Investigation by Polymerase Chain Reaction of Enteroviral Infection in Patients with Chronic Fatigue Syndrome

McArdle, Anne; McArdle, Francis; Jackson, MJ; Page, S.; Fahal, I. H.; Edwards, R. H. T.

doi:10.1042/cs0900295

Cited by 39 publications

(27 citation statements)

References 19 publications

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“…A significant reduction in citrate synthase, succinate reductase, and cytochrome-c oxidase was observed in the anterior tibialis muscle biopsy samples of CFS patients compared to healthy controls, which were attributed to the reduction in physical activity commonly present in CFS subjects [24]. A significant reduction in citrate synthase in the right quadriceps muscle biopsy samples from CFS subjects was also confirmed recently [37].…”

Section: Resultsmentioning

confidence: 59%

Association of mitochondrial dysfunction and fatigue: A review of the literature

et al. 2014

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Fatigue is often described by patients as a lack of energy, mental or physical tiredness, diminished endurance, and prolonged recovery after physical activity. Etiologic mechanisms underlying fatigue are not well understood; however, fatigue is a hallmark symptom of mitochondrial disease, making mitochondrial dysfunction a putative biological mechanism for fatigue. Therefore, this review examined studies that investigated the association of markers of mitochondrial dysfunction with fatigue and proposes possible research directions to enhance understanding of the role of mitochondrial dysfunction in fatigue. A thorough search using PubMed, Scopus, Web of Science, and Embase databases returned 1,220 articles. After application of inclusion and exclusion criteria, a total of 25 articles meeting eligibility criteria were selected for full review. Dysfunctions in the mitochondrial structure, mitochondrial function (mitochondrial enzymes and oxidative/nitrosative stress), mitochondrial energy metabolism (ATP production and fatty acid metabolism), immune response, and genetics were investigated as potential contributors to fatigue. Carnitine was the most investigated mitochondrial function marker. Dysfunctional levels were reported in all the studies investigating carnitine; however, the specific type of carnitine that was dysfunctional varied. Genetic profiles were the second most studied mitochondrial parameter. Six common pathways were proposed: metabolism, energy production, protein transport, mitochondrial morphology, central nervous system dysfunction and post-viral infection. Coenzyme Q10 was the most commonly investigated mitochondrial enzyme. Low levels of Coenzyme Q10 were consistently associated with fatigue. Potential targets for further investigation were identified as well as gaps in the current literature.

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Section: Resultsmentioning

confidence: 59%

Association of mitochondrial dysfunction and fatigue: A review of the literature

et al. 2014

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“…32 Alternatively, reduced glycolytic reserve in combination with reduced citrate synthase activity may promote pyruvate to be converted into lactate and removed from the cell. 4,19,31 This is essential as the accumulation of pyruvate may result in inhibition of glycolysis. ME/CFS patients have reported increased blood lactate, muscular lactate and ventricular lactate.…”

Section: Cd56mentioning

confidence: 99%

“…Interestingly, reduced citrate synthase activity has been reported in ME/CFS patients. 4,31 A reduction in citrate provides for the loss of allosteric regulation to inhibit glycolysis and facilitate glucose to be re-directed to the pentose phosphate pathway for NADPH production, which is essential for fatty acid synthesis. This pathway also compromises the availability of glutathione to remove hydrogen peroxide and may contribute to the evaluation of free radical, low fatty acids and high oxidized LDL antibodies reported in ME/CFS patients.…”

Section: Cd56mentioning

confidence: 99%

Reduced glycolytic reserve in isolated natural killer cells from Myalgic encephalomyelitis/chronic fatigue syndrome patients: A preliminary investigation

Nguyen

Staines

Johnston

et al. 2018

Asian Pac J Allergy Immunol

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Background: Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is medically unexplained post-exertional fatigue associated with significant reduction in natural killer cell (NK) cytotoxicity activity. Cytotoxic activity relies on glycolytic flux and mitochondrial respiration to fulfill energetic cellular demands. While mitochondrial dysfunction has been reported in ME/CFS patients, no previous investigation has examined the bioenergetic profile of isolated NK cells from ME/CFS patients.

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“…Depletion of muscle glycogen results in fatigue and impaired muscle performance and is a major determinant of endurance (2)(3)(4)(5). Likewise, the ineffective utilization of muscle glycogen, as in patients with McArdle disease, leads to impaired exercise tolerance (6). In their "glycogen shunt" hypothesis, Shulman and Rothman (7) propose that glycogenolysis is the predominant source of energy for muscle contraction with glycogen acting essentially as an intermediate for blood glucose to enter glycolysis.…”

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confidence: 99%

Exercise Capacity of Mice Genetically Lacking Muscle Glycogen Synthase

Pederson

Cope

Schroeder

et al. 2005

Journal of Biological Chemistry

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The glucose storage polymer glycogen is generally considered to be an important source of energy for skeletal muscle contraction and a factor in exercise endurance. A genetically modified mouse model lacking muscle glycogen was used to examine whether the absence of the polysaccharide affects the ability of mice to run on a treadmill. The MGSKO mouse has the GYS1 gene, encoding the muscle isoform of glycogen synthase, disrupted so that skeletal muscle totally lacks glycogen. The morphology of the soleus and quadriceps muscles from MGSKO mice appeared normal. MGSKO-null mice, along with wild type littermates, were exercised to exhaustion. There were no significant differences in the work performed by MGSKO mice as compared with their wild type littermates. The amount of liver glycogen consumed during exercise was similar for MGSKO and wild type animals. Fasting reduced exercise endurance, and after overnight fasting, there was a trend to reduced exercise endurance for the MGSKO mice. These studies provide genetic evidence that in mice muscle glycogen is not essential for strenuous exercise and has relatively little effect on endurance.The two major repositories of glycogen, the polymeric storage form of glucose, are in the liver and skeletal muscle (1). In humans, these carbohydrate reserves are an important determinant of endurance upon sustained exercise, and muscle glycogen has long been viewed as a critical energy source during muscular activity (2-4). Depletion of muscle glycogen results in fatigue and impaired muscle performance and is a major determinant of endurance (2-5). Likewise, the ineffective utilization of muscle glycogen, as in patients with McArdle disease, leads to impaired exercise tolerance (6). In their "glycogen shunt" hypothesis, Shulman and Rothman (7) propose that glycogenolysis is the predominant source of energy for muscle contraction with glycogen acting essentially as an intermediate for blood glucose to enter glycolysis. Increasing muscle glycogen by manipulating diet and exercise regimens, a procedure termed "carbohydrate loading" or "glycogen supercompensation" (8), is adopted by endurance athletes to delay the onset of fatigue (4, 9 -11).Although the importance of adequate muscle glycogen to sustain exercise in humans has been well documented, caution is needed in extrapolating findings in rodents to humans. For instance, the amount of muscle glycogen, expressed as a fraction of body mass, is ϳ10-fold lower in mice than in humans (12, 13), whereas the corresponding values for liver glycogen are comparable (14). Thus, the relative role of these two glycogen storage depots may be different between the two species. The relative importance of muscle and liver glycogen stores as fuel sources for exercise has been studied extensively in rats (15-17). Exhaustive exercise either by treadmill running or swimming resulted in a reduction of muscle glycogen by 70 or Ͼ90%, respectively (15, 16). Both exercise methods reduced liver glycogen Ͼ90%. Using less strenuous exercise regimens, muscle g...

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Investigation by Polymerase Chain Reaction of Enteroviral Infection in Patients with Chronic Fatigue Syndrome

Cited by 39 publications

References 19 publications

Association of mitochondrial dysfunction and fatigue: A review of the literature

Association of mitochondrial dysfunction and fatigue: A review of the literature

Reduced glycolytic reserve in isolated natural killer cells from Myalgic encephalomyelitis/chronic fatigue syndrome patients: A preliminary investigation

Exercise Capacity of Mice Genetically Lacking Muscle Glycogen Synthase

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