Dominic Stone
Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a complex and controversial clinical condition with no established causative factors. Muscle biopsies have been used to study the condition, revealing abnormal glycolytic metabolism and intramuscular pH, as well as the presence of enterovirus RNA in some patients. The role of enterovirus infection in CFS/ME has been suspected for decades, but data remains controversial. Muscle biopsies have also been used to study post-COVID exertion intolerance, revealing fewer capillaries, thicker capillary basement membranes, and increased numbers of CD169+ macrophages.
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What You'll Learn
Muscle hypersensitivity and fibre abnormalities
Research has shown that people with ME/CFS have abnormally fast muscle fibre conduction in the membranes of motor units at low static force load. This increased muscle membrane reactivity has also been observed in patients with fibromyalgia, a disorder with overlapping symptoms of muscular fatigue and pain. Studies have found that ME/CFS patients exhibit abnormal muscle membrane function, with increased muscle fibre conduction velocity (CV) compared to healthy individuals.
In addition to muscle hypersensitivity, ME/CFS patients may also experience muscle fibre abnormalities. Muscle biopsies have revealed a relative increase in type 2 glycolytic fibres in a small subgroup of patients. Furthermore, some studies have reported mitochondrial dysfunction in ME/CFS patients, with abnormal levels of key mitochondrial enzymes and reduced citrate synthase levels in muscle biopsy samples. While the exact cause of ME/CFS remains unknown, these muscle fibre abnormalities contribute to the severe fatigue and reduced functioning characteristic of the disease.
It is important to note that the presence of muscle hypersensitivity and fibre abnormalities in ME/CFS patients can vary, and not all patients will experience the same symptoms or severity. The underlying mechanisms of the disease are complex and involve interactions between various physiological systems, including the immune, oxidative, mitochondrial, and neuronal pathways.
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Mitochondrial dysfunction
Chronic Fatigue Syndrome (CFS), also known as myalgic encephalomyelitis (ME), is a debilitating disorder with no known origin. It is characterised by severe fatigue that is not alleviated by rest and may be exacerbated by physical or mental activity. CFS/ME patients often experience muscle pain, sleep disturbances, and cognitive dysfunction.
The diagnosis of CFS/ME is based on symptoms, and there are no specific laboratory tests available for confirmation. However, hospital-based investigations, such as blood tests, electromyography, and muscle biopsies, can be utilised to gain a better understanding of the condition. Muscle biopsies, in particular, play a crucial role in studying mitochondrial dysfunction, which is one of the underlying biological abnormalities associated with CFS/ME.
Mitochondria are the powerhouses within our cells, responsible for energy production. Mitochondrial dysfunction in CFS/ME has been a subject of debate, with conflicting findings. Some studies have reported deficiencies in the production of adenosine triphosphate (ATP) by mitochondria in CFS/ME patients, which could contribute to fatigue and post-exertional malaise. However, other studies have found no significant differences in ATP production rates compared to healthy individuals.
Additionally, research has identified abnormal levels of key mitochondrial enzymes in CFS/ME patients. For example, a study by Smits et al. found a significant reduction in citrate synthase in muscle biopsy samples from the quadriceps region of CFS/ME patients compared to healthy controls. Furthermore, studies have reported increased expression of genes involved in oxidative stress and decreased expression of genes involved in metabolic pathways in CFS/ME patients, which may be linked to mitochondrial dysfunction.
The investigation of mitochondrial dysfunction in CFS/ME is crucial, as it has important implications for understanding the disease and developing potential treatments. For instance, in a case study, a patient initially diagnosed with CFS was later found to have mitochondrial myopathy through a histochemical study of a muscle biopsy. This led to a successful treatment regimen with high doses of riboflavin and thiamine, resulting in significant improvement in fatigue and muscle symptoms.
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Muscle energy metabolism
The relative contribution of these metabolic pathways is primarily determined by the intensity and duration of exercise. For example, during short-lasting, intense exercise, such as 30 seconds to 3 minutes of exhausting bicycling, the anaerobic energy release in working muscles is activated. On the other hand, during longer-duration, lower-intensity exercise, the body relies more on aerobic energy release.
In individuals with chronic fatigue syndrome (CFS), also known as myalgic encephalomyelitis (ME), muscle biopsies have been used to study muscle energy metabolism. CFS/ME is characterised by severe disabling fatigue and can include symptoms such as muscle pain, disturbed sleep, and cognitive dysfunction. Research has identified underlying biological abnormalities, including mitochondrial dysfunction, which can be studied through muscle biopsies.
For instance, a study by Smits and colleagues reported a significant reduction in citrate synthase in muscle biopsies from the quadriceps region of CFS/ME patients compared to healthy controls. Additionally, a case study of a patient initially diagnosed with CFS found that further investigation through muscle biopsy, spectrophotometric analysis, and genetic studies revealed mitochondrial myopathy. This highlights the importance of muscle biopsies in differentiating between CFS and mitochondrial diseases, which can have overlapping symptoms, such as fatigue, muscle pain, and abdominal pain.
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Muscle pain and soreness
Research has shown that ME/CFS patients exhibit dysfunction of nociceptive inhibition during exercise, resulting in a decrease in pain threshold following exercise. This is abnormal, as typically, the release of endogenous opioids and additional inhibitory mechanisms during exercise lead to an increased pain threshold. Furthermore, studies have found lower electrical pain thresholds in muscle tissue sites for the ME/CFS group compared to healthy controls, suggesting the role of generalized hyperalgesia in ME/CFS.
ME/CFS patients often experience muscle pain and fatigue due to a perceived lack of energy, which can be severe enough to lead to the avoidance of physical activity. This muscle dysfunction can be understood through central and peripheral pathophysiological mechanisms, including the effects of the immune system, oxidative stress, mitochondrial dysfunction, and neuronal pathways. For example, abnormal levels of key mitochondrial enzymes have been reported in muscle biopsy studies of ME/CFS patients, indicating possible mitochondrial dysfunction.
Additionally, a study by Lane et al. revealed that a small subgroup (8%) of ME/CFS patients exhibited an increased blood lactate response to exercise, and muscle biopsies showed a relative increase in type 2 glycolytic fibers within this subgroup. These findings suggest that subgroups within the ME/CFS patient population exist, displaying abnormal glycolytic metabolism and intramuscular pH regulation.
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Muscle wasting
In such cases, a muscle biopsy may be performed as part of a diagnostic investigation to differentiate between ME/CFS and primary muscle or mitochondrial diseases. A muscle biopsy involves extracting a small sample of muscle tissue, typically from the quadriceps or vastus lateralis muscle, for laboratory analysis. This can help identify abnormalities in muscle structure, function, and metabolism that may underlie the patient's symptoms.
Several studies have utilised muscle biopsies to gain insights into the pathophysiology of ME/CFS. For example, muscle biopsy specimens from ME/CFS patients have shown indications of oxidative damage, with higher levels of free radicals associated with reduced energy production by the muscles. Gene expression studies on these specimens have also revealed altered expression of genes involved in mitochondrial functioning, oxidative stress, and muscle structure and fiber type.
Additionally, muscle biopsy analyses have identified abnormalities in muscle energy metabolism, with an association between abnormal lactate response to exercise and the presence of enterovirus sequences in the muscles of a subset of CFS patients. Furthermore, muscle biopsies have contributed to our understanding of post-COVID exertion intolerance, revealing reduced capillaries, thicker capillary basement membranes, and increased CD169+ macrophages in affected individuals.
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Frequently asked questions
A muscle biopsy is a procedure where a small sample of muscle is removed for analysis.
Muscle biopsies can help uncover the biochemical causes of ME/CFS. For example, muscle biopsies have shown that CFS skeletal muscle cells have lower levels of ATP and AMP-activated protein kinase dysfunction.
ME/CFS is a debilitating disorder of unknown aetiology, characterised by severe disabling fatigue in the absence of an alternative diagnosis. Diagnosis is nonspecific and symptom-based, and no laboratory tests can be used to diagnose CFS.
ME/CFS is characterised by profound fatigue that is not improved by rest and may be worsened by physical or mental activity. Other symptoms include muscle pain, disturbed sleep, and cognitive dysfunction.
