Sargent, Charli B App Sci, B Sc (Hons); Scroop, Garry MD, PhD

Medicine & Science in Sports & Exercise:
SPECIAL COMMUNICATIONS: Letters to the Editor-in-Chief
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Department of Thoracic Medicine

Royal Adelaide Hospital

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Dear Editor-in-Chief:

The consensus in the literature on chronic fatigue syndrome (CFS) is that maximal oxygen uptake (V̇O2max) is reduced and lactate production increased, as Jones and Heigenhauser intimate. When our study provided the contrary result we searched for reasons to explain the apparent conflict. We believe the major reason is that most previous studies have not employed true maximal exercise testing protocols in patient assessment.

During exercise testing, if the peak value for oxygen uptake (V̇O2peak) is to be regarded as the true maximal value (V̇O2max), the investigator must be assured that the subject exerted a maximal effort. There are well-accepted criteria for making this judgment in sedentary people (1,3), and these were detailed in our manuscript and rigorously applied in our study. The point we make in discussion is that such criteria have not been applied in most previous studies. Many have used symptom-limited protocols, which, by their very nature, frequently terminate before the criteria for a maximal effort have been met (5). Consequently, the V̇O2peak value achieved is often well below true V̇O2max and cannot define the subject’s aerobic capacity with any precision (5). Furthermore, the subjective nature of the point of termination in symptom-limited tests means that the metabolic measurements, as in any performance test, have poor reproducibility (4) and are an unsuitable platform for patient management. Since all CFS patients and control subjects tested in our study fulfilled the agreed criteria for a maximal effort, we are confident that our measurements represent true V̇O2max.

With regard to lactate metabolism, neither the lactate thresholds nor, more importantly, the rate constants describing the increase in plasma lactate relative to workload throughout incremental exercise were different from healthy sedentary controls. As we are unaware of any substantive evidence of altered muscle biochemistry in CFS patients (2), it is not immediately obvious why a handful of previous reports have described increased lactate levels. The answer may lie in the exponential nature of blood lactate accumulation during incremental exercise such that it is critically important to make all comparisons at the same relative workload (e.g. at the same percentage of each subject’s true V̇O2max).

In conclusion, while no one denies that exercise performance is impaired in CFS, the results presented in our paper provide compelling evidence that this is not due to an impairment of aerobic power or accelerated blood lactate accumulation during exercise. Therefore, it follows that the imposition of exercise training programs to correct a perceived loss of exercise capacity has no scientific basis and causes considerable patient distress.

Charli Sargent, B App Sci, B Sc (Hons)

Garry Scroop, MD, PhD

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