Abstract
Background: In this study the muscle bioenergetic function in response to exercise in severe ME was explored to see if the underlying metabolic problem in ME, responsible for the severe difficulties with trivial and the severe loss of muscle power, could be discovered. Methods: Inorganic phosphate, creatine kinase and lactate were measured in a former Dutch National Field Hockey Champion, who is now a patient bedridden with severe ME, before and 5 minutes after very trivial exercise, from which his muscles needed 12 hours to recover. Results: Inorganic phosphate and creatine kinase were both normal, however, lactate after this trivial exercise was very high, and further testing showed that a second batch of lactic acid was excreted after the same exercise with a 6-fold delay, showing that the lactic acid excretion was impaired and split into two. And this was delayed up to 11- fold by eating closer to the exercise. Conclusion: This study found that in severe ME, both the oxidative phosphorylation and the lactic acid excretion are impaired, and the combination of these two is responsible for the main characteristic of ME, the abnormally delayed muscle recovery after doing trivial things. The muscle recovery is further delayed by immune changes, including intracellular immune dysfunctions, and by lengthened and accentuated oxidative stress, but also by exercise metabolites, which work on the sensitive receptors in the dorsal root ganglions, which in severe ME are chronically inflamed, and are therefore much more sensitive to these metabolites, which are produced in high quantities in response to trivial which for ME patients, due to the underlining metabolic problem, is strenuous exercise. And a similar problem is most likely responsible for the abnormally delayed brain recovery after doing trivial things. This study also shows that the two metabolic problems are the result of an impaired oxygen uptake into the muscle cells or their mitochondria and in combination with the Norwegian Rituximab studies, which suggest that ME is an autoimmune disease, it is suggestive that antibodies are directly or indirectly blocking the oxygen uptake into the muscle cells or their mitochondria.
Highlights
In this study the muscle bioenergetic function in response to exercise in severe Myalgic Encephalomyelitis (ME) was explored to see if the underlying metabolic problem in ME, responsible for the severe difficulties with trivial exercise, and the severe loss of muscle power, could be discovered
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a chronic multi-system disease that can lead to striking debilitation [13]
The pathophysiology is related to activation of immunoinflammatory pathways and autoimmune responses underpinned by a state of energy depletion [4] and elderly patients with ME/CFS are at increased risk for non-Hodgkin’s lymphoma [5]
Summary
In this study the muscle bioenergetic function in response to exercise in severe ME was explored to see if the underlying metabolic problem in ME, responsible for the severe difficulties with trivial exercise, and the severe loss of muscle power, could be discovered. As reported by Jason et al the median age of death for cancer in the United States is 72 versus an average age of 47.8 if the person has ME/ CFS and the average age of death of heart failure is 83.1 versus 58.7 years if the person has ME/CFS [6] What this means is that ME/CFS patients who died of cancer or heart failure were considerable younger than what would have been expected from the general population, which means that ME/CFS increases the risk of death from these conditions dramatically [6], which constitutes indirect proof that ME/CFS is a physical disease. A quarter of ME/CFS patients have severe ME/CFS, are homebound or bedridden and suffer major functional impairments [2,7] to the point that some are tube fed due to dysphagia and /or dysparesis of the stomach caused by autonomic dysfunction which is a frequent finding in ME/CFS [8].
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