From the Journal of Workplace Health and Safety, 24 June 2013.[Epub ahead of print].
From Expert Opinion on Therapeutic Targets, 9 July 2013. [Epub ahead of print].
The role of mitochondrial dysfunctions due to oxidative and nitrosative stress in the chronic pain or chronic fatigue syndromes and fibromyalgia patients: peripheral and central mechanisms as therapeutic targets?
Meeus M, Nijs J, Hermans L, Goubert D, Calders P.
University of Antwerp, Faculty of Medicine and Health Sciences, Department of Rehabilitation Sciences and Physiotherapy, Pain in Motion Research Group, Antwerp, Belgium.
Abstract
INTRODUCTION
Chronic fatigue syndrome (CFS) and fibromyalgia (FM) are characterized by persistent pain and fatigue. It is hypothesized that reactive oxygen species (ROS), caused by oxidative and nitrosative stress, by inhibiting mitochondrial function can be involved in muscle pain and central sensitization as typically seen in these patients.
AREAS COVERED
The current evidence regarding oxidative and nitrosative stress and mitochondrial dysfunction in CFS and FM is presented in relation to chronic widespread pain. Mitochondrial dysfunction has been shown in leukocytes of CFS patients and in muscle cells of FM patients, which could explain the muscle pain. Additionally, if mitochondrial dysfunction is also present in central neural cells, this could result in lowered ATP pools in neural cells, leading to generalized hypersensitivity and chronic widespread pain.
EXPERT OPINION
Increased ROS in CFS and FM, resulting in impaired mitochondrial function and reduced ATP in muscle and neural cells, might lead to chronic widespread pain in these patients. Therefore, targeting increased ROS by antioxidants and targeting the mitochondrial biogenesis could offer a solution for the chronic pain in these patients. The role of exercise therapy in restoring mitochondrial dysfunction remains to be explored, and provides important avenues for future research in this area.
From Seminars in Arthritis and Rheumatism, 6 July 2013. [Epub ahead of print]
Heart rate variability in patients with fibromyalgia and patients with chronic fatigue syndrome: A systematic review.
Meeus M, Goubert D, De Backer F, Struyf F, Hermans L, Coppieters I, De Wandele I, Da Silva H, Calders P.
Department of Rehabilitation Sciences and Physiotherapy, Ghent University and Artevelde University College, Ghent Campus Heymans (UZ) 3 B3, De Pintelaan 185, Ghent, Belgium; “Pain in Motion” research group, Department of Rehabilitation Sciences and Physiotherapy, Faculty of Medicine and Health Sciences, University of Antwerp, Belgium. Electronic address: mira.meeus@artesis.be.
Abstract
OBJECTIVE
The goal of this systematic literature review is to determine whether there are differences and similarities in heart rate variability (HRV) between adult patients with Fibromyalgia (FM), Chronic Fatigue Syndrome (CFS), and healthy pain-free control subjects.
METHODS
To obtain relevant articles, PubMed and Web of Knowledge were searched for case-control studies. Selection of the literature was based on selection criteria ascertaining studies with adult human patient groups comparing HRV. Risk of bias and levels of evidence were determined.
RESULTS
Sixteen case-control studies were included, 10 comparing FM patients to controls and 6 comparing CFS patients to controls. Methodological quality was moderate to good. Both time domain and frequency domain measurements were used. The majority of the researchers observed lower HRV in FM patients compared to healthy control persons, as well as increased sympathetic activity and a blunted autonomic response to stressors. Resistance training improved HRV in FM patients. In CFS patients HRV was only reduced during sleep.
CONCLUSION
FM patients show more HRV aberrances and indices of increased sympathetic activity. Increased sympathetic activity is only present in CFS patients at night. Since direct comparisons are lacking and some confounders have to be taken into account, further research is warranted. The role of pain and causality can be subject of further research, as well as therapy studies directed to reduced HRV.
I look forward to this every Friday, Tony. I really appreciate it. 😀
But it did take me a long time to work it out – flipping between both sets, and forgetting where I was inbetween flips…
Hmmm. re. the first paper;
I do try to eat a load of antioxidant rich stuff.
I will NOT be attempting exercise “to enhance my mitochondrial functioning”.
11 years of evidence gathered by myself on myself, tells me this is the most stupid thing I could do.
I have to keep within anaerobic parameters, or I suffer for it.