I note however, that the lower workrate on the second day is NOT consistently associated with a delay or reduction in VO2 kinetics (as would be predicted by the hyperventilation hypothesis) see the summary table here:īut back to the gas exchange threshold, this point occurs in exercise where there is a ramped increase in power output. I instead focus on the reduction in workrate at the first ventilatory threshold aka the gas exchange threshold - this threshold has metabolic significance, namely it is the nonlinear point of oxygen extraction versus carbon dioxide output. Much ado was made about O2 dissociation curves and the Bohr effect due to hyperventilation, when the math suggests the effect on diffusion in the muscle is marginal at the physiological pressures they measured. Hyperventilation is actually normal past the second ventilatory threshold, due to respiratory compensation due to reduced blood PH. They make a big deal about hyperventilation as a possible cause even though their results don't really support it.

I am not a fan of his methodology, as they are ignoring the first ventilatory threshold (which is the most repeatable physiological threshold) and focusing on VO2peak which is subject to too many performance biases. These findings help to detangle the underlying mechanisms of CFS.Ĭlick to expand.I have commented, even on the thread about Systrom's most recent study. Central neural deregulation may contribute to these findings. Our results suggest disturbed membrane function in CFS patients, in their motor units involved in low force generation. In the CFS-group, the number of MUPs conveying very high conduction velocities increased abundantly with force and the MUPs narrowed. The CV of the CFS-group increased excessively with force ( P<0.001), whereas that of the controls increased only slightly and non-significantly, and that of the FM-group did not increase at all. The CV changes with force differed between CFS-group and both FM-group and controls ( P=0.01). The mean CV and motor unit potential (MUP) velocities with their statistical distribution were measured. We investigated whether CFS patients also show CV abnormalities.įemales with CFS (n=25), with FM (n=22), and healthy controls (n=21) underwent surface electromyography of the biceps brachii, loaded up to 20% of maximum strength, during short static contractions. Studies have shown increased muscle fiber conduction velocity (CV) in the non-painful muscles of FM patients. Chronic fatigue syndrome (CFS) and fibromyalgia (FM) are disorders of unknown etiology and unclear pathophysiology, with overlapping symptoms of – especially muscular –fatigue and pain.

Cfs units