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Fatigue: Biomedicine, Health & Behavior - Volume 2, Issue 2, 2014
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Titles and abstracts for the journal, Fatigue: Biomedicine, Health & Behavior, Volume 2, Issue 2, 2014. ==Volume 2, Issue 2, 2014== *The delayed fatigue effect in [[myalgic encephalomyelitis]]/[[chronic fatigue syndrome]] ([[ME/CFS]]) <blockquote> '''Abstract''' - '''Background''': [[Myalgic encephalomyelitis]]/[[chronic fatigue syndrome]] ([[ME/CFS]]) is a debilitating, long-term condition characterised by extreme fatigue (worsened by exertion), muscle and joint pain, and sleep disturbance. Post-exertional fatigue has been demonstrated previously following physical exercise, but not from mental exertion alone. '''Purpose''': The aim of this exploratory study was to assess the βdelayed fatigue effect,β in this instance fatigue two days post-challenge, following a cognitively fatiguing task. '''Methods''': Thirty-two participants (23 women; mean age 44, SDβ=β11.24; mean illness duration nine years, SDβ=β7.32) completed the Cambridge Neuropsychological Test Automated Battery, which acted as the cognitive challenge. Self-report measures were also completed that assessed fatigue (Multidimensional Fatigue Inventory; MFI), and anxiety and depression (Hospital Anxiety and Depression Scale; HADS) pre- and two days post-testing. '''Results''': Significant differences were found between pre- and post-test measures in three MFI sub-scales of fatigue (general, mental, and physical) and on the depression scale of the HADS. However, there were no significant changes in motivation, activity level, or self-reported anxiety scores. '''Conclusions''': These findings are suggestive of post-exertional symptom exacerbation following mental effort. This may have implications for working environments that present cognitive demands to individuals with ME/CFS."<ref name="Arroll, 2014" /></blockquote> *''Fatigue and body mass index in the Fragile X premutation carrier <blockquote> '''Abstract''' - '''Background''': Recent evidence has shown that mitochondrial dysfunction may be significant in carriers of the Fragile X premutation. '''Purpose''': The present study examined fatigue severity and body mass index (BMI) (two possible outcomes related to mitochondrial dysfunction) in premutation carriers with and without the Fragile X-associated Tremor Ataxia Syndrome (FXTAS) as compared to controls. '''Methods''': Surveys to gather data on height and weight and fatigue impact (Fatigue Severity Scale) were sent out to previous research trial participants with Fragile X premutation-related disorders. '''Results''': On the Fatigue Severity Scale, carriers with and without FXTAS had mean scores of 4.5 (SD 1.9) and 3.8 (SD 1.6), respectively, that differed significantly (pβ<β0.001) from the control mean score of 2.9 (SD 1.4). The mean BMI of carriers with FXTAS was 29.6β kg/m2 (SD 5.3) which differed significantly (pβ=β0.003) from the mean BMI of carriers without FXTAS of 26.9β kg/m2 (SD 5.1) and controls 26.7β kg/m2 (SD 4.4). However, premutation carriers without FXTAS did not differ significantly in BMI from controls. '''Conclusions''': The present study suggests potentially important clinical outcomes that may be related to the mitochondrial dysfunction seen in molecular studies previously done with premutation carriers.<ref>Summers, S. M., Cogswell, J., Goodrich, J. E., Mu, Y., Nguyen,D. V., Brass, S.D., & Hagerman, R. J. (2014). Fatigue and body mass index in the Fragile X premutation carrier. ''Fatigue: Biomedicine, Health & Behavior, 2'' (2), 64-72. doi:10.1080/21641846.2014.881155</ref></blockquote>'' *Acute and chronic hypoxia: implications for cerebral function and exercise tolerance.<blockquote> '''Abstract''' - '''Purpose''': To outline how hypoxia profoundly affects neuronal functionality and thus compromises exercise performance. '''Methods''': Investigations were reviewed and evaluated that used electroencephalography (EEG) and transcranial magnetic stimulation (TMS) to detect neuronal changes at rest and those studying fatiguing effects on whole-body exercise performance in acute (AH) and chronic hypoxia (CH). '''Results''': At rest during very early hypoxia (<1-h), slowing of cerebral neuronal activity is evident despite no change in corticospinal excitability. As time in hypoxia progresses (3-h), increased corticospinal excitability becomes evident; however, changes in neuronal activity are unknown. Prolonged exposure (3β5 d) causes a respiratory alkalosis which modulates Na+ channels, potentially explaining reduced neuronal excitability. Locomotor exercise in AH exacerbates the development of peripheral fatigue; as the severity of hypoxia increases, mechanisms of peripheral fatigue become less dominant and CNS hypoxia becomes the predominant factor. The greatest central fatigue in AH occurs when SaO2 is β€75%, a level that coincides with increasing impairments in neuronal activity. CH does not improve the level of peripheral fatigue observed in AH; however, it attenuates the development of central fatigue paralleling increases in cerebral O2 availability and corticospinal excitability. '''Conclusions''': The attenuated development of central fatigue in CH might explain the improvements in locomotor exercise performance commonly observed after acclimatisation to high altitude.<ref>Goodall, S., Twomey, R., & Amann, M. (2014). Acute and chronic hypoxia: implications for cerebral function and exercise tolerance. Fatigue: biomedicine, health & behavior, 2(2), 73-92. doi:10.1080/21641846.2014.909963</ref></blockquote> *[[Chronic Fatigue Syndrome]]: The Current Status and Future Potentials of Emerging [[Biomarker]]s [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4052724/ (Full text)]<blockquote> '''Abstract''' - [[Chronic fatigue syndrome]] ([[chronic fatigue syndrome|CFS]]) remains an incompletely characterized illness, in part due to controversy regarding its definition, biological basis and diagnosis. [[Biomarker]]s are objective measures that may lead to improvements in our understanding of CFS by providing a more coherent and consistent approach to study, diagnosis and treatment of the illness. Such metrics may allow us to distinguish between [[chronic fatigue syndrome|CFS]] subtypes β each defined by characteristic [[biomarker]]s β currently conflated under the single, heterogeneous condition of CFS. These delineations, in turn, may guide more granular, focused, and targeted treatment strategies based on more precise characterizations of the illness. Here, we review potential [[chronic fatigue syndrome|CFS]] [[biomarker]]s related to neurological and immunological components of the illness, and discuss how these [[biomarker]]s may be used to move the field of [[chronic fatigue syndrome|CFS]] forward, emphasizing clinical utility and potential routes of future research. <ref name="Fischer, 2014" /></blockquote> *Feasibility of a home-based self-management program for chronic fatigue <blockquote> '''Abstract''' - '''Purpose''': This study evaluated the feasibility of a 12-week home-based self-management program for unexplained chronic fatigue (UCF) or chronic fatigue syndrome (CFS). '''Methods''': Self-report outcomes included measures of fatigue impact, physical function, depression, and global change. A web diary measured daily compliance with self-management activities. '''Results''': Study withdrawals (20.8%) were due to time constraints, confidentiality concerns, or illness recovery. Subjects (Nβ=β19) showed excellent compliance (62.3%) on the web diary. Participant feedback indicated high satisfaction. Effect sizes were large for fatigue severity, physical functioning, and depression. '''Conclusions''': A home-based self-management program for UCF and CFS may offer improved patient access to treatment that may be unavailable, inconvenient, or costly. <ref>[[Fred Friedberg]], Ngan, M. C., & Chang, J. (2014). Feasibility of a home-based self-management program for chronic fatigue. ''Fatigue: Biomedicine, Health & Behavior, 2'' (2), 110-118. doi:10.1080/21641846.2014.904066</ref></blockquote> ==See also== *[[Fatigue: Biomedicine, Health & Behavior]] for other Issues ==References== <references> <ref name="Arroll, 2014">{{Citation | last1 = Arroll | first1 = M. A. | author-link1 = | last2 = Attree | first2 = E. A. | authorlink2 = | last3 = O'Leary | first3 = J.M. | author-link3 = | last4 = Dancey | first4 = C.P. | authorlink4 = | title = The delayed fatigue effect in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) | journal = Fatigue: Biomedicine, Health & Behavior | volume = 2 | issue = 2 | page = 57-63 | date = 2014 | pmid = | doi = 10.1080/21641846.2014.892755 }}</ref> <ref name="Fischer, 2014">{{Citation | last1 = Fischer | first1 = David B. | author-link1 = | last2 = William | first2 = Arsani H. | authorlink2 = | last3 = Strauss | first3 = Adam C. | authorlink3 = | last4 = Unger | first4 = Elizabeth R. | authorlink4 = Elizabeth Unger | last5 = Jason | first5 = Leonard | authorlink5 = Leonard Jason | last6 = Marshall, Jr | first6 = GailenD. | authorlink6 = Gailen Marshall | last7 = Dimitrakoff | first7 = JordanD. | author-link8 = Jordan Dimitrakoff | title = Chronic Fatigue Syndrome: The Current Status and Future Potentials of Emerging Biomarkers | journal = Fatigue: Biomedicine, Health & Behavior | volume = 2 | issue = 2 | page = 93-109 | date = 2014 | pmid = | doi = 10.1080/21641846.2014.906066 }}</ref> </references> [[Category:Journal issues]] [[Category: Fatigue: Biomedicine, Health & Behavior issues]]
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