Is physical deconditioning a perpetuting factor in chronic fatigue syndrome? A controlled study on maximal exercise performance and relations with fatigue, impairment, and physical activity

Department of Medical Psychology, University of Nijmegen, The Netherlands.
Psychological Medicine (Impact Factor: 5.94). 02/2001; 31(1):107-14. DOI: 10.1017/S0033291799003189
Source: PubMed


Chronic fatigue syndrome (CFS) patients often complain that physical exertion produces an increase of complaints, leading to a greater need for rest and more time spent in bed. It has been suggested that this is due to a bad physical fitness and that physical deconditioning is a perpetuating factor in CFS. Until now, studies on physical deconditioning in CFS have shown inconsistent results.
Twenty CFS patients and 20 matched neighbourhood controls performed a maximal exercise test with incremental load. Heart rate, blood pressure, respiratory tidal volume, O2 saturation, O2 consumption, CO2 production, and blood-gas values of arterialized capillary blood were measured. Physical fitness was quantified as the difference between the actual and predicted ratios of maximal workload versus increase of heart rate. Fatigue, impairment and physical activity were assessed to study its relationship with physical fitness.
There were no statistically significant differences in physical fitness between CFS patients and their controls. Nine CFS patients had a better fitness than their control. A negative relationship between physical fitness and fatigue was found in both groups. For CFS patients a negative correlation between fitness and impairment and a positive correlation between fitness and physical activity was found as well. Finally, it was found that more CFS patients than controls did not achieve a physiological limitation at maximal exercise.
Physical deconditioning does not seem a perpetuating factor in CFS.

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    • "Symptom exacerbation (i.e., PEM) related to even mild exercise has been reported to occur in greater than 95% of CFS patients.[2] In the literature, the patient reactions associated with PEM have included increased symptoms of pain and fatigue,[3] [4] [5] abnormal cardiopulmonary responses to exercise,[2] [6] [7] decreases in physical activity behaviors,[4] [8] [9] changes in cognitive function,[10] [11] and up-regulation of numerous biological variables.[12] [13] Although a number of studies have been conducted, consistent results and/or replication of findings have been rare.[14] "
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    ABSTRACT: Background: A primary complaint of chronic fatigue syndrome (CFS) patients is post-exertion malaise, which is a worsening of symptoms following activities such as exercise. Purpose: To examine the link between gene expression for metabolite, adrenergic, immune, and glucocorticoid receptors on leukocytes and symptoms (pain, fatigue, and mood) following a maximal exercise test. Methods: Thirteen CFS patients and 11 healthy participants matched on age and fitness underwent blood draws and completed questionnaires immediately before, and 15 minutes, 48 hours, and 72 hours following, maximal exercise. Symptom and genetic measures collected before and after exercise were compared using a doubly multivariate repeated-measures analysis of variance. Results: This comparison of CFS and healthy participants resulted in a significant multivariate main effect for Group (p textless 0.05). Univariate analyses indicated group differences for adrenergic α-2A and glucocorticoid (NR3C1) receptor messenger ribonucleic acid and symptoms of fatigue and confusion. Changes in gene expression were significantly correlated with symptoms. Conclusions: Results suggest that increased glucocorticoid sensitivity may contribute to the symptoms of post-exertion malaise in CFS. As NR3C1 interacts with other transcription factors, investigating the resulting cascades may lead to greater understanding of the biological mechanism of post-exertion malaise. This finding, if confirmed, could lead to novel approaches to prevent symptom exacerbation in CFS.
    10/2013; 1(4-4):190-209. DOI:10.1080/21641846.2013.838444
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    • "From previous studies in patients with CFS compared to healthy controls we know that groups of at least 10, preferably 20 patients per condition are sufficient to detect significant differences in (neuro)physiological parameters measured with sEMG, MRI, and exercise testing.[21,28,50,51] To identify (neuro)physiological characteristics of fatigue, a comparison of baseline measurements with an age, sex, and previous cancer treatment matched group of 20 non-fatigued patients is sufficient. "
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    ABSTRACT: Postcancer fatigue is a frequently occurring, severe, and invalidating problem, impairing quality of life. Although it is possible to effectively treat postcancer fatigue with cognitive behaviour therapy, the nature of the underlying (neuro)physiology of postcancer fatigue remains unclear. Physiological aspects of fatigue include peripheral fatigue, originating in muscle or the neuromuscular junction; central fatigue, originating in nerves, spinal cord, and brain; and physical deconditioning, resulting from a decreased cardiopulmonary function. Studies on physiological aspects of postcancer fatigue mainly concentrate on deconditioning. Peripheral and central fatigue and brain morphology and function have been studied for patients with fatigue in the context of chronic fatigue syndrome and neuromuscular diseases and show several characteristic differences with healthy controls. Fifty seven severely fatigued and 21 non-fatigued cancer survivors will be recruited from the Radboud University Nijmegen Medical Centre. Participants should have completed treatment of a malignant, solid tumour minimal one year earlier and should have no evidence of disease recurrence. Severely fatigued patients are randomly assigned to either the intervention condition (cognitive behaviour therapy) or the waiting list condition (start cognitive behaviour therapy after 6 months). All participants are assessed at baseline and the severely fatigued patients also after 6 months follow-up (at the end of cognitive behaviour therapy or waiting list). Primary outcome measures are fatigue severity, central and peripheral fatigue, brain morphology and function, and physical condition and activity. This study will be the first randomized controlled trial that characterizes (neuro)physiological factors of fatigue in disease-free cancer survivors and evaluates to which extent these factors can be influenced by cognitive behaviour therapy. The results of this study are not only essential for a theoretical understanding of this invalidating condition, but also for providing an objective biological marker for fatigue that could support the diagnosis and follow-up of treatment. The study is registered at (NCT01096641).
    BMC Cancer 06/2012; 12(1):256. DOI:10.1186/1471-2407-12-256 · 3.36 Impact Factor
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    • "According to some studies ME/CFS patients are ca pable of performing at the same level as sedentary controls (LaManca et al. 1999; Sargent et al. 2002; Bazelmans et al. 2001; Takken et al. 2007). However, when looking at the " high " performance levels of the ME/CFS patients in these latter studies, the deviant fin dings are most likely the result of differences in test samples, e.g. "
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    ABSTRACT: Benign Myalgic Encephalomyelitis (ME) / Chronic Fatigue Syndrome (CFS) is a debilitating disease which, despite numerous biological abnormalities has remained highly controversial. Notwithstanding the medical pathogenesis of ME/CFS, the (bio)psychosocial model is adopted by many governmental organizations and medical profes-sio-nals to legitimize the combination of Cognitive Behavioral Therapy (CBT) and Graded Exercise Therapy (GET) for ME/CFS. Justified by this model CBT and GET aim at eliminating presumed psychogenic and socially induced maintaining factors and reversing deconditioning, respectively. In this review we invalidate the (bio)psychosocial model for ME/CFS and demonstrate that the success claim for CBT/GET to treat ME/CFS is unjust. CBT/GET is not only hardly more effective than non-interventions or standard medical care, but many patients report that the therapy had affected them adversely, the majority of them even reporting substantial deterioration. Moreover, this review shows that exertion and thus GET most likely have a negative impact on many ME/CFS patients. Exertion induces post-exertional malaise with a decreased physical performan-ce/aerobic capacity, increased muscoskeletal pain, neurocognitive impairment, "fatigue", and weakness, and a long lasting "recovery" time. This can be explained by findings that exertion may amplify pre-existing pa-thophysiological abnormalities underpinning ME/CFS, such as inflammation, immune dysfunction, oxidative and nitrosative stress, channelopathy, defec-tive stress response mechanisms and a hypoactive hypothalamic-pituitary-adrenal axis. We conclude that it is unethical to treat patients with ME/CFS with ineffective, non-evidence-based and potentially harmful "rehabilitation therapies", such as CBT/GET.
    Neuro endocrinology letters 08/2009; 30(3):284-99. · 0.80 Impact Factor
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