&OV0312;O2max AND LACTATE PRODUCTION ARE NOT NORMAL IN ALL PATIENTS WITH CHRONIC FATIGUE

Dear Editor-in-Chief: While we may applaud the paper of Sargent et al. (1) for its careful study of patients with the Chronic Fatigue Syndrome (CFS), we believe many readers will judge its title to be ill-chosen, because it implies that V̇O2max and lactate production are normal in all patients with the condition, which on present evidence is patently wrong. Further, to infer that all reported studies did not meet so-called “gold standard” criteria for incremental maximal exercise testing will be hard to take for previous authors, who to most impartial reviewers have provided adequate evidence of both reductions in V̇O2max and increases in lactate production in a proportion of patients (2,3). In a Popperian sense, the hypothesis tested by Sargent et al. is falsified by even one exception. In our laboratory, many patients with CFS have undergone standardized exercise testing (4) in the past 30 yr, and a small proportion have shown severe reductions in V̇O2max with evidence of lactate production at low levels of power output. In an attempt to understand the mechanisms underlying these findings, we studied two male patients, aged 26 and 35, who satisfied the criteria for CFS used by Sargent et al., and in whom muscle strength (isokinetic ergometry), electromyography, and muscle ultrastructure were all normal. Maximal V̇O2 was reduced to 50 and 52% predicted (21.6 and 19.7 mL·kg−1·min−1), associated with peak recovery plasma [La−] of 9 and 11 mmol·L−1. At the end of 15 min submaximal steady-state exercise, muscle [La−] was increased in both subjects, to 33 and 148 mmol·kg−1dw, compared to control subjects (13 ± 5.8 mmol·kg−1), associated with reductions in the maximum activity of pyruvate dehydrogenase to1.36 and 1.41 mmol·min−1·kg−1dw (controls 3.3 ± 1.31 mmol·min−1·kg−1) (5), and reductions in creatine phosphate concentration to 56.3 and 4.3 mmol·min−1·kg−1dw (controls 80 ± 2.1 mmol·min−1·kg−1dw). We would be happy to provide other results to interested readers, but would use these results to indicate that in some CFS patients low V̇O2max is associated with excess lactate formation that is related to biochemical disturbances in exercising muscle. There seems to be general agreement that a number of mechanisms may contribute to the sensation of fatigue experienced by CFS sufferers (6), in ways that vary greatly from patient to patient. Exercise testing can provide a quantitative assessment of symptom intensity (7); identify some contributory mechanisms; provide a basis for reassurance and explanation of symptoms such as dyspnea, for patients; and allow a precise prescription of exercise rehabilitation where indicated. The assumption that exercise performance is normal in CFS patients is not warranted and limits the clinical options in their management. Norman L. Jones, MD, FRCP, FRCP(C) George J. F. Heigenhauser, PhD, FACSM

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