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Research in physiology and sports science has shown that fatigue, a complex psychophysiological phenomenon, has a relevant impact in performance and in the correct functioning of our motricity system, potentially being a cause of damage to the human organism. Fatigue can be seen as a subjective or objective phenomenon. Subjective fatigue corresponds to a mental and cognitive event, while fatigue referred as objective is a physical phenomenon. Despite the fact that subjective fatigue is often undervalued, only a physically and mentally healthy athlete is able to achieve top performance in a discipline. Therefore, we argue that physical training programs should address the preventive assessment of both subjective and objective fatigue mechanisms in order to minimize the risk of injuries. In this context, our paper presents a machine-learning system capable of extracting individual fatigue descriptors (IFDs) from electromyographic (EMG) and heart rate variability (HRV) measurements. Our novel approach, using two types of biosignals so that a global (mental and physical) fatigue assessment is taken into account, reflects the onset of fatigue by implementing a combination of a dimensionless (0-1) global fatigue descriptor (GFD) and a support vector machine (SVM) classifier. The system, based on 9 main combined features, achieves fatigue regime classification performances of 0.82 ± 0.24, ensuring a successful preventive assessment when dangerous fatigue levels are reached. Training data were acquired in a constant work rate test (executed by 14 subjects using a cycloergometry device), where the variable under study (fatigue) gradually increased until the volunteer reached an objective exhaustion state.
Fatigue related to Multiple Sclerosis (MS) is considered a multidimensional symptom, manifesting in several dimensions such as physical, cognitive, and psychosocial fatigue. This study investigated in 264 patients with severe primary MS-related fatigue (median MS duration 6.8 years, mean age 48.1 years, 75% women) whether subgroups can be distinguished based on these dimensions. Subsequently, we tested whether MS-related fatigue consists of a single common unidimensional factor. Subscale scores on four self-reported fatigue questionnaires, including the Checklist of Individual Strength, the Modified Fatigue Impact Scale, the Fatigue Severity Scale and the SF36 vitality, were used in a cluster analysis to identify patients with similar fatigue characteristics. Next, all 54 items were included in exploratory factor analysis to test unidimensionality. Study results show that in patients with a treatment indication for primary MS-related fatigue, fatigue profiles are based on severity and not on the various dimensions of fatigue. The three profiles found, suggested one underlying fatigue dimension, but this could not be confirmed. Factor analysis of all 54 items resulted in 8 factors, confirming the multidimensional construct of the included fatigue questionnaires.
Fatigue affects most cancer patients and has numerous potential causes, including cancer itself and cancer treatment. Cancer-related fatigue (CRF) is not relieved by rest, can decrease quality of life, and has no FDA-approved therapy. Thyrotropin-releasing hormone (TRH) has been proposed as a potential novel treatment for CRF, but its efficacy against CRF remains largely untested. Thus, we tested the TRH analog, taltirelin (TAL), in mouse models of CRF. To model fatigue, we used a mouse model of chemotherapy, a mouse model of radiation therapy, and mice bearing colon 26 carcinoma tumors. We used the treadmill fatigue test to assess fatigue-like behavior after treatment with TAL. Additionally, we used wild-type and TRH receptor knockout mice to determine which TRH receptor was necessary for the actions of TAL. Tumor-bearing mice displayed muscle wasting and all models caused fatigue-like behavior, with mice running a shorter distance in the treadmill fatigue test than controls. TAL reversed fatigue-like behavior in all three models and the mouse TRH1 receptor was necessary for the effects of TAL. These data suggest that TAL may be useful in alleviating fatigue in all cancer patients and provide further support for evaluating TAL as a potential therapy for CRF in humans.
A large number of fatigue scales exist and there is no consensus on which fatigue measuring scales that are most appropriate for use in assessment of fatigue in different diseases. We aimed to describe the use of fatigue scales in studies of disease-related fatigue during the last three decades. We searched databases from 1975 to 2004 for original studies reporting on disease-related fatigue and extracted information on method used to assess fatigue, diseases under study and year of publication. A total of 2285 papers reported measures of fatigue in chronic non-acute diseases of which 80% were published during the last decade. We identified 252 different ways to measure fatigue, of which 150 were use only once. Multi-symptom scales (n = 156) were used in 670 studies, while 71 scales specifically designed to measure fatigue were applied in 416 studies. The majority of these studies used scales with a multidimensional approach to fatigue, and most studies used scales that were disease-specific or only applied to few different diseases. Research in disease-related fatigue has increased exponentially during the last three decades, even if we adjust for the general increase in publishing activity. The number of scales has also increased and the majority of scales were developed for specific diseases. There is need for measure instruments with different sizes and dimensionality, and due to ceiling and floor effects, the same scale may not be useful for patients with different severity of fatigue. However, since fatigue is an unspecific symptom there should not be need for adopting disease specific fatigue scales for each individual disease. There may be differences in characteristics of fatigue between diseases and generic measurement instruments may facilitate documentation of such differences, which may be of clinical importance.
A lack of fatigue-related muscle contractile property changes at time of perceived physical exhaustion and greater central than peripheral fatigue detected by twitch interpolation technique have recently been reported in cancer survivors with fatigue symptoms. Based on these observations, it was hypothesized that compared to healthy people, myoelectrical manifestation of fatigue in the performing muscles would be less significant in these individuals while sustaining a prolonged motor task to self-perceived exhaustion (SPE) since their central fatigue was more prominent. The purpose of this study was to test this hypothesis by examining electromyographic (EMG) signal changes during fatiguing muscle performance.
Cognitive fatigue, or fatigue related to mental work, is a common experience. A growing body of work using functional neuroimaging has identified several regions that appear to be related to cognitive fatigue and that potentially comprise a "fatigue network". These include the striatum of the basal ganglia, the dorsolateral prefrontal cortex (DLPFC), the dorsal anterior cingulate cortex (dACC), the ventro-medial prefrontal cortex (vmPFC) and the anterior insula. However, no work has been conducted to assess whether the connectivity between these regions changes as a function of cognitive fatigue. We used a task-based functional neuroimaging paradigm to induce fatigue in 39 healthy individuals, regressed the signal associated with the task out of the data, and investigated how the functional connectivity between these regions changed as cognitive fatigue increased. We observed functional connectivity between these regions and other frontal regions largely decreased as cognitive fatigue increased while connectivity between these seeds and more posterior regions increased. Furthermore the striatum, the DLPFC, the insula and the vmPFC appeared to be central 'nodes' or hubs of the fatigue network. These findings represent the first demonstration that the functional connectivity between these areas changes as a function of cognitive fatigue.
The emerging applications of hydrogels in devices and machines require hydrogels to maintain robustness under cyclic mechanical loads. Whereas hydrogels have been made tough to resist fracture under a single cycle of mechanical load, these toughened gels still suffer from fatigue fracture under multiple cycles of loads. The reported fatigue threshold for synthetic hydrogels is on the order of 1 to 100 J/m2. We propose that designing anti-fatigue-fracture hydrogels requires making the fatigue crack encounter and fracture objects with energies per unit area much higher than that for fracturing a single layer of polymer chains. We demonstrate that the controlled introduction of crystallinity in hydrogels can substantially enhance their anti-fatigue-fracture properties. The fatigue threshold of polyvinyl alcohol (PVA) with a crystallinity of 18.9 weight % in the swollen state can exceed 1000 J/m2.
Background: Fatigue is a common complaint in patients with idiopathic pulmonary fibrosis (IPF) and has been reported in a considerable percentage of patients. Fatigue is also a registered side effect of pirfenidone, one of two approved antifibrotic drugs. The Fatigue Assessment Scale (FAS) was developed for assessment of fatigue in sarcoidosis and validated in patients with sarcoidosis. FAS has been used in a few IPF studies but has not been validated. Aims: To study the change in FAS after initiation of pirfenidone or nintedanib in the treatment of patients with IPF during a six-month period. Methods: Between April 2017 and January 2018, all incident patients with IPF starting antifibrotic treatment were invited to complete FAS before, four weeks, three, and six months after initiation of antifibrotic treatment. Baseline characteristics including lung function were registered. Results: Fifty-two patients were included, mean FVC% 84.8, mean DLCO% 51.4. Nintedanib was started in 25 patients; 27 patients started pirfenidone. Sixty-four percent of patients had a FAS score >22 indicating substantial fatigue at baseline. There was no statistically significant difference in FAS score for patients treated with nintedanib or pirfenidone at any time point. FAS score increased statistically significantly during the six-month follow-up. This change was driven by patients without substantial fatigue at baseline with an increase in FAS score of 8.4 points; patients with substantial fatigue at baseline experienced no statistically significant change. Conclusion: A majority of patients with IPF suffered from substantial fatigue at the time of diagnosis. Fatigue progressed over time and increasing fatigue was associated with younger age, nintedanib treatment and low degree of fatigue at baseline. There was no significant difference in FAS score between the two antifibrotic treatments at any time point, even though fatigue is not a registered side effect in nintedanib.
Q fever fatigue syndrome (QFS) is characterised by a state of prolonged fatigue that is seen in 20% of acute Q fever infections and has major health-related consequences. The molecular mechanisms underlying QFS are largely unclear. In order to better understand its pathogenesis, we applied a multi-omics approach to study the patterns of the gut microbiome, blood metabolome, and inflammatory proteome of QFS patients, and compared these with those of chronic fatigue syndrome (CFS) patients and healthy controls (HC).
Mental fatigue is an important aspect of alertness and wellbeing. Existing fatigue tests are subjective and/or time-consuming. Here, we show that smartphone-based gaze is significantly impaired with mental fatigue, and tracks the onset and progression of fatigue. A simple model predicts mental fatigue reliably using just a few minutes of gaze data. These results suggest that smartphone-based gaze could provide a scalable, digital biomarker of mental fatigue.
The adhesion of soft connective tissues (tendons, ligaments, and cartilages) on bones in many animals can maintain high toughness (∽800 J m-2) over millions of cycles of mechanical loads. Such fatigue-resistant adhesion has not been achieved between synthetic hydrogels and engineering materials, but is highly desirable for diverse applications such as artificial cartilages and tendons, robust antifouling coatings, and hydrogel robots. Inspired by the nanostructured interfaces between tendons/ligaments/cartilages and bones, we report that bonding ordered nanocrystalline domains of synthetic hydrogels on engineering materials can give a fatigue-resistant adhesion with an interfacial fatigue threshold of 800 J m-2, because the fatigue-crack propagation at the interface requires a higher energy to fracture the ordered nanostructures than amorphous polymer chains. Our method enables fatigue-resistant hydrogel coatings on diverse engineering materials with complex geometries. We further demonstrate that the fatigue-resistant hydrogel coatings exhibit low friction and low wear against natural cartilages.
The mass digitization of books is changing the way information is created, disseminated and displayed. Electronic book readers (e-readers) generally refer to two main display technologies: the electronic ink (E-ink) and the liquid crystal display (LCD). Both technologies have advantages and disadvantages, but the question whether one or the other triggers less visual fatigue is still open. The aim of the present research was to study the effects of the display technology on visual fatigue. To this end, participants performed a longitudinal study in which two last generation e-readers (LCD, E-ink) and paper book were tested in three different prolonged reading sessions separated by--on average--ten days. Results from both objective (Blinks per second) and subjective (Visual Fatigue Scale) measures suggested that reading on the LCD (Kindle Fire HD) triggers higher visual fatigue with respect to both the E-ink (Kindle Paperwhite) and the paper book. The absence of differences between E-ink and paper suggests that, concerning visual fatigue, the E-ink is indeed very similar to the paper.
Heart rate variability (HRV) is an objective, non-invasive tool to assessing autonomic dysfunction in chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME). People with CFS/ME tend to have lower HRV; however, in the literature there are only a few previous studies (most of them inconclusive) on their association with illness-related complaints. To address this issue, we assessed the value of different diurnal HRV parameters as potential biomarker in CFS/ME and also investigated the relationship between these HRV indices and self-reported symptoms in individuals with CFS/ME.
Motor neuron diseases as amyotrophic lateral sclerosis and post-polio syndrome are characterized by prominent muscular weakness and severe motor disability. The prevalence of fatigue in motor neuron diseases is remarkably high, and may contribute significantly to patients' disability and a poor quality of life. Despite its high prevalence, fatigue is an understudied clinical problem in motor neuron diseases and is often overlooked. The present review will attempt to explain the pathogenic mechanisms of muscle fatigue in amyotrophic lateral sclerosis and post-polio syndrome, to cover the various methods of quantification of fatigue that measure both subjective and physiological components, and to summarize the evidence regarding therapeutic interventions that can be used in order to minimize this symptom.
Although fatigue is an important nonmotor symptom in Parkinson's Disease (PD) patients, little is known about the pathophysiological details of fatigue in PD, and it is still unknown whether fatigue correlates with PD prognosis. In this study, we investigated whether fatigue in PD correlates with clinical manifestations, treatment, or patient prognosis.
Reduced basal ganglia function has been associated with fatigue in neurologic disorders, as well as in patients exposed to chronic immune stimulation. Patients with chronic fatigue syndrome (CFS) have been shown to exhibit symptoms suggestive of decreased basal ganglia function including psychomotor slowing, which in turn was correlated with fatigue. In addition, CFS patients have been found to exhibit increased markers of immune activation. In order to directly test the hypothesis of decreased basal ganglia function in CFS, we used functional magnetic resonance imaging to examine neural activation in the basal ganglia to a reward-processing (monetary gambling) task in a community sample of 59 male and female subjects, including 18 patients diagnosed with CFS according to 1994 CDC criteria and 41 non-fatigued healthy controls. For each subject, the average effect of winning vs. losing during the gambling task in regions of interest (ROI) corresponding to the caudate nucleus, putamen, and globus pallidus was extracted for group comparisons and correlational analyses. Compared to non-fatigued controls, patients with CFS exhibited significantly decreased activation in the right caudate (p = 0.01) and right globus pallidus (p = 0.02). Decreased activation in the right globus pallidus was significantly correlated with increased mental fatigue (r2 = 0.49, p = 0.001), general fatigue (r2 = 0.34, p = 0.01) and reduced activity (r2 = 0.29, p = 0.02) as measured by the Multidimensional Fatigue Inventory. No such relationships were found in control subjects. These data suggest that symptoms of fatigue in CFS subjects were associated with reduced responsivity of the basal ganglia, possibly involving the disruption of projections from the globus pallidus to thalamic and cortical networks.
Accumulating data indicates a link between a pro-inflammatory status and occurrence of chronic disease-related fatigue. The questions are whether the observed inflammatory profile can be (a) improved by anti-inflammatory diets, and (b) if this improvement can in turn be translated into a significant fatigue reduction. The aim of this narrative review was to investigate the effect of anti-inflammatory nutrients, foods, and diets on inflammatory markers and fatigue in various patient populations. Next to observational and epidemiological studies, a total of 21 human trials have been evaluated in this work. Current available research is indicative, rather than evident, regarding the effectiveness of individuals' use of single nutrients with anti-inflammatory and fatigue-reducing effects. In contrast, clinical studies demonstrate that a balanced diet with whole grains high in fibers, polyphenol-rich vegetables, and omega-3 fatty acid-rich foods might be able to improve disease-related fatigue symptoms. Nonetheless, further research is needed to clarify conflicting results in the literature and substantiate the promising results from human trials on fatigue.
The role of immune or infective triggers in the pathogenesis of Chronic Fatigue Syndrome (CFS) is not yet fully understood. Barriers to obtaining immune measures at baseline (i.e., before the trigger) in CFS and post-infective fatigue model cohorts have prevented the study of pre-existing immune dysfunction and subsequent immune changes in response to the trigger. This study presents interferon-alpha (IFN-α)-induced persistent fatigue as a model of CFS. IFN-α, which is used in the treatment of chronic Hepatitis C Virus (HCV) infection, induces a persistent fatigue in some individuals, which does not abate post-treatment, that is, once there is no longer immune activation. This model allows for the assessment of patients before and during exposure to the immune trigger, and afterwards when the original trigger is no longer present. Fifty-five patients undergoing IFN-α treatment for chronic HCV were assessed at baseline, during the 6-12 months of IFN-α treatment, and at six-months post-treatment. Measures of fatigue, cytokines and kynurenine pathway metabolites were obtained. Fifty-four CFS patients and 57 healthy volunteers completed the same measures at a one-off assessment, which were compared with post-treatment follow-up measures from the HCV patients. Eighteen patients undergoing IFN-α treatment (33%) were subsequently defined as having 'persistent fatigue' (the proposed model for CFS), if their levels of fatigue were higher six-months post-treatment than at baseline; the other 67% were considered 'resolved fatigue'. Patients who went on to develop persistent fatigue experienced a greater increase in fatigue symptoms over the first four weeks of IFN-α, compared with patients who did not (Δ Treatment Week (TW)-0 vs. TW4; PF: 7.1 ± 1.5 vs. RF: 4.0 ± 0.8, p = 0.046). Moreover, there was a trend towards increased baseline interleukin (IL)-6, and significantly higher baseline IL-10 levels, as well as higher levels of these cytokines in response to IFN-α treatment, alongside concurrent increases in fatigue. Levels increased to more than double those of the other patients by Treatment Week (TW)4 (p = 0.011 for IL-6 and p = 0.001 for IL-10). There was no evidence of an association between persistent fatigue and peripheral inflammation six-months post-treatment, nor did we observe peripheral inflammation in the CFS cohort. While there were changes in kynurenine metabolites in response to IFN-α, there was no association with persistent fatigue. CFS patients had lower levels of the ratio of kynurenine to tryptophan and 3-hydroxykynurenine than controls. Future studies are needed to elucidate the mechanisms behind the initial exaggerated response of the immune system in those who go on to experience persistent fatigue even if the immune trigger is no longer present, and the change from acute to chronic fatigue in the absence of continued peripheral immune activation.
Fatigue is the subjective sensation of weariness, increased sense of effort, or exhaustion and is pervasive in neurologic illnesses. Despite its prevalence, we have a limited understanding of the neurophysiological mechanisms underlying fatigue. The cerebellum, known for its role in motor control and learning, is also involved in perceptual processes. However, the role of the cerebellum in fatigue remains largely unexplored. We performed two experiments to examine whether cerebellar excitability is affected after a fatiguing task and its association with fatigue. Using a crossover design, we assessed cerebellar inhibition (CBI) and perception of fatigue in humans before and after "fatigue" and "control" tasks. Thirty-three participants (16 males, 17 females) performed five isometric pinch trials with their thumb and index finger at 80% maximum voluntary capacity (MVC) until failure (force <40% MVC; fatigue) or at 5% MVC for 30 s (control). We found that reduced CBI after the fatigue task correlated with a milder perception of fatigue. In a follow-up experiment, we investigated the behavioral consequences of reduced CBI after fatigue. We measured CBI, perception of fatigue, and performance during a ballistic goal-directed task before and after the same fatigue and control tasks. We replicated the observation that reduced CBI after the fatigue task correlated with a milder perception of fatigue and found that greater endpoint variability after the fatigue task correlated with reduced CBI. The proportional relation between cerebellar excitability and fatigue indicates a role of the cerebellum in the perception of fatigue, which might come at the expense of motor control.SIGNIFICANCE STATEMENT Fatigue is one of the most common and debilitating symptoms in neurologic, neuropsychiatric, and chronic illnesses. Despite its epidemiological importance, there is a limited understanding of the neurophysiological mechanisms underlying fatigue. In a series of experiments, we demonstrate that decreased cerebellar excitability relates to lesser physical fatigue perception and worse motor control. These results showcase the role of the cerebellum in fatigue regulation and suggest that fatigue- and performance-related processes might compete for cerebellar resources.
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