Abstract
.The temporal evolution of cortical activation and connectivity patterns during a fatiguing handgrip task were studied by functional near-infrared spectroscopy (fNIRS). Twenty-three young adults (18 to 35 years old) were recruited to use a handheld force sensor to perform intermittent handgrip contractions with their dominant hand at their personal maximum voluntary contraction force level for 3.5 s followed by 6.5 s of rest for 120 blocks. Subjects were divided into self-reported physically active and inactive groups, and their hemodynamic activity over the prefrontal and sensory-motor cortices (111 channels) was mapped while they performed this task. Using this fNIRS setup, a more detailed time sequence of cortical activation and connectivity patterns was observed compared to prior studies. A temporal evolution sequence of hemodynamic activation patterns was noted, which was different between the active and the inactive groups. Physically active subjects demonstrated delayed fatigue onset and significantly longer-lasting and more spatially extended functional connectivity (FC) patterns, compared to inactive subjects. The observed differences in activation and FC suggested differences in cortical network adaptation patterns as fatigue set in, which were dependent on subjects’ physical activity. The findings of this study suggest that physical activity increases FC with regions involved in motor task control and correlates to extended fatigue onset and enhanced performance.
Highlights
When performing physical exercise, the contracting muscles elicit demand for oxygen, which is supplied by increased blood flow
In the second half of the task, rDLPFC was not significant and instead activation was seen in the lDLPFC [Fig. 3(f)], opposite to what was seen for inactive subjects [Fig. 3(e)]
We propose that active subjects have stronger, persistent functional connectivity (FC) between rDLPFC and lDLPFC, bilateral PMC, and bilateral M1/S1 because they were able to inhibit bodily afferences that arise with fatigue more successfully than their inactive counterparts.[11]
Summary
The contracting muscles elicit demand for oxygen, which is supplied by increased blood flow. The brain must register and simultaneously integrate input from feedforward (i.e., central command) and feedback (e.g., exercise pressor reflex) neural mechanisms to make necessary cardiovascular adjustments to meet the metabolic demand of the exercise.[1,2] During exercise involving the arms, peripheral fatigue sets in, as characterized by reduced force-generating capability of the muscles that subsequently evolves into central fatigue, resulting in decreased neural drive to the muscles, after prolonged physical activity.[1,2,3,4,5,6] Central fatigue’s contribution to peripheral fatigue is less understood and functional brain imaging during fatiguing exercises is being investigated as a tool to help elucidate the underlying mechanisms.[3,4,5,6,7,8,9,10,11] Neural pathways gradually alter their connectivity (neuroplasticity), which affects regulation of the cardiovascular system both at rest and during exercise. Active individuals exhibit exercise-related neuroplasticity and have improved cardiovascular health, whereas inactive individuals may be predisposed to higher incidences of cardiovascular disease.[1,5,12]
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