Cognitive functioning in chronic fatigue syndrome and the role of depression, anxiety and fatigue

Objective: This study was designed to investigate the role of depression, anxiety, and fatigue in Chronic Fatigue Syndrome (CFS) sufferers' objective and subjective cognitive performance. Methods: Twenty-three CFS sufferers and 23 healthy control participants were compared on objective and subjective assessments of cognitive performance. Depression, anxiety, and fatigue were also evaluated. Results: CFS sufferers did not demonstrate any impairment in objective cognitive functioning compared to the control group, and objective performance was not related to their higher levels of depression or their level of fatigue. Depression scores only accounted for a small amount of the variance in CFS sufferers' lower subjective assessment of their cognitive performance compared to control participants. There were no differences between the groups on anxiety scores. Conclusion: The results are discussed in terms of the heterogeneity of the CFS population and the complex interaction of symptomatological factors that characterise CFS.

A contested disease state : chronic fatigue syndrome

This paper aims firstly to look at characteristics of the condition, and current issues related to the symptomatology and presentation of ME-CFS. Secondly, it identifies methodological problems in researching ME/CFS and demonstrates that the experimental approach to researching the condition can be informed by more qualitative, constructivist approaches. Thirdly, it argues that ME-CFS is a contested state whose acceptance by the medical profession requires the legitimation of a demonstrated biomedical basis

Physical activity, emotional stress, sleep disturbances, and daily fluctuations in chronic fatigue symptomatology

The current study explored the relationships between physical and emotional stress and the symptomatology of chronic fatigue syndrome (CFS). Fifty-four CFS patients were studied using a longitudinal design. A self-report format was used to collect daily measures of major physical (sleep disturbance and physical activity) and emotional (subjective emotional stress level) stressors, as well as measures of levels of fatigue and secondary symptoms. The variables accounted for a moderate variance at the individual and occasion levels. Sleep disturbance and emotional stress were found to be positively associated with levels of fatigue and symptomatology, whereas physical activity was found to have a negative relationship with fatigue only. The severity of fatigue and symptoms were found to fluctuate daily in relation with the variables, indicating the complex nature of the associations.

The limits of medicine and the social consequences for sufferers of chronic fatigue syndrome

Chronic fatigue syndrome (CFS) appears to be made up of several clusters of illness categories acting alone or in tandem to cause the decline of health through; fatigue/exhaustion, sensitivity/allergies, pain, general muscle and joint pains, cognitive impairment and gastrointestinal problems. This study investigated how patients interpret, evaluate and respond to the complex and varied symptoms of chronic fatigue syndrome. Data were collected from persons with CFS using a survey (n=90) and an interview (n=45). The researchers investigated how chronic fatigue syndrome is diagnosed by medical practitioners, how the label of CFS is determined and the social consequences for the patient. The results confirm the limited ability of the biomedical paradigm to diagnose adequately and treat effectively 'socially constructed' and medically ambiguous illnesses like CFS. In the absence of a legitimated regime of medical treatment for CFS, a range of often expensive treatments are employed by CFS sufferers, from formal use of pharmaceutical drugs through to 'alternative' therapies, including herbal, vitamin, homeopathic, esoteric meditative techniques, spiritual healing and general counselling are taken in no particular order.

The effect of laser power density on the fatigue life of laser-shock-peened 7050 aluminium alloy

Laser shock peening (LSP) is an innovative surface treatment method that can result in significant improvement in the fatigue life of many metallic components. The process produces very little or no surface profile modification while producing a considerably deeper compressive residual stress layer than traditional shot peening operations. The work discussed here was designed to: (a) quantify the fatigue life improvement achieved by LSP in a typical high strength aircraft aluminium alloy and (b) identify any technological risks associated with its use. It is shown that when LSP conditions are optimal for the material and specimen configuration, a —three to four times increase in fatigue life over the as-machined specimens could be achieved for a representative fighter aircraft loading spectrum when applied at a representative load level. However, if the process parameters are not optimal for the material investigated here, fatigue lives of LSP treated specimens may be reduced instead of increased due to the occurrence of internal cracking. This paper details the effect of laser power density on fatigue life of 7050-T7451 aluminium alloy by experimental and numerical analysis.

Effect of susceptibility to interfacial fracture on fatigue properties of spot-welded high strength sheet steel

While advanced high strength steels (AHSS) have numerous advantages for the automotive industry, they can be susceptible to interfacial fracture when spot-welded. In this study, the susceptibility of interfacial fracture to spot-weld microstructure and hardness is examined, as well as the corresponding relationships between fatigue, overload performance, and interfacial fracture for a TRIP (transformation induced plasticity) steel. Simple post-weld heat-treatments were used to alter the weld microstructure. The effect on interfacial fracture of diluting the weld pool by welding the TRIP material to non-TRIP steel was examined, along with the effect of altering the base material microstructure. Results show that weld hardness is not a good indicator of either the susceptibility to interfacial fracture, or the strength of the joint, and that interfacial fracture does not necessarily lead to a decrease in strength compared to conventional weld-failure mechanisms, i.e. button pullout. It was also found that while interfacial fracture does affect low cycle to failure behavior, there was no effect on high cycle fatigue.

Depressed Na+-K+-ATPase activity in skeletal muscle at fatigue is correlated with increased Na+-K+-ATPase mRNA expression following intense exercise

We investigated whether depressed muscle Na⁺-K⁺-ATPase activity with exercise reflected a loss of Na⁺-K⁺-ATPase units, the time course of its recovery postexercise, and whether this depressed activity was related to increased Na⁺-K⁺-ATPase isoform gene expression. Fifteen subjects performed fatiguing, knee extensor exercise at ~40% maximal work output per contraction. A vastus lateralis muscle biopsy was taken at rest, fatigue, 3 h, and 24 h postexercise and analyzed for maximal Na⁺-K⁺-ATPase activity via 3-O-methylfluorescein phosphatase (3-O-MFPase) activity, Na⁺-K⁺-ATPase content via [3H]ouabain binding sites, and Na⁺-K⁺-ATPase α1-, α2-, α3-, ß1-, ß2- and ß3-isoform mRNA expression by real-time RT-PCR. Exercise [352 (SD 267) s] did not affect [³H]ouabain binding sites but decreased 3-O-MFPase activity by 10.7 (SD 8)% (P < 0.05), which had recovered by 3 h postexercise, without further change at 24 h. Exercise elevated α1-isoform mRNA by 1.5-fold at fatigue (P < 0.05). This increase was inversely correlated with the percent change in 3-O-MFPase activity from rest to fatigue (%Δ3-O-MFPaserest-fatigue) (r = –0.60, P < 0.05). The average postexercise (fatigue, 3 h, 24 h) {alpha}1-isoform mRNA was increased 1.4-fold (P < 0.05) and approached a significant inverse correlation with %Δ3-O-MFPaserest-fatigue (r = –0.56, P = 0.08). Exercise elevated α2-isoform mRNA at fatigue 2.5-fold (P < 0.05), which was inversely correlated with %Δ3-O-MFPaserest-fatigue (r = –0.60, P = 0.05). The average postexercise α2-isoform mRNA was increased 2.2-fold (P < 0.05) and was inversely correlated with the %Δ3-O-MFPaserest-fatigue (r = –0.68, P < 0.05). Nonsignificant correlations were found between %Δ3-O-MFPaserest-fatigue and other isoforms. Thus acute exercise transiently decreased Na^+-K⁺-ATPase activity, which was correlated with increased Na⁺-K⁺-ATPase gene expression. This suggests a possible signal-transduction role for depressed muscle Na⁺-K⁺-ATPase activity with exercise.

The effect of prestrain and bake hardening on the low-cycle fatigue properties of TRIP steel

The scope of this study was to examine the effects of plane strain prestrain, induced via cold-rolling, and subsequent automotive paint bake hardening cycle on both tensile and fatigue properties of a hot rolled TRIP780 multiphase steel. Strain-life data has been generated for as-received (0% prestrain), 10% and 20% prestrained samples, in both baked and unbaked conditions. Cold rolling  increased the number of strain reversals to failure at high cyclic strain amplitudes with no effect at low strain amplitudes. Bake hardening increased the number of reversals to failure at high cyclic strain amplitudes. The prestrained material exhibited partial cyclic softening, with some residual strength increase. The residual strength increase was attributed to the austenite to martensite transformation that occurred during the prestraining process.

Microstructural analysis of pre-strained TRIP steel after fatigue testing

The widespread introduction of multiphase sheet steels in the automotive industry has led to considerable interest in the fatigue properties of these materials. The different microstructural phases within matelials such as TRIP steels can influence the fatigue behaviour due to the manner in which the cyclic strain is accommodated within these phases. In this study fully reversed straincontrolled fatigue tests were perfonnrmed on a commercially-produced uncoated TRIP 780 steel both in the as-received and 20 % prestrained condition. The pre-strained TRIP steel showed significant cyclic softening at higher strain amplitudes, whereas some initial work hardening was observed at lower strain amplitudes before cyclic softening. The cyclic stabilised strength of the pre-strained TRIP steel was independent of strain amplitude, while the cyclic stabilised strength of the as-received TRIP steel increased with strain amplitude. Transmission Electron Microscopy TEM was used to examine the effect of the cyclic deformation on the microstructure of the different conditions, with the differences in fatigue behaviour explained based on the differences in the deformation structure formed within the steel (i.e. dislocation density and sub-structure and microband formation).

Fighting fatigue whilst fighting bushfire : an overview of factors contributing to firefighter fatigue during bushfire suppression

Aching muscles and joints, lethargy, and sleepiness are all signs of firefighter fatigue during bushfire suppression. If not managed, fatigue may lead to injury or illness for the individual, which may also compromise the safety and productivity of their crew. Understanding the many sources of firefighter fatigue is, therefore, fundamental for all Australian fire agencies. This article will briefly address  several factors thought to contribute to firefighter fatigue including; sleep loss, firefighter’s work activity, their hydration, and nutrition, the hot and smoky  working environment, firefighter’s physical fitness and their experience. This brief overview draws on findings from firefighting research and the broader scientific literature.

Integrity of the circadian time-keeping system in chronic fatigue syndrome

Chronic Fatigue Syndrome (CFS) is a debilitating condition in which severe, ongoing fatigue is the most prominent of a complex of somatic, psychological and neuropsychological symptoms. The aetiology of CFS remains uncertain and, to date, efforts to distinguish a clear pathophysiological profile for the disorder have been unsuccessful. Current evidence suggests that, rather than being a discrete disease entity with a single cause, CFS is a clinical condition resulting from the interaction of a number of pathophysiological factors, including acute infections, stress and psychiatric disorder. Recently, there has been some interest in the proposition that disordered circadian time-keeping may contribute to the development and/or course of the illness. The rationale for the investigation of circadian factors in CFS is based on the fact that disorders known to be associated with circadian dysregulation, such as jet lag and shiftwork related syndromes have a high degree of symptomatological overlap with CFS. Also, the presence of circadian disturbance could account, in part, for other phenomenological aspects of CFS, including the high rates of comorbid affective disturbance, and the reports of low-level immune dyregulation among sufferers. While several recent studies have produced some evidence of chronobiological dysregulation in CFS patients, much work remains before conclusions can be drawn about the presence, nature and clinical significance of circadian disturbance in CFS. This thesis describes a series of studies that were designed to systematically investigate: 1. whether CFS is associated with a state of circadian dysregulation, and 2. whether circadian dysregulation contributes significantly to the symptomatology of CFS. The first of the 5 studies reported here compared the circadian patterns of sleep-activity of CFS sufferers with those of healthy controls. Results indicated that CFS patients' sleep-activity cycles were significantly phase delayed compared to controls, and that some aspects of their circadian profiles of sleep-activity were related to some measures of sleep-disturbance and well-being. Studies 2 and 3 investigated the relationship between rhythms of sleep-wake and core temperature in CFS patients and healthy controls. The major finding from these studies was that sleep-wake and core temperature rhythms appear to be less effectively synchronised. Further evidence was collected that suggested that there was a relationship between circadian parameters and symptom measures in the CFS group. While this indicated that circadian dysregulation is linked in some way to the symptoms of CFS, assessment of the actual clinical significance of circadian disturbances required the use of a prospective methodology. The final two studies, therefore, report on a placebo-controlled trial of clinical interventions that were designed to restore circadian integrity to CFS patients, in order to see whether this would lead to a reduction in symptom number or severity. Results indicated that, although patients experienced improvements across a range of measures of symptoms and functional capacity, these were small in magnitude, of unlikely clinical significance, and no greater, in general, to improvements reported by patients who underwent placebo treatment. These results, along with those of the earlier studies, are discussed with respect to their implications regarding the presence and significance of circadian dysregulation. It is concluded that, while they provide evidence that CFS is associated with a degree of both internal and external circadian desynchrony, these findings suggest that circadian dysregulation is likely to be only a peripheral, contributor to the processes that generate and maintain the symptom complex. These findings are discussed with respect to how they contribute to our overall understanding of this multi-dimensional condition, and the implications they have for the continuing effort to investigate the causes and treatment of CFS.