Neural Contributions to Muscle Fatigue

Abstract

During exercise, there is a progressive reduction in the ability to produce muscle forces. Processes within the nervous system, as well as within the muscles contribute to this fatigue. In addition to impaired function of the motor system, sensations associated with fatigue, and impairment of homeostasis can contribute to impairment of performance during exercise. This review discusses some of the neural changes that accompany exercise and the development of fatigue. The role of brain monoaminergic neurotransmitter systems in whole-body endurance performance is discussed, particularly with regard to exercise in hot environments. Next, fatigue-related alterations in the neuromuscular pathway are discussed in terms of changes in motor unit firing, motoneuron excitability and motor cortical excitability. These changes have mostly been investigated during single-limb isometric contractions. Finally, the small-diameter muscle afferents that increase firing with exercise and fatigue are discussed. These afferents have roles in cardiovascular and respiratory responses to exercise, and in impairment of exercise performance through interaction with the motor pathway, as well as providing sensations of muscle discomfort. Thus, changes at all levels of the nervous system including the brain, spinal cord, motor output, sensory input and autonomic function occur during exercise and fatigue. The mix of influences and the importance of their contribution varies with the type of exercise being performed.

Influence of Lumbar Muscle Fatigue on Trunk Adaptations during Sudden External Perturbations

“…Muscle fatigue is characterized by an increase of active motor units (De Luca, 1997), which is usually reflected by an increase in EMG amplitude signals in submaximal muscle contractions. A recent review has shown that muscle fatigue induced by a submaximal isometric contraction is associated with variable responses in motor units firing rates according to the intensity of the fatiguing task (Taylor et al, 2016). For example, motor unit behavior during submaximal isometric contraction at moderate intensity (50% MVC), which correspond to the Sorensen test (Demoulin et al, 2006), is first associated with a decrease in firing rate followed by an increased motor units recruitment (Heckman and Enoka, 2012).…”

Corticospinal excitability during fatiguing whole body exercise

“…This centrally-mediated increase in central motor drive would also increase perceived effort (Finn et al, 2018; McNeil et al, 2011). If an increase in neural drive into the cortex or motoneuron is not possible (e.g., during a maximal voluntary contraction, MVC) or insufficient to compensate for the diminished corticospinal excitability, the ability of the central nervous system to recruit motor units would be reduced and result in a lower muscle activation which is generally referred to as central fatigue (Klass et al, 2008; Martin et al, 2006; Petersen et al, 2003; Taylor et al, 2016). As central fatigue limits single-joint and whole body exercise performance (Hureau et al, 2018b; Taylor et al, 2006), it is important to understand how physical activity and associated fatigue influences the integrity of the corticospinal pathway.…”

Anodal and cathodal transcranial direct current stimulation can decrease force output of knee extensors during an intermittent MVC fatiguing task in young healthy male participants

“…Although the use of an intermittent MVC task was necessary to estimate the variation of VA throughout the task and between treatments, the large amount of peripheral fatigue generated, as estimated by the decrease of Ptw (see Figures 2 and 3), may have partially masked tDCS effects. Indeed, in such a condition, the limiting factor of performance may be more peripheral than central (Taylor et al, 2016), which could have limited the centrally mediated action of tDCS on performance.…”

“…Central fatigue can be defined as "a progressive reduction in voluntary activation of muscle during exercise" (Gandevia, 2001). A part of the central fatigue can be explained by a progressive reduction of the brain capacity to activate the muscle maximally (Taylor, Amann, Duchateau, Meeusen, & Rice, 2016). Interestingly, studies on tDCS have sometimes reported opposite effects.…”

“…The rationale behind the use of such specific task is that it allowed, for the first time, to assess the effect of tDCS on maximal muscle activation in different fatigue states, that is, nonfatigued during the first MVCs to highly fatigued at the end of the task. During an intermittent MVC task, a rapid drop of force is observed (Pethick, Winter, & Burnley, 2015), which can be explained by a large decline in motor unit firing rate, possibly related to a decrease in neural drive, changes in intrinsic motoneuron properties and inhibitory peripheral mechanisms (Taylor et al, 2016). We hypothesized that anodal tDCS could limit the reduction of force by facilitating the neural drive toward the muscles that can compensate at least partly fatigue mechanisms.…”