Does motoneuron adaptation contribute to muscle fatigue?

Abstract

To help reduce the gap between the cellular physiology of motoneurons (MNs) as studied "bottom-up" in animal preparations and the "top-down" study of the firing patterns of human motor units (MUs), this article addresses the question of whether motoneuron adaptation contributes to muscle fatigue. Findings are reviewed on the intracellularly recorded electrophysiology of spinal MNs as studied in vivo and in vitro using animal preparations, and the extracellularly recorded discharge of MUs as studied in conscious humans. The latter "top-down" approach, combined with kinetic measurements, has provided most of what is currently known about the neurobiology of muscle fatigue, including its task and context dependencies. It is argued that although the question addressed is still open, it should now be possible to design new "bottom-up" research paradigms using animal preparations that take advantage of what has been learned with the use of relatively noninvasive quantitative procedures in conscious humans.

Adjustments Differ Among Low-Threshold Motor Units During Intermittent, Isometric Contractions

“…The extrinsic synaptic input needed to recruit a motor neuron may change during a fatiguing contraction. Over short time intervals of motor unit activity, persistent inward currents in the dendrites may reduce the current required from extrinsic synaptic sources to reach recruitment threshold (Fuglevand et al 2006;Gorassini et al 2002;Heckman et al 2005;Nordstrom et al 2007). Longer intervals of motor unit activity, however, may elicit slow inactivation of Ca 2ϩ and Na ϩ persistent inward currents that conversely increase the synaptic current required to reach threshold (Heckman et al 2005).…”

Unraveling the neurophysiology of muscle fatigue

“…As the H-reflex area (normalized to the maximal M wave) decreases despite an increase in the amplitude of the surface EMG, the reduction in size likely represents a decrease in transmission along the pathway from the site of action potential generation in the Ia axons to the motor neurons (Duchateau et al, 2002;Kuwabara et al, 2002). The decline in H-reflex size is typically attributed to adjustments in motor neuron properties, such as adaptation (Kernell and Monster, 1982;Nordstrom et al, 2007), and modulation of afferent feedback to the motor neuron pool (Bongiovanni and Hagbarth, 1990;Kostyukov et al, 2005;Macefield et al, 1991;Pettorossi et al, 1999). Given that the same motor unit can exhibit significantly different declines in discharge rate in different loading conditions (Mottram et al, 2005;Rudroff et al, 2010a,b), withdrawal of facilitation to the motor neuron pool due to a depression of afferent feedback appears to be the more dominant mechanism responsible for the decline in H-reflex size during fatiguing contractions.…”

High-frequency submaximal stimulation over muscle evokes centrally generated forces in human upper limb skeletal muscles

“…Through persistent inward currents, the relationship between input current and firing frequency becomes nonlinear and motoneurons can sustain firing for prolonged periods, outlasting any excitatory inputs (3,27,35,44,46,48). Because it is not feasible to perform intracellular motoneurons recordings in able-bodied humans, there is only indirect evidence suggesting the presence of sustained motoneuron firing associated with plateau potentials in humans (8, 9, 16, 18, 26, 31, 41, 43; for review see 42).…”