Another characteristic mentioned in the CDCP definition is a substantial reduction of the premorbid activity level (1), evidenced by clinical research (2,3). In addition to the reduced activity level compared to the premorbid level or to healthy controls. people with CFS display an abnormal activity pattern their lifestyle appears to be characterised by activity peaks and longer bouts of rest after activity (3). The latter is in line with a physiological study showing a delayed recovery from exercise in CFS patients (4). Clinical studies revealed that overly vigorous exercise (5, 6) or even a 30% increase in activity (7), frequently triggers a relapse. However, the cause of this post_exertional malaise and the altered or reduced activity level remains unclear.
It is hypothesised that nitric oxide (NO) is involved in these phenomena of altered and reduced activity level and of exercise intolerance. It is known that patients with CFS present elevated levels of blood NO (8). Excessive NO concentrations are detrimental for physiological functions via the derivative peroxynitrite (9). Peroxynitrite is not a free radical, but leaves the hallmarks of oxidation typical of free radicals (9). Furthermore, NO as a mediator of vasodilatation, is critical for basal blood flow across many organs. In consequence, elevated amounts of NO in CFS can cause hypotension (10). As previously suggested (11), this may explain part of the abnormal exercise response in CFS. NO-induced vasodilatation may limit the capacity of the human body to increase blood flow during physical activity, limiting activity performance in CFS-patients. In addition, physical activity further increases NO amounts and vasodilatation and thus hypotension (12-14). In CFS patients this effect could be aggravated by the already elevated amounts of NO, explaining the malaise and the delayed recovery after physical activity (4). Secondly, pathological overproduction of NO will decrease oxygen consumption (15) and increase anaerobic glycolysis (lactate production) by modulating mitochondrial respiration (16) and iron metabolism (17). Finally, NO could alter muscular morphology and function by oxidative damage of cell membranes (18), structural proteins such as actin (9), and DNA (19), causing muscle weakness, soreness and fatigue. All these mechanisms compromise exercise capacity and worsen physical activity responses.
Therefore, it was hypothesised that NO plays an aetiological role in the reduced activity level and fluctuating symptom pattern in people with CFS. Either people with CFS are not capable of being physically active due to elevated NO amounts, or an activity peak could trigger NO release accompanied by post_exertional malaise.
In summary, the goal of this study was to investigate whether NO concentration in the serum was related to physical activity level in people with CFS and healthy sedentary controls.
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(spell-checker was going crazy here so I haven't gone through this but hopefully enough information for people to be able to recognise the study)
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