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ME/CFS Mitochondria/Energy Research

"There is no word in the the English lexicon that describes the lack of stamina, the paucity of energy, the absolute malaise and turpitude that accompanies this illness."
-Dr. Charles Lapp-

One of the differences that sets ME definitions apart from CFS definitions is the major criteria and hallmark symptom of post-exertional worsening of symptoms, even with minor mental or physical exertion.  Crushing exhaustion on top of already crushing exhaustion even at rest is one of the things that so disables the ME or CFS-labeled patient.  Figuring out where the molecular "short" is in cells' "batteries" (the mitochondria) has been a complex task over the decades.  But scientists are getting closer to finding  answers as to what is happening to "cut the current" in ME and CFS patients' cells, leaving them unable to perform normal daily activities that most people take for granted.

Listed below are research studies investigating this phenomenon in ME/CFS.  As you browse the other research categories in the NAME-US.org website, you will see how these studies interrelate with the functioning in the other body systems (particularly the cardiovascular system) affected by this disease.

2007 - 2005 - 2002 - 1999 - 1998 - 1996 - 1995 - 1994 - 1992 - 1991

   

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Research Overview
Neurology
Immunology
Circulatory/Cardio
Mitochondria/Energy
Genetics
DePaul Univ/Jason
Oxidative Stress
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"I asked Cheney about mitochrondrial myopathy and CFS. He confirmed what I suspected: in CFS there is so much injury to the mitochondria that CFS could be called a mitochrondrial disease."
Dr. Paul Cheney on Mitochondrial Myopathy, MRS Brain Scans and Chronic Fatigue Syndrome
by Carol Sieverling

Dr. Cheney states:
"Never, never exercise in mitochondrial myopathy."


“The most important thing is not to have (patients) do aerobic exercise. I believe that even progressive aerobic exercise is counter-productive. If you have a defect in mitochondrial function and you push the mitochondria by exercise, you kill the DNA.”

-Paul Cheney at the 1999 International Congress of Bioenergetic Medicine-


Exercise related abnormalities of function have been demonstrated... including a failure to coordinate oxidative metabolism with anaerobic glycolysis causing abnormally early intracellular acidosis, consistent with early fatigability and the slow recovery from exercise in M.E.
-Dr. E.G. Dowsett-
The Clinical and Scientific Basis of M.E./CFS


"What is the etiology, the cause, of this cardiac output problem?  The short version is that cardiac muscles have lost power because their mitochondria are dysfunctional."
-Dr. Paul Cheney-


Online Medical Dictionary


Background Image:
Inside a mitochondrion; mitochondria are the "batteries" of living cells.

 
         
 

2007

Post-exertional Symptomology In Chronic Fatigue Syndrome (Abstract)
Stiles, Travis L.; Snell, Christopher R.; Stevens, Staci R.; Moran, Megan; VanNess, J. Mark (CFS Medicine & Science in Sports & Exercise: Volume 39(5) Supplement, May 2007  "The results of this study indicate that CFS patients suffer symptom exacerbation following physical stress. As with MS, lupus and RA, post-exertional symptom exacerbation appears to be both a real and incapacitating feature of the syndrome. The delayed recovery response evoked by a single bout of exercise stress is distinctly different from that of sedentary controls."

2005

Exercise capacity and immune function in male and female patients with chronic fatigue syndrome (CFS).  (Abstract) Snell CR, Vanness JM, Strayer DR, Stevens SR. University of the Pacific, Department of Sport Sciences, Stockton, CA 95211-0197, USA.  "These results implicate abnormal immune activity in the pathology of exercise intolerance in CFS and are consistent with a channelopathy involving oxidative stress and nitric oxide-related toxicity."

Chronic fatigue syndrome: assessment of increased oxidative stress and altered muscle excitability in response to incremental exercise. (Abstract) Jammes Y, Steinberg JG, Mambrini O, Bregeon F, Delliaux S. Laboratoire de Physiopathologie Respiratoire (UPRES EA 2201), Faculte de Medecine, Institut Federatif de Recherche Jean Roche, Marseille, France.  "The response of CFS patients to incremental exercise associates a lengthened and accentuated oxidative stress together with marked alterations of the muscle membrane excitability. These two objective signs of muscle dysfunction are sufficient to explain muscle pain and postexertional malaise reported by our patients."

2002

Brain regions involved in fatigue sensation: reduced acetylcarnitine uptake into the brain. (Abstract) Kuratsune H, Yamaguti K, Lindh G, Evengard B, Hagberg G, Matsumura K, Iwase M, Onoe H, Takahashi M, Machii T, Kanakura Y, Kitani T, Langstrom B, Watanabe Y. Department of Molecular Medicine, Hematology and Oncology, Osaka University Graduate School of Medicine, C9, 2-2 Yamada-oka, Suita, Osaka 565-0871, Japan.  "These findings suggest that the levels of biosynthesis of neurotransmitters through acetylcarnitine might be reduced in some brain regions of chronic fatigue patients and that this abnormality might be one of the keys to unveiling the mechanisms of the chronic fatigue sensation."

1999

Demonstration of delayed recovery from fatiguing exercise in chronic fatigue syndrome. (Abstract) Paul L, Wood L, Behan WM, Maclaren WM. (1999) Department of Physiotherapy, Glasgow Caledonian University, Glasgow, Scotland.  "These findings support the clinical complaint of delayed recovery after exercise in patients with CFS."
 

Impaired oxygen delivery to muscle in chronic fatigue syndrome.  (Abstract) McCully KK, Natelson BH. Department of Medicine, Medical College of Pennsylvania and Hahnemann University, Philadelphia, PA 19129  "In conclusion, oxygen delivery was reduced in CFS patients compared with that in sedentary controls. This result is consistent with previous studies showing abnormal autonomic control of blood flow."

In vitro Study of Muscle Aerobic Metabolism in Chronic Fatigue Syndrome (Abastract) Wilhelmina M.H. Behan, Senior Lecturer, Pathology, Glasgow University, Glasgow, Scotland, U.K.; Ian J. Holt, Royal Society University Research Fellow, Department of Biochemical Medicine, Ninewells Medical School, Dundee, Scotland, U.K.; David H. Kay, House Officer, Western Infirmary, Glasgow, Scotland, U.K. Pamela Moonie, Research Assistant, Department of Biochemical Medicine, Ninewells Medical School , Dundee, Scotland, U.K. "This in vitro study confirms that there is convincing evidence of mild aerobic defects in skeletal muscle in some cases of CFS."
(Full Article)

1998

Influence of exhaustive treadmill exercise on cognitive functioning in chronic fatigue syndrome.  (Abstract)  LaManca JJ, Sisto SA, DeLuca J, Johnson SK, Lange G, Pareja J, Cook S, Natelson BH.  Chronic Fatigue Syndrome Cooperative Research Center, University of Medicine and Dentistry of New Jersey-New Jersey Medical School, Newark, USA. "We conclude that after physically demanding exercise, CFS subjects demonstrated impaired cognitive processing compared with healthy individuals."

 

1996

Reduced oxidative muscle metabolism in chronic fatigue syndrome.  (Abstract) McCully KK, Natelson BH, Iotti S, Sisto S, Leigh JS Jr. Department of Medicine, Medical College of Pennsylvania, Philadelphia 19131, USA.  "In conclusion, oxidative metabolism is reduced in CFS patients compared to sedentary controls."

 

1995

Unusual pattern of mitochondrial DNA deletions in skeletal muscle of an adult human with chronic fatigue syndrome. Zhang C, Baumer A, Mackay IR, Linnane AW, Nagley P. Human Molecular Genetics 1995; 4(4): 751-4. (Abstract not available)

1994

Acetylcarnitine deficiency in chronic fatigue syndrome.  (Abstract)  Kuratsune H, Yamaguti K, Takahashi M, Misaki H, Tagawa S, Kitani T. Osaka University Medical School, Japan. "...the concentration of serum acylcarnitine in patients with CFS tended to increase to the normal level with the recovery of general fatigue. Therefore, the measurement of acylcarnitine would be a useful tool for the diagnosis and assessment of the degree of clinical manifestation in patients with CFS."

1992

Skeletal muscle metabolism in the chronic fatigue syndrome. In vivo assessment by 31P nuclear magnetic resonance spectroscopy.  (Abstract) Wong R, Lopaschuk G, Zhu G, Walker D, Catellier D, Burton D, Teo K, Collins-Nakai R, Montague T. Department of Medicine, University of Alberta, Edmonton, Canada.  "Patients with CFS and normal control subjects have similar skeletal muscle metabolic patterns during dynamic exercise and reach similar clinical and metabolic end points. However, CFS patients reach exhaustion much more rapidly than normal subjects, at which point they also have relatively reduced intracellular concentrations of ATP. These data suggest a defect of oxidative metabolism with a resultant acceleration of glycolysis in the working skeletal muscles of CFS patients. This metabolic defect may contribute to the reduced physical endurance of CFS patients. Its etiology is unknown. Whether CFS patients' overwhelming tiredness at rest has a similar metabolic pathophysiology or etiology also remains unknown."

1991

Mitochondrial abnormalities in the postviral fatigue syndrome. (Abstract)  Behan WM, More IA, Behan PO. Department of Pathology, University of Glasgow, Scotland.  "We have examined the muscle biopsies of 50 patients who had postviral fatigue syndrome (PFS) for from 1 to 17 years. We found mild to severe atrophy of type II fibres in 39 biopsies, with a mild to moderate excess of lipid. On ultrastructural examination, 35 of these specimens showed branching and fusion of mitochondrial cristae. Mitochondrial degeneration was obvious in 40 of the biopsies with swelling, vacuolation, myelin figures and secondary lysosomes. These abnormalities were in obvious contrast to control biopsies, where even mild changes were rarely detected. The findings described here provide the first evidence that PFS may be due to a mitochondrial disorder precipitated by a virus infection."

 

   
 

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