Despite flourishing interest in the topic of fatigue—as indicated by the many presentations on fatigue at the 2015 annual meeting of the American College of Sports Medicine—surprisingly little is known about its impact on human performance. There are two main reasons for this dilemma: (1) the inability of current terminology to accommodate the scope of the conditions ascribed to fatigue, and (2) a paucity of validated experimental models. In contrast to current practice, a case is made for a unified definition of fatigue to facilitate its management in health and disease. Based on the classic two-domain concept of Mosso, fatigue is defined as a disabling symptom in which physical and cognitive function is limited by interactions between performance fatigability and perceived fatigability. As a symptom, fatigue can only be measured by self-report, quantified as either a trait characteristic or a state variable. One consequence of such a definition is that the word fatigue should not be preceded by an adjective (e.g., central, mental, muscle, peripheral, and supraspinal) to suggest the locus of the changes responsible for an observed level of fatigue. Rather, mechanistic studies should be performed with validated experimental models to identify the changes responsible for the reported fatigue. As indicated by three examples (walking endurance in old adults, time trials by endurance athletes, and fatigue in persons with multiple sclerosis) discussed in the review, however, it has proven challenging to develop valid experimental models of fatigue. The proposed framework provides a foundation to address the many gaps in knowledge of how laboratory measures of fatigue and fatigability impact real-world performance.

A number of studies over the last few decades have established that the control strategy employed by the nervous system during lengthening (eccentric) differs from those used during shortening (concentric) and isometric contractions. The purpose of this review is to summarize current knowledge on the neural control of lengthening contractions. After a brief discussion of methodological issues that can confound the comparison between lengthening and shortening actions, the review provides evidence that untrained individuals are usually unable to fully activate their muscles during a maximal lengthening contraction and that motor unit activity during submaximal lengthening actions differs from that during shortening actions. Contrary to common knowledge, however, more recent studies have found that the recruitment order of motor units is similar during submaximal shortening and lengthening contractions, but that discharge rate is systematically lower during lengthening actions. Subsequently, the review examines the mechanisms responsible for the specific control of maximal and submaximal lengthening contractions as reported by recent studies on the modulation of cortical and spinal excitability. As similar modulation has been observed regardless of contraction intensity, it appears that spinal and corticospinal excitability are reduced during lengthening compared with shortening and isometric contractions. Nonetheless, the modulation observed during lengthening contractions is mainly attributable to inhibition at the spinal level.

The purpose of this study was to determine the adjustments in the level of coactivation during a steadiness task performed by young and old adults after the torque-generating capacity of the antagonist muscles was reduced by a fatiguing contraction. Torque steadiness (coefficient of variation) and electromyographic activity of the extensor and flexor carpi radialis muscles were measured as participants matched a wrist extensor target torque (10% maximum) before and after sustaining an isometric contraction (30% maximum) with wrist flexors to task failure. Time to failure was similar (P = 0.631) for young (417 ± 121 s) and old (452 ± 174 s) adults. The reduction in maximal voluntary contraction torque (%initial) for the wrist flexors after the fatiguing contraction was greater (P = 0.006) for young (32.5 ± 13.7%) than old (21.8 ± 6.6%) adults. Moreover, maximal voluntary contraction torque for the wrist extensors declined for old (-13.7 ± 12.7%; P = 0.030), but not young (-5.4 ± 13.8%; P = 0.167), adults. Torque steadiness during the matching task with the wrist extensors was similar before and after the fatiguing contraction for both groups, but the level of coactivation increased after the fatiguing contraction for old (P = 0.049) but not young (P = 0.137) adults and was twice the amplitude for old adults (P = 0.002). These data reveal that old adults are able to adjust the amount of antagonist muscle activity independent of the agonist muscle during steady submaximal contractions.

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