Abnormal blood lactate accumulation during repeated exercise testing in myalgic encephalomyelitis/chronic fatigue syndrome.
Lien, Katarina, Johansen, Bjørn, Veierød, Marit B et al. · Physiological reports · 2019 · DOI
Quick Summary
This study looked at how the bodies of ME/CFS patients handle repeated exercise tests done 24 hours apart. Researchers measured how much oxygen patients used and tracked a substance called lactate in their blood during exercise. They found that ME/CFS patients performed worse on the second test and had higher lactate levels, opposite to what happened in healthy people, whose bodies actually recovered better the second time.
Why It Matters
This study provides objective physiological evidence that post-exertional malaise in ME/CFS involves abnormal lactate metabolism, suggesting that the body's inability to clear metabolic byproducts after exercise may contribute to delayed recovery. These findings support the biological basis of exercise intolerance in ME/CFS and could help guide rehabilitation approaches and validate patient experiences of worsening symptoms after exertion.
Observed Findings
ME/CFS patients showed lower oxygen uptake (VO₂peak) than controls on the first test, with further decline on the second test 24 hours later.
Lactate levels relative to power output were abnormally high in ME/CFS patients on both tests and increased further after 24 hours, whereas healthy controls showed decreased lactate on the second test.
Patients had lower oxygen uptake and power output at the gas exchange threshold on both tests, with additional reductions on the second test.
Healthy controls showed normal physiological adaptation with reduced lactate at the threshold during the second test, indicating recovery and improved efficiency.
Inferred Conclusions
Previous exercise deteriorates physical performance in ME/CFS patients and abnormally increases blood lactate during subsequent exercise, contrasting with healthy subjects who show improved lactate clearance with recovery.
The abnormal lactate accumulation suggests impaired metabolic recovery or mitochondrial dysfunction in ME/CFS that persists beyond 24 hours.
Post-exertional malaise may involve failure of normal exercise-induced physiological adaptations that occur in healthy individuals.
Remaining Questions
What mechanisms underlie the abnormal lactate accumulation—are they related to mitochondrial dysfunction, impaired lactate clearance, or altered metabolic pathways?
What This Study Does Not Prove
This study does not establish the mechanisms causing abnormal lactate accumulation, nor does it prove that lactate itself causes post-exertional malaise symptoms. The small sample size (18 patients) and female-only population limit generalizability. Correlation between lactate changes and symptom severity was not directly measured, so causality remains unclear.
Does the degree of lactate elevation correlate with symptom severity and the magnitude of post-exertional malaise experienced by patients?
Do longer recovery periods (beyond 24 hours) allow lactate metabolism to normalize, and how does this relate to individual variation in post-exertional malaise recovery times?
Are these lactate abnormalities present in male ME/CFS patients and across different age groups, or are they specific to the female population studied?