A cardiometabolic perspective on [PEM] in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and Long COVID, 2026, Westermeier et al

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A cardiometabolic perspective on post-exertional malaise in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and Long COVID

Westermeier, Francisco; Pretorius, Etheresia; Untersmayr, Eva; Bertinat, Romina; Sepúlveda, Nuno; Fisman, Enrique

Abstract
Post-exertional malaise (PEM), the defining feature of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), is increasingly recognized in individuals with Long COVID.

Although traditionally viewed as symptom exacerbation and/or emergence of new symptoms following exertion, PEM may reflect disrupted coordination across interconnected physiological systems operating over distinct post-exertional timescales. Such disruption may result in altered post-exertional physiological trajectories that contribute to multisystem manifestations and potential cardiometabolic consequences.

This perspective outlines a conceptual approach for investigating PEM through longitudinal assessment of post-exertional physiological trajectories while considering disease severity and underlying cardiometabolic health, including obesity and type 2 diabetes. Integrating these dimensions may help contextualize post-exertional responses, inform future longitudinal cardiometabolic profiling, facilitate patient stratification, and provide a framework for future mechanistic and interventional studies in ME/CFS and Long COVID.

Web | DOI | PDF | Cardiovascular Diabetology | Open Access
 
I cannot find any specific content in this paper. The full paper does not say anything more specific than the abstract. There is a suggestion that the concept of PEM should change from a clinical observation to a multisystem physiologic dysregulation, but without saying what that might be there seems no point.
 
I cannot find any specific content in this paper. The full paper does not say anything more specific than the abstract. There is a suggestion that the concept of PEM should change from a clinical observation to a multisystem physiologic dysregulation, but without saying what that might be there seems no point.
I agree... a whole lot of words but not much more.

I was going to say that I also don't understand why this is published in Cadiovascular Diabetology, but perhaps this explains why:
 

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Dr. David Systrom and his group have done extensive research on this and does icpet testing to test the lactate in people with PEM.

Thanks, we are very familiar with Systrom's publications here. We have several threads including the one above. The problem is that all these tests measure something correlated, at best, with PEM situations (I am not sure you do a second day CPET with PEM). PEM is defined in symptom terms. Nothing I have seen so far strongly suggests that those symptoms have a cardiometabolic basis. Apart from anything they occur at rest.
 
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