Muscle fatigability: Difference between revisions
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== Possible causes of muscle fatigability in ME/CFS == | == Possible causes of muscle fatigability in ME/CFS == | ||
Muscle biopsies have shown evidence of mitochondrial degeneration <ref>Behan WMH, More IAR, Behan PO. [http://www.ncbi.nlm.nih.gov/pubmed/1792865/ Mitochondrial abnormalities in the postviral fatigue syndrome]. Acta Neuropathol (Berl) 1991;83:61–65.</ref>, deletions of mitochondrial DNA <ref>http://www.ncbi.nlm.nih.gov/pubmed/8859904</ref><ref>http://www.ncbi.nlm.nih.gov/pubmed/7633428</ref>, and the reduction of mitochondrial activity <ref>http://www.ncbi.nlm.nih.gov/pubmed/8859904</ref>. | Muscle biopsies have shown evidence of mitochondrial degeneration <ref>Behan WMH, More IAR, Behan PO. [http://www.ncbi.nlm.nih.gov/pubmed/1792865/ Mitochondrial abnormalities in the postviral fatigue syndrome]. Acta Neuropathol (Berl) 1991;83:61–65.</ref>, deletions of mitochondrial DNA <ref>[http://www.ncbi.nlm.nih.gov/pubmed/8859904 Sensory characterization of somatic parietal tissues in humans with chronic fatigue syndrome.]</ref><ref>[http://www.ncbi.nlm.nih.gov/pubmed/7633428 Unusual pattern of mitochondrial DNA deletions in skeletal muscle of an adult human with chronic fatigue syndrome.]</ref>, and the reduction of mitochondrial activity <ref>[http://www.ncbi.nlm.nih.gov/pubmed/8859904 Sensory characterization of somatic parietal tissues in humans with chronic fatigue syndrome.]</ref>. | ||
In addition, evidence of oxidative damage to muscles has been found in CFS. <ref>http://www.ncbi.nlm.nih.gov/pubmed/11118815</ref> | In addition, evidence of oxidative damage to muscles has been found in CFS. <ref>[http://www.ncbi.nlm.nih.gov/pubmed/11118815 Specific oxidative alterations in vastus lateralis muscle of patients with the diagnosis of chronic fatigue syndrome.]</ref> | ||
Studies have found reduced levels of serum [[carnitine]] which return to normal after recovery and correlate with symptom severity. <ref>http://www.ncbi.nlm.nih.gov/pubmed/8148455 | Studies have found reduced levels of serum [[carnitine]] which return to normal after recovery and correlate with symptom severity. <ref>[http://www.ncbi.nlm.nih.gov/pubmed/8148455 Acylcarnitine deficiency in chronic fatigue syndrome.]</ref> | ||
Exercise has also been found to induce both early and excessive lactic acid formation in the muscles <ref>http://www.ncbi.nlm.nih.gov/pubmed/8544970</ref> with a reduced intraceullar concentrations of [[ATP]] and acceleration of [[glycolysis]].<ref>http://www.ncbi.nlm.nih.gov/pubmed/8618560</ref> | Exercise has also been found to induce both early and excessive lactic acid formation in the muscles <ref>[http://www.ncbi.nlm.nih.gov/pubmed/8544970 Serum levels of carnitine in chronic fatigue syndrome: clinical correlates.]</ref> with a reduced intraceullar concentrations of [[ATP]] and acceleration of [[glycolysis]].<ref>[http://www.ncbi.nlm.nih.gov/pubmed/8618560 Reduced oxidative muscle metabolism in chronic fatigue syndrome.]</ref> | ||
[[Peter Behan]] noted that ME patients were found to lack an important muscle enzyme called myoadenylate deaminase. An attempt has not been made to reproduce this finding in published research. | [[Peter Behan]] noted that ME patients were found to lack an important muscle enzyme called myoadenylate deaminase. An attempt has not been made to reproduce this finding in published research. | ||
Revision as of 08:48, December 9, 2015
Muscle fatigability in ME is a symptom in which muscles become weaker after minor exertion and a long period (3-5 days or longer) may elapse before full muscle power is restored. According to Melvin Ramsay, it is the defining feature of myalgic encephalomyelitis, without which a diagnosis of ME should not be made,[1] though this symptom is noted to improve during remission. Similar muscle effects are known to occur in other neurological diseases such as Multiple Sclerosis[2] and post-polio syndrome[3].
Possible causes of muscle fatigability in ME/CFS[edit | edit source]
Muscle biopsies have shown evidence of mitochondrial degeneration [4], deletions of mitochondrial DNA [5][6], and the reduction of mitochondrial activity [7].
In addition, evidence of oxidative damage to muscles has been found in CFS. [8]
Studies have found reduced levels of serum carnitine which return to normal after recovery and correlate with symptom severity. [9]
Exercise has also been found to induce both early and excessive lactic acid formation in the muscles [10] with a reduced intraceullar concentrations of ATP and acceleration of glycolysis.[11]
Peter Behan noted that ME patients were found to lack an important muscle enzyme called myoadenylate deaminase. An attempt has not been made to reproduce this finding in published research.
See Also[edit | edit source]
References[edit | edit source]
<references>
- ↑ The Clinical Features of Myalgic Encephalomyelitis
- ↑ http://mssociety.ca/en/information/symptoms_mng_fatigue.htm
- ↑ The Late Effects of Polio: An Overview
- ↑ Behan WMH, More IAR, Behan PO. Mitochondrial abnormalities in the postviral fatigue syndrome. Acta Neuropathol (Berl) 1991;83:61–65.
- ↑ Sensory characterization of somatic parietal tissues in humans with chronic fatigue syndrome.
- ↑ Unusual pattern of mitochondrial DNA deletions in skeletal muscle of an adult human with chronic fatigue syndrome.
- ↑ Sensory characterization of somatic parietal tissues in humans with chronic fatigue syndrome.
- ↑ Specific oxidative alterations in vastus lateralis muscle of patients with the diagnosis of chronic fatigue syndrome.
- ↑ Acylcarnitine deficiency in chronic fatigue syndrome.
- ↑ Serum levels of carnitine in chronic fatigue syndrome: clinical correlates.
- ↑ Reduced oxidative muscle metabolism in chronic fatigue syndrome.
