Metabolic changes in chronic fatigue syndrome
Metabolic functions are one of the principal determinants of energy expenditure and are exquisitely susceptible to the effects of circulating hormones and chemical changes. Consequently, clinical experiments based on energy expenditure and metabolic functions were considered to be valid approaches to the present research. Significant abnormalities were found in the proton magnetic resonance spectroscopy of basal ganglia in CFS patients. Automatic cardiovascular responses to exercise are also impaired in a subset of CFS patients. Finally, plasma membrane injury appears to be a possible explanation for a range of observations made in this research. Subjective fatigue is a complex symptom. It is the outcome of a variable combination of physiological and neuropsychological changes induced by the primary disease process. Downstream links between brain, neuromuscular and the cardiorespiratory functions are implicated in the neural control of force output during exercises in health and disease. Higher perceived fatigue in CFS is probably caused by the central mechanisms while the sensory input to these neural regulatory mechanisms may limit endurance to maximal and submaximal exercises. Based on these findings and more indirect evidence from other studies, changes in cell membrane properties affecting neuronal signalling in the basal ganglia seem to emerge as one of the likely pathophysiological mechanisms in CFS. There is also evidence of an imbalance of the central autonomic tone in a subset of CFS patients. Surely, research in CFS has the potential to unravel the biology of central fatigue and may bridge the gap that exists between the borderland of neurology and psychiatry.