Nikhil Prasad Fact checked by:Thailand Medical News Team Jul 29, 2026 47 minutes ago
Medical News: For years, many healthcare professionals have believed that the muscle weakness and poor exercise tolerance experienced by people with long COVID and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) were mainly the result of prolonged inactivity. A groundbreaking new study is now challenging that belief, showing that the muscle abnormalities in these patients are fundamentally different from the changes caused by extended bed rest. The findings suggest that these illnesses involve unique biological processes rather than simple physical deconditioning.
Researchers found that the muscle abnormalities seen in long COVID and ME/CFS are biologically distinct from
the changes caused by prolonged inactivity or bed rest
The study was conducted by researchers from the Department of Human Movement Sciences at Vrije Universiteit Amsterdam, the Amsterdam University Medical Center, the Amsterdam Institute of Infectious Disease, the Technical University of Munich, Lancaster University, Manchester Metropolitan University, Lithuanian Sports University, Flevoziekenhuis Almere, and other collaborating institutions in the Netherlands, Germany, Lithuania, and the United Kingdom.
Comparing Long COVID and ME/CFS with Prolonged Bed Rest
To determine whether inactivity alone explains the reduced physical capacity seen in patients, researchers compared two very different groups. One consisted of healthy volunteers who underwent an exceptionally strict 60-day bed rest program. The other included patients with long COVID and ME/CFS, along with healthy volunteers matched for age and sex.
Although both the bed rest participants and the patient groups demonstrated similarly reduced aerobic fitness and exercise capacity, the biological changes inside their muscles were remarkably different. This indicates that while inactivity can certainly reduce physical fitness, it does not reproduce the muscle abnormalities found in long COVID and ME/CFS.
Disease-Specific Muscle Changes
One of the clearest findings was that prolonged bed rest caused generalized muscle wasting across all muscle fiber types. However, patients with long COVID did not experience this widespread muscle shrinkage. Instead, people with ME/CFS showed selective shrinking of slow-twitch (Type I) muscle fibers, which normally support endurance activities.
Researchers also found that both long COVID and ME/CFS patients had fewer Type I muscle fibers and a higher proportion of fast-twitch glycolytic fibers that tire more quickly. Importantly, this shift in muscle fiber composition did not occur after prolonged bed rest, suggesting it is linked to the diseases themselves rather than inactivity.
Mitochondria and Oxygen Use Are Impaired
The study uncovered important differences in the muscles' energy-producing machinery. Bed rest reduced mitochondrial capacity mainly because overall mitochondrial content declined as muscles became smaller.
Patients with long COVID and ME/CFS showed something very different. Their mitochondria appeared to function abnormally even after accounting for mitochondrial content, indicatin
g intrinsic defects in cellular energy production. This could help explain why many patients experience profound fatigue after even minimal physical activity.
This
Medical News report also highlights another significant discovery. Researchers found that the normal relationship between mitochondrial function and overall exercise capacity disappeared in both patient groups. In healthy people, better mitochondrial performance is normally associated with better physical fitness. That relationship remained intact even after prolonged bed rest but was completely absent in long COVID and ME/CFS, suggesting additional disease mechanisms are interfering with the body's ability to produce and utilize energy.
Blood Supply to Muscles May Also Be Compromised
The investigators discovered further evidence that oxygen delivery to muscles is impaired. Patients with ME/CFS had fewer capillaries supplying their muscle fibers, reducing their ability to deliver oxygen and nutrients while removing metabolic waste products.
Even long COVID patients whose capillary numbers appeared relatively normal showed altered relationships between blood vessel supply and muscle fiber size. Combined with abnormal heart rate responses during exercise and reduced oxygen pulse, these findings suggest that defects in oxygen delivery and extraction contribute to the exercise intolerance seen in both illnesses.
Challenging Long-Held Assumptions
The study's findings directly challenge the idea that long COVID and ME/CFS patients are simply deconditioned because they avoid activity. While inactivity undoubtedly contributes to declining fitness, it cannot explain the unique muscle fiber changes, mitochondrial abnormalities, altered capillary structure, and distinctive cardiovascular responses identified in this research.
The researchers believe these diseases involve complex biological disturbances affecting muscles, blood vessels, and energy production. Their findings also suggest that rehabilitation programs based solely on gradually increasing exercise may not fully address the underlying pathology.
Conclusion
The study provides compelling evidence that long COVID and ME/CFS cannot be dismissed as illnesses caused primarily by inactivity or prolonged bed rest. Instead, patients exhibit distinct biological abnormalities involving muscle fibers, mitochondrial function, oxygen delivery, and exercise physiology that differ fundamentally from ordinary deconditioning. These discoveries strengthen the case for developing targeted therapies that address the underlying disease mechanisms rather than relying exclusively on conventional exercise-based rehabilitation approaches.
The study findings were published in the peer reviewed journal: Nature Communications.
https://www.nature.com/articles/s41467-026-75725-y
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