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      Quantification of Neuromuscular Fatigue: What Do We Do Wrong and Why?

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      Sports Medicine
      Springer Science and Business Media LLC

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          Abstract

          Neuromuscular fatigue (NMF) is usually assessed non-invasively in healthy, athletic or clinical populations with the combination of voluntary and evoked contractions. Although it might appear relatively straightforward to magnetically or electrically stimulate at different levels (cortical/spinal/muscle) and to measure mechanical and electromyographic responses to quantify neuromuscular adjustments due to sustained/repeated muscle contractions, there are drawbacks that researchers and clinicians need to bear in mind. The aim of this opinion paper is to highlight the pitfalls inevitably faced when NMF is quantified. The first problem might arise from the definition of fatigue itself and the parameter(s) used to measure it; for instance, measuring power vs. isometric torque may lead to different conclusions. Another potential limitation is the delay between exercise termination and the evaluation of neuromuscular function; the possible underestimation of exercise-induced neural and contractile impairment and misinterpretation of fatigue etiology will be discussed, as well as solutions recently proposed to overcome this problem. Quantification of NMF can also be biased (or not feasible) because of the techniques themselves (e.g. results may depend on stimulation intensity for transcranial magnetic stimulation) or the way data are analyzed (e.g. M wave peak-to-peak vs first phase amplitude). When available, alternatives recently suggested in the literature to overcome these pitfalls are considered and recommendations about the best practices to assess NMF (e.g. paying attention to the delay between exercise and testing, adapting the method to the characteristics of the population to be tested and considering the limitations associated with the techniques) are proposed.

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          Most cited references67

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          Fatigue and fatigability in neurologic illnesses: proposal for a unified taxonomy.

          Fatigue is commonly reported in many neurologic illnesses, including multiple sclerosis, Parkinson disease, myasthenia gravis, traumatic brain injury, and stroke. Fatigue contributes substantially to decrements in quality of life and disability in these illnesses. Despite the clear impact of fatigue as a disabling symptom, our understanding of fatigue pathophysiology is limited and current treatment options rarely lead to meaningful improvements in fatigue. Progress continues to be hampered by issues related to terminology and assessment. In this article, we propose a unified taxonomy and a novel assessment approach to addressing distinct aspects of fatigue and fatigability in clinical and research settings. This taxonomy is based on our current knowledge of the pathophysiology and phenomenology of fatigue and fatigability. Application of our approach indicates that the assessment and reporting of fatigue can be clarified and improved by utilizing this taxonomy and creating measures to address distinct aspects of fatigue and fatigability. We review the strengths and weaknesses of several common measures of fatigue and suggest, based on our model, that many research questions may be better addressed by using multiple measures. We also provide examples of how to apply and validate the taxonomy and suggest directions for future research.
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            Translating Fatigue to Human Performance.

            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.
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              Changes in muscle contractile properties and neural control during human muscular fatigue.

              The factors limiting force production and exercise endurance time have been briefly described, together with some of the changes occurring at various sites within the muscle and central nervous system. Evidence is presented that, in fatigue of sustained maximal voluntary contractions (MVC) executed by well-motivated subjects, the reduction in force generating capacity need not be due to a decline in central nervous system (CNS) motor drive or to failing neuromuscular transmission, but can be attributed solely to contractile failure of the muscles involved. However, despite this conclusion, both the integrated electromyogram (EMG) and the mean firing rate of individual motor units do decline progressively during sustained MVC. This, however, does not necessarily result in loss of force since the parallel slowing of muscle contractile speed reduces tetanic fusion frequency. It is suggested that the range of motoneuron firing rates elicited by voluntary effort is regulated and limited for each muscle to the minimum required for maximum force generation, thus preventing neuromuscular transmission failure and optimizing motor control. Such a CNS regulating mechanism would probably require some reflex feedback from the muscle.
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                Author and article information

                Journal
                Sports Medicine
                Sports Med
                Springer Science and Business Media LLC
                0112-1642
                1179-2035
                November 12 2019
                Article
                10.1007/s40279-019-01203-9
                31713783
                474914f4-1214-4160-97d1-5f3459ee3735
                © 2019

                http://www.springer.com/tdm

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