Cortical and spinal compensatory mechanisms during neuromuscular fatigue

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Neuromuscular fatigue is defined as an activity-induced reduction in maximal muscle force and is associated with an increased sense of effort during submaximal force production. Mechanisms of fatigue include muscle failure, as well as reduced neural drive to muscle (central fatigue). There are a number of well-studied spinal and cortical mechanisms that contribute to central fatigue. In contrast, the mechanisms which serve to increase gain in the neural pathway from brain to muscle to offset failure are not well understood. Two possible compensatory systems include: i) cortical facilitation and ii) spinal motor neuron (MN) persistent inward current (PIC). The purpose of the proposed research is to assess the contribution of these two compensatory systems that may serve to increase gain to optimize motor output and reduce sense of force and effort during muscle activity.  Many regions of the motor cortex contribute to planning voluntary muscle activity, and the final output from these brain regions is delivered via corticospinal neurons of the primary motor cortex. The cortical facilitation system increases the excitability of these cells in a way that may compensate for failure upstream or downstream in the pathway from brain to muscle during fatigue.  This would reduce the drive necessary to maintain output, however, the cost of increased gain may be a reduction in the precision with which force is produced. Thus, it is likely that these mechanisms are employed in a way that is both state-dependent (fatigue, nonfatigued) as well as task-dependent (precision vs. nonprecision).  The 1st objective of the proposed work is to determine whether cortical facilitation is increased during fatigue when the task demands precision. This will be accomplished by assessing cortical facilitation using transcranial magnetic stimulation just prior to movements associated with both precision and power tasks of upper and lower limb muscles. At a spinal level, persistent inward currents (PIC) provide a powerful means to increase motor output across diverse pools of MNs controlling many muscle groups. No studies to date, however, have investigated how PIC is modulated during fatigue.  The current methodology is to estimate PIC during seated, static contractions. Therefore, a 2nd objective of this research is to develop a technique to estimate fatigue-associated changes in PIC during a functionally-relevant postural task. This will be accomplished by estimating PIC using intramuscular recordings of motor unit pairs in seated, static contractions and during standing forward postural-sway. This work will improve our understanding of task-dependent modulation of motor output during human fatigue. This is significant because until we understand the mechanisms that modulate motor output in healthy people, we cannot fully understand the mechanisms of impaired motor function in injury, ageing, and disease.