The neural basis of the sense of fatigue

Hartman, Mark
Major Professor
Panteleimon Ekkekakis
Committee Member
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Evidence suggests that the genesis and regulation of the sense of exertional fatigue is rooted within the same neural networks responsible for processing affective responses. One key mechanism proposed to be involved in the sense of exertional fatigue is the interaction between the cognitive inhibitory processes of the dorsolateral prefrontal cortex (DLPFC) and the interoceptive inputs to the amygdala. The primary purpose of this dissertation is to examine the development and progression of exertional fatigue during exercise by examining the interactions between the level of bodily perturbations evoked by the exercise, the activity of the DLPFC (Tissue Oxygenation Index [TOI] percentage), the amygdala (indexed by the acoustic startle eyeblink response [ASER] amplitude), and affective responses (Empirical Valence Scale [EVS] score). The secondary purpose is to modulate the interaction between the DLPFC TOI, the EVS scores, and the ASER amplitudes using transcranial direct current stimulation (tDCS), to explore its potential as a treatment for attenuating the sense of fatigue during physical exertion. Individual differences were also examined. Thirty healthy university students—12 women and 18 men—exercised on a cycle ergometer for up to 20 minutes or until volitional termination at (1) heavy-intensity exercise while receiving sham tDCS on the right and left DLPFC (H-Sham), (2) heavy-intensity exercise while receiving active tDCS (H-Active), (3) severe-intensity exercise while receiving sham tDCS (S-Sham), and (4) severe-intensity exercise while receiving active tDCS (S-Active). The rate of decline in EVS scores was significantly greater during severe-intensity exercise compared to heavy-intensity exercise. The decline in the right and left DLPFC TOI percentages was significantly greater during severe-intensity exercise compared to heavy-intensity exercise, and this decline was larger in the right DLPFC compared to the left DLPFC. During both exercise intensities, the strength of the correlations between EVS scores and the right and left DLPFC TOI percentages increased as the interoceptive cues intensified. tDCS significantly increased DLPFC TOI percentages and the pattern of the ASER amplitudes. In conjunction with the decline in EVS scores, the drop in TOI was most prominent during severe-intensity exercise when, on average, the right DLPFC TOI dropped below baseline and, therefore, the DLPFC entered a hypometabolic state. Individuals with a higher level of tolerance demonstrated a greater activation of the right DLPFC during the heavy-intensity exercise compared to individuals with lower tolerance. The findings of this dissertation suggest that affective responses during exercise were a function of both the severity of homeostatic perturbations and the level of inhibitory control exerted by the right DLPFC. These results support the model for hemispheric specialization of the right PFC in the cognitive inhibition of displeasure. The regulation of the sense of exertional fatigue is, therefore, likely controlled by the right DLPFC. Exertional fatigue emerged at a defined threshold. Accordingly, the physiological response pattern entered a non-steady-state, accompanied by feelings of greater displeasure (or less pleasure) and high perceived activation. Proximal to the point of termination, the hypometabolic state of the DLPFC and the decline in affective responses were not reversed with active tDCS. As such, near one’s physiological limits, if the deactivation of the DLPFC and the corresponding displeasure serve to protect the body from reaching dangerous levels of perturbation, then this mechanism appears to be immutable. Future work should evaluate the potential of therapies that target the modulation of DLPFC inhibitory control (top–down) or interoceptive sensitivity (bottom–up) networks in relation to types of fatigue (e.g., clinical).