Dr. Rob Wüst, a physiology professor at the Vrije de Universiteit (Amsterdam, Netherlands) and winner of a Solve Ramsay Research Grant, studies how diseases like Long Covid and ME/CFS affect muscle physiology. Recently, Dr. Wüst published a fascinating new study on how Long Covid and ME/CFS affect muscles and physical functioning in Trends in Endocrinology & Metabolism.
People often think that people with Long Covid or ME/CFS experience fatigue and post-exertional malaise because of deconditioning—physiological changes caused by being overly sedentary. By this reasoning, people with these diseases may feel fatigued for the same reasons that physically inactive people do so—with insufficient use, their muscles and cardiovascular systems have atrophied over time.
To test how much deconditioning explained these symptoms of Long Covid and ME/CFS, Dr. Wust’s team scrutinized the physiological effects of Long Covid and ME/CFS with those of deconditioning. They measured exercise capacities and muscle physiologies among healthy people; people with Long Covid; people with ME/CFS; and people with physical inactivity–induced deconditioning. (For this last group, the team used data from an earlier study designed to understand how deconditioning affects astronauts during spaceflight. In that study, participants underwent deconditioning by strictly resting in bed for a full two months!)
As expected, healthy people could exercise significantly better than people with either disease or people with bed rest–induced deconditioning. But how the diseases changed physiologies differed from how deconditioning changed them. For example, deconditioning caused muscles to atrophy in general; but these diseases did not. Instead, Long Covid and (especially) ME/CFS affected certain types of muscle fibers, the ones that are more resistant to fatigue (type I fibers).
Also, in people with Long Covid or ME/CFS, capillaries no longer properly sustained the muscles and muscle mitochondria were uniquely impaired. These changes did not happen in people with bed rest–induced deconditioning.
This work is important because it argues against the commonly held idea that people with Long Covid or ME/CFS struggle to exercise simply because they are generally less active. This suggests rehabilitation programs designed to reverse deconditioning-induced changes would be inappropriate for helping people with these diseases. More appropriate rehabilitation programs should account for how these diseases uniquely affect muscles and cardiovascular physiologies.
Dr. Wüst’s team noted some limitations to the study. First, it is true that people with Long Covid or ME/CFS are usually more sedentary than healthy people; thus, we must further understand how the combination of disease and deconditioning affect physiologies. Second, these results may not apply to people with severe symptoms of Long Covid or ME/CFS because people with severe symptoms could not easily volunteer to take part in this study. Finally, although some physiological effects for people with ME/CFS were more severe than those for people with Long Covid (perhaps because the people with ME/CFS had been sick for much longer), further work is needed to understand how the effects of Long Covid differ from those of ME/CFS.
Why This Study Matters to Our Community:
- 🧠 Speaks Against a Common Misbelief: Shows how mere physical inactivity cannot fully explain Long Covid– and ME/CFS–associated changes in physiology (associated with exercise intolerance and post-exertional malaise).
- 🧪 Lays the Groundwork for Better Treatments: Calls for designing rehabilitation programs that account for unique physiological changes among people with Long Covid or ME/CFS.
- 🧬 Advances Basic Understanding: Shows how these diseases change muscle fibers, muscle capillaries, and muscle mitochondria, which may inform new ways to diagnose and treat people.
Read more research study summaries like this in our Solve Science Spotlight archive here.
