocol (MVCpost). The fatiguing protocol consisted of repeated, 50-second long isometric knee extensions with the right leg at 30% MVC until failure. During the fatigue protocol, hemodynamic responses of the motor cortex were recorded at a sampling rate of 5.81 HZ using a continuous-wave functional near infrared spectroscopy system (fNIRS). Raw fNIRS signals were processed and converted to hemoglobin concentrations using HomER2 software, and the peak HbO (HbOpeak) was obtained from the final contraction before failure. MVCpre and MVCpost were used to calculate the percentage of change in maximal force from the fatiguing task (MVCdiff). A Pearson’s correlation between HbOpeak and MVC diff was calculated using SPSS. RESULTS: Paired samples t-test showed a significant difference (p <.05) between MVCpre (828.34±238.8 N) and MVCpost (743.99±227.56 N). Pearson’s correlation between HbOpeak (2.93±1.86E-8) of the ipsilateral motor cortex and MVCdiff (-9.86±12.11 %) of the unexercised leg was not statistically significant (R = -0.368, p = .265). CONCLUSION: We hypothesized that peaks in oxyhemoglobin on the ipsilateral motor cortex during a fatiguing task would explain, to some extent, the force deficits in the unexercised leg. It is worth noting that this study was underpowered for a correlation. However, it is also possible that if the contralateral force deficit is indeed due to neural factors, that it is not cortical in origin.

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