SkeletalMuscleMetabolism intheChronic FatigueSyndrome* In VivoAssessment by31@ Nuclear Magnetic Resonance Spectroscopy

Background: Previous study ofpatients with chronic fatigue syndrome (CFS) has demonstrated a markedly reduced dynamic exercise capacity, not limited by cardiac perform ance and in the absence of clinical neuromuscular dysfunc tion, suggesting the possibility of a subclinical defect of skeletal muscle. Methods: The in viva metabolism of the gastrocnemius muscles of 22 CFS patients and 21 normal control subjects was compared during rest, graded dynamic exercise to exhaustion and recovery, using @1P nuclear magnetic reso nance (NMR) spectroscopy to reflect minute-to-minute intracellular high-energy phosphate metabolism Results: Duration of exercise was markedly shorter in the CFS patients (8.1 ±2.8mm) compared with the normal subjects (11.3±4.3 mm) (pO.005). There were large changes in phosphocreatine(PCr),inorganicphosphate(Pi), and pH from rest to clinical fatigue in all subjects, reflecting the high intensity of the exercise.The temporal metabolic patterns were qualitatively similar in the CFS patients and normal subjects. There were early and continuous changes in PCr and Pi that peaked at the point offatigue and rapidly reversed after exercise. In contrast, pH was relatively static in early exercise, not declining noticeably until 50 percent of total exercise duration was achieved, and reaching a nadir at 2 mm postexercise, before rapidly reversing. There were no differences in pH at rest (7.08±0.04 vs 7.10±OA)4), exhaustion(6.85±0.17vs &76±O.17) or early (6.64±0.25 vs 6.56±0.24)or late recovery (7.09±0.04vs 7.10±0.05), CFS patientsvs normalsubjects, respectively (NS). Neither were there intergroup differences (NS) in PCr or Pi. Although,quantitatively,the changes in PCr, Pi, and pH were marked and similar in both groups from rest to exhaustion,the changes all occurred much more rapidly in the CFS patients. Moreover,adenosine triphosphate(AlP) was significantly (p= 0.007) less at exhaustion in the CFS group. Conclusions: Patients with CFS and normal control subjects have similar skeletal muscle metabolic patterns during dynamic exercise and reach similar clinical and metabolic end points. However,CFS patients reach exhaustionmuch more rapidlythan normalsubjects, at which point they also have relativelyreduced intracellularconcentrationsof AlP. These data suggest a defect of oxidative metabolismwith a resultant accelerationof glycolysisin the workingskeletal muscles of CFS patients. This metabolic defect may con tribute to the reduced physical endurance of CFS patients. Its etiology is unknown.Whether CFS patients'overwhelm ingtirednessat rest has a similarmetabolicpathophysiology or etiology also remains unknown. (Chest 1992; 102:1716-22)