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Post‐exertional malaise and delayed recovery are hallmark symptoms of myalgic encephalomyelitis/chronic fatigue syndrome ( ME / CFS ). Studies on repeated cardiopulmonary exercise testing ( CPET ) show that previous exercise negatively affects oxygen uptake ( VO 2 ) and power output ( PO ) in ME / CFS . Whether this affects arterial lactate concentrations ([La a ]) is unknown. We studied 18 female patients (18–50 years) fulfilling the Canadian Consensus Criteria for ME / CFS and 15 healthy females (18–50 years) who underwent repeated CPET s 24 h apart ( CPET 1 and CPET 2 ) with [La a ] measured every 30th second. VO 2 at peak exercise ( VO 2peak ) was lower in patients than in controls on CPET 1 ( P < 0.001) and decreased in patients on CPET 2 ( P < 0.001). However, the difference in VO 2peak between CPET s did not differ significantly between groups. [La a ] per PO was higher in patients during both CPET s ( P interaction < 0.001), but increased in patients and decreased in controls from CPET 1 to CPET 2 ( P interaction < 0.001). Patients had lower VO 2 ( P = 0.02) and PO ( P = 0.002) at the gas exchange threshold ( GET , the point where CO 2 production increases relative to VO 2 ), but relative intensity (% VO 2peak ) and [La a ] at GET did not differ significantly from controls on CPET 1 . Patients had a reduction in VO 2 ( P = 0.02) and PO ( P = 0.01) at GET on CPET 2 , but no significant differences in % VO 2peak and [La a ] at GET between CPET s. Controls had no significant differences in VO 2 , PO or % VO 2peak ...

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating disease usually presenting after infection. Emerging evidence supports that energy metabolism is affected in ME/CFS, but a unifying metabolic phenotype has not been firmly established. We performed global metabolomics, lipidomics, and hormone measurements, and we used exploratory data analyses to compare serum from 83 patients with ME/CFS and 35 healthy controls. Some changes were common in the patient group, and these were compatible with effects of elevated energy strain and altered utilization of fatty acids and amino acids as catabolic fuels. In addition, a set of heterogeneous effects reflected specific changes in 3 subsets of patients, and 2 of these expressed characteristic contexts of deregulated energy metabolism. The biological relevance of these metabolic phenotypes (metabotypes) was supported by clinical data and independent blood analyses. In summary, we report a map of common and context-dependent metabolic changes in ME/CFS, and some of them presented possible associations with clinical patient profiles. We suggest that elevated energy strain may result from exertion-triggered tissue hypoxia and lead to systemic metabolic adaptation and compensation. Through various mechanisms, such metabolic dysfunction represents a likely mediator of key symptoms in ME/CFS and possibly a target for supportive intervention.