Tag: deconditioning

Chronic fatigue syndrome: physical and cardiovascular deconditioning

Abstract:

We investigated whether chronic fatigue syndrome (CFS) patients have physical and/or cardiovascular de-conditioning, in 273 CFS patients and 72 healthy controls.

We used laboratory tests to assess haematological, biochemical, endocrinological and immunological systems. The cardiovascular system was assessed by echocardiography and carotid echography. Body composition was determined by dual energy X-ray absorptiometry (DEXA).

CFS patients had smaller left ventricular end systolic (p < 0.001) and diastolic (p = 0.008) dimensions but thinner posterior walls (p = 0.02) than corresponding values in healthy controls. Left ventricular mass was also reduced in CFS patients (p = 0.006). Both maximum (p < 0.001) and minimum (p < 0.008) diameter of the carotid artery were smaller in CFS patients. The laboratory screening tests showed significant differences in serum albumin (p = 0.05), phosphate (p = 0.02), HDL-cholesterol (p = 0.03), HDL:total cholesterol ratio (p = 0.01), triglycerides (p = 0.02), neutrophils (p = 0.01) and thyroid-stimulating hormone (p = 0.04) between CFS patients and controls. Male CFS patients had an increased percentage of fat mass compared with healthy male subjects (p = 0.02).

This large group of CFS patients had evidence of physical and cardiovascular de-conditioning, suggesting that in these patients a graded exercise programme could lead to physical reconditioning and could increase their ability to perform physical activities.

 

Source: De Lorenzo F, Xiao H, Mukherjee M, Harcup J, Suleiman S, Kadziola Z, Kakkar VV. Chronic fatigue syndrome: physical and cardiovascular deconditioning. QJM. 1998 Jul;91(7):475-81. http://qjmed.oxfordjournals.org/content/91/7/475.long (Full article)

 

Physical fatigability and exercise capacity in chronic fatigue syndrome: association with disability, somatization and psychopathology

Abstract:

Physical fatigability and avoidance of physically demanding tasks in chronic fatigue syndrome (CFS) were assessed by the achievement or nonachievement of 85% of age-predicted maximal heart rate (target heart rate, THR) during incremental exercise. The association with functional status impairment, somatization, and psychopathology was examined.

A statistically significant association was demonstrated between this physical fatigability variable and impairment, and a trend was found for an association with somatization. No association was demonstrated with psychopathology. These results are in accordance with the cognitive-behavioral model of CFS, suggesting a major contribution of avoidance behavior to functional status impairment; however, neither anxiety nor depression seem to be involved in the avoidance behavior.

Aerobic work capacity was compared between CFS and healthy controls achieving THR. Physical deconditioning with early involvement of anaerobic metabolism was demonstrated in this CFS subgroup.

Half of the CFS patients who did not achieve THR did not reach the anaerobic threshold. This finding argues against an association in CFS between avoidance of physically demanding tasks and early anaerobic metabolism during effort.

 

Source: Fischler B, Dendale P, Michiels V, Cluydts R, Kaufman L, De Meirleir K. Physical fatigability and exercise capacity in chronic fatigue syndrome: association with disability, somatization and psychopathology. J Psychosom Res. 1997 Apr;42(4):369-78. http://www.ncbi.nlm.nih.gov/pubmed/9160276

 

Exercise responses and psychiatric disorder in chronic fatigue syndrome

Comment in: Exercise responses in the chronic fatigue syndrome. Objective assessment of study is difficult without knowledge of data. [BMJ. 1995]

 

Fatigue, exercise intolerance, and myalgia are cardinal symptoms of the chronic fatigue syndrome, but whether they reflect neuromuscular dysfunction or are a manifestation of depression or other psychiatric or psychological disorders diagnosed in a high proportion of fatigued patients in the community is unclear.’ In previous studies patients with the chronic fatigue syndrome showed exercise intolerance in incremental exercise tests, which seemed to be related to an increased perception of effort; also, blood lactate concentrations in some patients tended to increase more rapidly than normal at low work rates, implying inefficient aerobic muscle metabolism.2 We examined venous blood lactate responses to exercise at a work rate below the anaerobic threshold in relation to psychiatric disorder.

You can read the rest of this article here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2550606/pdf/bmj00607-0028.pdf

 

Source: Lane RJ, Burgess AP, Flint J, Riccio M, Archard LC. Exercise responses and psychiatric disorder in chronic fatigue syndrome. BMJ. 1995 Aug 26;311(7004):544-5. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2550606/pdf/bmj00607-0028.pdf

 

Lactate responses to exercise in chronic fatigue syndrome

Comment on: Exercise performance and fatiguability in patients with chronic fatigue syndrome. [J Neurol Neurosurg Psychiatry. 1993]

 

We were interested to read the recent account of exercise characteristics in patients with chronic fatigue syndrome by Gibson et al,’ which concluded that there was no abnormality of neuromuscular function in this condition. Patients reached the limits of exercise tolerance at lower heart rates than controls during incremental exercise to exhaustion but their peak work rates and duration of exercise did not differ significantly from the control group, although the total work done (the product of these variables) would appear to have been less; the authors had previously reported that patients with this condition showed a reduction in maximal work rate achieved in such tests.2 Despite this, plasma lactate levels at the end of exercise were as high in the patients as the controls.

In an earlier study using incremental exercise on a treadmill, Riley et a13 had found higher heart rates and increased lactate levels compared with normal controls at submaximal work rates but similarly noted no differences at peak exercise.

We have found that a proportion of patients with chronic fatigue syndrome exhibit abnormally raised lactate levels following steady state exercise at work rates below the anerobic threshold, corresponding to roughly half the peak work rates achieved in the incremental test paradigm.4 It is thus possible that lactate levels in some patients increase more rapidly than normal at lower work rates.

The cause of this apparent ‘left shift’ of the anaerobic threshold is unclear. Neither we nor Gibson et al 2 found evidence of “deconditioning” in terms of cardiac responses to exercise in our patients, and phosphorus spectroscopy of muscle in the syndrome has shown no consistent disturbance of muscle energy metabolism.5 The phenomenon may be of significance in the pathogenesis of “fatigue” in some patients, and it may be premature to conclude that neuromuscular function in all patients is normal, or that the “fatigue” is exclusively “central” in origin. Indeed, it may be presumptuous to consider chronic fatigue syndrome as a unitary entity.

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1072952/pdf/jnnpsyc00035-0134b.pdf

 

Source: Lane RJ, Woodrow D, Archard LC. Lactate responses to exercise in chronic fatigue syndrome. J Neurol Neurosurg Psychiatry. 1994 May;57(5):662-3. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1072952/

 

Chronic fatigue syndrome

Abstract:

Chronic Fatigue Syndrome appears to represent a spectrum of disorders in which a variety of pathophysiological mechanisms may operate. While the initiating event in the majority of patients is a pyrexial illness, possibly due to enterovirus infection, evidence of persisting infection or inflammatory changes in muscle and/or brain remain unconvincing.

CFS patients display a definite reduced aerobic work capacity compared to normal control subjects, but this may reflect a state of deconditioning resulting from prolonged physical inactivity. They also have an altered perception of their level of exertion and premorbid fitness.

The characteristic fluctuation in symptoms, with periods of relapses and partial remissions, may indicate that some central disorder of sensory perception is operational. It may be that a primary sleep disorder results in a reduced sensory threshold for afferent stimuli from muscle. This could well account for many of the subjective symptoms which patients experience. Much more research is clearly necessary if we are to achieve a better understanding of this distressing and at present enigmatic disorder.

 

Source: McCluskey DR, Riley MS. Chronic fatigue syndrome. Compr Ther. 1992 Apr;18(4):13-6. http://www.ncbi.nlm.nih.gov/pubmed/1628478