Category: Exercise

Muscle histopathology and physiology in chronic fatigue syndrome

Abstract:

Chronic fatigue syndrome (CFS) is characterized by fatigue at rest which is made worse by exercise. Previous biopsy studies on small numbers of CFS patients have shown a range of morphological changes to which have been attributed fatigue and myalgia.

We have now studied 108 patients with CFS or muscle pain and 22 normal volunteers by light and electron microscopy. There was no consistent correlation between symptoms and changes in fibre type prevalence, fibre size, degenerative or regenerative features, glycogen depletion, or mitochondrial abnormalities. Physiological contractile properties of quadriceps (maximal isometric force generation, frequency: force characteristics and relaxation rate) were also examined before and for up to 48 hours after a symptom-limited incremental cycle ergometer exercise test in 12 CFS patients and 12 normal volunteers.

Voluntary and stimulated force characteristics were normal at rest and during recovery. Exercise duration was similar in the two groups although CFS patients had higher perceived exertion scores in relation to heart rate during exercise, indicating a reduced effort sensation threshold. On physiological and pathological grounds it is clear that CFS is not a myopathy. Psychological/psychiatric factors appear to be of greater importance in this condition.

 

Source: Edwards RH1, Gibson H, Clague JE, Helliwell T. Muscle histopathology and physiology in chronic fatigue syndrome. Ciba Found Symp. 1993;173:102-17; discussion 117-31. http://www.ncbi.nlm.nih.gov/pubmed/8491096

 

Central basis of muscle fatigue in chronic fatigue syndrome

Abstract:

We studied whether muscle fatigue, metabolism, or activation are abnormal in the chronic fatigue syndrome (CFS). Subjects performed both an intermittent submaximal and a sustained maximal voluntary isometric exercise protocol of the tibialis anterior muscle.

The extent of fatigue, metabolic response, and changes in both M-wave amplitude and twitch tension during exercise were similar in patients and controls. The response to systemic exercise was also normal in the patients. However, voluntary activation of the tibialis was significantly lower in the patients during maximal sustained exercise.

The results indicate that patients with CFS have (1) normal fatigability and metabolism at both the intracellular and systemic levels, (2) normal muscle membrane function and excitation-contraction coupling, and (3) an inability to fully activate skeletal muscle during intense, sustained exercise. This failure of activation was well in excess of that found in controls, suggesting an important central component of muscle fatigue in CFS.

Comment in: Chronic fatigue syndrome. [Neurology. 1993]

 

Source: Kent-Braun JA, Sharma KR, Weiner MW, Massie B, Miller RG. Central basis of muscle fatigue in chronic fatigue syndrome. Neurology. 1993 Jan;43(1):125-31. http://www.ncbi.nlm.nih.gov/pubmed/8423875

 

Skeletal muscle metabolism in the chronic fatigue syndrome. In vivo assessment by 31P nuclear magnetic resonance spectroscopy

Abstract:

BACKGROUND: Previous study of patients with chronic fatigue syndrome (CFS) has demonstrated a markedly reduced dynamic exercise capacity, not limited by cardiac performance and in the absence of clinical neuromuscular dysfunction, suggesting the possibility of a subclinical defect of skeletal muscle.

METHODS: The in vivo metabolism of the gastrocnemius muscles of 22 CFS patients and 21 normal control subjects was compared during rest, graded dynamic exercise to exhaustion and recovery, using 31P nuclear magnetic resonance (NMR) spectroscopy to reflect minute-to-minute intracellular high-energy phosphate metabolism.

RESULTS: Duration of exercise was markedly shorter in the CFS patients (8.1 +/- 2.8 min) compared with the normal subjects (11.3 +/- 4.3 min) (p = 0.005). There were large changes in phosphocreatine (PCr), inorganic phosphate (Pi), and pH from rest to clinical fatigue in all subjects, reflecting the high intensity of the exercise. The temporal metabolic patterns were qualitatively similar in the CFS patients and normal subjects. There were early and continuous changes in PCr and Pi that peaked at the point of fatigue and rapidly reversed after exercise. In contrast, pH was relatively static in early exercise, not declining noticeably until 50 percent of total exercise duration was achieved, and reaching a nadir at 2 min postexercise, before rapidly reversing. There were no differences in pH at rest (7.08 +/- 0.04 vs 7.10 +/- 0.04), exhaustion (6.85 +/- 0.17 vs 6.76 +/- 0.17) or early (6.64 +/- 0.25 vs 6.56 +/- 0.24) or late recovery (7.09 +/- 0.04 vs 7.10 +/- 0.05), CFS patients vs normal subjects, respectively (NS). Neither were there intergroup differences (NS) in PCr or Pi. Although, quantitatively, the changes in PCr, Pi, and pH were marked and similar in both groups from rest to exhaustion, the changes all occurred much more rapidly in the CFS patients. Moreover, adenosine triphosphate (ATP) was significantly (p = 0.007) less at exhaustion in the CFS group.

CONCLUSIONS: 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.

 

Source: Wong R1, Lopaschuk G, Zhu G, Walker D, Catellier D, Burton D, Teo K, Collins-Nakai R, Montague T. Skeletal muscle metabolism in the chronic fatigue syndrome. In vivo assessment by 31P nuclear magnetic resonance spectroscopy. Chest. 1992 Dec;102(6):1716-22. http://www.ncbi.nlm.nih.gov/pubmed/1446478

 

Chronic fatigue syndrome: a joint paediatric-psychiatric approach

Comment in: Chronic fatigue syndrome: a joint paediatric-psychiatric approach. [Arch Dis Child. 1992]

 

Prolonged fatigue after an apparent viral infection, occurring sporadically or as an epidemic, has been described over the past 50 years. It has been given various names including Royal Free disease (1) and myalgic encephalomyelitis, but the preferred terms in the medical literature have been postviral fatigue syndrome (2) or chronic fatigue syndrome (CFS). (3)

However, the validity of this syndrome as a nosological entity has created a good deal of controversy and remains in doubt. (4) A constellation of symptoms make up the syndrome. There is fatigue of defined onset that is generally reported to follow a viral illness, often an influenza-like illness or an infection of the upper respiratory tract. The patient experiences profound fatigue with the initial illness and then fails to make the expected recovery, with fatigue that can persist over months or years. Fatigue is defined as a subjective sensation, which the patient often describes as tiredness or weariness and that occurs at rest. These patients also report a clear relationship of fatigue to activity. The term fatiguability has been used to describe the greater than normal fatigue that occurs after physical and sometimes after mental exertion in these patients. A great variety of associated symptoms have been described that include increased sleepiness, dizziness, vertigo, headache, difficulty in concentrating, sore throat, muscle weakness, and myalgia. The majority of patients have some emotional symptoms. There can be irritability and anxiety, tearfulness and depression. The fatigue and associated symptoms are of such severity as to impair significantly normal daily activities. There is a remarkable absence of physical signs and physical investigations fail to detect any organic pathology or current infection to account for the symptoms.

You can read the rest of this article here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1793327/pdf/archdisch00639-0088.pdf

 

Source: Vereker MI. Chronic fatigue syndrome: a joint paediatric-psychiatric approach. Arch Dis Child. 1992 Apr;67(4):550-5. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1793327/

 

Human quadriceps strength and fatiguability in patients with post viral fatigue

Abstract:

Quadriceps isometric strength, activation and fatiguability were measured in 11 patients with symptoms of fatigue three months after glandular fever or a glandular fever-like illness.

Predicted normal and lower limits of normal muscle strength were calculated from height and age. These measures and the fatigue index were compared with a group of healthy students of similar age.

Two of the patients were unable to activate fully their muscles. After allowing for this inhibition the group mean (SD) strength was 104 (22%) of predicted. Although there was no significant difference in the fatigue index between the patients and the control group, there was a trend for the patients to show less fatigue than controls.

There was no difference in the muscle results for those patients who were found to have Epstein-Barr virus infections and those who did not. The feelings of weakness and fatigue experienced by the patients could not be explained by either physiological muscle fatigue or lack of effort.

 

Source: Rutherford OM, White PD. Human quadriceps strength and fatiguability in patients with post viral fatigue. J Neurol Neurosurg Psychiatry. 1991 Nov;54(11):961-4. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1014616/ (Full article)

 

Muscle performance, voluntary activation, twitch properties and perceived effort in normal subjects and patients with the chronic fatigue syndrome

Abstract:

The decrease in maximal force-generating capacity, the degree of central activation of the muscle, and the subjective perception of effort were measured during prolonged submaximal isometric exercise in 12 male patients suffering from the ‘chronic fatigue syndrome’ and 13 naive, healthy male subjects.

Maximal voluntary isometric torque generated by the elbow flexors was measured before, and at 5 min intervals during an endurance sequence of 45 min of repetitive isometric contractions (6 s duration, 4 s rest interval) producing 30% of the initial maximal voluntary torque. Electrical stimuli were also delivered to the elbow flexors to measure the contractile force in the intervals between voluntary contractions. The degree of central motor activation during maximal voluntary contractions was assessed using a sensitive method of twitch interpolation.

In addition, the perceived effort required to achieve the target submaximal contractions was recorded using a standardized self-report scale. A high degree of central activation was achieved in maximal contractions during the endurance sequence both in the patients (mean of maximal force 93.6%; SD 7.8%), and in the control subjects (mean 90.9%; SD 9.5%).

The relative torque produced by either voluntary or electrically stimulated contractions was not significantly different between patients and control subjects throughout the test. There was no significant difference in the perceived exertion between the patients and control subjects.

These findings support the concept that neither poor motivation, nor muscle contractile failure is important in the pathogenesis of ‘fatigue’ in patients with the chronic fatigue syndrome.

 

Source: Lloyd AR, Gandevia SC, Hales JP. Muscle performance, voluntary activation, twitch properties and perceived effort in normal subjects and patients with the chronic fatigue syndrome. Brain. 1991 Feb;114 ( Pt 1A):85-98. http://www.ncbi.nlm.nih.gov/pubmed/1998892

 

Physiologic measurement of exercise and fatigue with special reference to chronic fatigue syndrome

Abstract:

Oxidative metabolism is the major source of energy for muscle activity, and maximal oxygen uptake (VO2max), the product of maximal cardiac output and maximal arteriovenous oxygen difference, indicates individual capacity for oxidative metabolism and performance of exercise by the large muscles.

Strength, a function of muscle cross-sectional area, motor-unit recruitment, and neuromuscular coordination, is the ability to develop force in a single, brief, maximal-effort voluntary contraction of rested muscle. Weakness is a diminished ability of rested muscle to exert maximal force. Fatigue is a loss of maximal force-generating capacity that develops during muscular activity, likely originates within muscle itself, and persists until muscle is fully recovered. Individual perception of motor effort can be determined with standardized rating scales.

These concepts are discussed in detail, their relevance to the pathophysiology of exercise in chronic fatigue syndrome is analyzed, and a general strategy of exercise evaluation pertinent to chronic fatigue syndrome is presented.

 

Source: Lewis SF, Haller RG. Physiologic measurement of exercise and fatigue with special reference to chronic fatigue syndrome. Rev Infect Dis. 1991 Jan-Feb;13 Suppl 1:S98-108. http://www.ncbi.nlm.nih.gov/pubmed/2020810

 

Aerobic work capacity in chronic fatigue syndrome

Comment on Aerobic work capacity in patients with chronic fatigue syndrome. [BMJ. 1990]

SIR,

The data of Dr Marshall S Riley and colleagues (1) are consistent with our findings (2) that most patients referred with the chronic fatigue syndrome have the effort syndrome-that is, chronic hyperventilation as a consequence of excessive effort and distress.(3)

May we draw attention to three points. Dr Riley and colleagues concluded that the patients could not be hyperventilating because their values of end-tidal partial pressure of carbon dioxide at rest and at peak exercise did not differ significantly from those of the controls.

In our opinion the values published for the controls (35 8 mmHg at rest and 36-3 mmHg at peak exercise) are too low to be accepted as normal. The finding that the patients reached their anaerobic threshold far quicker than did the controls is consistent with the early acidosis on exertion known to occur in chronic hyperventilation. This is a consequence of the depletion of the body’s buffer base reserves,(4) brought about by renal compensation for chronic respiratory alkalosis.(5)

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1664329/pdf/bmj00207-0055b.pdf

 

Source: Rosen SD, King JC, Wilkinson JB, Nixon PG. Aerobic work capacity in chronic fatigue syndrome. BMJ. 1990 Nov 24;301(6762):1217. [Comment] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1664329/

 

Aerobic work capacity in patients with chronic fatigue syndrome

Abstract:

OBJECTIVE: To determine the aerobic work capacity of patients with the chronic fatigue syndrome and compare it with that of two control groups, and to assess the patients’ perception of their level of activity before and during illness.

DESIGN: A symptom limited exercise treadmill test with on line gas analysis and blood sampling was used. Subjects were assessed by one investigator, who was blind to the group which they were in.

SETTING: Department of medicine, Royal Victoria Hospital, Belfast.

SUBJECTS: 13 Patients (10 women, three men) who fulfilled the diagnostic criteria for chronic fatigue syndrome. Two control groups of similar age, sex, and body weight: 13 normal subjects (10 women, three men) and seven patients (five women, two men) with the irritable bowel syndrome.

MAIN OUTCOME MEASURES: Aerobic work capacity as assessed by several variables such as length of time on treadmill, heart rate, and biochemical measurements; Borg score; and visual analogue scores of perceived level of physical activity.

RESULTS: The patients with the chronic fatigue syndrome had a reduced exercise capacity compared with that of the other subjects, spending a significantly shorter time on the treadmill. They had a significantly higher heart rate at submaximal levels of exertion and at stage III exertion had significantly higher blood lactate concentrations. Using a Borg score, they showed a significantly altered perception of their degree of physical exertion with a mean score of 8.2 compared with 6.6 and 5.3 for the normal subjects and patients with the irritable bowel syndrome respectively. Using a visual analogue scale they indicated that they had a greater capacity for activity before illness than had the patients with the irritable bowel syndrome, but the scores were not significantly different between the two groups. Both groups of patients indicated reduced activity at the time of testing. Normal controls and patients with the irritable bowel syndrome aspired to a greater level of activity than their current level, but the patients with the chronic fatigue syndrome aspired to a level similar to that which they had had before their illness.

CONCLUSIONS: Patients with the chronic fatigue syndrome have reduced aerobic work capacity compared with normal subjects and patients with the irritable bowel syndrome. They also have an altered perception of their degree of exertion and their premorbid level of physical activity.

 

Source: Riley MS, O’Brien CJ, McCluskey DR, Bell NP, Nicholls DP. Aerobic work capacity in patients with chronic fatigue syndrome. BMJ. 1990 Oct 27;301(6758):953-6. http://www.ncbi.nlm.nih.gov/pubmed/2249024

Note: You can read the full article here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1664147/

 

Patient management of post-viral fatigue syndrome

Abstract:

A case definition for post-viral fatigue syndrome is proposed within which various subgroups of patients exist. Any one treatment may not apply to all the subgroups. In particular, patients’ experiences do not show that avoidance of exercise is maladaptive. It is proposed that the recently ill often try to exercise to fitness whereas the chronically ill have learnt to avoid exercise. Recovery is more likely to be achieved if patients learn about their illness and do not exhaust their available energy.

 

Source: Ho-Yen DO. Patient management of post-viral fatigue syndrome. Br J Gen Pract. 1990 Jan;40(330):37-9. http://www.ncbi.nlm.nih.gov/pubmed/2107839

Note: You may read the full article here:  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1371214/